alpha-Crystallin A Chain
alpha-Crystallin B Chain
Molecular Sequence Data
Polymerase Chain Reaction
Amino Acid Sequence
Receptors, Adrenergic, beta
Proto-Oncogene Proteins c-maf
Native Polyacrylamide Gel Electrophoresis
Electrophoresis, Polyacrylamide Gel
Reverse Transcriptase Polymerase Chain Reaction
Immunoglobulin Light Chains
Transforming Growth Factor beta
Immunoglobulin Heavy Chains
Heat-Shock Proteins, Small
Electrophoresis, Gel, Two-Dimensional
Sequence Homology, Amino Acid
Gene Expression Regulation
Protein Structure, Secondary
Myosin Heavy Chains
Integrin beta Chains
beta 2-Glycoprotein I
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Chromatography, High Pressure Liquid
Receptors, Adrenergic, beta-2
Myosin Light Chains
Eye Diseases, Hereditary
Receptors, Adrenergic, beta-1
Magnetic Resonance Spectroscopy
Promoter Regions, Genetic
Protein Structure, Quaternary
Paired Box Transcription Factors
Amino Acid Substitution
Protein Structure, Tertiary
Glycogen Synthase Kinase 3
Transforming Growth Factor beta1
In Situ Hybridization
Estrogen Receptor beta
Receptors, Adrenergic, beta-3
Lens Cortex, Crystalline
Chromatography, Ion Exchange
Tumor Cells, Cultured
Fluorescent Antibody Technique, Indirect
Gene Expression Regulation, Developmental
Enhancer Elements, Genetic
Protein Processing, Post-Translational
HSP20 Heat-Shock Proteins
Retinal Pigment Epithelium
DNA Polymerase beta
Disease Models, Animal
Sphingolipid Activator Proteins
Sequence Analysis, DNA
SOXB1 Transcription Factors
Receptors, Transforming Growth Factor beta
Enzyme-Linked Immunosorbent Assay
Recombinant Fusion Proteins
Spectrometry, Mass, Electrospray Ionization
Dose-Response Relationship, Drug
Characterization of a sodium deoxycholate-activatable proteinase activity associated with betaA3/A1-crystallin of human lenses. (1/42)A human lens proteinase was purified by a five-step procedure that included two consecutive size-exclusion agarose A 1.5 m chromatographies, a preparative non-denaturing gel-electrophoretic separation, HPLC on a size-exclusion column (TSK G-3000 PW(XL)) followed by preparative isoelectric focusing. A 2300-fold purified enzyme showed a major band of 22 kDa during SDS-PAGE, a pH optimum of 7.8, pI between 4.5 and 5.0, a loss of activity above 45 degrees C and a serine type nature. The partial N-terminal sequence of the enzyme, i.e. P-M-P-G-S-L-G-P-W, matched with the sequence of human lens betaA3/A1-crystallin starting at residue No. 23. Based on the Western blot results of the enzyme with five different site-specific polyclonal antibodies raised against betaA3/A1-crystallin, it was concluded that the 22 kDa crystallin enzyme had a cleaved N-terminus but an intact C-terminus. The betaA3/A1-crystallin, isolated from human lenses, also exhibited proteinase activity following detergent activation and size-exclusion chromatography. The mouse recombinant betaA3/A1-crystallin proteinase was purified by the above five-step procedure, from a homogenate of Sf-9 cells transfected with baculovirus containing the full length coding sequence of betaA3/A1-crystallin. The mouse 22 kDa species also exhibited proteinase activity and immunoreactivity with anti-betaA3/A1-C-terminal antibody. Together, the data suggest that a truncated species of betaA3/A1-crystallin exhibits proteinase activity. (+info)
Identification and properties of anti-chaperone-like peptides derived from oxidized bovine lens betaL-crystallins. (2/42)Thermal aggregation of betaL-crystallin was higher in the presence of peptide fragments generated from oxidized and trypsin-digested betaL-crystallin compared with thermal aggregation of the control proteins without oxidized betaL-crystallin fragments. Increased aggregation of betaL-crystallin was also observed despite the presence of alpha-crystallin (which has anti-aggregating properties) in the system. Self-aggregation of the oxidized betaL-crystallin fragments per se was not observed under the experimental conditions. Reverse-phase HPLC analysis of the precipitate obtained after heating a mixture of betaL-crystallin and oxidized betaL-crystallin fragments revealed that more than one peptide co-precipitates with betaL-crystallin. Electrospray mass spectrometry analysis of the peptides revealed that the molecular weight(s) of the peptides ranged from 1400-1800. Tandem mass spectrometry and a data base search revealed that two of the peptides originated from betaA4-crystallin (LTIFEQENFLGR, residues 121-132) and betaB3-crystallin (AINGTWVGYEFPGYR, residues 153-167) respectively. Oxidized synthetic peptides representing the same sequence were also found to enhance the aggregation of betaL-crystallin in a manner similar to oxidized lens betaL-crystallin peptides. These data suggest that the polypeptides generated after oxidation and proteolysis of betaL-crystallins interact with denaturing proteins and facilitate their aggregation and light scattering, thus behaving like anti-chaperones. (+info)
