A subclass of ubiquitously-expressed lamins having an acidic isoelectric point. They are found to remain bound to nuclear membranes during mitosis.
A subclass of developmentally regulated lamins having a neutral isoelectric point. They are found to disassociate from nuclear membranes during mitosis.
Nuclear matrix proteins that are structural components of the NUCLEAR LAMINA. They are found in most multicellular organisms.
A type of H. influenzae isolated most frequently from biotype I. Prior to vaccine availability, it was a leading cause of childhood meningitis.
A lattice of fibrils which covers the entire inner surface of the nuclear envelope and interlinks nuclear pores (NUCLEAR PORE).
The membrane system of the CELL NUCLEUS that surrounds the nucleoplasm. It consists of two concentric membranes separated by the perinuclear space. The structures of the envelope where it opens to the cytoplasm are called the nuclear pores (NUCLEAR PORE).
An abnormal congenital condition, associated with defects in the LAMIN TYPE A gene, which is characterized by premature aging in children, where all the changes of cell senescence occur. It is manifested by premature greying; hair loss; hearing loss (DEAFNESS); cataracts (CATARACT); ARTHRITIS; OSTEOPOROSIS; DIABETES MELLITUS; atrophy of subcutaneous fat; skeletal hypoplasia; elevated urinary HYALURONIC ACID; and accelerated ATHEROSCLEROSIS. Many affected individuals develop malignant tumors, especially SARCOMA.
A species of HAEMOPHILUS found on the mucous membranes of humans and a variety of animals. The species is further divided into biotypes I through VIII.
Vaccines or candidate vaccines containing antigenic polysaccharides from Haemophilus influenzae and designed to prevent infection. The vaccine can contain the polysaccharides alone or more frequently polysaccharides conjugated to carrier molecules. It is also seen as a combined vaccine with diphtheria-tetanus-pertussis vaccine.
Infections with bacteria of the genus HAEMOPHILUS.
Infections of the nervous system caused by bacteria of the genus HAEMOPHILUS, and marked by prominent inflammation of the MENINGES. HAEMOPHILUS INFLUENZAE TYPE B is the most common causative organism. The condition primarily affects children under 6 years of age but may occur in adults.
Two closely related polypeptides (molecular weight 7,000) isolated from the thymus gland. These hormones induce the differentiation of prothymocytes to thymocytes within the thymus. They also cause a delayed impairment of neuromuscular transmission in vivo and are therefore believed to be the agent responsible for myasthenia gravis.
A heterogenous group of inherited muscular dystrophy without the involvement of nervous system. The disease is characterized by MUSCULAR ATROPHY; MUSCLE WEAKNESS; CONTRACTURE of the elbows; ACHILLES TENDON; and posterior cervical muscles; with or without cardiac features. There are several INHERITANCE PATTERNS including X-linked (X CHROMOSOME), autosomal dominant, and autosomal recessive gene mutations.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
Aneurysm caused by a tear in the TUNICA INTIMA of a blood vessel leading to interstitial HEMORRHAGE, and splitting (dissecting) of the vessel wall, often involving the AORTA. Dissection between the intima and media causes luminal occlusion. Dissection at the media, or between the media and the outer adventitia causes aneurismal dilation.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
A species of anaerobic, gram-positive, rod-shaped bacteria in the family Clostridiaceae that produces proteins with characteristic neurotoxicity. It is the etiologic agent of BOTULISM in humans, wild fowl, HORSES; and CATTLE. Seven subtypes (sometimes called antigenic types, or strains) exist, each producing a different botulinum toxin (BOTULINUM TOXINS). The organism and its spores are widely distributed in nature.

