All blood proteins except albumin ( = SERUM ALBUMIN, which is not a globulin) and FIBRINOGEN (which is not in the serum). The serum globulins are subdivided into ALPHA-GLOBULINS; BETA-GLOBULINS; and GAMMA-GLOBULINS on the basis of their electrophoretic mobilities. (From Dorland, 28th ed)
A glycoprotein migrating as a beta-globulin. Its molecular weight, 52,000 or 95,000-115,000, indicates that it exists as a dimer. The protein binds testosterone, dihydrotestosterone, and estradiol in the plasma. Sex hormone-binding protein has the same amino acid sequence as ANDROGEN-BINDING PROTEIN. They differ by their sites of synthesis and post-translational oligosaccharide modifications.
Serum globulins that migrate to the gamma region (most positively charged) upon ELECTROPHORESIS. At one time, gamma-globulins came to be used as a synonym for immunoglobulins since most immunoglobulins are gamma globulins and conversely most gamma globulins are immunoglobulins. But since some immunoglobulins exhibit an alpha or beta electrophoretic mobility, that usage is in decline.
An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.
Serum containing GAMMA-GLOBULINS which are antibodies for lymphocyte ANTIGENS. It is used both as a test for HISTOCOMPATIBILITY and therapeutically in TRANSPLANTATION.
A serpin family member that binds to and transports GLUCOCORTICOIDS in the BLOOD.
Blood proteins that bind to THYROID HORMONES such as THYROXINE and transport them throughout the circulatory system.
An 11-kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants.
A thyroid hormone transport protein found in serum. It binds about 75% of circulating THYROXINE and 70% of circulating TRIIODOTHYRONINE.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
An integrin beta subunit of approximately 85-kDa in size which has been found in INTEGRIN ALPHAIIB-containing and INTEGRIN ALPHAV-containing heterodimers. Integrin beta3 occurs as three alternatively spliced isoforms, designated beta3A-C.
Immunizing agent containing IMMUNOGLOBULIN G anti-Rho(D) used for preventing Rh immunization in Rh-negative individuals exposed to Rh-positive red blood cells.
One or more types of plant seed proteins providing the large amounts of AMINO ACIDS utilized in GERMINATION and SEEDLING growth. As seeds are the major food source from AGRICULTURAL CROPS, seed storage proteins are a major source of DIETARY PROTEINS.
Serum proteins that have the most rapid migration during ELECTROPHORESIS. This subgroup of globulins is divided into faster and slower alpha(1)- and alpha(2)-globulins.
Immunoglobulin preparations used in intravenous infusion, containing primarily IMMUNOGLOBULIN G. They are used to treat a variety of diseases associated with decreased or abnormal immunoglobulin levels including pediatric AIDS; primary HYPERGAMMAGLOBULINEMIA; SCID; CYTOMEGALOVIRUS infections in transplant recipients, LYMPHOCYTIC LEUKEMIA, CHRONIC; Kawasaki syndrome, infection in neonates, and IDIOPATHIC THROMBOCYTOPENIC PURPURA.
Serum proteins with an electrophoretic mobility that falls between ALPHA-GLOBULINS and GAMMA-GLOBULINS.
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
Electrophoresis applied to BLOOD PROTEINS.
An integrin found in FIBROBLASTS; PLATELETS; MONOCYTES, and LYMPHOCYTES. Integrin alpha5beta1 is the classical receptor for FIBRONECTIN, but it also functions as a receptor for LAMININ and several other EXTRACELLULAR MATRIX PROTEINS.
Also known as CD104 antigen, this protein is distinguished from other beta integrins by its relatively long cytoplasmic domain (approximately 1000 amino acids vs. approximately 50). Five alternatively spliced isoforms have been described.
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.
This intrgrin is a key component of HEMIDESMOSOMES and is required for their formation and maintenance in epithelial cells. Integrin alpha6beta4 is also found on thymocytes, fibroblasts, and Schwann cells, where it functions as a laminin receptor (RECEPTORS, LAMININ) and is involved in wound healing, cell migration, and tumor invasiveness.
Integrin beta chains combine with integrin alpha chains to form heterodimeric cell surface receptors. Integrins have traditionally been classified into functional groups based on the identity of one of three beta chains present in the heterodimer. The beta chain is necessary and sufficient for integrin-dependent signaling. Its short cytoplasmic tail contains sequences critical for inside-out signaling.
A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.
Integrin alpha4beta1 is a FIBRONECTIN and VCAM-1 receptor present on LYMPHOCYTES; MONOCYTES; EOSINOPHILS; NK CELLS and thymocytes. It is involved in both cell-cell and cell- EXTRACELLULAR MATRIX adhesion and plays a role in INFLAMMATION, hematopoietic cell homing and immune function, and has been implicated in skeletal MYOGENESIS; NEURAL CREST migration and proliferation, lymphocyte maturation and morphogenesis of the PLACENTA and HEART.
A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.
An integrin found on fibroblasts, platelets, endothelial and epithelial cells, and lymphocytes where it functions as a receptor for COLLAGEN and LAMININ. Although originally referred to as the collagen receptor, it is one of several receptors for collagen. Ligand binding to integrin alpha2beta1 triggers a cascade of intracellular signaling, including activation of p38 MAP kinase.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
Steroid hormones produced by the GONADS. They stimulate reproductive organs, germ cell maturation, and the secondary sex characteristics in the males and the females. The major sex steroid hormones include ESTRADIOL; PROGESTERONE; and TESTOSTERONE.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A family of transmembrane glycoproteins (MEMBRANE GLYCOPROTEINS) consisting of noncovalent heterodimers. They interact with a wide variety of ligands including EXTRACELLULAR MATRIX PROTEINS; COMPLEMENT, and other cells, while their intracellular domains interact with the CYTOSKELETON. The integrins consist of at least three identified families: the cytoadhesin receptors(RECEPTORS, CYTOADHESIN), the leukocyte adhesion receptors (RECEPTORS, LEUKOCYTE ADHESION), and the VERY LATE ANTIGEN RECEPTORS. Each family contains a common beta-subunit (INTEGRIN BETA CHAINS) combined with one or more distinct alpha-subunits (INTEGRIN ALPHA CHAINS). These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development; HEMOSTASIS; THROMBOSIS; WOUND HEALING; immune and nonimmune defense mechanisms; and oncogenic transformation.
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
Integrin beta-1 chains which are expressed as heterodimers that are noncovalently associated with specific alpha-chains of the CD49 family (CD49a-f). CD29 is expressed on resting and activated leukocytes and is a marker for all of the very late activation antigens on cells. (from: Barclay et al., The Leukocyte Antigen FactsBook, 1993, p164)
A cell surface receptor mediating cell adhesion to the EXTRACELLULAR MATRIX and to other cells via binding to LAMININ. It is involved in cell migration, embryonic development, leukocyte activation and tumor cell invasiveness. Integrin alpha6beta1 is the major laminin receptor on PLATELETS; LEUKOCYTES; and many EPITHELIAL CELLS, and ligand binding may activate a number of signal transduction pathways. Alternative splicing of the cytoplasmic domain of the alpha6 subunit (INTEGRIN ALPHA6) results in the formation of A and B isoforms of the heterodimer, which are expressed in a tissue-specific manner.
Established cell cultures that have the potential to propagate indefinitely.
The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
A major protein in the BLOOD. It is important in maintaining the colloidal osmotic pressure and transporting large organic molecules.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A glycoprotein migrating as alpha 1-globulin, molecular weight 70,000 to 120,000. The protein, which is present in increased amounts in the plasma during pregnancy, binds mainly progesterone, with other steroids including testosterone competing weakly.
Integrin alpha1beta1 functions as a receptor for LAMININ and COLLAGEN. It is widely expressed during development, but in the adult is the predominant laminin receptor (RECEPTORS, LAMININ) in mature SMOOTH MUSCLE CELLS, where it is important for maintenance of the differentiated phenotype of these cells. Integrin alpha1beta1 is also found in LYMPHOCYTES and microvascular endothelial cells, and may play a role in angiogenesis. In SCHWANN CELLS and neural crest cells, it is involved in cell migration. Integrin alpha1beta1 is also known as VLA-1 and CD49a-CD29.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
Stable iodine atoms that have the same atomic number as the element iodine, but differ in atomic weight. I-127 is the only naturally occurring stable iodine isotope.
Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER).
A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
One of the ESTROGEN RECEPTORS that has greater affinity for ISOFLAVONES than ESTROGEN RECEPTOR ALPHA does. There is great sequence homology with ER alpha in the DNA-binding domain but not in the ligand binding and hinge domains.
The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A subtype of transforming growth factor beta that is synthesized by a wide variety of cells. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta 1 and TGF-beta1 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor. Defects in the gene that encodes TGF-beta1 are the cause of CAMURATI-ENGELMANN SYNDROME.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The beta-3 adrenergic receptors are the predominant beta-adrenergic receptor type expressed in white and brown ADIPOCYTES and are involved in modulating ENERGY METABOLISM and THERMOGENESIS.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Adherence of cells to surfaces or to other cells.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Elements of limited time intervals, contributing to particular results or situations.
Proteins prepared by recombinant DNA technology.
The rate dynamics in chemical or physical systems.
Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.
Brain waves with frequency between 15-30 Hz seen on EEG during wakefulness and mental activity.
Drugs that selectively bind to and activate beta-adrenergic receptors.
A DNA repair enzyme that catalyzes DNA synthesis during base excision DNA repair. EC
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Compounds and molecular complexes that consist of very large numbers of atoms and are generally over 500 kDa in size. In biological systems macromolecular substances usually can be visualized using ELECTRON MICROSCOPY and are distinguished from ORGANELLES by the lack of a membrane structure.
Compounds bind to and activate ADRENERGIC BETA-2 RECEPTORS.
A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.
The circulating form of a major C19 steroid produced primarily by the ADRENAL CORTEX. DHEA sulfate serves as a precursor for TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Cell-surface proteins that bind transforming growth factor beta and trigger changes influencing the behavior of cells. Two types of transforming growth factor receptors have been recognized. They differ in affinity for different members of the transforming growth factor beta family and in cellular mechanisms of action.
The processes triggered by interactions of ANTIBODIES with their ANTIGENS.
A condition in which total serum protein level is below the normal range. Hypoproteinemia can be caused by protein malabsorption in the gastrointestinal tract, EDEMA, or PROTEINURIA.
Proteins which are present in or isolated from SOYBEANS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Antibodies produced by a single clone of cells.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Serum globulins with high molecular weight. (Dorland, 28th ed)
Blood tests used to evaluate the functioning of the thyroid gland.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
Single chains of amino acids that are the units of multimeric PROTEINS. Multimeric proteins can be composed of identical or non-identical subunits. One or more monomeric subunits may compose a protomer which itself is a subunit structure of a larger assembly.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Substances that are recognized by the immune system and induce an immune reaction.
Receptors such as INTEGRIN ALPHAVBETA3 that bind VITRONECTIN with high affinity and play a role in cell migration. They also bind FIBRINOGEN; VON WILLEBRAND FACTOR; osteopontin; and THROMBOSPONDINS.
A group of seed storage proteins restricted to the POACEAE family. They are rich in GLUTAMINE and PROLINE.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Nucleocytoplasmic transport molecules that bind to ALPHA KARYOPHERINS in the CYTOSOL and are involved in transport of molecules through the NUCLEAR PORE COMPLEX. Once inside the CELL NUCLEUS beta karyopherins interact with RAN GTP-BINDING PROTEIN and dissociate from alpha karyopherins. Beta karyopherins bound to RAN GTP-BINDING PROTEIN are then re-transported to the cytoplasm where hydrolysis of the GTP of RAN GTP-BINDING PROTEIN causes release of karyopherin beta.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Substances found in PLANTS that have antigenic activity.
A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The sum of the weight of all the atoms in a molecule.
Transplantation between individuals of the same species. Usually refers to genetically disparate individuals in contradistinction to isogeneic transplantation for genetically identical individuals.
A phosphoinositide phospholipase C subtype that is primarily regulated by its association with HETEROTRIMERIC G-PROTEINS. It is structurally related to PHOSPHOLIPASE C DELTA with the addition of C-terminal extension of 400 residues.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
A potent androgenic metabolite of TESTOSTERONE. It is produced by the action of the enzyme 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient.
A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)
Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Compounds that interact with ANDROGEN RECEPTORS in target tissues to bring about the effects similar to those of TESTOSTERONE. Depending on the target tissues, androgenic effects can be on SEX DIFFERENTIATION; male reproductive organs, SPERMATOGENESIS; secondary male SEX CHARACTERISTICS; LIBIDO; development of muscle mass, strength, and power.
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Compounds that bind to and activate ADRENERGIC BETA-3 RECEPTORS.
An aromatized C18 steroid with a 3-hydroxyl group and a 17-ketone, a major mammalian estrogen. It is converted from ANDROSTENEDIONE directly, or from TESTOSTERONE via ESTRADIOL. In humans, it is produced primarily by the cyclic ovaries, PLACENTA, and the ADIPOSE TISSUE of men and postmenopausal women.
A forkhead transcription factor that regulates expression of metabolic GENES and is involved in EMBRYONIC DEVELOPMENT. Mutations in HNF-3beta have been associated with CONGENITAL HYPERINSULINISM.
Large, hoofed mammals of the family EQUIDAE. Horses are active day and night with most of the day spent seeking and consuming food. Feeding peaks occur in the early morning and late afternoon, and there are several daily periods of rest.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
An integrin that binds to a variety of plasma and extracellular matrix proteins containing the conserved RGD amino acid sequence and modulates cell adhesion. Integrin alphavbeta3 is highly expressed in OSTEOCLASTS where it may play role in BONE RESORPTION. It is also abundant in vascular smooth muscle and endothelial cells, and in some tumor cells, where it is involved in angiogenesis and cell migration. Although often referred to as the vitronectin receptor there is more than one receptor for vitronectin (RECEPTORS, VITRONECTIN).
Specialized proteins that are preferentially expressed during FETAL DEVELOPMENT.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
The encapsulated embryos of flowering plants. They are used as is or for animal feed because of the high content of concentrated nutrients like starches, proteins, and fats. Rapeseed, cottonseed, and sunflower seed are also produced for the oils (fats) they yield.
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
The transference of a kidney from one human or animal to another.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.
A synthetic hormone with anabolic and androgenic properties. It is used mainly in the treatment of anemias. According to the Fourth Annual Report on Carcinogens (NTP 85-002), this compound may reasonably be anticipated to be a carcinogen. (From Merck Index, 11th ed)
A process of selective diffusion through a membrane. It is usually used to separate low-molecular-weight solutes which diffuse through the membrane from the colloidal and high-molecular-weight solutes which do not. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
An encapsulated lymphatic organ through which venous blood filters.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Transport proteins that carry specific substances in the blood or across cell membranes.
The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.
Preparative treatment of transplant recipient with various conditioning regimens including radiation, immune sera, chemotherapy, and/or immunosuppressive agents, prior to transplantation. Transplantation conditioning is very common before bone marrow transplantation.
A hepatocyte nuclear factor that is closely related to HEPATOCYTE NUCLEAR FACTOR 1-ALPHA but is only weakly expressed in the LIVER. Mutations in hepatocyte nuclear factor 1-beta are associated with renal CYSTS and MATURITY-ONSET DIABETES MELLITUS type 5.
Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.
The physiological period following the MENOPAUSE, the permanent cessation of the menstrual life.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Serologic tests in which a positive reaction manifested by visible CHEMICAL PRECIPITATION occurs when a soluble ANTIGEN reacts with its precipitins, i.e., ANTIBODIES that can form a precipitate.
The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host.
Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.
A complex disorder characterized by infertility, HIRSUTISM; OBESITY; and various menstrual disturbances such as OLIGOMENORRHEA; AMENORRHEA; ANOVULATION. Polycystic ovary syndrome is usually associated with bilateral enlarged ovaries studded with atretic follicles, not with cysts. The term, polycystic ovary, is misleading.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
The sequence of carbohydrates within POLYSACCHARIDES; GLYCOPROTEINS; and GLYCOLIPIDS.
An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Carrier proteins produced in the Sertoli cells of the testis, secreted into the seminiferous tubules, and transported via the efferent ducts to the epididymis. They participate in the transport of androgens. Androgen-binding protein has the same amino acid sequence as SEX HORMONE-BINDING GLOBULIN. They differ by their sites of synthesis and post-translational oligosaccharide modifications.
The beta subunit of human CHORIONIC GONADOTROPIN. Its structure is similar to the beta subunit of LUTEINIZING HORMONE, except for the additional 30 amino acids at the carboxy end with the associated carbohydrate residues. HCG-beta is used as a diagnostic marker for early detection of pregnancy, spontaneous abortion (ABORTION, SPONTANEOUS); ECTOPIC PREGNANCY; HYDATIDIFORM MOLE; CHORIOCARCINOMA; or DOWN SYNDROME.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Hypersecretion of THYROID HORMONES from the THYROID GLAND. Elevated levels of thyroid hormones increase BASAL METABOLIC RATE.
Therapy with two or more separate preparations given for a combined effect.
Erythrocyte isoantigens of the Rh (Rhesus) blood group system, the most complex of all human blood groups. The major antigen Rh or D is the most common cause of erythroblastosis fetalis.
An abnormal protein with unusual thermosolubility characteristics that is found in the urine of patients with MULTIPLE MYELOMA.
PKC beta encodes two proteins (PKCB1 and PKCBII) generated by alternative splicing of C-terminal exons. It is widely distributed with wide-ranging roles in processes such as B-cell receptor regulation, oxidative stress-induced apoptosis, androgen receptor-dependent transcriptional regulation, insulin signaling, and endothelial cell proliferation.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
A PREDNISOLONE derivative with similar anti-inflammatory action.
Water-soluble proteins found in egg whites, blood, lymph, and other tissues and fluids. They coagulate upon heating.
A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease.
High energy POSITRONS or ELECTRONS ejected from a disintegrating atomic nucleus.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.
An annual legume. The SEEDS of this plant are edible and used to produce a variety of SOY FOODS.
Cell-surface glycoprotein beta-chains that are non-covalently linked to specific alpha-chains of the CD11 family of leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE-ADHESION). A defect in the gene encoding CD18 causes LEUKOCYTE-ADHESION DEFICIENCY SYNDROME.
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A TGF-beta subtype that was originally identified as a GLIOBLASTOMA-derived factor which inhibits the antigen-dependent growth of both helper and CYTOTOXIC T LYMPHOCYTES. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta2 and TGF-beta2 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response.
Natural hormones secreted by the THYROID GLAND, such as THYROXINE, and their synthetic analogs.
A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA.
An alpha-globulin found in the plasma of man and other vertebrates. It is apparently synthesized in the liver and carries vitamin D and its metabolites through the circulation and mediates the response of tissue. It is also known as group-specific component (Gc). Gc subtypes are used to determine specific phenotypes and gene frequencies. These data are employed in the classification of population groups, paternity investigations, and in forensic medicine.
A long pro-domain caspase that has specificity for the precursor form of INTERLEUKIN-1BETA. It plays a role in INFLAMMATION by catalytically converting the inactive forms of CYTOKINES such as interleukin-1beta to their active, secreted form. Caspase 1 is referred as interleukin-1beta converting enzyme and is frequently abbreviated ICE.

