Extracellular Matrix
Extracellular Matrix Proteins
Fibronectins
Collagen
Matrix Metalloproteinases
Matrix Metalloproteinase 2
Laminin
Tenascin
Cells, Cultured
Matrix Metalloproteinase 1
Matrix Metalloproteinase Inhibitors
Integrins
Fibroblasts
Matrix Metalloproteinase 3
Bone Matrix
Nuclear Matrix
Cell Movement
Collagen Type I
Matrix Metalloproteinase 14
Tissue Inhibitor of Metalloproteinases
Hyaluronic Acid
Glycosaminoglycans
RNA, Messenger
Basement Membrane
Tissue Inhibitor of Metalloproteinase-1
Transforming Growth Factor beta
Antigens, CD29
Tissue Inhibitor of Metalloproteinase-2
Immunohistochemistry
Collagen Type IV
Tissue Engineering
Matrix Metalloproteinase 13
Chondroitin Sulfate Proteoglycans
Signal Transduction
Gelatinases
Matrix Metalloproteinase 7
Molecular Sequence Data
Cartilage
Versicans
Decorin
Matrix Metalloproteinase 9
Antigens, CD147
Matrix Metalloproteinases, Membrane-Associated
Biglycan
Cell Differentiation
Tissue Scaffolds
Vitronectin
Fibrosis
Gelatin
Amino Acid Sequence
Thrombospondins
Blotting, Western
Transforming Growth Factor beta1
Reverse Transcriptase Polymerase Chain Reaction
Gene Expression Regulation
Fluorescent Antibody Technique
Glycoproteins
Heparan Sulfate Proteoglycans
Cell Adhesion Molecules
Matrix Metalloproteinase 12
Stress, Mechanical
Protein Binding
Osteonectin
Microscopy, Electron, Scanning
Matrix Metalloproteinases, Secreted
Models, Biological
Aggrecans
Cattle
Cell Division
Fibrillar Collagens
Biocompatible Materials
Collagen Type III
Gene Expression
Epithelial Cells
Heparitin Sulfate
Cytoskeleton
Hydrogels
Actins
Calcification, Physiologic
Cartilage, Articular
Connective Tissue
Chick Embryo
Microscopy, Electron
Receptors, Fibronectin
Skin
Matrilin Proteins
Matrix Metalloproteinase 10
Hyaluronoglucosaminidase
Cell Adhesion Molecules, Neuronal
Collagen Type VI
Dystroglycans
Focal Adhesions
Chondroitin Sulfates
Cell-Matrix Junctions
Up-Regulation
Morphogenesis
Mice, Knockout
Base Sequence
Tumor Cells, Cultured
Phenotype
Latent TGF-beta Binding Proteins
Heparin
Mechanotransduction, Cellular
Microscopy, Fluorescence
Cartilage Oligomeric Matrix Protein
Tissue Inhibitor of Metalloproteinase-3
Focal Adhesion Protein-Tyrosine Kinases
Dermis
Disease Models, Animal
Connective Tissue Growth Factor
Rats, Sprague-Dawley
Cell Communication
Cell Surface Extensions
Protein-Lysine 6-Oxidase
Gels
Procollagen
Glomerular Mesangium
Endothelium, Vascular
Transfection
Gene Expression Profiling
Epithelium
Integrin alpha5beta1
Brevican
Urokinase-Type Plasminogen Activator
Protease Inhibitors
Matrix Metalloproteinase 11
Myofibroblasts
In Situ Hybridization
Microscopy, Confocal
Elastic Tissue
Collagen Type II
Electrophoresis, Polyacrylamide Gel
Culture Media, Conditioned
Elastic Modulus
Focal Adhesion Kinase 1
Protein Structure, Tertiary
Metalloproteases
Endothelial Cells
Cell Survival
Stromal Cells
Biomimetic Materials
Keratan Sulfate
Osteoblasts
Antigens, CD44
Integrin alpha5
Receptors, Laminin
Immunoblotting
Blotting, Northern
Drug Combinations
Receptors, Vitronectin
Gene Expression Regulation, Developmental
Growth Substances
Chondrogenesis
Neovascularization, Physiologic
Binding Sites
Oligonucleotide Array Sequence Analysis
Enzyme Activation
Mesoderm
Microfilament Proteins
Gene Expression Regulation, Enzymologic
Biomechanical Phenomena
Intercellular Signaling Peptides and Proteins
Cell Membrane
Viral Matrix Proteins
Membrane Proteins
Lung
Receptors, Cell Surface
Trabecular Meshwork
Phosphorylation
Thrombospondin 1
Mesenchymal Stromal Cells
Plastics
Integrin alphaV
Cornea
Peptide Fragments
Fluorescent Antibody Technique, Indirect
Polarized distribution of Bcr-Abl in migrating myeloid cells and co-localization of Bcr-Abl and its target proteins. (1/9343)
Bcr-Abl plays a critical role in the pathogenesis of Philadelphia chromosome-positive leukemia. Although a large number of substrates and interacting proteins of Bcr-Abl have been identified, it remains unclear whether Bcr-Abl assembles multi-protein complexes and if it does where these complexes are within cells. We have investigated the localization of Bcr-Abl in 32D myeloid cells attached to the extracellular matrix. We have found that Bcr-Abl displays a polarized distribution, colocalizing with a subset of filamentous actin at trailing portions of migrating 32D cells, and localizes on the cortical F-actin and on vesicle-like structures in resting 32D cells. Deletion of the actin binding domain of Bcr-Abl (Bcr-AbI-AD) dramatically enhances the localization of Bcr-Abl on the vesicle-like structures. These distinct localization patterns of Bcr-Abl and Bcr-Abl-AD enabled us to examine the localization of Bcr-Abl substrate and interacting proteins in relation to Bcr-Abl. We found that a subset of biochemically defined target proteins of Bcr-Abl redistributed and co-localized with Bcr-Abl on F-actin and on vesicle-like structures. The co-localization of signaling proteins with Bcr-Abl at its sites of localization supports the idea that Bcr-Abl forms a multi-protein signaling complex, while the polarized distribution and vesicle-like localization of Bcr-Abl may play a role in leukemogenesis. (+info)Role of alphavbeta3 integrin in the activation of vascular endothelial growth factor receptor-2. (2/9343)
Interaction between integrin alphavbeta3 and extracellular matrix is crucial for endothelial cells sprouting from capillaries and for angiogenesis. Furthermore, integrin-mediated outside-in signals co-operate with growth factor receptors to promote cell proliferation and motility. To determine a potential regulation of angiogenic inducer receptors by the integrin system, we investigated the interaction between alphavbeta3 integrin and tyrosine kinase vascular endothelial growth factor receptor-2 (VEGFR-2) in human endothelial cells. We report that tyrosine-phosphorylated VEGFR-2 co-immunoprecipitated with beta3 integrin subunit, but not with beta1 or beta5, from cells stimulated with VEGF-A165. VEGFR-2 phosphorylation and mitogenicity induced by VEGF-A165 were enhanced in cells plated on the alphavbeta3 ligand, vitronectin, compared with cells plated on the alpha5beta1 ligand, fibronectin or the alpha2beta1 ligand, collagen. BV4 anti-beta3 integrin mAb, which does not interfere with endothelial cell adhesion to vitronectin, reduced (i) the tyrosine phosphorylation of VEGFR-2; (ii) the activation of downstream transductor phosphoinositide 3-OH kinase; and (iii) biological effects triggered by VEGF-A165. These results indicate a new role for alphavbeta3 integrin in the activation of an in vitro angiogenic program in endothelial cells. Besides being the most important survival system for nascent vessels by regulating cell adhesion to matrix, alphavbeta3 integrin participates in the full activation of VEGFR-2 triggered by VEGF-A, which is an important angiogenic inducer in tumors, inflammation and tissue regeneration. (+info)Inhibition of transforming growth factor beta production by nitric oxide-treated chondrocytes: implications for matrix synthesis. (3/9343)