Apoptosis in hematopoietic cells (FL5.12) caused by interleukin-3 withdrawal: relationship to caspase activity and the loss of glutathione. (1/319)

The mechanism of cell death caused by cytokine deprivation remains largely unknown. FL5.12 cells (a murine prolymphocytic cell line), following interleukin-3 (IL-3) withdrawal, undergo a decrease in intracellular glutathione (GSH) that precedes the onset of apoptosis. In the present study, the induction of apoptosis following IL-3 withdrawal or GSH depletion with DL-buthionine-[S,R,]-sulfoximine (BSO) was examined. Both conditions caused time-dependent increases in phosphatidylserine externalization, acridine orange and ethidium bromide staining, decreases in mitochondrial membrane potential, processing and activation of caspase-3 and proteolysis of the endogenous caspase substrate poly(adenosine diphosphate ribose)polymerase (PARP). Apoptosis induced by IL-3 deprivation but not BSO also caused lamin B1 cleavage, suggesting activation of caspase-6. Despite a more profound depletion of GSH after BSO than withdrawal of IL-3, the extent of apoptosis was somewhat lower. Benzyloxycarbonyl-Val-Ala-Asp(OMe)fluoromethyl ketone (z-VAD.fmk) blocked this caspase activity and prevented cell death after BSO exposure but not after IL-3 deprivation. Following IL-3 withdrawal, the caspase inhibitors z-VAD.fmk and boc-asp(OMe)fluoromethylketone (boc-asp.fmk) prevented the cleavage and activation of caspase-3, the breakdown of lamin B1 and partially mitigated PARP degradation. However, the externalization of phosphatidylserine, the fall in mitochondrial membrane potential and subsequent apoptotic cell death still occurred. These results suggest that IL-3 withdrawal may mediate cell death by a mechanism independent of both caspase activation and the accompanying loss of GSH.  (+info)

Apoptosis and cell-cycle arrest in human and murine tumor cells are initiated by isoprenoids. (2/319)

Diverse classes of phytochemicals initiate biological responses that effectively lower cancer risk. One class of phytochemicals, broadly defined as pure and mixed isoprenoids, encompasses an estimated 22,000 individual components. A representative mixed isoprenoid, gamma-tocotrienol, suppresses the growth of murine B16(F10) melanoma cells, and with greater potency, the growth of human breast adenocarcinoma (MCF-7) and human leukemic (HL-60) cells. beta-Ionone, a pure isoprenoid, suppresses the growth of B16 cells and with greater potency, the growth of MCF-7, HL-60 and human colon adenocarcinoma (Caco-2) cells. Results obtained with diverse cell lines differing in ras and p53 status showed that the isoprenoid-mediated suppression of growth is independent of mutated ras and p53 functions. beta-Ionone suppressed the growth of human colon fibroblasts (CCD-18Co) but only when present at three-fold the concentration required to suppress the growth of Caco-2 cells. The isoprenoids initiated apoptosis and, concomitantly arrested cells in the G1 phase of the cell cycle. Both suppress 3-hydroxy-3-methylglutaryl CoA reductase activity. beta-Ionone and lovastatin interfered with the posttranslational processing of lamin B, an activity essential to assembly of daughter nuclei. This interference, we postulate, renders neosynthesized DNA available to the endonuclease activities leading to apoptotic cell death. Lovastatin-imposed mevalonate starvation suppressed the glycosylation and translocation of growth factor receptors to the cell surface. As a consequence, cells were arrested in the G1 phase of the cell cycle. This rationale may apply to the isoprenoid-mediated G1-phase arrest of tumor cells. The additive and potentially synergistic actions of these isoprenoids in the suppression of tumor cell proliferation and initiation of apoptosis coupled with the mass action of the diverse isoprenoid constituents of plant products may explain, in part, the impact of fruit, vegetable and grain consumption on cancer risk.  (+info)

Strong association of autoantibodies to human nuclear lamin B1 with lupus anticoagulant antibodies in systemic lupus erythematosus. (3/319)