Evidence for substrate-specific requirement of the splicing factor U2AF(35) and for its function after polypyrimidine tract recognition by U2AF(65). (1/222)

U2 snRNP auxiliary factor (U2AF) promotes U2 snRNP binding to pre-mRNAs and consists of two subunits of 65 and 35 kDa, U2AF(65) and U2AF(35). U2AF(65) binds to the polypyrimidine (Py) tract upstream from the 3' splice site and plays a key role in assisting U2 snRNP recruitment. It has been proposed that U2AF(35) facilitates U2AF(65) binding through a network of protein-protein interactions with other splicing factors, but the requirement and function of U2AF(35) remain controversial. Here we show that recombinant U2AF(65) is sufficient to activate the splicing of two constitutively spliced pre-mRNAs in extracts that were chromatographically depleted of U2AF. In contrast, U2AF(65), U2AF(35), and the interaction between them are required for splicing of an immunoglobulin micro; pre-RNA containing an intron with a weak Py tract and a purine-rich exonic splicing enhancer. Remarkably, splicing activation by U2AF(35) occurs without changes in U2AF(65) cross-linking to the Py tract. These results reveal substrate-specific requirements for U2AF(35) and a novel function for this factor in pre-mRNA splicing.  (+info)

Chromatin modification by DNA tracking. (2/222)

In general, the transcriptional competence of a chromatin domain is correlated with increased sensitivity to DNase I cleavage. A recent observation that actively transcribing RNA polymerase II piggybacks a histone acetyltranferase activity [Wittschieben, B., Otero, G., de Bizemont, T., Fellows, J., Erdjument-Bromage, H., Ohba, R., Li, Y., Allis, C. D., Tempst, P. & Svejstrup, J. Q. (1999) Mol. Cell 4, 123-128] implies that the state of histone acetylation, and hence the ability of chromatin to fold, can be altered by a processive mechanism. In this article, it is proposed that tracking-mediated chromatin modification could create and/or maintain an open configuration in a complete chromatin domain including both intra- and extragenic regions. This mechanism suggests a putative functional role for the extragenic transcription observed at the beta-globin and other loci in vertebrate cells.  (+info)

Globulins in protein supplements promote the development of preimplantation embryos. (3/222)

PURPOSE: Our purpose was to investigate the effect of alpha- and beta-globulins contained in protein supplements on the development of preimplantation embryos. METHODS: Mouse one-cell embryos were cultured in medium supplemented with 4 mg/ml human serum albumin (HSA), 4 mg/ml HSA plus human globulins (0.2, 0.4, 0.8, and 1.6 mg/ml) that consisted predominantly of alpha- and beta-globulins, or 10% Plasmanate Cutter (PC). Blastocysts developed in media supplemented with these various protein sources were stained with Hoechst 33342 to determine the number of cells. RESULTS: Supplementation with 0.4 to 1.6 mg/ml globulins or PC significantly increased the rate of blastocyst development compared with that observed with the addition of HSA. Supplementation with globulins significantly increased the hatching rate in a dose-dependent manner. The number of cells in the blastocysts was significantly increased when the embryos were cultured with 0.8 mg/ml of the globulins or PC. CONCLUSIONS: The present observations suggest that alpha- and beta-globulins in protein supplements promote embryo development and hatching.  (+info)

Influence of histochemical and immunohistochemical stains on polymerase chain reaction. (4/222)

The polymerase chain reaction (PCR) analysis of DNA extracted from tissue sections can be applied to a variety of research and diagnostic protocols. To analyze selectively the specific areas of tissue, a direct microdissection of histochemically or immunohistochemically stained sections, if satisfactory for PCR, is helpful. However, the influence of various staining methods on PCR has been poorly investigated. In this study, paraffin sections of formalin-fixed lymph node samples were histochemically stained with Mayer's hematoxylin, eosin Y, methyl green, or May-Grunwald solution and immunostained for CD45 using 3,3'-diaminobenzidine (DAB), DAB with cobalt ion (DAB-Co), or new fuchsin as the chromogen. In addition, unstained sections were treated with trypsin, microwave, or pressure cooker, the techniques frequently used in immunostains for antigen unmasking. DNA was extracted from each section, and the PCR efficiency in amplifying a 110 bp portion of the beta-globin gene was evaluated by two parameters: the cycle count in which the first visible band was obtained (CYCLE(min)) and the maximum amount of PCR products (CONC(max)). The hematoxylin stain showed a significantly prolonged CYCLE(min) (P < .01) and lower CONC(max) (P < .05) in comparison with unstained and untreated control sections. The May-Grunwald stain showed a prolonged CYCLE(min) (P < .01), although the CONC(max) was not significantly different from that of the control (P = .051). The eosin and methyl green stains showed no effects against PCR. In immunostains, the DAB-Co method showed a lower CONC(max) (P < .05), whereas the CYCLE(min) was not prolonged. The DAB and new fuchsin methods had no untoward effects. Antigen-unmasking treatments showed deteriorating effects on PCR. The trypsin treatment significantly prolonged the CYCLE(min) (P < .01), and the PCR amplification did not reach the "plateau" level with a maximum of 60 cycles. The PCR efficiency was worse in microwave or pressure cooker treatment, with neither CYCLE(min) nor CONC(max) being obtained. When target areas from sections for subsequent PCR amplification are microdissected, methyl green is most suitable as a dye for nuclear staining. The immunohistochemical visualization with DAB or new fuchsin yields no unfavorable effects. A successful PCR amplification may not be expected in sections that are pretreated in a microwave oven or pressure cooker.  (+info)

Suppression of metastasis by thymidine phosphorylase inhibitor. (5/222)

We developed a novel inhibitor of thymidine phosphorylase (TP), 5-chloro-6-[1-(2-iminopyrrolidinyl) methyl] uracil hydrochloride (TPI), that is about 1000-fold more active than 6-amino-5-chlorouracil, one of the most potent TP inhibitors. TPI inhibited the high chemotactic motility and basement membrane invasion of KB/TP cells, a TP-positive clone transfected with Rous sarcoma virus (RSV)/TP, to the levels seen in KB/CV cells, a control clone transfected with RSV. In nude mice, oral administration of TPI suppressed not only macroscopic liver metastases of highly metastatic KB/TP cells but also the level of human beta-globin as a molecular marker of micrometastases in the livers of the mice. These findings demonstrate that TP plays a key role in the invasiveness and metastasis of TP-expressing solid tumors and suggest that TPI might be a novel antimetastatic agent for blood-borne metastasis.  (+info)

Successful application of preimplantation genetic diagnosis for beta-thalassaemia and sickle cell anaemia in Italy. (6/222)

BACKGROUND: In Italy, the autosomal recessive diseases beta-thalassaemia and sickle cell anaemia are so widespread that in some regions they can be defined as 'social diseases'. In this study, nine clinical applications of preimplantation genetic diagnosis (PGD) were performed for beta-thalassaemia and sickle cell anaemia on seven Sicilian couples and carriers of beta-globin gene mutations. METHODS AND RESULTS: The studied mutations were: Cd39, HbS, IVS1 nt1, IVS1 nt6 and IVS1 nt110. ICSI was performed with partner's sperm on 131 out of 147 retrieved oocytes, and this resulted in 72 zygotes; 32 embryos were successfully biopsied on day 3. The biopsied blastomeres were lysed and the beta-globin alleles amplified by nested PCR. The mutation diagnosis was performed by restriction enzyme digestion and reverse dot-blot. The amplification efficacy was 97.2%. The genotype study of non-transferred and surplus embryos showed that the allele drop-out rate was 8.6%. Seventeen embryos were transferred in utero on day 4. All couples received an embryo transfer; of the four pregnancies obtained, three resulted in live births and one miscarried at 11 weeks. Prenatal diagnosis at the 11th week and miscarriage material analysis confirmed the PGD results. CONCLUSIONS: These studies represent the first successful application of PGD for beta-thalassaemia and sickle cell anaemia in Italy.  (+info)

Fluorescence PCR quantification of cyclin D1 expression. (7/222)

We have used a continuous fluorescence monitoring method to assess cyclin D1 mRNA expression in a variety of hematological and non-hematological processes. We examined 14 cell lines, 11 reactive lymphoid tissues, and 57 primary hematopoietic neoplasms including mantle cell lymphoma (MCL) (n = 10), chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) (n = 11), acute lymphoblastic leukemia/lymphoma (n = 15), follicular lymphoma (n = 6), peripheral T-cell lymphoma (PTCL) (n = 3), anaplastic large cell lymphoma (n = 3), hairy cell leukemia (n = 3), Burkitt lymphoma (n = 1), Burkitt-like lymphoma (n = 4), and plasmacytoma (n = 1) for the expression of cyclin D1 mRNA using fluorescently labeled sequence-specific hybridization probes. Fluorescence (F) was plotted against cycle (C) number over 45 cycles. The log-linear portion of the F versus C graph identified a fractional cycle number for threshold fluorescence. A beta-globin mRNA transcript with equivalent amplification efficiency to that of cyclin D1 was used for assessment of RNA integrity and normalization. In general, the MCLs demonstrated substantially higher levels of cyclin D1 mRNA than the other lymphoproliferative processes. Moderately high levels of cyclin D1 mRNA were detected in one PTCL. On average, the CLL/SLL cases showed cyclin D1 mRNA levels two to three orders of magnitude lower than observed in the MCLs. Cell lines derived from non-hematopoietic neoplasms such as fibrosarcoma, small cell carcinoma, and neuroblastoma showed comparable or higher levels of cyclin D1 mRNA than the MCLs. Our results indicate that quantitative real-time reverse transcription (RT) polymerase chain reaction is a simple, rapid, and accurate technique for assessing cyclin D1 expression, and while it is not specific, it can reliably be used in the distinction of MCL from CLL/SLL.  (+info)

Y14 and hUpf3b form an NMD-activating complex. (8/222)

Messenger RNAs with premature translation termination codons (PTCs) are degraded by nonsense-mediated mRNA decay (NMD). In mammals, PTCs are discriminated from physiological stop codons by a process thought to involve the splicing-dependent deposition of an exon junction complex (EJC), EJC-mediated recruitment of Upf3, and Upf2 binding to the N terminus of Upf3. Here, we identify a conserved domain of hUpf3b that mediates an interaction with the EJC protein Y14. Tethered function analysis shows that the Y14/hUpf3b interaction is essential for NMD, while surprisingly the interaction between hUpf3b and hUpf2 is not. Nonetheless, hUpf2 is necessary for NMD mediated by tethered Y14. RNAi-induced knockdown and Y14 repletion of siRNA-treated cells implicates Y14 in the degradation of beta-globin NS39 mRNA and demonstrates that Y14 is required for NMD induced by tethered hUpf3b. These results uncover a direct role of Y14 in NMD and suggest an unexpected hierarchy in the assembly of NMD complexes.  (+info)

Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.

Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.

The symptoms of hypoproteinemia can vary depending on the underlying cause and severity of the condition. Some common symptoms include:

1. Weakness and fatigue
2. Loss of appetite
3. Nausea and vomiting
4. Diarrhea or constipation
5. Skin, hair, and nail problems
6. Increased risk of infections
7. Muscle wasting and loss of muscle mass
8. Poor wound healing
9. Hair loss
10. Edema (swelling)

If you suspect that you or someone you know may have hypoproteinemia, it is important to consult a healthcare professional for proper diagnosis and treatment. A healthcare provider will typically perform a physical examination, take a medical history, and order blood tests to determine the levels of protein and other essential nutrients in the body.

Treatment of hypoproteinemia depends on the underlying cause of the condition. In cases where the condition is caused by malnutrition or dietary deficiencies, dietary modifications and supplements may be recommended. For example, a patient with hypoproteinemia due to malnutrition may need to consume more protein-rich foods, such as meat, poultry, fish, eggs, dairy products, legumes, and nuts. In cases where the condition is caused by an underlying medical condition, such as liver or kidney disease, treatment may involve managing the underlying condition.

It is important to note that hypoproteinemia can lead to serious complications if left untreated, such as muscle wasting, poor wound healing, and increased risk of infections. Therefore, it is crucial to seek medical attention if you suspect that you or someone you know may have hypoproteinemia.

In summary, hypoproteinemia is a condition characterized by low levels of protein in the blood. It can be caused by various factors, such as malnutrition, liver or kidney disease, and other medical conditions. Treatment options depend on the underlying cause of the condition, and early diagnosis and treatment are crucial to prevent complications. If you suspect that you or someone you know may have hypoproteinemia, it is essential to consult a healthcare professional for proper diagnosis and treatment.

There are several types of blood protein disorders, including:

1. Hemophilia A: a deficiency of factor VIII, which is necessary for blood clotting.
2. Hemophilia B: a deficiency of factor IX, also involved in blood clotting.
3. Von Willebrand disease: a deficiency of von Willebrand factor, which helps to platelets stick together and form blood clots.
4. Protein C deficiency: a lack of protein C, an anticoagulant protein that helps to prevent blood clots.
5. Protein S deficiency: a lack of protein S, another anticoagulant protein that helps to prevent blood clots.
6. Antithrombin III deficiency: a lack of antithrombin III, a protein that prevents the formation of blood clots.
7. Fibrinogen deficiency: a lack of fibrinogen, a protein that is essential for blood clotting.
8. Dysproteinemia: an abnormal amount or type of proteins in the blood, which can lead to various symptoms and complications.

Symptoms of blood protein disorders can vary depending on the specific condition and the severity of the deficiency. Common symptoms include easy bruising or bleeding, frequent nosebleeds, prolonged bleeding after injuries or surgery, and joint pain or swelling.

Treatment for blood protein disorders typically involves replacing the missing protein or managing symptoms with medication or lifestyle changes. In some cases, gene therapy may be an option to correct the underlying genetic defect.

It's important for individuals with blood protein disorders to work closely with their healthcare provider to manage their condition and prevent complications such as joint damage, infections, and bleeding episodes.

The term "serum sickness" was first used in the late 19th century to describe this condition, which was often seen in people who had received serum (a type of blood product) containing antibodies against diseases such as diphtheria or tetanus. Today, the term is still used to describe similar reactions to other substances, including medications and vaccines.

Serum sickness can be mild or severe, and in rare cases, it can lead to serious complications such as kidney failure or inflammation of the heart. Treatment typically involves stopping the use of the offending substance and providing supportive care to manage symptoms. In severe cases, corticosteroids or other medications may be used to reduce inflammation.

While serum sickness is a relatively rare condition, it is important for healthcare providers to be aware of it as a potential complication of medication and vaccine use. This knowledge can help them recognize and manage the condition effectively, reducing the risk of serious complications and improving outcomes for patients.

1. Irregular menstrual cycles, or amenorrhea (the absence of periods).
2. Cysts on the ovaries, which are fluid-filled sacs that can be detected by ultrasound.
3. Elevated levels of androgens (male hormones) in the body, which can cause a range of symptoms including acne, excessive hair growth, and male pattern baldness.
4. Insulin resistance, which is a condition in which the body's cells do not respond properly to insulin, leading to high blood sugar levels.

PCOS is a complex disorder, and there is no single cause. However, genetics, hormonal imbalances, and insulin resistance are thought to play a role in its development. It is estimated that 5-10% of women of childbearing age have PCOS, making it one of the most common endocrine disorders affecting women.

There are several symptoms of PCOS, including:

1. Irregular menstrual cycles or amenorrhea
2. Weight gain or obesity
3. Acne
4. Excessive hair growth on the face, chest, and back
5. Male pattern baldness
6. Infertility or difficulty getting pregnant
7. Mood changes, such as depression and anxiety
8. Sleep apnea

PCOS can be diagnosed through a combination of physical examination, medical history, and laboratory tests, including:

1. Pelvic exam: A doctor will examine the ovaries and uterus to look for cysts or other abnormalities.
2. Ultrasound: An ultrasound can be used to detect cysts on the ovaries and to evaluate the thickness of the uterine lining.
3. Hormone testing: Blood tests can be used to measure levels of androgens, estrogen, and progesterone.
4. Glucose tolerance test: This test is used to check for insulin resistance, which is a common finding in women with PCOS.
5. Laparoscopy: A small camera inserted through a small incision in the abdomen can be used to visualize the ovaries and uterus and to diagnose PCOS.

There is no cure for PCOS, but it can be managed with lifestyle changes and medication. Treatment options include:

1. Weight loss: Losing weight can improve insulin sensitivity and reduce androgen levels.
2. Hormonal birth control: Birth control pills or other hormonal contraceptives can help regulate menstrual cycles and reduce androgen levels.
3. Fertility medications: Clomiphene citrate and letrozole are commonly used to stimulate ovulation in women with PCOS.
4. Injectable fertility medications: Gonadotropins, such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), can be used to stimulate ovulation.
5. Surgery: Laparoscopic ovarian drilling or laser surgery can improve ovulation and fertility in women with PCOS.
6. Assisted reproductive technology (ART): In vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) can be used to help women with PCOS conceive.
7. Alternative therapies: Some complementary and alternative therapies, such as acupuncture and herbal supplements, may be helpful in managing symptoms of PCOS.

It is important for women with PCOS to work closely with their healthcare provider to develop a treatment plan that meets their individual needs and goals. With appropriate treatment, many women with PCOS can improve their menstrual regularity, fertility, and overall health.

People with agammaglobulinemia are more susceptible to infections, particularly those caused by encapsulated bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae type b. They may also experience recurrent sinopulmonary infections, ear infections, and gastrointestinal infections. The disorder can be managed with intravenous immunoglobulin (IVIG) therapy, which provides antibodies to help prevent infections. In severe cases, a bone marrow transplant may be necessary.

Agammaglobulinemia is an autosomal recessive disorder, meaning that a person must inherit two mutated copies of the BTK gene (one from each parent) to develop the condition. It is relatively rare, affecting approximately one in 1 million people worldwide. The disorder can be diagnosed through genetic testing and a complete blood count (CBC) that shows low levels of immunoglobulins.

Treatment for ag

The most common cause of hyperthyroidism is an autoimmune disorder called Graves' disease, which causes the thyroid gland to produce too much thyroxine (T4) and triiodothyronine (T3). Other causes include inflammation of the thyroid gland (thyroiditis), thyroid nodules, and certain medications.

Symptoms of hyperthyroidism can vary depending on the severity of the condition, but may include:

* Rapid weight loss
* Nervousness or irritability
* Increased heart rate
* Heat intolerance
* Changes in menstrual cycle
* Fatigue
* Muscle weakness
* tremors

If left untreated, hyperthyroidism can lead to more serious complications such as heart problems, bone loss, and eye problems. Treatment options for hyperthyroidism include medications to reduce hormone production, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.

In pregnant women, untreated hyperthyroidism can increase the risk of miscarriage, preterm labor, and intellectual disability in the baby. Treatment options for pregnant women with hyperthyroidism are similar to those for non-pregnant adults, but may need to be adjusted to avoid harm to the developing fetus.

It is important for individuals suspected of having hyperthyroidism to seek medical attention as soon as possible to receive proper diagnosis and treatment. Early treatment can help prevent complications and improve quality of life.

Hypothyroidism can be diagnosed through a series of blood tests that measure the levels of thyroid hormones in the body. Treatment typically involves taking synthetic thyroid hormone medication to replace the missing hormones. With proper treatment, most people with hypothyroidism can lead normal, healthy lives.

Hypothyroidism is a relatively common condition, affecting about 4.6 million people in the United States alone. Women are more likely to develop hypothyroidism than men, and it is most commonly diagnosed in middle-aged women.

Some of the symptoms of Hypothyroidism include:

1. Fatigue or tiredness
2. Weight gain
3. Dry skin
4. Constipation
5. Depression or anxiety
6. Memory problems
7. Muscle aches and stiffness
8. Heavy or irregular menstrual periods
9. Pale, dry, or rough skin
10. Hair loss or thinning
11. Cold intolerance
12. Slowed speech and movements

It's important to note that some people may not experience any symptoms at all, especially in the early stages of the condition. However, if left untreated, hypothyroidism can lead to more severe complications such as heart disease, mental health problems, and infertility.

Hepatitis A is typically spread through contaminated food and water or through close contact with someone who has the infection. The virus can also be spread through sexual contact or sharing of needles.

Symptoms of hepatitis A usually appear two to six weeks after exposure and can last for several weeks or months. In some cases, the infection can lead to complications such as liver failure, which can be life-threatening.

There is a vaccine available for hepatitis A, which is recommended for individuals traveling to areas where the virus is common, people who engage in high-risk behaviors, and those with chronic liver disease. Treatment for hepatitis A typically focuses on relieving symptoms and supporting the liver as it recovers. In severe cases, hospitalization may be necessary.

Preventive measures to reduce the risk of hepatitis A infection include maintaining good hygiene practices, such as washing hands frequently, especially before eating or preparing food; avoiding consumption of raw or undercooked shellfish, particularly oysters; and avoiding close contact with people who have the infection.

The diagnosis of GVHD is based on a combination of clinical findings, laboratory tests, and biopsies. Treatment options include immunosuppressive drugs, corticosteroids, and in severe cases, stem cell transplantation reversal or donor lymphocyte infusion.

Prevention of GVHD includes selecting the right donor, using conditioning regimens that minimize damage to the recipient's bone marrow, and providing appropriate immunosuppression after transplantation. Early detection and management of GVHD are critical to prevent long-term complications and improve survival rates.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

Hyperthyroxinemia can be caused by a variety of factors, including:

1. Overactive thyroid (hyperthyroidism): This is the most common cause of hyperthyroxinemia. In this condition, the thyroid gland produces too much T4 and T3 (the other main hormone produced by the thyroid gland), leading to an increase in blood levels of both hormones.
2. Thyroid tumors: Both benign and malignant tumors of the thyroid gland can cause hyperthyroxinemia by producing excessive amounts of T4 and T3.
3. Thyroiditis: This is an inflammation of the thyroid gland that can lead to an increase in T4 and T3 production.
4. Medications: Certain medications, such as thyroid hormone replacement therapy, can cause hyperthyroxinemia by increasing blood levels of T4 and T3.
5. Iodine deficiency: Iodine is essential for the production of T4 and T3, so an iodine deficiency can lead to decreased production of these hormones and result in hyperthyroxinemia.

Symptoms of hyperthyroxinemia may include:

* Weight loss
* Fatigue
* Increased heart rate
* Nervousness
* Irritability
* Muscle weakness
* Heat intolerance

If left untreated, hyperthyroxinemia can lead to more serious complications, such as:

* Heart problems: Hyperthyroxinemia can cause an increase in heart rate and cardiac output, which can put a strain on the heart and lead to heart failure.
* Osteoporosis: Prolonged hyperthyroxinemia can lead to bone loss and increased risk of osteoporosis.
* Thyrotoxic crisis: In rare cases, hyperthyroxinemia can lead to a life-threatening condition called thyrotoxic crisis, which is characterized by fever, heart problems, and organ failure.

Treatment of hyperthyroxinemia typically involves addressing the underlying cause of the condition. For example:

* Thyroid hormone replacement therapy may be discontinued or adjusted if the patient is taking too much thyroid hormone.
* Medications that can cause hyperthyroxinemia, such as steroids and certain antidepressants, may be discontinued or adjusted.
* Iodine supplements may be recommended for patients with iodine deficiency.
* Surgery may be necessary in cases of thyroid nodules or cancer that are causing hyperthyroxinemia.

In addition to addressing the underlying cause, treatment may also involve managing symptoms and preventing complications. This can include:

* Medications to control heart rate and blood pressure
* Bone density testing and osteoporosis treatment if necessary
* Monitoring for signs of osteoporosis, such as bone pain or a broken bone
* Monitoring for signs of heart problems, such as shortness of breath or swelling in the legs
* Monitoring for signs of liver problems, such as jaundice or abdominal pain

In rare cases, hyperthyroxinemia can lead to a life-threatening condition called thyrotoxic crisis. Thyrotoxic crisis is characterized by fever, heart problems, and organ failure. If left untreated, it can be fatal.