OBJECTIVE: Nitric oxide (NO) is generated copiously by articular chondrocytes activated by interleukin-1beta (IL-1beta). If NO production is blocked, much of the IL-1beta inhibition of proteoglycan synthesis is prevented. We tested the hypothesis that this inhibitory effect of NO on proteoglycan synthesis is secondary to changes in chondrocyte transforming growth factor beta (TGFbeta). METHODS: Monolayer, primary cultures of lapine articular chondrocytes and cartilage slices were studied. NO production was determined as nitrite accumulation in the medium. TGFbeta bioactivity in chondrocyte- and cartilage-conditioned medium (CM) was measured with the mink lung epithelial cell bioassay. Proteoglycan synthesis was measured as the incorporation of 35S-sodium sulfate into macromolecules separated from unincorporated label by gel filtration on PD-10 columns. RESULTS: IL-1beta increased active TGFbeta in chondrocyte CM by 12 hours; by 24 hours, significant increases in both active and latent TGFbeta were detectable. NG-monomethyl-L-arginine (L-NMA) potentiated the increase in total TGFbeta without affecting the early TGFbeta activation. IL-1beta stimulated a NO-independent, transient increase in TGFbeta3 at 24 hours; however, TGFbeta1 was not changed. When NO synthesis was inhibited with L-NMA, IL-1beta increased CM concentrations of TGFbeta1 from 24-72 hours of culture. L-arginine (10 mM) reversed the inhibitory effect of L-NMA on NO production and blocked the increases in TGFbeta1. Anti-TGFbeta1 antibody prevented the restoration of proteoglycan synthesis by chondrocytes exposed to IL-1beta + L-NMA, confirming that NO inhibition of TGFbeta1 in IL-1beta-treated chondrocytes effected, in part, the decreased proteoglycan synthesis. Furthermore, the increase in TGFbeta and proteoglycan synthesis seen with L-NMA was reversed by the NO donor S-nitroso-N-acetylpenicillamide. Similar results were seen with cartilage slices in organ culture. The autocrine increase in CM TGFbeta1 levels following prior exposure to TGFbeta1 was also blocked by NO. CONCLUSION: NO can modulate proteoglycan synthesis indirectly by decreasing the production of TGFbeta1 by chondrocytes exposed to IL-1beta. It prevents autocrine-stimulated increases in TGFbeta1, thus potentially diminishing the anabolic effects of this cytokine in chondrocytes. (+info)Role of thrombin receptor in breast cancer invasiveness. (4/9343)
Invasion, the ability of an epithelial cancer cell to detach from and move through a basement membrane, is a central process in tumour metastasis. Two components of invasion are proteolysis of extracellular matrix and cellular movement through it. A potential promoter of these two processes is thrombin, the serine proteinase derived from the ubiquitous plasma protein prothrombin. Thrombin promotes the invasion of MDA-MB231 breast tumour cells (a highly aggressive cell line) in an in vitro assay. Invasion by MDA-MB436 and MCF-7 cells, less aggressive cell lines, is not promoted by thrombin. Thrombin, added to the cells, is a stimulator of cellular movement; fibroblast-conditioned medium is the chemotaxin. Thrombin-promoted invasion is inhibited by hirudin. Stimulation of invasion is a receptor-mediated process that is mimicked by a thrombin receptor-activating peptide. Thrombin has no effect on chemotaxis in vitro. Thrombin receptor is detectable on the surface of MDA-MB231 cells, but not on the other two cell lines. Introduction of oestrogen receptors into MDA-MB231 cells by transfection with pHEO had no effect on thrombin receptor expression, in the presence or absence of oestradiol. This paper demonstrates that thrombin increases invasion by the aggressive breast cancer cell line MDA-MB231 by a thrombin receptor-dependent mechanism. (+info)Extracellular matrix remodelling in the endometrium and its possible relevance to the pathogenesis of endometriosis. (5/9343)
Essential features of endometrial physiology involve the extracellular matrix (ECM). In the pathogenesis of endometriosis, interactions of endometriosis cells with ECM can be postulated. Two systems of secreted proteases in the endometrium, the plasmin(ogen) activator/inhibitor and the matrix metalloproteinases and their inhibitors were examined in cell cultures of uterine endometrial cells from women with and without endometriosis. Soluble urokinase receptor secretion is increased, and mRNA transcription of tissue inhibitor of metalloproteinases-2 (TIMP-2) is upregulated by progestin in endometriosis. These findings are compatible with an altered ECM turnover in the endometrium of these patients that may explain a higher invasive potential of retrogradely menstruated endometrial fragments. (+info)Mechanisms and mediators in coal dust induced toxicity: a review. (6/9343)