OBJECTIVE: To determine the frequency and clinical significance of high titers of IgG autoantibodies to nuclear lamin B1 in a large number of unselected and well-characterized systemic lupus erythematosus (SLE) patients, disease controls, and normal healthy controls. METHODS: A cross-sectional study of anti-lamin B1 autoantibodies, as measured by enzyme-linked immunosorbent assay using human recombinant lamin B1 autoantigen, was performed on serum samples obtained at first evaluation of 238 consecutive French Canadian adults: 61 healthy control subjects, 20 patients with osteoarthritis, 22 with ankylosing spondylitis, 11 with autoimmune hepatitis, 30 with rheumatoid arthritis, and 94 with SLE. SLE patients were studied for 57 disease manifestations. A case-control study was performed to analyze the relationship between anti-lamin B1 status and thrombotic manifestations between SLE onset and last followup. RESULTS: High titers of anti-lamin B1 were strikingly restricted to a subset of 8 SLE patients (8.5%). The mean anti-lamin B1 titer was higher in this subset than in the other SLE patients or any control group (P<0.001). By univariate analysis and stepwise multiple logistic regression, the most striking association of anti-lamin B1 was with lupus anticoagulant (LAC) antibodies (P = 0.00001). Although LAC were significantly associated with thrombosis in our SLE patients, anti-lamin B1 was not. The frequency of thrombosis in SLE patients expressing both LAC and anti-lamin B1 was similar to that in patients without LAC (P = 1.0). However, patients expressing LAC without anti-lamin B1 had a greater frequency of thrombosis (P = 0.018). CONCLUSION: High titers of IgG anti-lamin B1 autoantibodies are highly specific for a subset of SLE patients whose clinical characteristics include the presence of LAC and other laboratory manifestations of the antiphospholipid syndrome. The presence of LAC without anti-lamin B1 may define a subset of SLE patients at greater risk for thrombosis.  (+info)

Translational control of nuclear lamin B1 mRNA during oogenesis and early development of Xenopus. (4/319)

Cytoplasmic polyadenylation of specific mRNAs is commonly correlated with their translational activation during development. A canonical nuclear polyadenylation element AAUAAA (NPE) and cytoplasmic polyadenylation element(s) (CPE) are necessary and sufficient for polyadenylation during egg maturation. We have characterized cis-acting sequences of Xenopus nuclear lamin B1 mRNA that mediate translational regulation. By injection of synthetic RNAs into oocytes we show that the two CPE-like elements found in the 3'-untranslated region of B1 mRNA act as translational repressors in oocytes. The same CPEs in conjunction with the NPE confer transient polyadenylation and translational activation during egg maturation. Poly(A) length determination of the endogenous lamin B1 mRNA reveals a gradual increase of poly(A) tail length in early development up to mid-blastula, and a shortening of poly(A) tails during gastrulation and neurulation. The same kinetic and extent of polyadenylation and poly(A) tail shortening is observed with synthetic RNAs injected into fertilized eggs. Polyadenylation and translational activation of these RNAs is independent of the two CPEs and a NPE during early development. While translational regulation of lamin B1 mRNA functions in parts via established mechanisms, the pattern of polyadenylation and deadenylation during early development points to a novel mode of translational regulation.  (+info)

Decreased and aberrant nuclear lamin expression in gastrointestinal tract neoplasms. (5/319)

BACKGROUND: Altered expression of lamins A/C and B1, constituent proteins of the nuclear lamina, may occur during differentiation and has also been reported in primary lung cancer. AIMS: To examine the expression of these proteins in gastrointestinal neoplasms. PATIENTS: Archival human paraffin wax blocks and frozen tissue from patients undergoing surgical resection or endoscopic biopsy. METHODS: Immunohistochemistry and western blotting using polyclonal antisera against A type lamins and lamin B1. RESULTS: The expression of lamin A/C was reduced and was frequently undetectable by immunohistochemistry in all primary colon carcinomas and adenomas, and in 7/8 primary gastric cancers. Lamin B1 expression was reduced in all colon cancers, 16/18 colonic adenomas, and 6/8 gastric cancers. Aberrant, cytoplasmic labelling with both antibodies occurred in some colonic cancers and around one third of colonic adenomas. Cytoplasmic lamin A/C expression was detected in 3/8 gastric cancers. Lamin expression was reduced in gastric dysplasia, but not intestinal metaplasia, atrophy, or chronic gastritis. Lamin expression was low in carcinomas of oesophagus, prostate, breast, and uterus, but not pancreas. CONCLUSIONS: Reduced expression of nuclear lamins, sometimes together with aberrant, cytoplasmic immunoreactivity is common in gastrointestinal neoplasms. Altered lamin expression may be a biomarker of malignancy in the gastrointestinal tract.  (+info)

