Cell Migration Assays
Cell Migration Assays, Macrophage
Cell Movement
Cell Migration Assays, Leukocyte
Cells, Cultured
Signal Transduction
Leukocytes
Cell Migration Inhibition
Leukocyte Rolling
Chemotaxis, Leukocyte
Chemotaxis
Leukocyte Count
Focal Adhesions
RNA, Small Interfering
Endothelial Cells
Fibronectins
Integrins
Chemokine CXCL12
Blotting, Western
Receptors, CXCR4
Endothelium, Vascular
Animal Migration
Actins
Neutrophils
Pseudopodia
Phosphorylation
RNA Interference
Laminin
Cell Adhesion Molecules
rac1 GTP-Binding Protein
Reverse Transcriptase Polymerase Chain Reaction
Foreign-Body Migration
Transfection
Antigens, CD29
Focal Adhesion Protein-Tyrosine Kinases
Matrix Metalloproteinase 9
Gene Knockdown Techniques
RNA, Messenger
Cell Polarity
Gene Expression Regulation, Neoplastic
Mice, Knockout
Extracellular Matrix
Fibroblasts
Epithelial Cells
Diffusion Chambers, Culture
Up-Regulation
Immunohistochemistry
Neovascularization, Physiologic
Neoplasm Metastasis
Cytoskeleton
Flow Cytometry
Paxillin
Chemokines, CXC
Tumor Cells, Cultured
Matrix Metalloproteinase 2
rac GTP-Binding Proteins
Neovascularization, Pathologic
Cell Surface Extensions
Epithelium, Corneal
Protein Binding
Chemokines
Microscopy, Fluorescence
Enzyme Activation
Collagen
Cadherins
Dose-Response Relationship, Drug
Phosphatidylinositol 3-Kinases
Molecular Sequence Data
Vitronectin
Vascular Endothelial Growth Factor A
Cell Differentiation
Down-Regulation
Cell Division
Platelet-Derived Growth Factor
rho GTP-Binding Proteins
Umbilical Veins
Myocytes, Smooth Muscle
rhoA GTP-Binding Protein
Proto-Oncogene Proteins c-akt
Antigens, CD
Monocytes
Receptors, Chemokine
Enzyme Inhibitors
Chemotactic Factors
Neural Crest
cdc42 GTP-Binding Protein
Gene Expression Regulation
Focal Adhesion Kinase 1
Amino Acid Sequence
Microscopy, Video
Antigens, CD18
Models, Biological
Disease Models, Animal
Gene Expression
Venules
Macrophage Migration-Inhibitory Factors
Membrane Proteins
Apoptosis
Culture Media, Conditioned
Time-Lapse Imaging
Cell Survival
Glioma
Stem Cells
Real-Time Polymerase Chain Reaction
Secretory Leukocyte Peptidase Inhibitor
Epidermal Growth Factor
Leukocyte Elastase
Microfilament Proteins
Mice, Nude
Coculture Techniques
Angiogenesis Inhibitors
Transendothelial and Transepithelial Migration
Intercellular Signaling Peptides and Proteins
Keratinocytes
P-Selectin
Lysophospholipids
Melanoma
Intercellular Adhesion Molecule-1
Ligands
Chemokine CCL2
Trophoblasts
Phenotype
Cell Communication
Cytoskeletal Proteins
Leukocyte Transfusion
Macrophages
Mitogen-Activated Protein Kinase 3
Fibroblast Growth Factor 2
Mutation
Inflammation
src-Family Kinases
Antibodies
Proto-Oncogene Proteins c-met
Crk-Associated Substrate Protein
rho-Associated Kinases
Dendritic Cells
Rats, Sprague-Dawley
Cytokines
NIH 3T3 Cells
Lymphocyte Function-Associated Antigen-1
Morphogenesis
Extracellular Signal-Regulated MAP Kinases
Cattle
Mesenchymal Stromal Cells
Enzyme-Linked Immunosorbent Assay
Protein Structure, Tertiary
L-Selectin
Gene Expression Regulation, Developmental
Guanine Nucleotide Exchange Factors
Integrin alpha5beta1
MAP Kinase Signaling System
Protein-Tyrosine Kinases
Integrin alpha4
Actin Cytoskeleton
Stress Fibers
Bone Marrow Cells
Zebrafish
Integrin alpha4beta1
Embryo, Nonmammalian
Antigens, CD44
Activation of protein tyrosine kinases and matrix metalloproteinases causes blood-brain barrier injury: Novel mechanism for neurodegeneration associated with alcohol abuse. (1/45)
Blood-brain barrier (BBB) formed by brain microvascular endothelial cells (BMVEC) regulates the passage of molecules and leukocytes in and out of the brain. Activation of matrix metalloproteinases (MMPs) and alteration of basement membrane (BM) associated with BBB injury was documented in stroke patients. While chronic alcoholism is a risk factor for developing stroke, underlying mechanisms are not well understood. We hypothesized that ethanol (EtOH)-induced protein tyrosine kinase (PTK) signaling resulted a loss of BBB integrity via MMPs activation and degradation of BM component, collagen IV. Treatment of BMVEC with EtOH or acetaldehyde (AA) for 2-48 h increased MMP-1, -2 and -9 activities or decreased the levels of tissue inhibitors of MMPs (TIMP-1, -2) in a PTK-dependent manner without affecting protein tyrosine phosphatase