Chronic inhalation of coal dust can cause several lung disorders, including simple coal workers pneumoconiosis (CWP), progressive massive fibrosis (PMF), chronic bronchitis, lung function loss, and emphysema. This review focuses on the cellular actions and interactions of key inflammatory cells and target cells in coal dust toxicity and related lung disorders, i.e. macrophages and neutrophils, epithelial cells, and fibroblasts. Factors released from or affecting these cells are outlined in separate sections, i.e. (1) reactive oxygen species (ROS) and related antioxidant protection mechanisms, and (2) cytokines, growth factors and related proteins. Furthermore, (3) components of the extracellular matrix (ECM), including the modifying role of ROS, cytokines, proteases and antiproteases are discussed in relation to tissue damage and remodelling in the respiratory tract. It is recognised that inhaled coal dust particles are important non-cellular and cellular sources of ROS in the lung, and may be significantly involved in the damage of lung target cells as well as important macromolecules including alpha-1-antitrypsin and DNA. In vitro and in vivo studies with coal dusts showed the up-regulation of important leukocyte recruiting factors, e.g. Leukotriene-B4 (LTB4), Platelet Derived Growth Factor (PDGF), Monocyte Chemotactic Protein-1 (MCP-1), and Tumor Necrosis Factor-alpha (TNF alpha), as well as the neutrophil adhesion factor Intercellular Adhesion Molecule-1 (ICAM-1). Coal dust particles are also known to stimulate the (macrophage) production of various factors with potential capacity to modulate lung cells and/or extracellular matrix, including O2-., H2O2, and NO, fibroblast chemoattractants (e.g. Transforming Growth Factor-beta (TGF beta), PDGF, and fibronectin) and a number of factors that have been shown to stimulate and/or inhibit fibroblast growth or collagen production such as (TNF alpha, TGF beta, PDGF, Insulin Like Growth Factor, and Prostaglandin-E2). Further studies are needed to clarify the in vivo kinetics and relative impact of these factors. (+info)Matrix valency regulates integrin-mediated lymphoid adhesion via Syk kinase. (7/9343)
Lymphocytes accumulate within the extracellular matrix (ECM) of tumor, wound, or inflammatory tissues. These tissues are largely comprised of polymerized adhesion proteins such as fibrin and fibronectin or their fragments. Nonactivated lymphoid cells attach preferentially to polymerized ECM proteins yet are unable to attach to monomeric forms or fragments of these proteins without previous activation. This adhesion event depends on the appropriate spacing of integrin adhesion sites. Adhesion of nonactivated lymphoid cells to polymeric ECM components results in activation of the antigen receptor-associated Syk kinase that accumulates in adhesion-promoting podosomes. In fact, activation of Syk by antigen or agonists, as well as expression of an activated Syk mutant in lymphoid cells, facilitates their adhesion to monomeric ECM proteins or their fragments. These results reveal a cooperative interaction between signals emanating from integrins and antigen receptors that can serve to regulate stable lymphoid cell adhesion and retention within a remodeling ECM. (+info)alphaSU2, an epithelial integrin that binds laminin in the sea urchin embryo. (8/9343)
At gastrulation in the sea urchin embryo dramatic cell adhesion changes contribute to primary mesenchyme cell ingression movements and to cell rearrangements during archenteron invagination. At ingression, quantitative adhesion assays demonstrated previously that primary mesenchyme cells (PMCs) change their affinity for neighboring cells, for a fibronectin-like substrate, and for the hyaline layer. To investigate the molecular basis for these and other differential cell affinities at gastrulation, we have identified an integrin that appears to be responsible for specific alterations in cell-substrate adhesion to laminin. During early cleavage stages blastomeres adhere poorly to laminin substrates. Around hatching there is a large increase in the ability of blastomeres to bind to laminin and this increase correlates temporally with the expression of an integrin on the basal surface all blastomeres. PMCs, after undergoing their epithelial-mesenchymal transition, have a strongly reduced affinity for laminin relative to ectoderm cells and, correspondingly, do not stain for the presence of the integrin. We identified the alpha integrin cDNA from Lytechinus variegatus by RT-PCR. Overlapping clones were obtained from a midgastrula cDNA library to provide a complete sequence for the integrin. The composite cDNA encoded a protein that was most similar to the alpha5 subgroup of vertebrate integrins, but there was not a definitive vertebrate integrin homolog. Northern blots and Western immunoblots showed that the sea urchin integrin, which we have named alphaSU2, is present in eggs and during all stages of development. Immunolocalization with specific polyclonal antibodies showed that alphaSU2 first appears on the basal cell surface of epithelia at the midblastula stage, at a time correlating with the increase in adhesive affinity for laminin. The protein remains at high levels on the basal surface of ectoderm cells but is temporarily reduced or eliminated from endoderm cells during their convergent-extension movements. To confirm integrin binding specificity, alphaSU2 was transfected into an alpha-integrin-deficient CHO cell line. alphaSU2-expressing CHO cells bound well to isolated sea urchin basal lamina and to purified laminin. The transfected cells bound weakly or not at all to fibronectin, type I collagen, and type IV collagen. This is consistent with the hypothesis that alphaSU2 integrin functions by binding epithelial cells to laminin in the basal lamina. In vivo, modulation of alphaSU2 integrin expression correlates with critical adhesive changes during cleavage and gastrulation. Thus, this protein appears to be an important contributor to the morphogenetic rearrangements that characterize gastrulation in the sea urchin embryo. (+info)Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.
Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.
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.
Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
During ventricular remodeling, the heart muscle becomes thicker and less flexible, leading to a decrease in the heart's ability to fill with blood and pump it out to the body. This can lead to shortness of breath, fatigue, and swelling in the legs and feet.
Ventricular remodeling is a natural response to injury, but it can also be exacerbated by factors such as high blood pressure, diabetes, and obesity. Treatment for ventricular remodeling typically involves medications and lifestyle changes, such as exercise and a healthy diet, to help manage symptoms and slow the progression of the condition. In some cases, surgery or other procedures may be necessary to repair or replace damaged heart tissue.
The process of ventricular remodeling is complex and involves multiple cellular and molecular mechanisms. It is thought to be driven by a variety of factors, including changes in gene expression, inflammation, and the activity of various signaling pathways.