The apoptotic effects and synergistic interaction of sodium butyrate and MG132 in human retinoblastoma Y79 cells. (6/319)

This study deals with the apoptotic effect exerted on human retinoblastoma Y79 cells by both sodium butyrate and an inhibitor of 26S proteasome [z-Leu-Leu-Leu-CHO (MG132)] and their synergistic effect. Exposure to sodium butyrate (1-4 mM) induced an accumulation of cells in the G2-M phase that was already visible after 24 h of treatment, when morphological and biochemical signs of apoptosis appeared only in a small number of cells (5-10%). Thereafter, the apoptotic effects increased progressively with slow kinetics, reaching a maximum after 72 h of exposure, when they concerned a large fraction of cells (>75% with 4 mM sodium butyrate). Sodium butyrate stimulated the conversion of procaspase-3 into caspase-3 and also induced the cleavage of poly-(ADP-ribose) polymerase and lamin B, two hallmarks of apoptosis. All of the apoptotic signals were suppressed by benzyloxy carbonyl-Val-Ala-Asp-fluoromethylketone (a general inhibitor of caspase activities), whereas acetyl-Asp-Glu-Val-Asp aldehyde, a specific inhibitor of caspase-3 activity, only induced a partial reversion of the apoptotic effects. Sodium butyrate also decreased the Bcl-2 level, whereas it increased the Bax level and stimulated the release of cytochrome c from the mitochondria, an event that was most likely responsible for the activation of caspase-3. Finally, sodium butyrate activated 26S proteasome, the major extralysosomal degradative machinery, which is responsible for the degradation of short-lived proteins. Consequently, the levels of p53, N-myc, and IkappaBalpha (factors that play regulatory roles in apoptosis) diminished, whereas the nuclear level of nuclear factor kappaB concomitantly increased. Treatment of Y79 cells with MG132 induced apoptosis with more rapid kinetics than with sodium butyrate. The effects appeared after 8 h of incubation, reaching a maximum at 24 h, and they were accompanied by increased levels of N-myc, p53, and IkappaBalpha. MG132 also favored the release of cytochrome c from the mitochondria and increased the activity of caspase-3. When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB. Moreover, an increase in the level of Bax and an enhancement in the release of cytochrome c from the mitochondria were observed. Clear synergistic effects concerning the activation of both caspase-3 and apoptosis were induced by a combination of suboptimal doses of sodium butyrate and MG132. The results support the conclusion that MG132 potentiates the apoptotic effect of sodium butyrate by suppressing its stimulatory effect on 26S proteasome activity. Synergistic interactions between butyrate and inhibitors of proteasome could represent a new important tool in tumor therapy and, in particular, the treatment of retinoblastoma.  (+info)

Colocalization of intranuclear lamin foci with RNA splicing factors. (7/319)

The lamins form a fibrous network underlying the inner nuclear membrane termed the nuclear lamina. In order to gain insights into the role of lamins in nuclear organization, we have characterized a monoclonal antibody (LA-2H10) raised against recombinant rat lamin A that labels nuclei in a speckled pattern in all cells of unsynchronized populations of HeLa and rat F-111 fibroblast cells, unlike the typical nuclear periphery staining by another monoclonal antibody to lamin A, LA-2B3. In immunolocalization studies the lamin A speckles or foci were found to colocalize with the RNA splicing factors SC-35 and U5-116 kD, but not with p80 coilin found in coiled bodies. Lamin B1 was also associated with these foci. These foci dispersed when cells entered mitosis and reformed during anaphase. The differential reactivity of LA-2H10 and LA-2B3 was retained after nuclei were extracted with detergents, nucleases and salt to disrupt interactions of lamins with chromatin and other nuclear proteins. Using deletion fragments of recombinant lamin A, the epitope recognized by LA-2H10 was located between amino acids 171 and 246. Our findings are consistent with a structural role for lamins in supporting nuclear compartments containing proteins involved in RNA splicing.  (+info)