Cleavage of the A site mRNA codon during ribosome pausing provides a mechanism for translational quality control. (3/42)Cells employ many mechanisms to ensure quality control during protein biosynthesis. Here, we show that, during the pausing of a bacterial ribosome, the mRNA being translated is cleaved at a site within or immediately adjacent to the A site codon. The extent of this A site mRNA cleavage is correlated with the extent of ribosome pausing as assayed by tmRNA-mediated tagging of the nascent polypeptide. Cleavage does not require tmRNA, the ribosomal alarmone (p)ppGpp, or bacterial toxins such as RelE which have been shown to stimulate a similar activity. Translation is required for cleavage, suggesting that the ribosome participates in the reaction in some fashion. When normal protein synthesis is compromised, A site mRNA cleavage and the tmRNA system provide a mechanism for reducing translational errors and the production of aberrant and potentially harmful polypeptides. (+info)
Characterization of the G91del CRYBA1/3-crystallin protein: a cause of human inherited cataract. (4/42)Congenital cataract is a leading cause of visual disability in children. Inherited isolated (non-syndromic) cataract represents a significant proportion of cases and the identification of genes responsible for inherited cataract will lead to a better understanding of the mechanism of cataract formation at the molecular level both in congenital and age-related cataract. Crystallins are abundantly expressed in the developing human lens and represent excellent candidate genes for inherited cataract. A genome-wide search of a five-generation family with autosomal dominant lamellar cataract demonstrated linkage to the 17p12-q11 region. Screening of the CRYBA1/3 gene showed a 3 bp deletion, which resulted in a G91del mutation within the tyrosine corner, that co-segregated with disease and was not found in 96 normal controls. In order to understand the molecular basis of cataract formation, the mutant protein was expressed in vitro and its unfolding and refolding characteristics assessed using far-UV circular dichroism spectroscopy. Defective folding and a reduction in solubility were found. As the wild-type protein did not refold into the native conformation following unfolding, a corresponding CRYBB2 mutant was genetically engineered and its refolding characteristics analysed and compared with wild-type CRYBB2. Its biophysical properties support the hypothesis that removal of the glycine residue from the tyrosine corner impairs the folding and solubility of beta-crystallin proteins. This study represents the first comprehensive description of the biophysical consequences of a mutant beta-crystallin protein that is associated with human inherited cataract. (+info)
CRYBA3/A1 gene mutation associated with suture-sparing autosomal dominant congenital nuclear cataract: a novel phenotype. (5/42)PURPOSE: To identify the genetic defect leading to the congenital nuclear cataract affecting a large five-generation Swiss family. METHODS: Family history and clinical data were recorded. The phenotype was documented by both slit lamp and Scheimpflug photography. One cortical lens was evaluated by electron microscopy after cataract extraction. Lenticular phenotyping and genotyping were performed independently with short tandem repeat polymorphism. Linkage analysis was performed, and candidate genes were PCR amplified and screened for mutations on both strands using direct sequencing. RESULTS: Affected individuals had a congenital nuclear lactescent cataract in both eyes. Linkage was observed on chromosome 17 for DNA marker D17S1857 (lod score: 3.44 at theta = 0). Direct sequencing of CRYBA3/A1, which maps to the vicinity, revealed an in-frame 3-bp deletion in exon 4 (279delGAG). This mutation involved a deletion of glycine-91, cosegregated in all affected individuals, and was not observed in unaffected individuals or in 250 normal control subjects from the same ethnic background. Electron microscopy showed that cortical lens fiber morphology was normal. CONCLUSIONS: The DeltaG91 mutation in CRYBA3/A1 is associated with an autosomal dominant congenital nuclear lactescent cataract. A splice mutation (IVS3+1G/A) in this gene has been reported in a zonular cataract with sutural opacities. These results indicate phenotypic heterogeneity related to mutations in this gene. (+info)