Overall, ventricular remodeling is an important condition that can have significant consequences for patients with heart disease. Understanding its causes and mechanisms is crucial for developing effective treatments and improving outcomes for those affected by this condition.
Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.
Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.
Keloids can be caused by a variety of factors, including:
* Trauma or injury to the skin, such as cuts, burns, or bites
* Surgery or other medical procedures
* Piercings or tattoos
* Skin conditions like acne or chickenpox
Keloids can appear in different shapes and sizes, and may be:
* Red or purple in color
* Raised and irregularly shaped
* Soft and rubbery to the touch
* Itchy or painful
There is no cure for keloids, but there are several treatment options available, including:
* Steroid injections to reduce inflammation and flatten the scar tissue
* Silicone gel or sheeting to help flatten and soften the scar
* Surgery to remove the keloid and repair the underlying tissue
* Laser therapy to reduce the size and color of the keloid
It's important to note that while these treatments can help improve the appearance of keloids, they may not completely eliminate them. In some cases, keloids may return after treatment.
Cicatrix is a term used to describe the scar tissue that forms after an injury or surgery. It is made up of collagen fibers and other cells, and its formation is a natural part of the healing process. The cicatrix can be either hypertrophic (raised) or atrophic (depressed), depending on the severity of the original wound.
The cicatrix serves several important functions in the healing process, including:
1. Protection: The cicatrix helps to protect the underlying tissue from further injury and provides a barrier against infection.
2. Strength: The collagen fibers in the cicatrix give the scar tissue strength and flexibility, allowing it to withstand stress and strain.
3. Support: The cicatrix provides support to the surrounding tissue, helping to maintain the shape of the affected area.
4. Cosmetic appearance: The appearance of the cicatrix can affect the cosmetic outcome of a wound or surgical incision. Hypertrophic scars are typically red and raised, while atrophic scars are depressed and may be less noticeable.
While the formation of cicatrix is a normal part of the healing process, there are some conditions that can affect its development or appearance. For example, keloid scars are raised, thick scars that can form as a result of an overactive immune response to injury. Acne scars can also be difficult to treat and may leave a lasting impression on the skin.
In conclusion, cicatrix is an important part of the healing process after an injury or surgery. It provides protection, strength, support, and can affect the cosmetic appearance of the affected area. Understanding the formation and functions of cicatrix can help medical professionals to better manage wound healing and improve patient outcomes.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient 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.
The exact cause of osteoarthritis is not known, but it is thought to be due to a combination of factors such as genetics, wear and tear on joints over time, and injuries or trauma to the joint. Osteoarthritis can affect any joint in the body, but it most commonly affects the hands, knees, hips, and spine.
The symptoms of osteoarthritis can vary depending on the severity of the condition and which joint is affected. Common symptoms include:
* Pain or tenderness in the joint
* Stiffness, especially after periods of rest or inactivity
* Limited mobility or loss of flexibility
* Grating or crackling sensations when the joint is moved
* Swelling or redness in the affected joint
* Muscle weakness or wasting
There is no cure for osteoarthritis, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These include:
* Pain relief medications such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
* Physical therapy to improve mobility and strength
* Lifestyle modifications such as weight loss, regular exercise, and avoiding activities that exacerbate the condition
* Bracing or orthotics to support the affected joint
* Corticosteroid injections or hyaluronic acid injections to reduce inflammation and improve joint function
* Joint replacement surgery in severe cases where other treatments have failed.
Early diagnosis and treatment of osteoarthritis can help manage symptoms, slow the progression of the disease, and improve quality of life for individuals with this condition.
There are several types of pulmonary fibrosis, including:
1. Idiopathic pulmonary fibrosis (IPF): This is the most common and severe form of the disease, with no known cause or risk factors. It is characterized by a rapid decline in lung function and poor prognosis.
2. Connective tissue disease-associated pulmonary fibrosis: This type is associated with conditions such as rheumatoid arthritis, systemic lupus erythematosus, and scleroderma.
3. Drug-induced pulmonary fibrosis: Certain medications, such as amiodarone and nitrofurantoin, can cause lung damage and scarring.
4. Radiation-induced pulmonary fibrosis: Exposure to high doses of radiation, especially in childhood, can increase the risk of developing pulmonary fibrosis later in life.
5. Environmental exposures: Exposure to pollutants such as silica, asbestos, and coal dust can increase the risk of developing pulmonary fibrosis.
Symptoms of pulmonary fibrosis include shortness of breath, coughing, and fatigue. The disease can be diagnosed through a combination of imaging tests such as chest X-rays, computed tomography (CT) scans, and magnetic resonance imaging (MRI), as well as lung biopsy.
Treatment options for pulmonary fibrosis are limited and vary depending on the underlying cause of the disease. Medications such as pirfenidone and nintedanib can help slow the progression of the disease, while lung transplantation may be an option for advanced cases.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
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.
The exact cause of fibrosarcoma is not known, but it is believed to be linked to genetic mutations that occur during a person's lifetime. Some risk factors for developing fibrosarcoma include previous radiation exposure, chronic inflammation, and certain inherited conditions such as neurofibromatosis type 1 (NF1).
The symptoms of fibrosarcoma can vary depending on the location and size of the tumor. In some cases, there may be no symptoms until the tumor has grown to a significant size. Common symptoms include pain, swelling, and limited mobility in the affected limb. If the tumor is near a nerve, it can also cause numbness or tingling sensations in the affected area.
Diagnosis of fibrosarcoma typically involves a combination of imaging tests such as X-rays, CT scans, and MRI scans, as well as a biopsy to confirm the presence of cancer cells. Treatment options for fibrosarcoma may include surgery, radiation therapy, and chemotherapy, depending on the size and location of the tumor, as well as the patient's overall health.
Prognosis for fibrosarcoma is generally good if the tumor is caught early and treated aggressively. However, if the cancer has spread to other parts of the body (metastasized), the prognosis is generally poorer. In some cases, the cancer can recur after treatment, so it is important for patients to follow their doctor's recommendations for regular check-ups and follow-up testing.
Overall, fibrosarcoma is a rare and aggressive form of cancer that can be challenging to diagnose and treat. However, with early detection and appropriate treatment, many people with this condition can achieve long-term survival and a good quality of life.