Start sites of bidirectional DNA synthesis at the human lamin B2 origin. (8/319)

The initiation sites of bidirectional synthesis at the DNA replication origin located at the 3' end of the human lamin B2 gene were investigated. RNA-primed nascent DNA molecules were subjected to second-strand synthesis with appropriate primers, amplified by ligation-mediated polymerase chain reaction, and size fractionated. Evidence for precise start sites was obtained. Exploration of close to 1 kilobase, coupled to inhibition of Okazaki fragment synthesis, demonstrates that the leading strands initiate at precise nucleotides on either helix, overlapping by three base pairs, within the area bound to a protein complex possibly analogous to the prereplicative complex of yeast.  (+info)

I'm sorry for any confusion, but "Lamin Type B" is not a recognized medical term or concept in human physiology or pathology. The term "lamin" refers to proteins that are part of the nuclear lamina, a filamentous network found inside the nucleus of cells. There are three types of lamin proteins: A, B, and C.

Lamin A and Lamin C are produced from the LMNA gene, while Lamin B1 and Lamin B2 are produced from the LMNB1 and LMNB2 genes, respectively. Therefore, "Lamin Type B" is not a specific designation, but rather encompasses two distinct proteins: Lamin B1 and Lamin B2.

If you have any questions about lamins or another medical topic, please provide more context or clarify your question so I can give you a more accurate answer.

Lamin Type A, also known as LMNA, is a gene that provides instructions for making proteins called lamins. These proteins are part of the nuclear lamina, a network of fibers that lies just inside the nuclear envelope, which is the membrane that surrounds the cell's nucleus. The nuclear lamina helps maintain the shape and stability of the nucleus and plays a role in regulating gene expression and DNA replication.

Mutations in the LMNA gene can lead to various diseases collectively known as laminopathies, which affect different tissues and organs in the body. These conditions include Emery-Dreifuss muscular dystrophy, limb-girdle muscular dystrophy, dilated cardiomyopathy with conduction system disease, and a type of premature aging disorder called Hutchinson-Gilford progeria syndrome. The specific symptoms and severity of these disorders depend on the particular LMNA mutation and the tissues affected.

Lamins are type V intermediate filament proteins that play a structural role in the nuclear envelope. They are the main components of the nuclear lamina, a mesh-like structure located inside the inner membrane of the nuclear envelope. Lamins are organized into homo- and heterodimers, which assemble into higher-order polymers to form the nuclear lamina. This structure provides mechanical support to the nucleus, helps maintain the shape and integrity of the nucleus, and plays a role in various nuclear processes such as DNA replication, transcription, and chromatin organization. Mutations in the genes encoding lamins have been associated with various human diseases, collectively known as laminopathies, which include muscular dystrophies, neuropathies, cardiomyopathies, and premature aging disorders.

Haemophilus influenzae type b (Hib) is a bacterial subtype that can cause serious infections, particularly in children under 5 years of age. Although its name may be confusing, Hib is not the cause of influenza (the flu). It is defined medically as a gram-negative, coccobacillary bacterium that is a member of the family Pasteurellaceae.

Hib is responsible for several severe and potentially life-threatening infections such as meningitis (inflammation of the membranes surrounding the brain and spinal cord), epiglottitis (swelling of the tissue located at the base of the tongue that can block the windpipe), pneumonia, and bacteremia (bloodstream infection).

Before the introduction of the Hib vaccine in the 1980s and 1990s, Haemophilus influenzae type b was a leading cause of bacterial meningitis in children under 5 years old. Since then, the incidence of invasive Hib disease has decreased dramatically in vaccinated populations.