Proteomic and sequence analysis of chicken lens crystallins reveals alternate splicing and translational forms of beta B2 and beta A2 crystallins. (6/42)PURPOSE: To characterize the adult chicken lens proteome using mass spectrometry and two-dimensional gel electrophoresis (2-DE). METHODS: Lens proteins from 10-week old chickens were separated by gel filtration and reversed-phase chromatography, and whole protein masses were measured with electrospray mass spectrometry. Water-soluble lens proteins were separated by 2-DE and identified by tandem mass spectrometry of in-gel digests. RESULTS: Whole protein masses were consistent with all major chicken lens crystallin sequences, except for beta B2 and beta B3. Subsequent cDNA sequencing revealed errors in published sequences translating into 2- and 7-amino-acid differences, respectively, for beta B2 and beta B3, which were in better agreement with the measured masses. Previously uncharacterized forms of beta A2 and beta B2 were observed. The novel form of beta A2 had four fewer amino acids, was more abundant, and resulted from translation at a second start codon. The novel form of beta B2 contained 14 additional amino acids in the interdomain linker and resulted from alternate splicing within intron 4 of the transcript. All examined crystallins, except beta A3, for which data could not be obtained, were N-terminally acetylated, and all beta-crystallins lacked an initial methionine, except for the smaller beta A2 form. In-gel digests identified 29 proteins on the 2-DE map and indicated that truncation occurs within N-terminal extensions of beta-crystallins during lens maturation. CONCLUSIONS: The complementary techniques 2-DE, mass spectrometry, and DNA sequencing were used to provide the most complete description of the adult chicken lens proteome to date and identified alternate forms of beta A2 and beta B2. (+info)
Crystallins in water soluble-high molecular weight protein fractions and water insoluble protein fractions in aging and cataractous human lenses. (7/42)PURPOSE: The aim of the study was to comparatively analyze crystallin fragments in the water soluble high molecular weight (WS-HMW) and in the water insoluble (WI) protein fractions of human cataractous (with nuclear opacity) and age matched normal lenses to determine the identity of crystallin species that show cataract specific changes such as truncation and post-translational modifications. Because these changes were cataract specific and not aging specific, the results were expected to provide information regarding potential mechanisms of age related cataract development. METHODS: The WS-alpha-crystallin, WS-HMW protein, and WI protein fractions were isolated from normal lenses of different ages and from cataractous lenses. The three fractions were subjected to two dimensional (2D) gel electrophoresis (IEF in the first dimension and SDS-PAGE in the second dimension). Individual spots from 2D gels were trypsin digested and the tryptic fragments were analyzed by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry. RESULTS: The 2D protein profiles of WS-alpha-crystallin fractions of normal human lenses showed an age related increase in the number of crystallin fragments. In young normal lenses, the WS-alpha-crystallin fragments were mostly C-terminally truncated, but in older lenses these were both N- and C-terminally truncated. The WS-HMW protein fraction from normal lenses contained mainly fragments of alphaA- and alphaB-crystallin, whereas additional fragments of betaB1- and betaA3-crystallin were present in this fraction from cataractous lenses. Similarly, the WI proteins in normal lenses contained fragments of alphaA- and alphaB-crystallin, but cataractous lenses contained additional fragments of betaA3- and betaB1-crystallin. The modifications identified in the WS-HMW and WI crystallin species of cataractous lenses were truncation, oxidation of Trp residues, and deamidation of Asn to Asp residues. CONCLUSIONS: The results show that the components of WS-HMW and WI protein fractions of cataractous lenses differed from normal lenses. Selective insolubilization of fragments of betaA3/A1- and betaB1-crystallin occurred during cataract development compared to normal lenses. Further, the crystallin species of cataractous lenses showed increased truncation, deamidation of Asn to Asp residues, and oxidation of Trp residue. (+info)