There are several types of diabetic nephropathy, including:
1. Mesangial proliferative glomerulonephritis: This is the most common type of diabetic nephropathy and is characterized by an overgrowth of cells in the mesangium, a part of the glomerulus (the blood-filtering unit of the kidney).
2. Segmental sclerosis: This type of diabetic nephropathy involves the hardening of some parts of the glomeruli, leading to decreased kidney function.
3. Fibrotic glomerulopathy: This is a rare form of diabetic nephropathy that is characterized by the accumulation of fibrotic tissue in the glomeruli.
4. Membranous nephropathy: This type of diabetic nephropathy involves the deposition of immune complexes (antigen-antibody complexes) in the glomeruli, leading to inflammation and damage to the kidneys.
5. Minimal change disease: This is a rare form of diabetic nephropathy that is characterized by minimal changes in the glomeruli, but with significant loss of kidney function.
The symptoms of diabetic nephropathy can be non-specific and may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Diagnosis is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies such as ultrasound or CT scans.
Treatment for diabetic nephropathy typically involves managing blood sugar levels through lifestyle changes (such as diet and exercise) and medication, as well as controlling high blood pressure and other underlying conditions. In severe cases, dialysis or kidney transplantation may be necessary. Early detection and management of diabetic nephropathy can help slow the progression of the disease and improve outcomes for patients with this condition.
There are several types of hypertrophy, including:
1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).
Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.
In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.
There are several types of melanoma, including:
1. Superficial spreading melanoma: This is the most common type of melanoma, accounting for about 70% of cases. It usually appears as a flat or slightly raised discolored patch on the skin.
2. Nodular melanoma: This type of melanoma is more aggressive and accounts for about 15% of cases. It typically appears as a raised bump on the skin, often with a darker color.
3. Acral lentiginous melanoma: This type of melanoma affects the palms of the hands, soles of the feet, or nail beds and accounts for about 5% of cases.
4. Lentigo maligna melanoma: This type of melanoma usually affects the face and is more common in older adults.
The risk factors for developing melanoma include:
1. Ultraviolet (UV) radiation exposure from the sun or tanning beds
2. Fair skin, light hair, and light eyes
3. A history of sunburns
4. Weakened immune system
5. Family history of melanoma
The symptoms of melanoma can vary depending on the type and location of the cancer. Common symptoms include:
1. Changes in the size, shape, or color of a mole
2. A new mole or growth on the skin
3. A spot or sore that bleeds or crusts over
4. Itching or pain on the skin
5. Redness or swelling around a mole
If melanoma is suspected, a biopsy will be performed to confirm the diagnosis. Treatment options for melanoma depend on the stage and location of the cancer and may include surgery, chemotherapy, radiation therapy, or a combination of these. Early detection and treatment are key to successful outcomes in melanoma cases.
In conclusion, melanoma is a type of skin cancer that can be deadly if not detected early. It is important to practice sun safety, perform regular self-exams, and seek medical attention if any suspicious changes are noticed on the skin. By being aware of the risk factors, symptoms, and treatment options for melanoma, individuals can take steps to protect themselves from this potentially deadly disease.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
The condition can be caused by a variety of factors, including excessive alcohol consumption, viral hepatitis, non-alcoholic fatty liver disease, and certain medications. It can also be a complication of other diseases such as hemochromatosis and Wilson's disease.
The symptoms of liver cirrhosis can vary depending on the severity of the disease, but may include fatigue, loss of appetite, nausea, abdominal swelling, and pain in the upper right side of the abdomen. As the disease progresses, it can lead to complications such as esophageal varices, ascites, and liver failure, which can be life-threatening.
There is no cure for liver cirrhosis, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control swelling and pain, dietary changes, and in severe cases, liver transplantation. In some cases, a liver transplant may be necessary if the disease has caused significant damage and there is no other option to save the patient's life.
In conclusion, liver cirrhosis is a serious and potentially life-threatening condition that can cause significant damage to the liver and lead to complications such as liver failure. It is important for individuals to be aware of the risk factors and symptoms of the disease in order to seek medical attention if they suspect they may have liver cirrhosis. With proper treatment and management, it is possible to slow the progression of the disease and improve the patient's quality of life.
Symptoms of Intervertebral Disc Degeneration may include:
* Back pain
* Neck pain
* Stiffness in the back and neck
* Limited range of motion
* Muscle spasms
* Tingling or numbness in the arms or legs
Treatment for Intervertebral Disc Degeneration can vary depending on the severity of the condition and may include:
* Conservative treatments such as physical therapy, pain medication, and lifestyle changes
* Injections of corticosteroids or hyaluronic acid to reduce inflammation and relieve pain
* Surgery to remove the damaged disc and fuse the adjacent vertebrae together.
It's important to seek medical attention if you experience any symptoms of Intervertebral Disc Degeneration, as early diagnosis and treatment can help to manage the condition and prevent further damage.
The symptoms of Marfan syndrome can vary widely among individuals with the condition, but typically include:
1. Tall stature (often over 6 feet 5 inches)
2. Long limbs and fingers
3. Curvature of the spine (scoliosis)
4. Flexible joints
5. Eye problems, such as nearsightedness, glaucoma, and detached retinas
6. Heart problems, such as mitral valve prolapse and aortic dilatation
7. Blood vessel problems, such as aneurysms and dissections
8. Lung problems, such as pneumothorax (collapsed lung)
9. Other skeletal problems, such as pectus excavatum (a depression in the chest wall) and clubfoot
Marfan syndrome is usually diagnosed through a combination of clinical evaluation, family history, and genetic testing. Treatment for the condition typically involves managing its various symptoms and complications, such as with medication, surgery, or lifestyle modifications. Individuals with Marfan syndrome may also need to avoid activities that could exacerbate their condition, such as contact sports or heavy lifting.
While there is currently no cure for Marfan syndrome, early diagnosis and appropriate management can help individuals with the condition live long and relatively healthy lives. With proper care and attention, many people with Marfan syndrome are able to lead fulfilling lives and achieve their goals.
Airway remodeling is a complex process that involves changes in the structure and function of the airways, as well as an immune response. It is characterized by the following features:
* Airway wall thickening and inflammation
* Increased mucus production
* Narrowing of the airway lumina due to smooth muscle hypertrophy and fibrosis
* Increased airway resistance and decreased lung function.