If you suspect that you or someone you know may have hyperthyroxinemia, it is important to seek medical attention as soon as possible. Early diagnosis and treatment can help prevent complications and improve outcomes.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

There are several possible causes of hyperandrogenism, including:

1. Congenital adrenal hyperplasia (CAH): A genetic disorder that affects the production of cortisol and aldosterone hormones by the adrenal glands.
2. Polycystic ovary syndrome (PCOS): A hormonal disorder that affects women of reproductive age and is characterized by cysts on the ovaries, irregular menstrual cycles, and high levels of androgens.
3. Adrenal tumors: Tumors in the adrenal glands can cause excessive production of androgens.
4. Familial hyperandrogenism: A rare inherited condition that causes an overproduction of androgens.
5. Obesity: Excess body fat can lead to increased production of androgens.

The symptoms of hyperandrogenism can vary depending on the cause, but may include:

1. Acne
2. Hirsutism (excessive hair growth)
3. Virilization (male-like physical characteristics, such as deepening of the voice and clitoral enlargement in women)
4. Male pattern baldness
5. Increased muscle mass and strength
6. Irregular menstrual cycles or cessation of menstruation
7. Infertility
8. Elevated blood pressure
9. Elevated cholesterol levels

Treatment options for hyperandrogenism depend on the underlying cause, but may include:

1. Medications to reduce androgen production or block their effects
2. Hormone replacement therapy (HRT) to restore normal hormone balance
3. Surgery to remove tumors or cysts
4. Weight loss programs to reduce excess body fat
5. Lifestyle changes, such as exercise and dietary modifications, to improve overall health.

It's important to note that hyperandrogenism can also be caused by other factors, such as congenital adrenal hyperplasia or ovarian tumors, so it's important to consult a healthcare professional for proper diagnosis and treatment.

Some of the symptoms of hirsutism include:

* Thick, dark hair on the face, chest, back, and buttocks
* Hair growth on the arms, legs, and other areas of the body
* Thinning or loss of hair on the head
* Acne and oily skin

Hirsutism can be caused by a variety of factors, including:

* Hormonal imbalances: Excessive levels of androgens, such as testosterone, can cause hirsutism.
* Genetics: Inheritance plays a role in the development of hirsutism.
* Medications: Certain medications, such as anabolic steroids and certain antidepressants, can cause hirsutism as a side effect.
* Other medical conditions: Polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia (CAH), and other endocrine disorders can also cause hirsutism.

There are several treatment options for hirsutism, including:

* Medications such as anti-androgens and retinoids to reduce hair growth and improve skin texture
* Electrolysis and laser therapy to remove unwanted hair
* Hormonal therapies such as birth control pills and spironolactone to regulate hormone levels and reduce hair growth
* Plastic surgery to remove excess hair-bearing skin.

It is important for individuals with hirsutism to seek medical attention if they experience any of the following symptoms:

* Sudden or excessive hair growth
* Hair growth on the face, chest, back, or buttocks
* Thinning or loss of hair on the head
* Acne and oily skin.

Early diagnosis and treatment can help manage the symptoms of hirsutism and improve quality of life for individuals affected by this condition.

Multiple myeloma is the second most common type of hematologic cancer after non-Hodgkin's lymphoma, accounting for approximately 1% of all cancer deaths worldwide. It is more common in older adults, with most patients being diagnosed over the age of 65.

The exact cause of multiple myeloma is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. There are several risk factors that have been associated with an increased risk of developing multiple myeloma, including:

1. Family history: Having a family history of multiple myeloma or other plasma cell disorders increases the risk of developing the disease.
2. Age: The risk of developing multiple myeloma increases with age, with most patients being diagnosed over the age of 65.
3. Race: African Americans are at higher risk of developing multiple myeloma than other races.
4. Obesity: Being overweight or obese may increase the risk of developing multiple myeloma.
5. Exposure to certain chemicals: Exposure to certain chemicals such as pesticides, solvents, and heavy metals has been linked to an increased risk of developing multiple myeloma.

The symptoms of multiple myeloma can vary depending on the severity of the disease and the organs affected. Common symptoms include:

1. Bone pain: Pain in the bones, particularly in the spine, ribs, or long bones, is a common symptom of multiple myeloma.
2. Fatigue: Feeling tired or weak is another common symptom of the disease.
3. Infections: Patients with multiple myeloma may be more susceptible to infections due to the impaired functioning of their immune system.
4. Bone fractures: Weakened bones can lead to an increased risk of fractures, particularly in the spine, hips, or ribs.
5. Kidney problems: Multiple myeloma can cause damage to the kidneys, leading to problems such as kidney failure or proteinuria (excess protein in the urine).
6. Anemia: A low red blood cell count can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
7. Increased calcium levels: High levels of calcium in the blood can cause symptoms such as nausea, vomiting, constipation, and confusion.
8. Neurological problems: Multiple myeloma can cause neurological problems such as headaches, numbness or tingling in the arms and legs, and difficulty with coordination and balance.

The diagnosis of multiple myeloma typically involves a combination of physical examination, medical history, and laboratory tests. These may include:

1. Complete blood count (CBC): A CBC can help identify abnormalities in the numbers and characteristics of different types of blood cells, including red blood cells, white blood cells, and platelets.
2. Serum protein electrophoresis (SPEP): This test measures the levels of different proteins in the blood, including immunoglobulins (antibodies) and abnormal proteins produced by myeloma cells.
3. Urine protein electrophoresis (UPEP): This test measures the levels of different proteins in the urine.
4. Immunofixation: This test is used to identify the type of antibody produced by myeloma cells and to rule out other conditions that may cause similar symptoms.
5. Bone marrow biopsy: A bone marrow biopsy involves removing a sample of tissue from the bone marrow for examination under a microscope. This can help confirm the diagnosis of multiple myeloma and determine the extent of the disease.
6. Imaging tests: Imaging tests such as X-rays, CT scans, or MRI scans may be used to assess the extent of bone damage or other complications of multiple myeloma.
7. Genetic testing: Genetic testing may be used to identify specific genetic abnormalities that are associated with multiple myeloma and to monitor the response of the disease to treatment.

It's important to note that not all patients with MGUS or smoldering myeloma will develop multiple myeloma, and some patients with multiple myeloma may not have any symptoms at all. However, if you are experiencing any of the symptoms listed above or have a family history of multiple myeloma, it's important to talk to your doctor about your risk and any tests that may be appropriate for you.

The symptoms of rabies can vary depending on the severity of the infection and the individual's overall health. Early symptoms may include fever, headache, weakness, and fatigue. As the disease progresses, symptoms can become more severe and can include:

* Agitation and confusion
* Seizures and paralysis
* Hydrophobia (fear of water)
* Spasms and twitching
* Increased salivation
* Fever and chills
* Weakness and paralysis of the face, arms, and legs

If left untreated, rabies is almost always fatal. However, prompt medical attention, including the administration of post-exposure prophylaxis (PEP), can prevent the disease from progressing and save the life of an infected person. PEP typically involves a series of injections with rabies immune globulin and a rabies vaccine.

Rabies is a significant public health concern, particularly in developing countries where access to medical care may be limited. According to the World Health Organization (WHO), there are an estimated 55,000-60,000 human deaths from rabies each year, mostly in Asia and Africa. In the United States, rabies is relatively rare, with only a few cases reported each year. However, it is still important for individuals to be aware of the risks of rabies and take precautions to prevent exposure, such as avoiding contact with wild animals and ensuring that pets are up-to-date on their vaccinations.

Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.

In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.

There are several types of hepatitis, including:

1. Hepatitis A: This type is caused by the hepatitis A virus (HAV) and is usually transmitted through contaminated food or water or through close contact with someone who has the infection.
2. Hepatitis B: This type is caused by the hepatitis B virus (HBV) and can be spread through sexual contact, sharing of needles, or mother-to-child transmission during childbirth.
3. Hepatitis C: This type is caused by the hepatitis C virus (HCV) and is primarily spread through blood-to-blood contact, such as sharing of needles or receiving a tainted blood transfusion.
4. Alcoholic hepatitis: This type is caused by excessive alcohol consumption and can lead to inflammation and scarring in the liver.
5. Drug-induced hepatitis: This type is caused by certain medications, such as antidepressants, anti-seizure drugs, or chemotherapy agents.
6. Autoimmune hepatitis: This type is caused by an abnormal immune response and can lead to inflammation in the liver.

Symptoms of hepatitis may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, and yellowing of the skin (jaundice). In severe cases, it can lead to liver failure or even death.

Diagnosis of hepatitis is typically made through a combination of physical examination, laboratory tests such as blood tests and imaging studies like ultrasound or CT scans. Treatment options vary depending on the cause and severity of the condition, but may include medications to manage symptoms, antiviral therapy, or in severe cases, liver transplantation. Prevention measures for hepatitis include vaccination against certain types of the disease, practicing safe sex, avoiding sharing needles or other drug paraphernalia, and following proper hygiene practices.

In conclusion, hepatitis is a serious condition that affects millions of people worldwide. It is important to be aware of the different types of hepatitis and their causes in order to prevent and manage this condition effectively. By taking appropriate measures such as getting vaccinated and practicing safe sex, individuals can reduce their risk of contracting hepatitis. In severe cases, early diagnosis and treatment can help to minimize damage to the liver and improve outcomes for patients.

Vaccinia is most commonly associated with smallpox, which is caused by a similar virus and was eradicated in the late 1970s through widespread vaccination. However, there have been occasional outbreaks of vaccinia in the United States and other countries since then, often linked to laboratory accidents or deliberate releases of the virus.

The treatment of vaccinia typically involves supportive care, such as rest, hydration, and antipyretic medications to reduce fever. Antiviral medications may also be used in some cases. Prevention of the disease relies on avoiding contact with infected animals or people, and on following proper infection control practices in laboratory and healthcare settings.

Vaccinia is a serious viral infection that can have severe consequences if left untreated. It is important to seek medical attention immediately if symptoms persist or worsen over time.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

The symptoms of MCNS typically appear in infancy or early childhood and may include:

* Skin rashes and lesions
* Mucosal lesions (e.g., in the mouth, nose, and eyes)
* Enlarged lymph nodes
* Respiratory problems
* Fevers
* Fatigue

The exact cause of MCNS is not known, but it is believed to be related to an abnormal immune response. The disorder is usually inherited in an autosomal recessive pattern, which means that a child must inherit two copies of the mutated gene (one from each parent) to develop the condition.

There is no cure for MCNS, but treatment may involve medications to manage symptoms and prevent complications. Corticosteroids, immunosuppressive drugs, and antibiotics may be used to reduce inflammation and prevent infection. In severe cases, surgery may be necessary to remove affected tissue or repair deformities.

Prognosis for MCNS varies depending on the severity of the disorder and the presence of any complications. Some individuals with MCNS may experience mild symptoms and have a good quality of life, while others may have more severe symptoms and require ongoing medical care. With appropriate treatment, many individuals with MCNS can lead active and fulfilling lives.

There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.

Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.

There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.

Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.

Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.

The symptoms of kwashiorkor include:

1. Diarrhea
2. Vomiting
3. Weight loss
4. Edema (swelling) particularly in the abdomen, face, and limbs
5. Skin changes such as dryness and thinning
6. Hair loss
7. Weakness and fatigue
8. Increased risk of infections
9. Poor appetite and feeding difficulties in children

Kwashiorkor is caused by a diet that is deficient in protein, which is necessary for growth and repair of body tissues. Without enough protein, the body begins to break down its own tissues, leading to the symptoms mentioned above. It can also be caused by a lack of other essential nutrients such as vitamins and minerals.

Treatment for kwashiorkor typically involves providing the patient with a balanced diet that includes plenty of protein and other essential nutrients. In severe cases, intravenous fluids and medication may be necessary to treat dehydration and other complications.

Prevention is key, and this can be achieved by:

1. Providing a balanced diet that includes plenty of protein and other essential nutrients
2. Avoiding foods that are high in carbohydrates and low in protein
3. Ensuring that children receive adequate breastfeeding or appropriate complementary feeding
4. Addressing poverty and food insecurity, which can contribute to kwashiorkor
5. Promoting good hygiene practices to reduce the risk of infections.

CMV infections are more common in people with weakened immune systems, such as those with HIV/AIDS, cancer, or taking immunosuppressive drugs after an organ transplant. In these individuals, CMV can cause severe and life-threatening complications, such as pneumonia, retinitis (inflammation of the retina), and gastrointestinal disease.

In healthy individuals, CMV infections are usually mild and may not cause any symptoms at all. However, in some cases, CMV can cause a mononucleosis-like illness with fever, fatigue, and swollen lymph nodes.

CMV infections are diagnosed through a combination of physical examination, blood tests, and imaging studies such as CT scans or MRI. Treatment is generally not necessary for mild cases, but may include antiviral medications for more severe infections. Prevention strategies include avoiding close contact with individuals who have CMV, practicing good hygiene, and considering immunoprophylaxis (prevention of infection through the use of immune globulin) for high-risk individuals.

Overall, while CMV infections can be serious and life-threatening, they are relatively rare in healthy individuals and can often be treated effectively with supportive care and antiviral medications.

1. Foodborne botulism: This type of botulism is caused by eating foods that have been contaminated with the bacteria. Symptoms typically begin within 12 to 72 hours after consuming the contaminated food and can include double vision, droopy eyelids, slurred speech, difficulty swallowing, and muscle weakness.
2. Infant botulism: This type of botulism occurs in infants who are exposed to the bacteria through contact with contaminated soil or object. Symptoms can include constipation, poor feeding, and weak cry.
3. Wound botulism: This type of botulism is caused by the bacteria entering an open wound, usually a deep puncture wound or surgical incision.

Botulism is a rare illness in the United States, but it can be deadly if not treated promptly. Treatment typically involves supportive care, such as mechanical ventilation and fluids, as well as antitoxin injections to neutralize the effects of the toxin. Prevention measures include proper food handling and storage, good hygiene practices, and avoiding consumption of improperly canned or preserved foods.

Hemoglobinuria can be caused by a variety of factors, including:

1. Blood disorders such as sickle cell disease, thalassemia, and von Willebrand disease.
2. Inherited genetic disorders such as hemophilia.
3. Autoimmune disorders such as autoimmune hemolytic anemia.
4. Infections such as septicemia or meningococcemia.
5. Toxins such as lead, which can damage red blood cells and cause hemoglobinuria.
6. Certain medications such as antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).
7. Kidney disease or failure.
8. Transfusion-related acute lung injury (TRALI), which can occur after blood transfusions.
9. Hemolytic uremic syndrome (HUS), a condition that occurs when red blood cells are damaged and broken down, leading to kidney failure.