Intrasarcoplasmic amyloidosis impairs proteolytic function of proteasomes in cardiomyocytes by compromising substrate uptake. (8/42)The presence of increased ubiquitinated proteins and amyloid oligomers in failing human hearts strikingly resembles the characteristic pathology in the brain of many neurodegenerative diseases. The ubiquitin-proteasome system (UPS) is responsible for degradation of most cellular proteins and plays essential roles in virtually all cellular processes. UPS impairment by aberrant protein aggregation was previously shown in cell culture but remains to be demonstrated in intact animals. Mechanisms underlying the impairment are poorly understood. We report here that UPS proteolytic function is severely impaired in the heart of a mouse model of intrasarcoplasmic amyloidosis caused by cardiac-restricted expression of a human desmin-related myopathy-linked missense mutation of alphaB-crystallin (CryAB(R120G)). The UPS impairment was detected before cardiac hypertrophy, and failure became discernible, suggesting that defective protein turnover likely contributes to cardiac remodeling and failure in this model. Further analyses reveal that the impairment is likely attributable to insufficient delivery of substrate proteins into the 20S proteasomes, and depletion of key components of the 19S subcomplex may be responsible. The derangement is likely caused by aberrant protein aggregation rather than loss of function of the CryAB gene because UPS malfunction was not evident in CryAB-null hearts and inhibition of aberrant protein aggregation by Congo red or a heat shock protein significantly attenuated CryAB(R120G)-induced UPS malfunction in cultured cardiomyocytes. Because of the central role of the UPS in cell regulation and the high intrasarcoplasmic amyloidosis prevalence in failing human hearts, our data suggest a novel pathogenic process in cardiac disorders with abnormal protein aggregation. (+info)
There are different types of cataracts, including:
1. Nuclear cataract: This is the most common type of cataract and affects the center of the lens.
2. Cortical cataract: This type of cataract affects the outer layer of the lens and can cause a "halo" effect around lights.
3. Posterior subcapsular cataract: This type of cataract affects the back of the lens and is more common in younger people and those with diabetes.
4. Congenital cataract: This type of cataract is present at birth and can be caused by genetic factors or other conditions.
Symptoms of cataracts can include:
* Blurred vision
* Double vision
* Sensitivity to light
* Difficulty seeing at night
* Fading or yellowing of colors
Cataracts can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as ultrasound or optical coherence tomography (OCT).
Treatment for cataracts typically involves surgery to remove the clouded lens and replace it with an artificial one called an intraocular lens (IOL). The type of IOL used will depend on the patient's age, visual needs, and other factors. In some cases, cataracts may be removed using a laser-assisted procedure.
In addition to surgery, there are also non-surgical treatments for cataracts, such as glasses or contact lenses, which can help improve vision. However, these treatments do not cure the underlying condition and are only temporary solutions.
It's important to note that cataracts are a common age-related condition and can affect anyone over the age of 40. Therefore, it's important to have regular eye exams to monitor for any changes in vision and to detect cataracts early on.
In summary, cataracts are a clouding of the lens in the eye that can cause blurred vision, double vision, sensitivity to light, and other symptoms. Treatment typically involves surgery to remove the clouded lens and replace it with an artificial one, but non-surgical treatments such as glasses or contact lenses may also be used. Regular eye exams are important for detecting cataracts early on and monitoring vision health.
1. Retinitis pigmentosa (RP): a group of degenerative diseases that affect the retina and cause progressive vision loss.
2. Leber congenital amaurosis (LCA): a rare inherited disorder that causes blindness or severe visual impairment at birth or in early childhood.
3. Stargardt disease: a genetic disorder that affects the retina and can cause progressive vision loss, usually starting in childhood.
4. Juvenile macular degeneration (JMD): a group of inherited conditions that affect the macula, the part of the retina responsible for central vision.
5. Persistent hyperplastic primary vitreous (PHPV): a rare inherited condition where abnormal development of the eye can cause vision loss or blindness.