Airway remodeling is a hallmark of asthma and COPD, and it can lead to exacerbations and poor disease control if left untreated. The exact mechanisms driving airway remodeling are not fully understood, but it is believed that a combination of genetic and environmental factors contribute to its development.
There are several techniques used to assess airway remodeling in patients with respiratory diseases, including:
* Quantitative computed tomography (QCT) - This technique allows for the measurement of airway wall thickness and luminal area.
* Magnetic resonance imaging (MRI) - MRI can provide information on airway size and shape, as well as tissue composition.
* Bronchoscopy with biopsy - This procedure allows for the examination of airway tissue and the assessment of inflammation and fibrosis.
There are several treatments available for airway remodeling in patients with respiratory diseases, including:
* Medications such as bronchodilators, corticosteroids, and anti-inflammatory drugs
* Pulmonary rehabilitation - This includes exercises and education to help improve lung function and overall health.
* Lung transplantation - In severe cases of airway remodeling that do not respond to other treatments, lung transplantation may be considered.
It is important for patients with respiratory diseases to work closely with their healthcare provider to monitor their condition and adjust their treatment plan as needed. With appropriate management, many patients with airway remodeling can experience improved lung function and quality of life.
There are two main types of systemic scleroderma: diffuse cutaneous systemic sclerosis (DCSS) and limited cutaneous systemic sclerosis (LCSS). DCSS is characterized by skin thickening and scar formation over the trunk, arms, and legs, while LCSS is characterized by skin tightening and patches of scaly skin on the hands and face.
The symptoms of systemic scleroderma can include:
* Skin hardening and tightening
* Fatigue
* Joint pain and stiffness
* Muscle weakness
* Swallowing difficulties
* Heartburn and acid reflux
* Shortness of breath
* Raynaud's phenomenon (pale or blue-colored fingers and toes in response to cold temperatures or stress)
The exact cause of systemic scleroderma is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment options for systemic scleroderma include medications to manage symptoms such as pain, stiffness, and swallowing difficulties, as well as physical therapy and lifestyle modifications to improve quality of life.
In summary, systemic scleroderma is a chronic autoimmune disease that affects multiple systems in the body, causing skin hardening and thickening, fatigue, joint pain, and other symptoms. While there is no cure for systemic scleroderma, treatment options are available to manage symptoms and improve quality of life.
There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:
1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.
The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:
* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain
Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.
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%.
There are several subtypes of chondrosarcoma, including:
1. Grade 1 (low-grade) chondrosarcoma: This is a slow-growing tumor that is less likely to spread to other parts of the body.
2. Grade 2 (intermediate-grade) chondrosarcoma: This type of tumor grows more quickly than grade 1 and may be more likely to spread.
3. Grade 3 (high-grade) chondrosarcoma: This is an aggressive tumor that can grow quickly and spread to other parts of the body.
The symptoms of chondrosarcoma can vary depending on the location of the tumor, but may include pain in the affected area, swelling, and limited mobility. Treatment for chondrosarcoma typically involves surgery to remove the tumor, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells. The prognosis for chondrosarcoma varies depending on the grade of the tumor and the effectiveness of treatment.
Sources:
* American Cancer Society. (2020). Chondrosarcoma. Retrieved from
* Mayo Clinic. (2020). Chondrosarcoma. Retrieved from
* National Cancer Institute. (2020). Chondrosarcoma. Retrieved from
Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.
There are several types of arteriosclerosis, including:
1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.
Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.
Extracellular matrix
Extracellular matrix protein 2
Extracellular matrix protein 1
A. Hari Reddi
Interstitium
Ossein
Ground substance
Plant matrix metalloproteinase
Laminin
Tenascin
EMI domain
Chondroitinase treatment
Cell and Tissue Research
Aspein
Arterial stiffness
Mesoglea
Generative tissue
Keith Burridge
Cell wall
Mesangial cell
3D cell culture in wood-based nanocellulose hydrogel
Collagen, type I, alpha 1
Nanofiber
PAPLN
Cenderitide
McGill University Faculty of Dentistry
3D cell culture
Uveitic glaucoma
Collin Y. Ewald
Lung
TENM3
SGCA
Food web
Catenin
CD34
Trimeric autotransporter adhesin
Cerebral amyloid angiopathy
LDL receptor
Mary Cynthia Farach-Carson
Pyrobaculum
Lyme disease
Synemin
Postpartum psychosis
Collagen, type IV, alpha 2
BMP binding endothelial regulator
Trappin protein transglutaminase binding domain
PNN
Amelogenin
Samuel I. Stupp
Brain
Environmental DNA
AP-1 transcription factor
Liver support system
Glypican 6
Index of biochemistry articles
Philip Lazarovici
Industrial enzymes
HAPLN1
Heparan sulfate 2-O-sulfotransferase
TMEM125
PA-03-167: AGING MUSCULOSKELETAL AND SKIN EXTRACELLULAR MATRIX
Glycobiology and Extracellular Matrices
Cartilage and bone extracellular matrix - PubMed
Interactions of Cartilage Extracellular Matrix Macromolecules - PubMed
Extracellular Matrix and Immune Niches in Human Disease 2022 | Hindawi
NIH VideoCast - Biomedical Engineering Scientific Interest Group: Engineered Extracellular Matrix Models to Study Tumor...
Extracellular matrix Pre-coated Plates: R&D Systems
talks.cam : Mechanobiology of Cells and Extracellular Matrices
EMMPRIN (extracellular matrix metalloproteinase inducer) is a novel marker of poor outcome in serous ovarian carcinoma
Manufacturing considerations for producing and assessing decellularized extracellular matrix hydrogels. | California's Stem...
Functional ultrasound imaging for assessment of extracellular matrix scaffolds used for liver organoid formation
LTBP2 mutations cause Weill-Marchesani and Weill-Marchesani-like syndrome and affect disruptions in the extracellular matrix -...