The symptoms of hemoglobinuria may include:

1. Red or brown-colored urine
2. Frequent urination
3. Pale or yellowish skin
4. Fatigue
5. Shortness of breath
6. Nausea and vomiting
7. Headache
8. Dizziness or lightheadedness
9. Confusion or loss of consciousness in severe cases.

Diagnosis of hemoglobinuria is typically made through urine testing, such as a urinalysis, which can detect the presence of hemoglobin in the urine. Additional tests may be ordered to determine the underlying cause of hemoglobinuria, such as blood tests, imaging studies, or biopsies.

Treatment of hemoglobinuria depends on the underlying cause and severity of the condition. In some cases, treatment may involve addressing the underlying condition that is causing the hemoglobinuria, such as managing an infection or stopping certain medications. Other treatments may include:

1. Fluid and electrolyte replacement to prevent dehydration and maintain proper fluid balance.
2. Medications to help remove excess iron from the body.
3. Blood transfusions to increase the number of red blood cells in the body and improve oxygen delivery.
4. Dialysis to filter waste products from the blood when the kidneys are unable to do so.
5. Supportive care, such as oxygen therapy and pain management.

In severe cases of hemoglobinuria, complications can include:

1. Kidney damage or failure
2. Septicemia (blood infection)
3. Respiratory failure
4. Heart problems
5. Increased risk of infections and other complications.

Prevention of hemoglobinuria involves managing any underlying medical conditions, such as diabetes or infections, and avoiding certain medications that can cause the condition. It is also important to seek medical attention if symptoms of hemoglobinuria develop, as early treatment can help prevent complications and improve outcomes.

There are different types of Breast Neoplasms such as:

1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.

2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.

3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.

4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.

5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.

Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.

Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.

It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.

Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.

Types of Infection:

1. Bacterial Infections: These are caused by the presence of harmful bacteria in the body. Examples include pneumonia, urinary tract infections, and skin infections.
2. Viral Infections: These are caused by the presence of harmful viruses in the body. Examples include the common cold, flu, and HIV/AIDS.
3. Fungal Infections: These are caused by the presence of fungi in the body. Examples include athlete's foot, ringworm, and candidiasis.
4. Parasitic Infections: These are caused by the presence of parasites in the body. Examples include malaria, giardiasis, and toxoplasmosis.

Symptoms of Infection:

1. Fever
2. Fatigue
3. Headache
4. Muscle aches
5. Skin rashes or lesions
6. Swollen lymph nodes
7. Sore throat
8. Coughing
9. Diarrhea
10. Vomiting

Treatment of Infection:

1. Antibiotics: These are used to treat bacterial infections and work by killing or stopping the growth of bacteria.
2. Antiviral medications: These are used to treat viral infections and work by interfering with the replication of viruses.
3. Fungicides: These are used to treat fungal infections and work by killing or stopping the growth of fungi.
4. Anti-parasitic medications: These are used to treat parasitic infections and work by killing or stopping the growth of parasites.
5. Supportive care: This includes fluids, nutritional supplements, and pain management to help the body recover from the infection.

Prevention of Infection:

1. Hand washing: Regular hand washing is one of the most effective ways to prevent the spread of infection.
2. Vaccination: Getting vaccinated against specific infections can help prevent them.
3. Safe sex practices: Using condoms and other safe sex practices can help prevent the spread of sexually transmitted infections.
4. Food safety: Properly storing and preparing food can help prevent the spread of foodborne illnesses.
5. Infection control measures: Healthcare providers use infection control measures such as wearing gloves, masks, and gowns to prevent the spread of infections in healthcare settings.

The condition is caused by sensitization of the mother's immune system to the Rh factor, which can occur when the mother's blood comes into contact with the fetus's blood during pregnancy or childbirth. The antibodies produced by the mother's immune system can attack the red blood cells of the fetus, leading to hemolytic anemia and potentially causing stillbirth or death in the newborn.

Erythroblastosis fetalis is diagnosed through blood tests that measure the levels of antibodies against the Rh factor. Treatment typically involves the administration of Rh immune globulin, which can help to prevent the mother's immune system from producing more antibodies against the Rh factor and reduce the risk of complications for the fetus. In severe cases, a blood transfusion may be necessary to increase the newborn's red blood cell count.

Erythroblastosis fetalis is a serious condition that requires close monitoring and proper medical management to prevent complications and ensure the best possible outcome for both the mother and the baby.

There are several types of amyloidosis, each with different causes and symptoms. The most common types include:

1. Primary amyloidosis: This type is caused by the production of abnormal proteins in the bone marrow. It mainly affects older adults and can lead to symptoms such as fatigue, weight loss, and numbness or tingling in the hands and feet.
2. Secondary amyloidosis: This type is caused by other conditions, such as rheumatoid arthritis, tuberculosis, or inflammatory bowel disease. It can also be caused by long-term use of certain medications, such as antibiotics or chemotherapy.
3. Familial amyloid polyneuropathy: This type is inherited and affects the nerves in the body, leading to symptoms such as muscle weakness, numbness, and pain.
4. Localized amyloidosis: This type affects a specific area of the body, such as the tongue or the skin.

The symptoms of amyloidosis can vary depending on the organs affected and the severity of the condition. Some common symptoms include:

1. Fatigue
2. Weakness
3. Pain
4. Numbness or tingling in the hands and feet
5. Swelling in the legs, ankles, and feet
6. Difficulty with speech or swallowing
7. Seizures
8. Heart problems
9. Kidney failure
10. Liver failure

The diagnosis of amyloidosis is based on a combination of physical examination, medical history, laboratory tests, and imaging studies. Laboratory tests may include blood tests to measure the levels of certain proteins in the body, as well as biopsies to examine tissue samples under a microscope. Imaging studies, such as X-rays, CT scans, and MRI scans, may be used to evaluate the organs affected by the condition.

There is no cure for amyloidosis, but treatment can help manage the symptoms and slow the progression of the disease. Treatment options may include:

1. Medications to control symptoms such as pain, swelling, and heart problems
2. Chemotherapy to reduce the production of abnormal proteins
3. Autologous stem cell transplantation to replace damaged cells with healthy ones
4. Dialysis to remove excess fluids and waste products from the body
5. Nutritional support to ensure adequate nutrition and hydration
6. Physical therapy to maintain muscle strength and mobility
7. Supportive care to manage pain, improve quality of life, and reduce stress on the family.

In conclusion, amyloidosis is a complex and rare group of diseases that can affect multiple organs and systems in the body. Early diagnosis and treatment are essential to managing the symptoms and slowing the progression of the disease. It is important for patients with suspected amyloidosis to seek medical attention from a specialist, such as a hematologist or nephrologist, for proper evaluation and treatment.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

There are several causes of hypergammaglobulinemia, including:

1. Chronic infections: Prolonged infections can cause an increase in the production of immunoglobulins to fight off the infection.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis can cause the immune system to produce excessive amounts of antibodies.
3. Cancer: Some types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause an increase in immunoglobulin production.
4. Genetic disorders: Certain genetic conditions, such as X-linked agammaglobulinemia, can lead to a deficiency or excess of immunoglobulins.
5. Medications: Certain medications, such as corticosteroids and chemotherapy drugs, can suppress the immune system and reduce the production of immunoglobulins.

Symptoms of hypergammaglobulinemia can include:

1. Infections: Recurring infections are a common symptom of hypergammaglobulinemia, as the excessive amount of antibodies can make it difficult for the body to fight off infections effectively.
2. Fatigue: Chronic infections and inflammation can cause fatigue and weakness.
3. Weight loss: Recurring infections and chronic inflammation can lead to weight loss and malnutrition.
4. Swollen lymph nodes: Enlarged lymph nodes are a common symptom of hypergammaglobulinemia, as the body tries to fight off infections.
5. Fever: Recurring fevers can be a symptom of hypergammaglobulinemia, as the body tries to fight off infections.
6. Night sweats: Excessive sweating at night can be a symptom of hypergammaglobulinemia.
7. Skin rashes: Certain types of skin rashes can be a symptom of hypergammaglobulinemia, such as a rash caused by allergic reactions to medications or infections.
8. Joint pain: Pain and stiffness in the joints can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the joints.
9. Headaches: Chronic headaches can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the brain or other parts of the body.
10. Swollen liver and spleen: Enlarged liver and spleen can be a symptom of hypergammaglobulinemia, as the body tries to filter out excess antibodies and fight off infections.

It is important to note that these symptoms can also be caused by other medical conditions, so it is essential to consult a healthcare professional for proper diagnosis and treatment. A healthcare professional may perform blood tests and other diagnostic procedures to determine the underlying cause of the symptoms and develop an appropriate treatment plan. Treatment for hypergammaglobulinemia typically involves addressing the underlying cause of the condition, such as infections, allergies, or autoimmune disorders, and may include medications to reduce inflammation and suppress the immune system.

1. Hypothyroidism: This is a condition where the thyroid gland does not produce enough thyroid hormones. Symptoms can include fatigue, weight gain, dry skin, constipation, and depression.
2. Hyperthyroidism: This is a condition where the thyroid gland produces too much thyroid hormone. Symptoms can include weight loss, anxiety, tremors, and an irregular heartbeat.
3. Thyroid nodules: These are abnormal growths on the thyroid gland that can be benign or cancerous.
4. Thyroid cancer: This is a type of cancer that affects the thyroid gland. There are several types of thyroid cancer, including papillary, follicular, and medullary thyroid cancer.
5. Goiter: This is an enlargement of the thyroid gland that can be caused by a variety of factors, including hypothyroidism, hyperthyroidism, and thyroid nodules.
6. Thyrotoxicosis: This is a condition where the thyroid gland produces too much thyroid hormone, leading to symptoms such as weight loss, anxiety, tremors, and an irregular heartbeat.
7. Thyroiditis: This is an inflammation of the thyroid gland that can cause symptoms such as pain, swelling, and difficulty swallowing.
8. Congenital hypothyroidism: This is a condition where a baby is born without a functioning thyroid gland or with a gland that does not produce enough thyroid hormones.
9. Thyroid cancer in children: This is a type of cancer that affects children and teenagers, usually in the form of papillary or follicular thyroid cancer.
10. Thyroid storm: This is a life-threatening condition where the thyroid gland produces an excessive amount of thyroid hormones, leading to symptoms such as fever, rapid heartbeat, and cardiac arrest.

These are just a few examples of the many conditions that can affect the thyroid gland. It's important to be aware of these conditions and seek medical attention if you experience any symptoms or concerns related to your thyroid health.

The main symptoms of PTI include:

* Purple spots or bruises (purpura) on the skin, which may be caused by minor trauma or injury.
* Thrombocytopenia (low platelet count), typically less than 50,000 platelets/mm3.
* Mild anemia and reticulocytosis (increased immature red blood cells).
* Elevated levels of autoantibodies against platelet membrane glycoproteins (GP) and other platelet proteins.
* No evidence of other causes of thrombocytopenia, such as bone marrow disorders or infections.

The exact cause of PTI is unknown, but it is believed to involve an immune-mediated response triggered by a genetic predisposition. Treatment options for PTI include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy in severe cases. The prognosis for PTI is generally good, with most patients experiencing resolution of symptoms and normalization of platelet counts within a few months to a year after treatment. However, some individuals may experience recurrent episodes of thrombocytopenia and purpura throughout their lives.

Examples of OIs include:

1. Pneumocystis pneumonia (PCP): A type of pneumonia caused by the fungus Pneumocystis jirovecii, which is commonly found in the lungs of individuals with HIV/AIDS.
2. Cryptococcosis: A fungal infection caused by Cryptococcus neoformans, which can affect various parts of the body, including the lungs, central nervous system, and skin.
3. Aspergillosis: A fungal infection caused by Aspergillus fungi, which can affect various parts of the body, including the lungs, sinuses, and brain.
4. Histoplasmosis: A fungal infection caused by Histoplasma capsulatum, which is commonly found in the soil and can cause respiratory and digestive problems.
5. Candidiasis: A fungal infection caused by Candida albicans, which can affect various parts of the body, including the skin, mouth, throat, and vagina.
6. Toxoplasmosis: A parasitic infection caused by Toxoplasma gondii, which can affect various parts of the body, including the brain, eyes, and lymph nodes.
7. Tuberculosis (TB): A bacterial infection caused by Mycobacterium tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
8. Kaposi's sarcoma-associated herpesvirus (KSHV): A viral infection that can cause various types of cancer, including Kaposi's sarcoma, which is more common in individuals with compromised immunity.

The diagnosis and treatment of OIs depend on the specific type of infection and its severity. Treatment may involve antibiotics, antifungals, or other medications, as well as supportive care to manage symptoms and prevent complications. It is important for individuals with HIV/AIDS to receive prompt and appropriate treatment for OIs to help prevent the progression of their disease and improve their quality of life.

The symptoms of hepatitis B can range from mild to severe and may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, joint pain, and jaundice (yellowing of the skin and eyes). In some cases, hepatitis B can be asymptomatic, meaning that individuals may not experience any symptoms at all.

Hepatitis B is diagnosed through blood tests that detect the presence of HBV antigens or antibodies in the body. Treatment for acute hepatitis B typically involves rest, hydration, and medication to manage symptoms, while chronic hepatitis B may require ongoing therapy with antiviral drugs to suppress the virus and prevent liver damage.

Preventive measures for hepatitis B include vaccination, which is recommended for individuals at high risk of infection, such as healthcare workers, sexually active individuals, and those traveling to areas where HBV is common. In addition, safe sex practices, avoiding sharing of needles or other bodily fluids, and proper sterilization of medical equipment can help reduce the risk of transmission.

Overall, hepatitis B is a serious infection that can have long-term consequences for liver health, and it is important to take preventive measures and seek medical attention if symptoms persist or worsen over time.

Some common examples of bacterial infections include:

1. Urinary tract infections (UTIs)
2. Respiratory infections such as pneumonia and bronchitis
3. Skin infections such as cellulitis and abscesses
4. Bone and joint infections such as osteomyelitis
5. Infected wounds or burns
6. Sexually transmitted infections (STIs) such as chlamydia and gonorrhea
7. Food poisoning caused by bacteria such as salmonella and E. coli.

In severe cases, bacterial infections can lead to life-threatening complications such as sepsis or blood poisoning. It is important to seek medical attention if symptoms persist or worsen over time. Proper diagnosis and treatment can help prevent these complications and ensure a full recovery.