6. Anophthalmia/microphthalmia: a rare inherited condition where one or both eyes are absent or severely underdeveloped.
7. ocular albinism: a genetic condition that affects the development of pigment in the eye, leading to visual impairment and increased risk of eye conditions such as cataracts and glaucoma.
8. Peter's anomaly: a rare inherited condition where there is an abnormal development of the cornea and lens of the eye, leading to vision loss or blindness.
9. cone-rod dystrophy: a group of inherited conditions that affect the retina and can cause progressive vision loss, usually starting in childhood.
10. Retinal dystrophy: a general term for a group of inherited disorders that affect the retina and can cause progressive vision loss, usually starting in adulthood.
These are just a few examples of hereditary eye diseases. There are many other conditions that can be inherited and affect the eyes. Genetic testing and counseling can help identify the risk of inheriting these conditions and provide information on how to manage and treat them.
Anterior uveitis can be caused by a variety of factors, including infection, autoimmune disorders, and trauma. It is often diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and laboratory tests to rule out other conditions. Treatment options for anterior uveitis depend on the underlying cause and may include antibiotics, anti-inflammatory medications, and surgery to remove any affected tissue.
In summary, anterior uveitis is a type of inflammation that occurs in the front part of the eye, which can cause symptoms such as redness, pain, blurred vision, and sensitivity to light. It can be caused by a variety of factors and diagnosed through a combination of physical examination, imaging tests, and laboratory tests. Treatment options depend on the underlying cause and may include antibiotics, anti-inflammatory medications, and surgery.
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.
1. Keratoconus: This is a progressive thinning of the cornea that can cause it to bulge into a cone-like shape, leading to blurred vision and sensitivity to light.
2. Fuchs' dystrophy: This is a condition in which the cells in the innermost layer of the cornea become damaged, leading to clouding and blurred vision.
3. Bullous keratopathy: This is a condition in which there is a large, fluid-filled bubble on the surface of the cornea, which can cause blurred vision and discomfort.
4. Corneal ulcers: These are open sores on the surface of the cornea that can be caused by infection or other conditions.
5. Dry eye syndrome: This is a condition in which the eyes do not produce enough tears, leading to dryness, irritation, and blurred vision.
6. Corneal abrasions: These are scratches on the surface of the cornea that can be caused by injury or other conditions.
7. Trachoma: This is an infectious eye disease that can cause scarring and blindness if left untreated.
8. Ocular herpes: This is a viral infection that can cause blisters on the surface of the cornea and lead to scarring and vision loss if left untreated.
9. Endophthalmitis: This is an inflammation of the inner layer of the eye that can be caused by bacterial or fungal infections, and can lead to severe vision loss if left untreated.
10. Corneal neovascularization: This is the growth of new blood vessels into the cornea, which can be a complication of other conditions such as dry eye syndrome or ocular trauma.
These are just a few examples of the many different types of corneal diseases that can affect the eyes. It's important to seek medical attention if you experience any symptoms such as pain, redness, or blurred vision in one or both eyes. Early diagnosis and treatment can help prevent complications and preserve vision.
Heavy chain disease is also known as:
* Heavy chain defect
* Immunoglobulin (IgG) heavy chain disease
* Kappa chain disease
* Lambda chain disease
The main causes of heavy chain disease include:
* Genetic mutations in the IGH genes that code for the heavy chains of immunoglobulins
* Autoantibodies against the heavy chains of immunoglobulins
* Infections such as HIV, which can lead to the overproduction of certain types of immunoglobulins
The symptoms of heavy chain disease can vary depending on the type of heavy chain that is affected and the severity of the disease. Some common symptoms include:
* Weight loss
* Night sweats
* Swollen lymph nodes
* Enlarged spleen
Heavy chain disease can be diagnosed through a variety of tests, including:
* Blood tests to measure the levels of different types of immunoglobulins in the blood
* Genetic testing to identify genetic mutations in the IGH genes
* Immunophenotyping to study the expression of heavy chains on the surface of B cells
There is no cure for heavy chain disease, but treatment options are available to manage the symptoms and prevent complications. Some common treatments include:
* Corticosteroids to reduce inflammation and suppress the immune system
* Immunoglobulin therapy to replace deficient or abnormal immunoglobulins
* Chemotherapy to reduce the production of abnormal immunoglobulins
The prognosis for heavy chain disease varies depending on the type and severity of the disease. In general, the prognosis is good for patients with light chain disease who receive prompt and appropriate treatment. However, the prognosis is poorer for patients with heavy chain disease, particularly those with a high level of immunoglobulin M (IgM) production.