Identification of Molecules in Leech Extracellular Matrix that Promote Neurite Outgrowth - NASA/ADS
Expression of CD133 and Extracellular Matrix Molecules in Malignant Brain Tumors
Physicochemical properties of extracellular matrix: Key to function, Clue to mechanism
Rat pancreatic stellate cells secrete matrix metalloproteinases: implications for extracellular matrix turnover | Gut
Macrophage Deposition of Cholesterol into the Extracellular Matrix | NIH Research Festival
Fibroblast growth factor 21 (FGF21) alleviates senescence, apoptosis, and extracellular matrix degradation in osteoarthritis...
Figures and data in MITF reprograms the extracellular matrix and focal adhesion in melanoma | eLife
Adipose extracellular matrix promotes skin wound healing by inducing the differentiation of adipose‑derived stem cells into...
KEGG entry for human spondin 2, extracellular matrix protein SPON2
Effect of MeCP2 on TGF-β1-induced Extracellular Matrix Production in Nasal Polyp-derived Fibroblasts - Physician's Weekly
Hypohalous Acids Contribute to Renal Extracellular Matrix Damage in Experimental Diabetes | Diabetes | American Diabetes...
The musculotendinous transition of the extracellular matrix | Apunts Sports Medicine
Collagen and Endothelial Cell Coculture Improves β-Cell Functionality and Rescues Pancreatic Extracellular Matrix - NMI.de
The feelgood mutation in zebrafish dysregulates COPII-dependent secretion of select extracellular matrix proteins in skeletal...
Adhesion of eukaryotic cell lines on the gold surface modified with extracellular matrix proteins monitored by the...
Tranilast inhibits pulmonary fibrosis by suppressing TGFbeta-mediated extracellular matrix protein production
Extracellular matrix molecules and cell adhesion molecules induce neurites through different mechanisms. | Journal of Cell...
Proteins8
- The complexity of the extracellular matrix is not only reflected in the distribution of extracellular matrix proteins throughout different tissues and organs, but also during different physiological and pathological processes. (hindawi.com)
- R&D Systems offers a range of aseptically prepared microplates pre-coated with extracellular matrix (ECM) proteins for culturing adherent cell lines and quantifying cell adhesion. (rndsystems.com)
- We demonstrate that hypohalous acid-derived modifications of renal tissues and extracellular matrix (ECM) proteins are significantly elevated in experimental diabetic nephropathy. (diabetesjournals.org)
- Extracellular matrix (ECM) proteins are known to impact numerous reparative functions in the body. (nmi.de)
- The cells were adhered and grown on the gold surface of the sensor pre-coated with adsorbed layer of extracellular matrix proteins as vitronectin and laminin. (muni.cz)
- Cartilage contains numerous noncollagenous proteins in its extracellular matrix, including proteoglycans. (biomedcentral.com)
- The extracellular matrix of articular cartilage contains a large variety of noncollagenous proteins. (biomedcentral.com)
- Background: The over expression of fascin, extracellular matrix metalloproteinase inducer (EMMPRIN), and ezrin proteins has been associated with poor prognosis in various carcinomas and sarcomas. (who.int)
Molecules5
- Various cell types secrete different matrix molecules and the nature and the amount of these molecules change during developmental age. (nih.gov)
- EMMPRIN is a member of the immunoglobulin superfamily of adhesion molecules and has a role in the activation of several matrix metalloproteinases (MMP). (nih.gov)
- Extracellular matrix molecules and cell adhesion molecules induce neurites through different mechanisms. (rupress.org)
- It has recently become clear that both extracellular matrix (ECM) glycoproteins and various cell adhesion molecules (CAMs) can promote neurite outgrowth from primary neurons, though little is known of the intracellular mechanisms through which these signals are transduced. (rupress.org)
- Some of the molecules represent degradation products of larger precursors that accumulate because of their interaction with other matrix components. (biomedcentral.com)
Metalloproteinase inducer1
- IMSEAR at SEARO: Clinicopathologic significance of fascin, extracellular matrix metalloproteinase inducer, and ezrin expressions in colorectal adenocarcinoma. (who.int)
Macromolecules2
- The extracellular matrix (ECM) is a complex of self assembled macromolecules. (nih.gov)
- Extracellular matrix (ECM) is a three-dimensional network entity composed of extracellular macromolecules. (bvsalud.org)
Heterogeneity1
- The heterogeneity of extracellular matrix (ECM) of breast cancer has remained largely unexplored and underestimated. (bvsalud.org)
Tissues8
- Projects are encouraged that determine how cellular aging processes lead to altered matrix production and maintenance, and how aging-related altered matrix composition and organization affect the function of these tissues. (nih.gov)
- Cartilage and bone are classified as connective tissues and are composed largely of extracellular matrix. (nih.gov)
- The interaction of the epidermis and the muscle fibers with their associated connective tissue and, in particular, the extracellular matrix, is fundamental to the function of these tissues. (nih.gov)
- In most of these tissues there is evidence of increased turnover of extracellular matrix with age as well as changes in composition of the matrix with age. (nih.gov)
- Because these tissues depend on matrix for function and cell viability, these aging-associated changes in matrix are likely key to altered integrity and function of the musculoskeletal tissues and skin in the elderly. (nih.gov)
- Thus, matrix influences on blood vessels and nerves in aging tissues of the musculoskeletal system and skin may be important to understand, as vascular and neural function change. (nih.gov)
- We are soliciting applications from post-doctoral level scientists interested in developing and implementing novel MRI methods for studying water and ion transport mechanisms in extracellular matrix (ECM), tissue culture systems, or "engineered" tissues. (nih.gov)
- Extracellular matrix (ECM) from decellularized tissues provide a physical scaffolding and offers crucial biochemical and biomechanical cues for cellular constituents. (nih.gov)
Pathological3
- Turnover and degradation of normal and pathological matrices are dependent on the responses of the local cell to auto and paracrine anabolic and catabolic pathway. (nih.gov)
- Although we have a certain understanding of the basic structure of the extracellular matrix and its physiological and pathological functions, there are still many important questions to be answered in this field. (hindawi.com)
- Impact statement Expression analysis identifies hypoxia-induced pathological changes in extracellular matrix (ECM) homeostasis as potential targets to support β-cell transplants by encapsulation in biomaterials for the treatment of diabetes mellitus. (nmi.de)
Vesicles2
- Extracellular vesicles (EVs) are widely studied regarding their role in cell-to-cell communication and disease, as well as for applications as biomarkers or drug delivery vehicles. (nature.com)