activity. Enhanced PTK activity after EtOH exposure correlated with increased phosphorylated proteins of selective receptor and nonreceptor PTKs. Up-regulation of MMPs activities and protein contents paralleled a decrease in collagen IV content, and inhibitors of EtOH metabolism, MMP-2 and -9, or PTK reversed all these effects. Using human BMVEC assembled into BBB models, we found that EtOH/AA diminished barrier tightness, augmented permeability, and monocyte migration across the BBB via activation of PTKs and MMPs. These findings suggest that alcohol associated BBB injury could be mediated by MMPs via BM protein degradation and could serve as a comorbidity factor for neurological disorders like stroke or neuroinflammation. Furthermore, our preliminary experiments indicated that human astrocytes secreted high levels of MMP-1 and -9 following exposure to EtOH, suggesting the role of BM protein degradation and BBB compromise as a result of glial activation by ethanol. These results provide better understanding of multifaceted effects of alcohol on the brain and could help develop new therapeutic interventions. (+info)Neutrophil interactions with keratocytes during corneal epithelial wound healing: a role for CD18 integrins. (2/45)
PURPOSE: To determine the role of keratocytes and leukocyte beta(2) (CD18) integrins in neutrophil (PMN) migration through the corneal stroma after epithelial scrape injury. METHODS: Using C57BL/6 wild-type and CD18(-/-) mice, corneas were excised at 6 hours (wild-type) or 24 hours (CD18(-/-)) after central corneal epithelial abrasion, time points determined previously to have similar levels of emigrated PMNs. Corneas were prepared for ultrastructural morphometric analysis of PMNs, keratocyte networks, and collagen. RESULTS: Transmission electron microscopy revealed intact keratocyte networks within the paralimbus that were morphometrically similar, regardless of epithelial injury or mouse genotype. Secondary to epithelial abrasion, extravasated PMNs within the paralimbus developed close contacts with keratocytes and collagen. In wild-type mice, 40% of the PMN surface was in contact with the keratocyte surface, and this value decreased to 10% in CD18(-/-) mice. PMN contact with collagen was similar in wild-type and CD18(-/-) mice, with approximately 50% of the PMN surface contacting the collagen fibrils. Since corneal edema resulting from scrape injury was similar, regardless of genotype and did not involve structural changes in collagen fibrils, these data favor a direct role for CD18 in mediating PMN contact with keratocytes. CONCLUSIONS: The data show that in response to epithelial scrape injury, PMN migration in the corneal stroma involves close contact between keratocytes and collagen. Although PMN-keratocyte contacts require CD18 integrins, contact with collagen is CD18 independent. Fundamentally, PMN migration along keratocyte networks constitutes the beginning of a new experimental concept for understanding leukocyte migration within the wounded cornea. (+info)STAT1 signaling modulates HIV-1-induced inflammatory responses and leukocyte transmigration across the blood-brain barrier. (3/45)
The relationship among neuroinflammation, blood-brain barrier (BBB) dysfunction, and progressive HIV-1 infection as they affect the onset and development of neuroAIDS is incompletely understood. One possible link is signal transducers and activators of transcription (STATs) pathways. These respond to proinflammatory and regulatory factors and could affect neuroinflammatory responses induced from infected cells and disease-affected brain tissue. Our previous works demonstrated that HIV-1 activates pro-inflammatory and interferon-alpha-inducible genes in human brain microvascular endothelial cells (HBMECs) and that these genes are linked to the Janus kinase (JAK)/STAT pathway. We now demonstrate that HIV-1 activates STAT1, induces IL-6 expression, and diminishes expression of claudin-5, ZO-1, and ZO-2 in HBMECs. The STAT1 inhibitor, fludarabine, blocked HIV-1-induced IL-6, diminished HIV-1-induced claudin-5 and ZO-1 down-regulation, and blocked HIV-1- and IL-6-induced monocyte migration across a BBB model. Enhanced expression and activation of STAT1 and decreased claudin-5 were observed in microvessels from autopsied brains of patients with HIV-1-associated dementia. These data support the notion that STAT1 plays an integral role in HIV-1-induced BBB damage and is relevant to viral neuropathogenesis. Inhibition of STAT1 activation could provide a unique therapeutic strategy to attenuate HIV-1-induced BBB compromise and as such improve clinical outcomes. (+info)Immunomodulation by alpha(1)-proteinase inhibitor: lack of chemotactic effects of recombinant human alpha(1)-proteinase inhibitor from yeast on human peripheral blood granulocytes. (4/45)