The causes of heavy chain disease are not well understood, but it is believed to be related to genetic mutations in the IGH genes. There is no known prevention for heavy chain disease, and it is usually diagnosed in adults between the ages of 30 and 60.
Overall, heavy chain disease is a rare and complex disorder that can have a significant impact on quality of life. While there is no cure, early diagnosis and appropriate treatment can improve outcomes for patients with this condition.
There are several different types of uveitis, including:
1. Anterior uveitis: This type affects the front part of the eye and is the most common form of uveitis. It is often caused by an infection or injury.
2. Posterior uveitis: This type affects the back part of the eye and can be caused by a systemic disease such as sarcoidosis or juvenile idiopathic arthritis.
3. Intermediate uveitis: This type affects the middle layer of the eye and is often caused by an autoimmune disorder.
4. Panuveitis: This type affects the entire uvea and can be caused by a systemic disease such as vasculitis or Behçet's disease.
Symptoms of uveitis may include:
* Eye pain
* Redness and swelling in the eye
* Blurred vision
* Sensitivity to light
* Floaters (specks or cobwebs in your vision)
* Flashes of light
If you experience any of these symptoms, it is important to see an eye doctor as soon as possible. Uveitis can be diagnosed with a comprehensive eye exam, which may include imaging tests such as ultrasound or MRI. Treatment for uveitis depends on the cause and severity of the condition, but may include medication to reduce inflammation, antibiotics for infections, or surgery to remove any diseased tissue.
Early diagnosis and treatment are important to prevent complications such as cataracts, glaucoma, and blindness. If you have uveitis, it is important to follow your doctor's recommendations for treatment and monitoring to protect your vision.
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:
3. Heart disease
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.
Infertility can be classified into two main categories:
1. Primary infertility: This type of infertility occurs when a couple has not been able to conceive a child after one year of regular sexual intercourse, and there is no known cause for the infertility.
2. Secondary infertility: This type of infertility occurs when a couple has been able to conceive at least once before but is now experiencing difficulty in conceiving again.
There are several factors that can contribute to infertility, including:
1. Age: Women's fertility declines with age, especially after the age of 35.
2. Hormonal imbalances: Imbalances of hormones such as progesterone, estrogen, and thyroid hormones can affect ovulation and fertility.
3. Polycystic ovary syndrome (PCOS): A common condition that affects ovulation and can cause infertility.
4. Endometriosis: A condition in which the tissue lining the uterus grows outside the uterus, causing inflammation and scarring that can lead to infertility.
5. Male factor infertility: Low sperm count, poor sperm quality, and blockages in the reproductive tract can all contribute to infertility.
6. Lifestyle factors: Smoking, excessive alcohol consumption, being overweight or underweight, and stress can all affect fertility.
7. Medical conditions: Certain medical conditions such as diabetes, hypertension, and thyroid disorders can affect fertility.
8. Uterine or cervical abnormalities: Abnormalities in the shape or structure of the uterus or cervix can make it difficult for a fertilized egg to implant in the uterus.
9. Previous surgeries: Surgeries such as hysterectomy, tubal ligation, and cesarean section can affect fertility.
10. Age: Both male and female age can impact fertility, with a decline in fertility beginning in the mid-30s and a significant decline after age 40.
It's important to note that many of these factors can be treated with medical interventions or lifestyle changes, so it's important to speak with a healthcare provider if you are experiencing difficulty getting pregnant.
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:
4. Numbness or tingling in the hands and feet
5. Swelling in the legs, ankles, and feet
6. Difficulty with speech or swallowing
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 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.
There are several types of gliomas, including:
1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.
The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.
Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.
The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.
Plasmacytoma is a type of plasma cell dyscrasia, which is a group of diseases that affect the production and function of plasma cells. Plasma cells are a type of white blood cell that produces antibodies to fight infections. In plasmacytoma, the abnormal plasma cells grow and multiply out of control, leading to a tumor.