- Extracellular vesicles (EVs) are released by many cell types in vitro and in vivo and are present in most body fluids. (nature.com)
Cells8
- Reciprocally, the matrix and the mechanical and biochemical processes it is subject to, affect the cells. (nih.gov)
- In bone, as well as in cartilage, the ECM resident cells produce local factors, inflammatory mediators, and matrix-degrading enzymes. (nih.gov)
- Extracellular matrix (ECM) has a broad impact on the basic function of immune cells: affecting cell survival, growth and differentiation, and determining cell shape and migration. (hindawi.com)
- This Special Issue invites original research and review articles that further the understanding and clarify the related fundamental knowledge and underlying mechanism of the interplay between immune cells and their extracellular matrices, in order to explore new therapeutic strategies and improve clinical outcomes. (hindawi.com)
- In this study, we evaluate different manufacturing parameters for making an injectable biomaterial derived from skeletal muscle from pigs that has been stripped of all cells, leaving behind only the extracellular matrix of the tissue. (ca.gov)
- In the present study, it was hypothesized that adipose‑derived stem cells (ADSCs) could be induced by the adipose extracellular matrix (ECM) to differentiate into fibroblasts in order to promote skin wound healing. (spandidos-publications.com)
- As previously reported, several immune cells, including T cells, may be associated with scar formation, and epidermal cells have a critical role in wound healing by regulating the extracellular matrix (ECM) ( 4 ). (spandidos-publications.com)
- Breast cancer cells interact with tumor-derived extracellular matrix in a molecular subtype-specific manner. (bvsalud.org)
Apoptosis2
- The matrix is a mediator of signals for cell proliferation and differentiation, and for apoptosis. (nih.gov)
- In vitro, the results revealed that FGF21 administration alleviated apoptosis, senescence, and extracellular matrix (ECM) catabolism of the chondrocytes induced by tert-butyl hydroperoxide (TBHP) by mediating autophagy flux. (sens.org)
Homeostasis2
- It is becoming increasingly apparent that while the extracellular environment normally maintains tissue homeostasis, but when negatively perturbed, it may also contribute to disease progression and age-dependent pathologies. (harvard.edu)
- Extracellular matrix in synovium development, homeostasis and arthritis disease. (bvsalud.org)
Adipose1
- The National Institutes of Diabetes and Digestive and Kidney Diseases (NIDDK) announces a workshop focusing on the role of the adipose tissue niche in the development, maintenance and remodeling of different adipose tissue depots in healthy individuals, and how the extracellular matrix and cellular components of the niche are modified during the develop of diabetes, in the overfed state, and following other metabolic stressors. (nih.gov)
Protein2
- R&D Systems Extracellular Matrix (ECM) Protein Coated Plate assay template (left). (rndsystems.com)
- Latent transforming growth factor (TGF) beta-binding protein 2 (LTBP2) is an extracellular matrix (ECM) protein that associates with fibrillin-1 containing microfibrils. (nih.gov)
Proteoglycans1
- Cartilage ECM is composed mainly of two components defining its mechano-physical properties: the collagenous network, responsible for the tensile strength of the cartilage matrix, and the proteoglycans (mainly aggrecan), responsible for the osmotic swelling and the elastic properties of the cartilage tissue. (nih.gov)
Tumor1
- In addition, dynamic changes in the extracellular matrix network are also one of the basic features of the tumor microenvironment. (hindawi.com)
Responses3
- However, it is still unknown how the extracellular matrix contributes to tissue regeneration and how changes in the extracellular matrix induces differential cellular responses in diseases. (harvard.edu)
- In this talk, Varghese will discuss efforts to delineate the role of the extracellular matrix on cellular responses relevant to tissue repair, stem cell differentiation, and disease progression. (harvard.edu)
- However, these 3-D cell constructs are limited in that they do not integrate extracellular components within the structure important for more reliable and accurate biological responses. (nih.gov)
Composition2
- More needs to be done to understand the changes that take place in extracellular matrix composition and structure with age, why those changes occur and the mechanisms by which they result in altered tissue function. (nih.gov)
- Thus, changes in matrix composition with age could lead to altered local balances or effects of these factors. (nih.gov)
Interactions1
- Furthermore, there is evidence that the extracellular matrix acts as a reservoir of humoral factors such as hormones and growth factors, and mediates cell interactions with these factors. (nih.gov)
Accumulate1
- Our previous research has identified a novel macrophage cholesterol processing pathway, in which macrophages deposit excess cholesterol into the extracellular matrix where it can accumulate unless mobilized by HDL. (nih.gov)
Components1
- Its lectin-like properties suggest the possibility of interaction with other components of the extracellular matrix [ 3 ], though it has also been suggested that it is involved in intracellular trafficking during aggrecan synthesis. (biomedcentral.com)
Interaction1
- MITF depletion affects cell size and cell-matrix interaction. (elifesciences.org)
Cancer1
- Work in cancer shows that the matrix influences angiogenesis. (nih.gov)
Metalloproteinases2
- The objectives of this study were to investigate the relationship of CD133 and other remodeling factors such as matrix metalloproteinases (MMP) in the brain tumors. (scirp.org)
- The NOTCH pathway may be also related to many remodeling factors such as matrix metalloproteinases (MMP) in the brain tumors. (scirp.org)
Increasingly1
- Paradoxically, however, the matrix can become increasingly insoluble, less digestible and more cross- linked with age. (nih.gov)
Function3
- The extracellular matrix is involved in normal tissue function on a number of levels, including regulation of cell fate, growth and function within the tissue. (nih.gov)
- The extracellular matrix may have an influence on vascular function and neurological function, and the converse may also be true. (nih.gov)
- In this study, we examined the function of ATP-binding cassette transporter A1 (ABCA1) in ApoA-I mobilization of cholesterol deposited into the extracellular matrix by cholesterol-enriched macrophages. (nih.gov)
Network1
- The extracellular matrix (ECM) of cartilage consists of a fibrous collagen network, which is pre-stressed by the osmotic swelling pressure exerted by negatively charged proteoglycan aggregates embedded in the collagen network. (nih.gov)
Show1
- Conclusions: Our findings show that extracellular cholesterol deposited by macrophages can be mobilized by both ApoA-I and 5A, but that mobilization depends on macrophage ABCA1. (nih.gov)