The nuclear lamina is a protein network that lies beneath the inner nuclear membrane of the nuclear envelope in eukaryotic cells. It is primarily composed of type V intermediate filament proteins called lamins, which assemble into heteropolymeric filaments and provide structural support to the nucleus. The nuclear lamina plays essential roles in various nuclear processes, including DNA replication, gene expression, and nuclear division. Additionally, it serves as an attachment site for chromatin, nuclear pore complexes, and other nuclear envelope components, helping maintain the overall organization and integrity of the nucleus.

The nuclear envelope is a complex and double-membrane structure that surrounds the eukaryotic cell's nucleus. It consists of two distinct membranes: the outer nuclear membrane, which is continuous with the endoplasmic reticulum (ER) membrane, and the inner nuclear membrane, which is closely associated with the chromatin and nuclear lamina.

The nuclear envelope serves as a selective barrier between the nucleus and the cytoplasm, controlling the exchange of materials and information between these two cellular compartments. Nuclear pore complexes (NPCs) are embedded in the nuclear envelope at sites where the inner and outer membranes fuse, forming aqueous channels that allow for the passive or active transport of molecules, such as ions, metabolites, and RNA-protein complexes.

The nuclear envelope plays essential roles in various cellular processes, including DNA replication, transcription, RNA processing, and chromosome organization. Additionally, it is dynamically regulated during the cell cycle, undergoing disassembly and reformation during mitosis to facilitate equal distribution of genetic material between daughter cells.

Progeria, also known as Hutchinson-Gilford Progeria Syndrome (HGPS), is a rare and fatal genetic condition characterized by the rapid aging of children. The term "progeria" comes from the Greek words "pro," meaning prematurely, and "gereas," meaning old age.

Individuals with progeria typically appear normal at birth but begin to display signs of accelerated aging within the first two years of life. These symptoms can include growth failure, loss of body fat and hair, aged-looking skin, joint stiffness, hip dislocation, and cardiovascular disease. The most common cause of death in progeria patients is heart attack or stroke due to widespread atherosclerosis (the hardening and narrowing of the arteries).

Progeria is caused by a mutation in the LMNA gene, which provides instructions for making a protein called lamin A. This protein is essential for the structure and function of the nuclear envelope, the membrane that surrounds the cell's nucleus. The mutation leads to the production of an abnormal form of lamin A called progerin, which accumulates in cells throughout the body, causing premature aging.

There is currently no cure for progeria, and treatment is focused on managing symptoms and complications. Researchers are actively studying potential treatments that could slow or reverse the effects of the disease.

Haemophilus influenzae is a gram-negative, coccobacillary bacterium that can cause a variety of infectious diseases in humans. It is part of the normal respiratory flora but can become pathogenic under certain circumstances. The bacteria are named after their initial discovery in 1892 by Richard Pfeiffer during an influenza pandemic, although they are not the causative agent of influenza.

There are six main serotypes (a-f) based on the polysaccharide capsule surrounding the bacterium, with type b (Hib) being the most virulent and invasive. Hib can cause severe invasive diseases such as meningitis, pneumonia, epiglottitis, and sepsis, particularly in children under 5 years of age. The introduction of the Hib conjugate vaccine has significantly reduced the incidence of these invasive diseases.

Non-typeable Haemophilus influenzae (NTHi) strains lack a capsule and are responsible for non-invasive respiratory tract infections, such as otitis media, sinusitis, and exacerbations of chronic obstructive pulmonary disease (COPD). NTHi can also cause invasive diseases but at lower frequency compared to Hib.

Proper diagnosis and antibiotic susceptibility testing are crucial for effective treatment, as Haemophilus influenzae strains may display resistance to certain antibiotics.

Haemophilus vaccines are vaccines that are designed to protect against Haemophilus influenzae type b (Hib), a bacterium that can cause serious infections such as meningitis, pneumonia, and epiglottitis. There are two main types of Hib vaccines:

1. Polysaccharide vaccine: This type of vaccine is made from the sugar coating (polysaccharide) of the bacterial cells. It is not effective in children under 2 years of age because their immune systems are not yet mature enough to respond effectively to this type of vaccine.
2. Conjugate vaccine: This type of vaccine combines the polysaccharide with a protein carrier, which helps to stimulate a stronger and more sustained immune response. It is effective in infants as young as 6 weeks old.