There are several subtypes of plasmacytoma, including:
* solitary plasmacytoma: A single tumor that occurs in one location.
* multiple myeloma: A type of cancer that affects the bones and is characterized by an overgrowth of malignant plasma cells in the bone marrow.
* extramedullary plasmacytoma: A tumor that occurs outside of the bone marrow, such as in soft tissue or organs.
Plasmacytoma is usually diagnosed through a combination of physical examination, imaging tests such as X-rays or CT scans, and biopsy. Treatment typically involves chemotherapy and/or radiation therapy to destroy the abnormal cells. In some cases, surgery may be necessary to remove the tumor.
Plasmacytoma is a relatively rare cancer, but it can be aggressive and potentially life-threatening if left untreated. It is important for patients with symptoms of plasmacytoma to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.
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.
List of MeSH codes (D12.776)
List of A1 genes, proteins or receptors
Protease inhibitor (biology)
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- From NCBI Gene: Mammalian lens crystallins are divided into alpha, beta, and gamma families. (nih.gov)
- 15. Sequence characterization of gamma-crystallins from lip shark (Chiloscyllium colax): existence of two cDNAs encoding gamma-crystallins of mammalian and teleostean classes. (nih.gov)
- As the main structural protein in the mammalian lens, ßB1-crystallin has an important role in the maintenance of lens transparency. (bvsalud.org)
- Alpha crystallins can be induced by heat shock and are members of the small heat shock protein (HSP20) family. (nih.gov)
- The method is illustrated for a two-domain 177-amino-acid protein, S crystallin, using an experimental SAXS data set fitted at resolutions from 200 Å to 30 Å. (nih.gov)
- Our results reveal low solubility and structural stability of ßB1-L116P at physiological temperature, which markedly impaired the protein structure and the oligomerization of ßB1-crystallin. (bvsalud.org)
- The ß-crystallin protein family is the richest and most soluble structural protein in the lens. (bvsalud.org)
- However, it is the only protein of the ßÎ³-crystallin family that has been found in an extended conformation. (bvsalud.org)
- 6. Characterization of gamma-crystallin from the eye lens of bullfrog: complexity of gamma-crystallin multigene family as revealed by sequence comparison among different amphibian species. (nih.gov)
- 12. Homology modeling of rho-crystallin from bullfrog (Rana catesbeiana) lens. (nih.gov)
- 14. Purification and characterization of rho-crystallin from Japanese common bullfrog lens. (nih.gov)
- 17. Taxon-specific zeta -crystallin in Japanese tree frog (Hyla japonica) lens. (nih.gov)
- 19. Structural similarity of bovine lung prostaglandin F synthase to lens epsilon-crystallin of the European common frog. (nih.gov)
- indiana some person, the steady collection of chromophore and complex, insoluble crystallin aggregate indium the lens nucleus moderate to the formation of deoxyadenosine monophosphate brown nuclear cataract. (chickgolden.com)
- Congenital cataract, a common disease with lens opacification, causes blindness in the newborn worldwide and is mainly caused by abnormal aggregation of crystallin. (bvsalud.org)
- Human ßB2-crystallin (HßB2C) is found in high proportion in the eye lens, and its mutations are related to some cataracts. (bvsalud.org)
- 3. Sequence analysis of frog alpha B-crystallin cDNA: sequence homology and evolutionary comparison of alpha A, alpha B and heat shock proteins. (nih.gov)
- In fact, a wide variety of native proteins exhibited induced CR circular dichroism indicating that CR bound to representative proteins from different classes of secondary structure such as alpha (citrate synthase), alpha + beta (lysozyme), beta (concavalin A), and parallel beta-helical proteins (pectate lyase). (nih.gov)
- The cataract disease is correlated with conformational changes in key proteins called crystallins. (bvsalud.org)
- B2 Microglobulin Human Recombinant produced in E.Coli is a non-glycosylated polypeptide chain having a molecular mass of 11.76 kDa.The B2M is purified by proprietary chromatographic techniques. (neobiolab.com)