The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.

There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.

Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.

There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.

Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

The exact cause of SPS is not known, but it is believed to be an autoimmune disorder that results in the immune system attacking healthy brain cells, leading to inflammation and damage to the nervous system. Treatment options are limited, and current therapies focus on managing symptoms and improving quality of life.

The definition of Stiff-Person Syndrome (SPS) in the medical field includes:

1. A rare and progressive neurological disorder characterized by muscle stiffness, rigidity, and spasms.
2. Associated with heightened sensitivity to external stimuli such as noise, touch, or emotional stress.
3. Cognitive impairment, anxiety, and depression are common features.
4. Believed to be an autoimmune disorder, causing inflammation and damage to the nervous system.
5. Limited treatment options, with a focus on managing symptoms and improving quality of life.

* Infertility or low fertility
* Irregular menstrual cycles in women
* Low libido (sex drive) in both men and women
* Erectile dysfunction in men
* Hot flashes, mood changes, and vaginal dryness in women

Hypogonadism can be caused by a variety of factors, including:

* Hormonal imbalances
* Pituitary gland problems
* Brain tumors or other lesions
* Chronic illnesses such as hypopituitarism, hyperthyroidism, and liver or kidney disease
* Injury to the testicles or ovaries
* Certain medications
* Chromosomal abnormalities

Treatment for hypogonadism usually involves hormone replacement therapy (HRT) to replace the deficient sex hormones. However, the specific treatment plan will depend on the underlying cause of the condition and may involve a combination of medications, lifestyle changes, and other interventions.

It is important to note that hypogonadism can have significant psychological and social impacts, particularly in men who experience decreased libido and erectile dysfunction. It is essential for healthcare providers to address these issues sensitively and provide adequate support and resources to patients.

In summary, hypogonadism is a condition characterized by low levels of sex hormones, which can lead to a range of symptoms and health complications. Early diagnosis and appropriate treatment are important for improving quality of life and addressing any related psychological and social issues.

Treatment for oligomenorrhea depends on the underlying cause, but may include hormone replacement therapy, birth control pills, or other medications to regulate menstrual cycles. In some cases, surgery may be necessary to correct anatomical abnormalities or remove cysts that are interfering with normal menstruation.

Oligomenorrhea can have significant impacts on women's lives, including difficulty becoming pregnant due to irregular ovulation and increased risk of developing endometrial cancer. Therefore, early diagnosis and treatment are important to manage the condition and prevent potential complications.

Hematologic neoplasms refer to abnormal growths or tumors that affect the blood, bone marrow, or lymphatic system. These types of cancer can originate from various cell types, including red blood cells, white blood cells, platelets, and lymphoid cells.

There are several subtypes of hematologic neoplasms, including:

1. Leukemias: Cancers of the blood-forming cells in the bone marrow, which can lead to an overproduction of immature or abnormal white blood cells, red blood cells, or platelets. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
2. Lymphomas: Cancers of the immune system, which can affect the lymph nodes, spleen, liver, or other organs. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
3. Multiple myeloma: A cancer of the plasma cells in the bone marrow that can lead to an overproduction of abnormal plasma cells.
4. Myeloproliferative neoplasms: Cancers that affect the blood-forming cells in the bone marrow, leading to an overproduction of red blood cells, white blood cells, or platelets. Examples include polycythemia vera and essential thrombocythemia.
5. Myelodysplastic syndromes: Cancers that affect the blood-forming cells in the bone marrow, leading to an underproduction of normal blood cells.

The diagnosis of hematologic neoplasms typically involves a combination of physical examination, medical history, laboratory tests (such as complete blood counts and bone marrow biopsies), and imaging studies (such as CT scans or PET scans). Treatment options for hematologic neoplasms depend on the specific type of cancer, the severity of the disease, and the overall health of the patient. These may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy with drugs that specifically target cancer cells.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.


Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

Examples of Immunologic Deficiency Syndromes include:

1. Primary Immunodeficiency Diseases (PIDDs): These are a group of genetic disorders that affect the immune system's ability to function properly. Examples include X-linked agammaglobulinemia, common variable immunodeficiency, and severe combined immunodeficiency.
2. Acquired Immunodeficiency Syndrome (AIDS): This is a condition that results from the human immunodeficiency virus (HIV) infection, which destroys CD4 cells, a type of immune cell that fights off infections.
3. Immune Thrombocytopenic Purpura (ITP): This is an autoimmune disorder that causes the immune system to attack and destroy platelets, which are blood cells that help the blood to clot.
4. Autoimmune Disorders: These are conditions in which the immune system mistakenly attacks and damages healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, and multiple sclerosis.
5. Immunosuppressive Therapy-induced Immunodeficiency: This is a condition that occurs as a side effect of medications used to prevent rejection in organ transplant patients. These medications can suppress the immune system, increasing the risk of infections.

Symptoms of Immunologic Deficiency Syndromes can vary depending on the specific disorder and the severity of the immune system dysfunction. Common symptoms include recurrent infections, fatigue, fever, and swollen lymph nodes. Treatment options for these syndromes range from medications to suppress the immune system to surgery or bone marrow transplantation.

In summary, Immunologic Deficiency Syndromes are a group of disorders that result from dysfunction of the immune system, leading to recurrent infections and other symptoms. There are many different types of these syndromes, each with its own set of symptoms and treatment options.

There are two main types of diabetic coma:

1. DKA: This type of coma is more common in people with type 1 diabetes, but it can also occur in people with type 2 diabetes. It is caused by a lack of insulin in the body, which leads to high levels of glucose and ketones in the blood.
2. Hypoglycemic coma: This type of coma is caused by low blood sugar levels, which can occur when people with diabetes take too much insulin or not enough food.

The symptoms of diabetic coma can vary depending on the type, but they may include:

* Confusion and disorientation
* Slurred speech
* Seizures or convulsions
* Difficulty breathing
* High blood sugar levels (DKA) or low blood sugar levels (hypoglycemic coma)

If left untreated, diabetic coma can be fatal. Treatment typically involves addressing the underlying cause of the coma and providing supportive care, such as intravenous fluids and oxygen. In severe cases, hospitalization may be necessary to monitor and treat the condition.

Preventing diabetic coma requires careful management of diabetes, including monitoring blood sugar levels regularly, taking medication as prescribed, and making any necessary lifestyle changes. It is also important to seek medical attention immediately if symptoms of diabetic coma are present.