Hib vaccines are usually given as part of routine childhood immunizations starting at 2 months of age. They are administered through an injection into the muscle. The vaccine is safe and effective, with few side effects. Vaccination against Hib has led to a significant reduction in the incidence of Hib infections worldwide.

Haemophilus infections are caused by bacteria named Haemophilus influenzae. Despite its name, this bacterium does not cause the flu, which is caused by a virus. There are several different strains of Haemophilus influenzae, and some are more likely to cause severe illness than others.

Haemophilus infections can affect people of any age, but they are most common in children under 5 years old. The bacteria can cause a range of infections, from mild ear infections to serious conditions such as meningitis (inflammation of the membranes surrounding the brain and spinal cord) and pneumonia (infection of the lungs).

The bacterium is spread through respiratory droplets when an infected person coughs or sneezes. It can also be spread by touching contaminated surfaces and then touching the mouth, nose, or eyes.

Prevention measures include good hygiene practices such as handwashing, covering the mouth and nose when coughing or sneezing, and avoiding close contact with people who are sick. Vaccination is also available to protect against Haemophilus influenzae type b (Hib) infections, which are the most severe and common form of Haemophilus infection.

Haemophilus meningitis is a specific type of bacterial meningitis caused by the Haemophilus influenzae type b (Hib) bacteria. Meningitis is an inflammation of the membranes covering the brain and spinal cord, known as the meninges. Before the introduction of the Hib vaccine, Haemophilus influenzae type b was the leading cause of bacterial meningitis in children under 5 years old. However, since the widespread use of the Hib vaccine, the incidence of Haemophilus meningitis has significantly decreased.

Haemophilus influenzae type b bacteria can also cause other serious infections such as pneumonia, epiglottitis (inflammation of the tissue located at the base of the tongue that can obstruct the windpipe), and bacteremia (bloodstream infection). The Hib vaccine has been very effective in preventing these infections as well.

Symptoms of Haemophilus meningitis may include fever, headache, stiff neck, nausea, vomiting, confusion, and sensitivity to light. In severe cases, it can lead to seizures, coma, or even death. If you suspect someone has meningitis, seek immediate medical attention. Haemophilus meningitis is treated with antibiotics, and early treatment is crucial for a better prognosis.

Thymopoietins are a group of hormone-like polypeptides that play a crucial role in the development and differentiation of T-lymphocytes (T-cells) within the thymus gland. The term "thymopoietin" is often used to refer specifically to a particular polypeptide called thymopoietin alpha, which was first identified in the 1970s. Thymopoietin alpha helps to promote the differentiation of immature T-cells into mature T-cells, and it also contributes to the process of negative selection, whereby self-reactive T-cells are eliminated to prevent autoimmune disorders.

Other factors that contribute to thymopoiesis (the production of T-cells in the thymus) may also be referred to as thymopoietins, including interleukin-7 (IL-7), which is produced by stromal cells in the thymus and helps to support the survival and proliferation of immature T-cells.

Overall, thymopoietins play a critical role in maintaining immune homeostasis and preventing the development of autoimmune diseases.

Emery-Dreifuss muscular dystrophy (EDMD) is a genetic disorder characterized by the triad of 1) early contractures of the elbow and Achilles tendons, 2) slowly progressive muscle weakness and wasting, which begins in the muscles around the shoulder and pelvis and later involves the arms and legs, and 3) cardiac conduction defects that can lead to serious heart rhythm abnormalities.

EDMD is caused by mutations in one of several genes, including the EMD, LMNA, FHL1, and SYNE1/2 genes. These genes provide instructions for making proteins that are important for maintaining the structure and function of muscle cells, as well as the electrical activity of the heart.

The symptoms of EDMD can vary in severity and age of onset, even among family members with the same genetic mutation. Treatment typically focuses on managing the symptoms of the disease, including physical therapy to maintain mobility, bracing or surgery for contractures, and medications to manage cardiac arrhythmias. In some cases, a heart transplant may be necessary.