- 8. Characterization of gamma-crystallin from a catfish: structural characterization of one major isoform with high methionine by cDNA sequencing. (nih.gov)
- 5. Sequence analysis of one major basic beta-crystallin (beta Bp) of amphibian lenses: evolutionary comparison and phylogenetic relatedness between beta- and gamma-crystallins. (nih.gov)
- 10. Characterization of gammaS-crystallin isoforms from a catfish: evolutionary comparison of various gamma-, gammaS-, and beta-crystallins. (nih.gov)
- 11. Characterization of gamma S-crystallin isoforms from lip shark (Chiloscyllium colax): evolutionary comparison between gamma S and beta/gamma crystallins. (nih.gov)
- 16. Characterization of gamma-crystallins from a hybrid teleostean fish: multiplicity of isoforms as revealed by cDNA sequence analysis. (nih.gov)
- crystallin beta-gamma domain containin. (gsea-msigdb.org)
- Two additional functions of alpha crystallins are an autokinase activity and participation in the intracellular architecture. (nih.gov)
- 4. Characterization, cloning, and expression of porcine alpha B crystallin. (nih.gov)
- Hsp20/alpha crystallin family [Interproscan]. (ntu.edu.sg)
- 2 microglobulin associates with class I-like molecules such as CD1 and Qa as well as with the alpha chain of MHC class I molecules. (neobiolab.com)
- Therefore, we hypothesize that the extended conformation is not energetically favourable and that HßB2C may adopt a closed (completely folded) conformation, similar to the other members of the ßÎ³-crystallin family. (bvsalud.org)
- Inclusion of these data during structure refinement decreases the backbone coordinate root-mean-square difference between the derived model and the high-resolution crystal structure of a 54% homologous B crystallin from 1.96 ( 0.07 Å to 1.31 ( 0.04 Å. (nih.gov)
- CD8 T cells cannot develop in the absence of MHC class I.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 proteinaemia, renal failure, or kidney transplants. (neobiolab.com)
- Human Beta 2 microglobulin levels can rise either because its rate of synthesis has increased (e.g. in AIDS, malignant monoclonal plasma cell dyscrasia, solid tumors and autoimmune disease) or because of impaired renal filtration (e.g. due to renal insufficiency, graft rejection or nephrotoxicity induced by post-transplantation immunosuppressive therapy). (neobiolab.com)
- Amyloid fibrils from insulin and the variable domain of Ig light chain demonstrate induced CD spectra upon binding to Congo red. (nih.gov)
- A number of components of the mycobacterial cell wall such as glycopeptidolipids, short chain mycolic acids, monomeromycolyl diacylglycerol, etc. have been shown to play an important role in formation of pellicle biofilms. (microbialcell.com)
- Conclusion: T1D and T2D likely share a final common pathway for beta cell dysfunction that includes secretion of interleukin-1? (gsea-msigdb.org)
- Comparison of avian delta-crystallins with and without endogenous argininosuccinate lyase activity. (nih.gov)
- Surprisingly, the native conformations of insulin and Ig light chain also induced Congo red circular dichroism, but with different spectral shapes than those from fibrils. (nih.gov)
- Abcam ab74008 Mouse monoclonal [G88] to Kappa light chain 125ug 3996 Kappa light chain 抗体 一抗 Dog,Ferret,Fox,Mink (Mustela). (thesixteendigital.com)
- and prostaglandins by immune effector cells, exacerbating existing beta cell dysfunction, and causing further hyperglycemia. (gsea-msigdb.org)
- Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. (neobiolab.com)
- Inclusion of these data during structure refinement decreases the backbone coordinate root-mean-square difference between the derived model and the high-resolution crystal structure of a 54% homologous B crystallin from 1.96 ( 0.07 Å to 1.31 ( 0.04 Å. (nih.gov)
- Two additional functions of alpha crystallins are an autokinase activity and participation in the intracellular architecture. (nih.gov)
- 9. mTORC1 and mTORC2 Complexes Regulate the Untargeted Metabolomics and Amino Acid Metabolites Profile through Mitochondrial Bioenergetic Functions in Pancreatic Beta Cells. (nih.gov)
- Increased line width resulting from slower majority of the resonances necessary for defining the requisite rotational diffusion leads to a decrease in signal-to-noise ratio, side-chain-mediated interdomain NOE contacts. (nih.gov)