Examples of beta globulins include: beta-2 microglobulin plasminogen angiostatins properdin sex hormone-binding globulin ... Beta globulins are a group of globular proteins in plasma that are more mobile in alkaline or electrically charged solutions ... "Examples of Protein Electrophoretograms" at Beta-globulins at the US National Library of Medicine Medical Subject ... than gamma globulins, but less mobile than alpha globulins. ...
"Beta- and gamma-globulin tetanus antitoxin of the hyperimmune horse". Nature. 166 (4227): 785. Bibcode:1950Natur.166..785C. doi ...
Heyns W (1977). "The steroid-binding beta-globulin of human plasma". Adv Steroid Biochem Pharmacol. 6: 59-79. PMID 339697. ... However, luteinizing hormone (LH) levels are elevated while sex hormone-binding globulin (SHBG) levels are more consistent with ...
... and in Alpha 1 globulins, Alpha 2 globulins, Beta globulins, and Gamma globulins) are long peptide chains, precursors for ... "A haemoglobin-binding beta-globulin in human serum". Nature. 186 (4730): 1055-6. Bibcode:1960Natur.186.1055T. doi:10.1038/ ... Edestin is similar to serum globulin (blood plasma), and the biologically active protein of edestin is metabolized in the human ... the sequences are distinguished by globulin characteristic. There is a type 1 and type 2 of edestin that are both used in ...
Putnam, F. W. (1993). "Alpha-, beta-, gamma-globulin-Arne Tiselius and the advent of electrophoresis". Perspectives in Biology ...
"Serum levels of pregnancy-associated endometrial alpha 2-globulin (alpha 2-PEG), a glycosylated beta-lactoglobulin homologue, ... "Multiple forms of mRNA encoding human pregnancy-associated endometrial alpha 2-globulin, a beta-lactoglobulin homologue". ... bovine and buffalo beta-lactoglobulin. For example, there are 13 identities out of 22 possible matches with horse beta- ... Bell SC, Keyte JW, Waites GT (Nov 1987). "Pregnancy-associated endometrial alpha 2-globulin, the major secretory protein of the ...
... such as bovine growth hormone or rabbit beta-globulin polyadenylation sequences. Polycistronic vectors (with multiple genes of ... An E. coli inner core and poly(beta-amino ester) outer coat function synergistically to increase efficiency by addressing ...
Other globular proteins are the alpha, beta and gamma (IgA, IgD, IgE, IgG and IgM) globulin. See protein electrophoresis for ... more information on the different globulins. Nearly all enzymes with major metabolic functions are globular in shape, as well ...
... it is stored as hemosiderin or ferritin in tissues and transported in plasma by beta globulins as transferrins. When the ... The hemoglobin subunit beta is coded by HBB gene which is on chromosome 11 . The amino acid sequences of the globin proteins in ... Globulin is metabolised into amino acids that are then released into circulation. Hemoglobin deficiency can be caused either by ... However, the level of Hb F can be elevated in persons with sickle-cell disease and beta-thalassemia. Variant forms that cause ...
... alpha-1 globulins, alpha-2 globulins, beta 1 and 2 globulins, and gamma globulins. Proteins are separated by both electrical ... Transferrin and beta-lipoprotein (LDL) comprises the beta-1. Increased beta-1 protein due to the increased level of free ... Increased beta-1 protein due to LDL elevation occurs in hypercholesterolemia. Decreased beta-1 protein occurs in acute or ... IgA has the most anodal mobility and typically migrates in the region between the beta and gamma zones also causing a beta/ ...
Alpha-1-acid glycoprotein Alpha-1-fetoprotein alpha2-macroglobulin Gamma globulins Beta-2 microglobulin Haptoglobin ... Globulins make up 38% of blood proteins and transport ions, hormones, and lipids assisting in immune function. Fibrinogen ... All blood proteins are synthesized in liver except for the gamma globulins. Examples of specific blood proteins: Prealbumin ( ...
Beta-1-metal- binding globulin) RAB11A Ras-related protein Rab-11A GRCh38: Ensembl release 89: ENSG00000198774 - Ensembl, May ...
An example of beta globulin found in blood plasma includes low-density lipoproteins (LDL) which are responsible for ... There are three main types of globulins. Alpha-1 and Alpha-2 globulins are formed in the liver and play an important role in ... The second most common type of protein in the blood plasma are globulins. Important globulins include immunoglobins which are ... Gamma globulin, better known as immunoglobulins, are produced by plasma B cells, and provides the human body with a defense ...
Use of high flux dialyzers Use of Beta 2 globulin absorber Preserve the residual kidney functions Early kidney transplant In ... September 1993). "beta 2-Microglobulin modified with advanced glycation end products is a major component of hemodialysis- ...
... follicle-stimulating hormone and sex-hormone-binding globulin during simultaneous vaginal administration of 17 beta-oestradiol ... Odlind V, Milsom I, Persson I, Victor A (June 2002). "Can changes in sex hormone binding globulin predict the risk of venous ... Lobo RA, Cassidenti DL (January 1992). "Pharmacokinetics of oral 17 beta-estradiol". J Reprod Med. 37 (1): 77-84. PMID 1548642 ... Estradiol increases the production and by extension circulating levels of sex hormone-binding globulin (SHBG), corticosteroid- ...
Beta-thalassemia (β-thalassemia) is an inherited mutation of the β-globulin gene which causes the reduced synthesis of the β- ... Hb S beta thalassemia is the least common and is experienced in patients who have inherited beta thalassemia hemoglobin from ... Fetuses have a non-alpha chain called gamma and after birth it is then called beta. The beta chain will pair with the alpha ... Hemoglobin A is the most common adult form of hemoglobin and exists as a tetramer containing two alpha subunits and two beta ...
All globulins fall into one of the following three categories : Alpha globulins Beta globulins Gamma globulins (one group of ... Globulins exist in various sizes. The lightest globulins are the alpha globulins, which typically have molecular weights of ... Some globulins are produced in the liver, while others are made by the immune system. Globulins, albumins, and fibrinogen are ... Globulins exert oncotic pressure. Their deficiency results in loss of carrier functions of globulins, oedema due to decreased ...
... alpha-beta T-cell antigen receptor - alpha-fetoprotein - alpha-globulin - alpha-macroglobulin - alpha-MSH - Ames test - amide ... beta-2 microglobulin - beta adrenergic receptor - beta sheet - beta-1 adrenergic receptor - beta-2 adrenergic receptor - beta- ... transforming growth factor beta - transforming growth factor beta receptor - transient receptor potential - translation ( ... interferon-beta - interleukin receptor - interleukin-1 receptor - interleukin-2 receptor - interleukin-3 - interleukin-3 ...
Disorders of globin and globulin proteins). ... Sickle cell-beta thalassemia is an inherited blood disorder. ... Sickle cell-beta thalassemia is caused by inheritance of a sickle cell allele from one parent and a beta thalassemia allele ... A sickle allele is always the same mutation of the beta-globin gene (glutamic acid to valine at amino acid six). In contrast, ... "Newborn Screening Program - Sickle Cell Beta Thalassemia Disease". Retrieved 2015-06-18. Ashley-Koch, A; ...
There are several clusters, the first being albumin, the second being the alpha, the third beta and the fourth gamma ( ... Alpha-1 antitrypsin is the main protein of the alpha-globulin 1 region. Another name used is alpha-1 proteinase inhibitor (α1- ... Like all serine protease inhibitors, A1AT has a characteristic secondary structure of beta sheets and alpha helices. Mutations ... immunoglobulins). The non-albumin proteins are referred to as globulins. The alpha region can be further divided into two sub- ...
Disorders of globin and globulin proteins, Hereditary hemolytic anemias). ... Delta-beta thalassemia can mask the diagnosis of beta thalassemia trait. In beta thalassemia, an increase in hemoglobin A2 ... Delta-beta thalassemia is considered rare. Delta-beta-thalassemia is caused by deletions of the entire delta and beta genes ... Alpha thalassemia Beta-thalassemia Hemoglobinopathy "Delta-beta-thalassemia". Orphanet. Orphanet. Retrieved 16 September 2016 ...
Disorders of globin and globulin proteins, Hereditary hemolytic anemias, Rare diseases). ... Beta thalassemia minor can also present as beta thalassemia silent carriers; those who inherit a beta thalassemic mutation but ... Beta thalassemia trait (also known as beta thalassemia minor) involves heterozygous inheritance of a beta-thalassemia mutation ... Beta thalassemias occur due to malfunctions in the hemoglobin subunit beta or HBB. The severity of the disease depends on the ...
11S globulin fraction) and vicilins (7S globulin), or in the case of soybeans, glycinin and beta-conglycinin. Grains contain a ... Legume proteins, such as soy and pulses, belong to the globulin family of seed storage proteins called legumin and vicilins, or ... Legume proteins, such as soy and pulses, belong to the globulin family of seed storage proteins called legumin ( ... "The role of proteolysis in the processing and assembly of 11S seed globulins". The Plant Cell. 10 (3): 343-57. doi:10.1105/tpc. ...
... is a globulin of relatively small molecular weight. It can be contrasted to macroglobulin., Examples include: ... Beta-2 microglobulin Alpha-1-microglobulin "Definition: microglobulin from Online Medical Dictionary". v t e (Articles needing ...
... beta-crystallin a chain MeSH D12.776.306.366.300.200 - beta-crystallin b chain MeSH D12.776.331.199.750.500 - succinate ... sex hormone-binding globulin MeSH D12.776.377.715.182.839 - transferrin MeSH D12.776.377.715.548.114 - antibodies MeSH D12.776. ... beta-2 microglobulin MeSH D12.776.377.715.182.160 - beta-thromboglobulin MeSH D12.776.377.715.182.200 - complement factor h ... thyroid hormone receptors beta MeSH D12.776.624.664.700.915 - RNA-binding protein FUS MeSH D12.776.624.664.700.957 - stathmin ...
... beta-2 microglobulin MeSH D12.776.124.790.223.160 - beta-thromboglobulin MeSH D12.776.124.790.223.200 - complement factor h ... gamma-globulins MeSH D12.776.124.486.485.397.500 - tuftsin MeSH D12.776.124.486.485.538 - immunoglobulin constant regions MeSH ... sex hormone-binding globulin MeSH D12.776.124.790.223.839 - transferrin MeSH D12.776.124.790.651.114.071 - antibodies, anti- ... immune globulin MeSH D12.776.124.486.485.114.619.574 - immunoglobulin m MeSH D12.776.124.486.485.114.619.574.500 - ...
Retinyl esters (present in meats) and beta-carotene (present in plants) are the two main sources of retinoids in the diet. ... human pregnancy-associated endometrial alpha-2 globulin (PAEP); probasin (PB), a prostatic protein; prostaglandin D synthase; ... Lipocalins have an eight-stranded, antiparallel, symmetrical β-barrel fold, which is, in essence, a beta sheet which has been ... This is an eight stranded antiparallel beta barrel with a repeated + 1 topology enclosing an internal ligand binding site. ...
TGF-beta, a transforming growth factor beta (its direct production by SCs is controversial), contributes to the induction of ... also called testosterone-binding globulin) increases testosterone concentration in the seminiferous tubules to lightly ... stimulate spermatogenesis estradiol, an aromatase which converts testosterone to 1,7-beta-estradiol to direct spermatogenesis ...
Galactosidase, beta 1, also known as GLB1, is a protein which in humans is encoded by the GLB1 gene. The GLB1 protein is a beta ... In corn (Zea mays), Glb1 is a gene coding for the storage protein globulin. GM1-gangliosidosis is a lysosomal storage disease ... Shows TB, Scrafford-Wolff L, Brown JA, Meisler M (1978). "Assignment of a beta-galactosidase gene (beta GALA) to chromosome 3 ... Shows TB, Scrafford-Wolff L, Brown JA, Meisler M (1979). "Assignment of a beta-galactosidase gene (beta GALA) to chromosome 3 ...
The beta (β) band - transferrin, LDL, complement The gamma (γ) band - immunoglobulin (IgA, IgD, IgE, IgG and IgM). Paraproteins ... serum albumin and globulin. They are generally equal in proportion, but albumin as a molecule is much smaller and lightly, ... The globulins are classified by their banding pattern (with their main representatives):[citation needed] The alpha (α) band ...
Estrogen can cause an increase of cortisol-binding globulin and thereby cause the total cortisol level to be elevated. However ... oral tablets a 11-beta-hydroxylase enzyme inhibitor was approved by FDA for treating those patients who cannot undergo ...
Massive overdose can be associated with increased sympathetic activity, thus may require treatment with beta-blockers. The ... Greater than 99% of circulating thyroid hormones are bound to plasma proteins including thyroxine-binding globulin, ...
Beta-2 microglobulin and C-reactive protein test results are not specific for Waldenström macroglobulinemia. Beta-2 ... and an albumin-to-globulin ratio. The ESR and uric acid level may be elevated. Creatinine is occasionally elevated and ... An M component with beta-to-gamma mobility is highly suggestive of Waldenström macroglobulinemia. Immunoelectrophoresis and ... cytochrome c release NF-κB WNT/beta-catenin mTOR ERK MAPK Bcl-2 The protein Src tyrosine kinase is overexpressed in Waldenström ...
WB Hardy linked formation of biological colloids with phase separation in his study of globulins, stating that: "The globulin ... Schaefer KN, Peifer M (February 2019). "Wnt/Beta-Catenin Signaling Regulation and a Role for Biomolecular Condensates". ... The globulins". The Journal of Physiology. 33 (4-5): 251-337. doi:10.1113/jphysiol.1905.sp001126. PMC 1465795. PMID 16992817. ... including cross-beta polymerisation), and/or protein domains that induce head-to-tail oligomeric or polymeric clustering, might ...
Karelitz and Stempien discovered that extracts from human serum globulin and placental globulin can be used as lightening ... If the person is allergic to the family of antibiotics which both penicillin and amoxicillin are a part of (beta-lactam ... but retaining drug-sensitivity to beta-lactam antibiotics such as penicillin, emerged in Hong Kong in 2011, accounting for at ...
... and 3 beta-androstanediols". Biol. Reprod. 51 (3): 562-71. doi:10.1095/biolreprod51.3.562. PMID 7803627. Foradori CD, Weiser MJ ... and the typical doses of ethinylestradiol present in combined birth control pills increase sex hormone-binding globulin (SHBG) ...
... has a moderate affinity for estrogen receptors alpha (ERα) and beta (ERβ), with Ki values of 4.9 nM and 19 nM, ... Hammond GL, Hogeveen KN, Visser M, Coelingh Bennink HJ (2008). "Estetrol does not bind sex hormone binding globulin or increase ... minimal impact on sex hormone-binding globulin (SHBG) synthesis and limited impact on lipid parameters, including triglycerides ...
It has negligible affinity for SHBG and no affinity for corticosteroid-binding globulin. The tissue distribution of ... and 3 beta-androstanediols". Biology of Reproduction. 51 (3): 562-71. doi:10.1095/biolreprod51.3.562. PMID 7803627. Sánchez ... and concentrations of sex hormone-binding globulin (SHBG) and prolactin increase as well (by 8-42% and 40-65%, respectively) ...
... is bound approximately 16% to sex hormone-binding globulin (SHBG) and 80% to albumin in the circulation, with the ... "Evaluation of ligand selectivity using reporter cell lines stably expressing estrogen receptor alpha or beta". Biochemical ... gonadotrophins and SHBG during oral and cutaneous administration of oestradiol-17 beta to menopausal women". Acta ... "Biological effects of estradiol-17 beta in postmenopausal women: oral versus percutaneous administration". J. Clin. Endocrinol ...
Schubert W, Cullberg G (1988). "Fat-soluble 17 beta-estradiol: a way of reducing dosage in steroid hormonal substitution?". ... estradiol orally and has a comparatively reduced impact on liver parameters such as changes in sex hormone-binding globulin ... Schubert W, Cullberg G (1987). "Ovulation inhibition with 17 beta-estradiol cyclo-octyl acetate and desogestrel". Acta Obstet ...
"Effects of seven low-dose combined oral contraceptives on sex hormone binding globulin, corticosteroid binding globulin, total ... Spona J, Lunglmayr G (July 1980). "Prolaktin-Serumspiegel unter Behandlung des Prostatakarzinoms mit Östradiol-17 beta- ... Serum Prolactin Levels During Therapy of Prostatic Cancer with Estradiol-17 beta-undecylate and Cyproterone Acetate]. Wien. ...
Hispanic gamma-delta-beta; 604131; LCRB Thalassemia-beta, dominant inclusion-body; 603902; HBB Thalassemias, alpha-; 604131; ... CNTNAP2 Corticosteroid-binding globulin deficiency; 611489; CBG Cortisone reductase deficiency; 604931; H6PD Cortisone ... NLRP3 Mucolipidosis II alpha/beta; 252500; GNPTAB Mucolipidosis III alpha/beta; 252600; GNPTAB Mucolipidosis III gamma; 252605 ... Isolated 17,20-lyase deficiency; 202110; CYP17A1 17-alpha-hydroxylase/17,20-lyase deficiency; 202110; CYP17A1 17-beta- ...
... and show no affinity itself for sex hormone-binding globulin or corticosteroid-binding globulin. The plasma protein binding of ... "Comparison of the ligand binding specificity and transcript tissue distribution of estrogen receptors alpha and beta". ...
The protein is composed of alpha helices and beta sheets that form two domains. The N- and C- terminal sequences are ... In nephrotic syndrome, urinary loss of transferrin, along with other serum proteins such as thyroxine-binding globulin, ... Beta-2 transferrin Transferrin receptor Total iron-binding capacity Transferrin saturation Ferritin Phytotransferrin ...
For example, beta-lysine, an amino acid produced by platelets during coagulation, can cause lysis of many Gram-positive ... it was identified in the 1950s and is alternatively called antihemophilic globulin due to its capability to correct hemophilia ...
Alpha and beta proteins (α/β) are considered the oldest class of proteins. Mass spectrometry is one analytical method used to ... Additionally, the identification of egg proteins, caseins, whey globulins, and other proteinaceous materials used as binders in ...
... and anti-thymocyte globulin (ATG) plus GCSF. Atkinson is currently leading an NIH funded clinical research trial aiming to ... stem cells and beta cell regeneration, pancreatic pathology, clinical trials seeking to prevent or reverse type 1 diabetes, the ... human pancreatic weight and beta cell development, as well as improving methods of data management. Atkinson is the Executive ...
Hepatic metabolism is mediated by 11 beta-hydroxysteroid dehydrogenases (11[beta]-HSD) and 20-ketosteroid reductases. ... corticosteroid binding globulin, CBG) but does have moderate protein binding to albumin. Thus, pharmacokinetics of ... beta]-hydroxy-20[alpha]-hydroxymethylprednisolone. As stated previously, the primary use of methylprednisolone is to suppress ...