Nuclear proteins are a category of proteins that are primarily found in the nucleus of a eukaryotic cell. They play crucial roles in various nuclear functions, such as DNA replication, transcription, repair, and RNA processing. This group includes structural proteins like lamins, which form the nuclear lamina, and regulatory proteins, such as histones and transcription factors, that are involved in gene expression. Nuclear localization signals (NLS) often help target these proteins to the nucleus by interacting with importin proteins during active transport across the nuclear membrane.

A dissecting aneurysm is a serious and potentially life-threatening condition that occurs when there is a tear in the inner layer of the artery wall, allowing blood to flow between the layers of the artery wall. This can cause the artery to bulge or balloon out, leading to a dissection aneurysm.

Dissecting aneurysms can occur in any artery, but they are most commonly found in the aorta, which is the largest artery in the body. When a dissecting aneurysm occurs in the aorta, it is often referred to as a "dissecting aortic aneurysm."

Dissecting aneurysms can be caused by various factors, including high blood pressure, atherosclerosis (hardening and narrowing of the arteries), genetic disorders that affect the connective tissue, trauma, or illegal drug use (such as cocaine).

Symptoms of a dissecting aneurysm may include sudden severe chest or back pain, which can feel like ripping or tearing, shortness of breath, sweating, lightheadedness, or loss of consciousness. If left untreated, a dissecting aneurysm can lead to serious complications, such as rupture of the artery, stroke, or even death.

Treatment for a dissecting aneurysm typically involves surgery or endovascular repair to prevent further damage and reduce the risk of rupture. The specific treatment approach will depend on various factors, including the location and size of the aneurysm, the patient's overall health, and their medical history.

The cell nucleus is a membrane-bound organelle found in the eukaryotic cells (cells with a true nucleus). It contains most of the cell's genetic material, organized as DNA molecules in complex with proteins, RNA molecules, and histones to form chromosomes.

The primary function of the cell nucleus is to regulate and control the activities of the cell, including growth, metabolism, protein synthesis, and reproduction. It also plays a crucial role in the process of mitosis (cell division) by separating and protecting the genetic material during this process. The nuclear membrane, or nuclear envelope, surrounding the nucleus is composed of two lipid bilayers with numerous pores that allow for the selective transport of molecules between the nucleoplasm (nucleus interior) and the cytoplasm (cell exterior).

The cell nucleus is a vital structure in eukaryotic cells, and its dysfunction can lead to various diseases, including cancer and genetic disorders.

'Clostridium botulinum' is a gram-positive, rod-shaped, anaerobic bacteria that produces one or more neurotoxins known as botulinum toxins. These toxins are among the most potent naturally occurring biological poisons and can cause a severe form of food poisoning called botulism in humans and animals. Botulism is characterized by symmetrical descending flaccid paralysis, which can lead to respiratory and cardiovascular failure, and ultimately death if not treated promptly.

The bacteria are widely distributed in nature, particularly in soil, sediments, and the intestinal tracts of some animals. They can form spores that are highly resistant to heat, chemicals, and other environmental stresses, allowing them to survive for long periods in adverse conditions. The spores can germinate and produce vegetative cells and toxins when they encounter favorable conditions, such as anaerobic environments with appropriate nutrients.

Human botulism can occur through three main routes of exposure: foodborne, wound, and infant botulism. Foodborne botulism results from consuming contaminated food containing preformed toxins, while wound botulism occurs when the bacteria infect a wound and produce toxins in situ. Infant botulism is caused by the ingestion of spores that colonize the intestines and produce toxins, mainly affecting infants under one year of age.

Prevention measures include proper food handling, storage, and preparation practices, such as cooking and canning foods at appropriate temperatures and for sufficient durations. Wound care and prompt medical attention are crucial in preventing wound botulism. Vaccines and antitoxins are available for prophylaxis and treatment of botulism in high-risk individuals or in cases of confirmed exposure.

No FAQ available that match "lamin type b"

No images available that match "lamin type b"