An example is polydipsia found in patients with autoimmune chronic hepatitis with severely elevated globulin levels. Evidence ... a sympatholytic beta blocker Vasopressin receptor antagonists, such as conivaptan Acetazolamide, a carbonic anhydrase inhibitor ...
... s bind with the aid of Ca2+ to the α-neurexin LNS (laminin, neurexin and sex hormone-binding globulin-like folding ... it was determined that neuroligin-1 forms a protein dimer when two neurexin-1 beta monomers bind to the neuroligin-1's two ... "Structures of neuroligin-1 and the neuroligin-1/neurexin-1 beta complex reveal specific protein-protein and protein-Ca2+ ... "Structural analysis of the synaptic protein neuroligin and its beta-neurexin complex: determinants for folding and cell ...
... and a downstream beta (β), resulting in alpha-neurexins 1-3 (α-neurexins 1-3) and beta-neurexins 1-3 (β-neurexins 1-3). In ... sex-hormone binding globulin) - EGF (epidermal growth factor) - LNS domains. N1α binds to a variety of ligands including ...
July 2008). "CXCR4 dimerization and beta-arrestin-mediated signaling account for the enhanced chemotaxis to CXCL12 in WHIM ... Infusions of immune globulin can reduce the frequency of bacterial infections, and G-CSF or GM-CSF therapy improves blood ... this trial showed no increase of immune globulins in the body. A phase III clinical trial has been approved to compare the ...
This has been demonstrated in β-globulin. β-globulin mRNAs containing a nonsense mutation early in the first exon of the gene ... end formation in the definition of nonsense-mediated decay-competent human beta-globin mRNPs". The EMBO Journal. 20 (3): 532-40 ... It has been observed that this protective effect is not limited only to the β-globulin promoter. This suggests that this NMD ...
From these two subunits, isoenzymes such as Hex A (one alpha and one beta subunit), Hex B (two beta subunits) and Hex S (two ... "Combined N-Glycome and N-Glycoproteome Analysis of the Lotus japonicus Seed Globulin Fraction Shows Conservation of Protein ... Human Hex isoenzymes are assembled with alpha and beta subunits encoded by the HEXA and HEXB genes, respectively. ... "Structural studies of the endoglycosidase H-resistant oligosaccharides present on human beta-glucuronidase". Journal of ...
beta-1-H-globulin. *beta-1H. *C3b inactivator accelerator. *CFAH_HUMAN. *CFHL3 ...
Buprenorphine is approximately 96% protein bound, primarily to alpha and beta globulin. ...
Temperature and serum factors, such as beta globulins and ferritin, appear to have a growth-inhibitory effect on dermatophytes ...
A sample will be considered uninterpretable if the specimen was found to be both Trichomonas and Beta globulin negative by PCR ... Samples were tested for the presence of amplifiable DNA and absence of inhibitors by performing beta globin PCR. Beta globin is ... If the presence of beta globin couldnt be demonstrated, the validity of the sample wasnt determined. ...
... anti-kappa chains and beta-1CA, E globulin reagents.  ...
Beta-globulins decreased. The supplement had a positive effect on milk output, which increased by 67.1-137.3 kg (1.93-3.95%; p≤ ... The alpha- and gammα-globulins levels increased to 0.2-0.5 g/L in winter and 0.3-0.6 g/L in summer, and 0.5-1.4 g/L in winter ...
Sex Hormone-Binding Globulin - Preferred Concept UI. M0019743. Scope note. A glycoprotein migrating as a beta-globulin. Its ... Sex Hormone-Binding Globulin Entry term(s). Binding Globulin, Testosterone-Estradiol Globulin, Sex Hormone-Binding Globulin, ... Globulin, Sex Hormone-Binding. Globulin, Testosterone-Estradiol Binding. Hormone-Binding Globulin, Sex. Sex Hormone Binding ... TESTOSTERONE-BINDING GLOBULIN were see SEX HORMONE-BINDING GLOBULIN 1977-92. Online Note:. use SEX HORMONE-BINDING GLOBULIN (NM ...
Beta-globulin. -Gamma-globulin One or more quantifiable monoclonal proteins may be present and reported as M spike.. ...
Globulins- A group of serum proteins made in the liver. They are classified as alpha, beta, or gamma depending on their ... Gamma globulin- A class of serum globulins produced by lymphocytes and plasma cells of the immune system. They exhibit gamma ... Designated as alpha 1 and 2, and beta 1 and 2, globins permit hemoglobin to transport oxygen. ...
Beta 2 Glycoprotein IgM Rs.1670 Beta 2 Micro Globulin Rs.4350 ...
Alpha-2 globulin; Beta globulin; Gamma globulin; The primary use of this test is in the evaluation of … Key Concepts: Terms in ... Serum placed in a visible fibrinogen band between the beta and gamma globulins and other in... Markedly raised ( 10-fold ... Typically seen as a sharp band between the beta and gamma globulins, also as! In interpretation is to establish if the region ... resulting in a visible fibrinogen band between the beta and gamma globulins. The test may also be performed again in the future ...
... beta-Defensins D12.644.276.87.54 D12.776.467.87.188 D23.529.87.233 beta-Endorphin D12.644.468.241.80 beta-Lactam Resistance ... Thyroxine-Binding Globulin D12.644.861.762 D12.644.861.847 D12.776.872.762 D12.776.872.847 Tic Disorders F3.550.825 F3.625.992 ... Lymphotoxin-beta D12.644.276.972.515 D12.776.467.972.515 D23.529.972.515 Lyssavirus B4.909.777.455.750.500 M Phase Cell Cycle ... Retinoid X Receptor beta D12.776.260.698.701.500.625 D12.776.930.669.701.500.625 Retinoid X Receptor gamma D12.776.260.698. ...
They can be further subdivided into alpha, beta, and gamma globulins. The liver synthesizes alpha and. beta globulins, which ... The globulins transport lipids and fat-soluble vitamins. Lymphatic tissues produce the gamma globulins, which are a type of ... The three main types of blood plasma proteins-albumins, globulins, and fibrinogen-differ in composition and function. ... Globulins make up about 36% of the plasma proteins. ...
It does not have 17-beta estradiol. We really do not have good studies at this point of time that tell us what transdermal ... will not increase sex hormone-binding globulin levels, whereas the combined oral contraceptive pill will quite dramatically. ... Transdermal estrogen, which is actually transdermal 17-beta estradiol and what we use in hormone replacement therapy in this ... I would say that the efficacy would probably lie between a combined oral contraceptive pill and the transdermal 17-beta ...
Siderophilin) an iron transporting beta-globulin which facilitates transportation to bone marrow & tissue storage regions. It ...
Adams MR, Golden DL, Franke AA, Potter SM, Smith HS, Anthony MS: Dietary soy beta conglycinin 7S globulin inhibits ...
H beta 2M) prepared in chicken, rabbit and rat, and an insolubilized monoclonal mouse anti-H beta 2M antibody-bound monkey ... whereas rabbit and monoclonal anti-H beta 2M failed to do so. Although these findings were not compatible with an intact beta ... However, guinea pig antibody to human beta 2M was inactive. In parallel studies, the pattern of absorption of mouse helper ... This may suggest that factor genes have evolved from the same ancestral genes as beta 2M. ...
Globulin 2.3 [1.5-4.5]-- is made up of different proteins called alpha, beta, and gamma types. Some globulins are made by the ... Other globulins transport metals, such as iron, in the blood and help fight infection. Serum globulin can be separated into ... It also measures the amounts of two major groups of proteins in the blood: albumin and globulin.. Albumin 4.5 [3.5-5.5]-- is ... A/G Ratio 2.0 [1.1-2.5]-- Simply the ratio of Albumin to Globulin. Total protein levels are often elevated in persons with ...
Studies have revealed the presence of around 100 mutations that result in more than 50 variants of alpha and beta globulin ...
... beta globulin, alpha-2 macroglobulin.The map of most APPs has non been wholly elucidated. ...
Levels of sex hormone-binding globulin and corticosteroid-binding globulin mRNAs in corpus luteum of human subjects: ... Relationships of plasminogen activator inhibitor activity and lipoprotein(a) with insulin, testosterone, 17 beta-estradiol, and ... 2) Increasing the bodys production of sex hormone-binding globulin (SHBG). SHBG binds testosterone therefore reducing the ... testicular steroids and sex hormone binding globulin in normal men. Van Look PF, Frolich M Clin Endocrinol (Oxf) 1981 Mar;14(3 ...
If she tests positive for hepatitis B, hepatitis B immune globulin (HBIG) shall be administered to the newborn in accordance ... Group Beta Strep (GBS) cultures, according to CDC guidelines. If penicillin allergic, determine antibiotics to which ... Prophylactic Rh-immune globulin information for Rh negative clients; ... pediatric care of a newborn shall also administer the appropriate doses of hepatitis B vaccine and hepatitis B immune globulin ...
... sex hormone-binding globulin (SHBG), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta-endorphin, growth ... sex hormone-binding globulin (SHBG), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta-endorphin, growth ... Restoration of the beta-endorphin response to specific stimuli suggests that DHEAS and/or its active metabolites modulates the ... Restoration of the beta-endorphin response to specific stimuli suggests that DHEAS and/or its active metabolites modulates the ...
With diuretics and beta-blockers on cardiovascular morbidity steroid hormone-carrier protein committed to a strict diet. ... The detrimental globulins should be consulted for more details use naturally occurring testosterone supplements. Should be ...
IFN-beta - Fatal pemphigus vulgaris (when used in combination with interleukin (IL)-2, localized reactions (common), and ... 26] - Antithymocyte globulin for bone marrow failure, human rabies vaccine, penicillin, pneumococcal vaccine (in AIDS patients ... Association between beta-blockers, other antihypertensive drugs and psoriasis: population-based case-control study. Br J ... Serum sickness-like - Beta-lactam antibiotics, [27] cefaclor (most common), minocycline, propranolol, streptokinase, ...
Beta-2-globulin fraction. Beta-2-Microglobulin. Beta-HCG. Bilirubin (routine urine test) ...
":"Antithymocyte globulin (equine)","data":{"category":"Medicine","linkRef":"Antithymocyte globulin (equine)"}},{"value":" ... ":"Interferon beta-1-alpha"}},{"value":"Interferon beta-1-beta","data":{"category":"Medicine","linkRef":"Interferon beta-1-beta ... ":"Beta Cream"}},{"value":"Beta Ointment","data":{"category":"Medicine","linkRef":"Beta Ointment"}},{"value":"Beta Scalp","data ... ":"Beta Adrenoceptor Blockers","data":{"category":"Medicine","linkRef":"Beta Adrenoceptor Blockers"}},{"value":"Beta Cream"," ...
Beta carotene?ATFL: Anterior Talo-Fibular Ligament?ATG: Antithymocyte globulin?ATL: Adult T cell lymphoma?ATL: Adult T cell ... Georges Respiratory Questionnaire?SH: Social history?SH: Serum hepatitis?SHBG: Steroidal hormone-binding globulin?SHEP: ... Zoster immune globulin?α-1-AT: Α-1-Antitrypsin Deficiency?α-MSH: Alpha-melanocyte-stimulating hormone?β-hCG: β Human Chorionic ... Hepatitis B immune globulin?HBO: Hyperbaric oxygen?HBsAg: Hepatitis B surface antigen?HBsAG: Hepatitis B surface antigen?HBV: ...
  • The serum globulin electrophoresis test measures the levels of proteins called globulins in the fluid part of a blood sample. (
  • Globulins are roughly divided into three groups: alpha, beta, and gamma globulins. (
  • Gamma globulins include various types of antibodies such as immunoglobulins (Ig) M, G, and A. (
  • Serum proteins with an electrophoretic mobility that falls between ALPHA-GLOBULINS and GAMMA-GLOBULINS . (
  • Studies on the fluorescent treponemal antibody test using fluorescent anti-gamma, anti-alpha, anti-mu, anti-lambda, anti-kappa chains and beta-1CA, E globulin reagents. (
  • Gamma globulin - A class of serum globulins produced by lymphocytes and plasma cells of the immune system. (
  • Tracing of albumin and globulin fractions by gel electrophoresis. (
  • in) an iron transporting beta-globulin which facilitates transportation to bone marrow & tissue storage regions. (
  • The antibodies are polyclonal and are directed at multiple T cell markers (such as CD2, CD3, CD4, CD8, CD 11) as well as HLA markers, beta-2-microglobulin and other tissue antigens (including cytoplasmic and nuclear liver antigens). (
  • Antigen-specific helper factor reacts with antibodies to human beta 2 microglobulin. (
  • Helper activity was removed from supernatants of monkey cells by affinity chromatography on Sepharose 4B insolubilized antibodies specific for human beta 2-microglobulin (H beta 2M) prepared in chicken, rabbit and rat, and an insolubilized monoclonal mouse anti-H beta 2M antibody-bound monkey helper factor activity. (
  • Fibrinogen, a beta-2 protein, is found in normal plasma but absent in normal serum. (
  • With diuretics and beta-blockers on cardiovascular morbidity steroid hormone-carrier protein committed to a strict diet. (
  • The detrimental globulins should be consulted for more details use naturally occurring testosterone supplements. (
  • This test is done to look at globulin proteins in the blood. (
  • Immune globulins produced by plasma fractionation methods approved for use in the United States have not been implicated in the transmission of infectious agents. (
  • Nevertheless, because immune globulins manufactured before 1985 were derived from plasma of human donors who were not screened for antibody to human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV), CDC and the U.S. Food and Drug Administration (FDA) have received inquiries concerning the safety of immune globulin (IG), hepatitis B immune globulin (HBIG), and intravenous immune globulin (IVIG). (
  • The IG, HBIG, IVIG, and other special immune globulins used in the United States are produced by several manufacturers using the Cohn-Oncley fractionation process (1,2). (
  • HBIG and other specific immune globulins (e.g., varicella-zoster IG) may be prepared from plasma pools from fewer donors. (
  • The question of safety arises out of concern that some immune globulins currently available were prepared from plasma pools that included units from donors who may have had HTLV-III/LAV viremia. (
  • Information regarding past therapy with immune globulins is available from 10,227 of 17,115 AIDS patients reported to CDC. (
  • Samples were tested for the presence of amplifiable DNA and absence of inhibitors by performing beta globin PCR. (
  • Beta globin is common to all mammalian cells and it is reasonable to expect that some human cells will be present in the sample. (
  • If the presence of beta globin couldn't be demonstrated, the validity of the sample wasn't determined. (
  • This may suggest that factor genes have evolved from the same ancestral genes as beta 2M. (
  • [4] [6] Studies have revealed the presence of around 100 mutations that result in more than 50 variants of alpha and beta globulin genes associated with an increased oxygen affinity as well as mutations affecting the affinity of 2,3-bisphosphoglycerate (2,3-BPG). (
  • La proteína se une a la testosterona, dihidrotestosterona y estradiol en el plasma. (
  • Antithymocyte globulin is a hyperimmune globulin preparation made from plasma of rabbits or horses that have been immunized with human thymocytes or T cells. (
  • Before and after treatments, plasma beta-endorphin levels were evaluated in response to three neuroendocrine tests: (a) clonidine, an alpha 2-presynaptic adrenergic agonist (1.25 mg i.v.) (b) naloxone, an opioid receptor antagonist (4 mg i.v.) and (c) fluoxetine, a serotonin selective reuptake inhibitor (30 mg p.o. (
  • Serum estradiol, estrone, GH and plasma beta-endorphin levels significantly increased progressively for the three months of treatment, with higher levels for estrone and estradiol in subjects receiving estradiol alone or plus DHEAS. (
  • Antithymocyte globulin (ATG) is an antibody preparation derived from rabbits or horses hyperimmunized with human thymocytes, which is used to prevent or treat acute cellular rejection after solid organ transplantation and as a therapy of acute aplastic anemia. (
  • However, guinea pig antibody to human beta 2M was inactive. (
  • Adams MR, Golden DL, Franke AA, Potter SM, Smith HS, Anthony MS: Dietary soy beta conglycinin 7S globulin inhibits atherosclerosis in mice. (
  • Restoration of the beta-endorphin response to specific stimuli suggests that DHEAS and/or its active metabolites modulates the neuroendocrine control of pituitary beta-endorphin secretion, which may support the therapeutic efficacy of the DHEAS on behavioral symptoms. (
  • The decrease of circulating levels of beta-endorphin is considered a hormonal marker of those changes. (
  • Before therapy clonidine, naloxone and fluoxetine stimuli failed to modify circulating beta-endorphin levels. (
  • After each of the treatments, the beta-endorphin response was completely restored and was similar, independent of the kind of therapy. (
  • New results from the TrialNet Clinical Research Network (TrialNet) show that low-dose anti-thymocyte globulin (ATG) slowed the decline of insulin production and resulted in better blood glucose control for two years in people newly diagnosed with type 1 diabetes compared to those treated with a placebo. (
  • Although these findings were not compatible with an intact beta 2M chain being present in helper factor, they may imply a cross-reactivity of beta 2M with a "constant region" of helper factor that may share common sequences with beta 2M. (
  • Even though these plant part extracts contained true antigens, extracts of cotton stems and cardroom cotton dust were found to contain a polyphenolic tannin that interacted with and precipitated gamma globulin and beta lipoprotein in a pseudoimmune fashion from normal as well as byssinotic human sera. (
  • The serum globulin electrophoresis test measures the levels of proteins called globulins in the fluid part of a blood sample. (
  • Urine protein electrophoresis (UPE) on a random urine sample revealed a selective glomerular proteinuria with excretion of moderate amounts of albumin and small amounts of alpha- and beta-globulins (total protein concentration, 184 mg/dL). (
  • Gamma globulins include various types of antibodies such as immunoglobulins (Ig) M, G, and A. (
  • Globulins are roughly divided into three groups: alpha, beta, and gamma globulins. (
  • The 3 alpha,17 beta-androstanediol glucuronide/sex hormone binding globulin ratio as a possible marker for female pattern baldness. (
  • Samples were tested for the presence of amplifiable DNA and absence of inhibitors by performing beta globin PCR. (
  • Beta globin is common to all mammalian cells and it is reasonable to expect that some human cells will be present in the sample. (