INTRODUCTION: Recombinant alpha(1)-proteinase inhibitor, clinically developed for inhalative augmentation therapy in patients with alpha(1)-proteinase inhibitor deficiency or cystic fibrosis, may directly contribute to leukocyte accumulation as it may function as a chemoattractant. The migratory effects of yeast-derived human recombinant alpha(1)-proteinase inhibitor on human peripheral blood neutrophils and eosinophils were therefore tested in vitro. MATERIALS AND METHODS: Human peripheral blood leukocytes were prepared from forearm venous blood and tested for migration toward various preparations of yeast-derived recombinant alpha(1)-proteinase inhibitor in modified Boyden-chamber micropore filter assays. RESULTS: No direct effects of yeast-derived recombinant human alpha(1)-proteinase inhibitor on in vitro migration of isolated neutrophils or eosinophils were seen. CONCLUSIONS: The lack of direct chemotactic effects of recombinant human alpha(1)-proteinase inhibitor despite anti-inflammatory effects in other biological activities of leukocytes may contribute to the preserved antibacterial defense mechanisms observed in patients under experimental augmentation therapy with inhaled alpha(1)-proteinase inhibitor. (+info)C-terminal repeats of Clostridium difficile toxin A induce production of chemokine and adhesion molecules in endothelial cells and promote migration of leukocytes. (5/45)
The C-terminal repeating sequences of Clostridium difficile toxin A (designated ARU) are homologous to the carbohydrate-binding domain of streptococcal glucosyltransferases (GTFs) that were recently identified as potent modulins. To test the hypothesis that ARU might exert a similar biological activity on endothelial cells, recombinant ARU (rARU), which was noncytotoxic to cell cultures, was analyzed using human umbilical vein endothelial cells. The rARU could bind directly to endothelial cells in a serum- and calcium-dependent manner and induce the production of interleukin-6 (IL-6), IL-8, and monocyte chemoattractant protein 1 in a dose-dependent manner. An oligosaccharide binding assay indicated that rARU, but not GTFC, binds preferentially to Lewis antigens and 3'HSO3-containing oligosaccharides. Binding of rARU to human endothelial or intestinal cells correlated directly with the expression of Lewis Y antigen. Bound rARU directly activated mitogen-activated protein kinases and the NF-kappaB signaling pathway in endothelial cells to release biologically active chemokines and adhesion molecules that promoted migration in a transwell assay and the adherence of polymorphonuclear and mononuclear cells to the endothelial cells. These results suggest that ARU may bind to multiple carbohydrate motifs to exert its biological activity on human endothelial cells. (+info)Infection of endothelial cells with virulent Rickettsia prowazekii increases the transmigration of leukocytes. (6/45)
(+info)Epstein-Barr virus lytic transactivator Zta enhances chemotactic activity through induction of interleukin-8 in nasopharyngeal carcinoma cells. (7/45)
(+info)Comparative study of the usefulness of the drug-induced lymphocyte stimulation test and the leukocyte migration test in drug allergies. (8/45)
In 133 patients suspected of hypersensitivity to drugs and 102 control patients without hypersensitivity to drugs, the identification of allergenic drugs was performed by the drug-induced lymphocyte stimulation test (DLST) and the leukocyte migration test (LMT) to compare their usefulness in identifying drug allergies. In the 133 subject patients, the positive rate was 24.8% on the DLST and 60.9% on the LMT (agreement rate; 77.4%); thus, the LMT showed a significantly higher positive rate than the DLST (p<0.000001, chi(2)-test). In the 102 control patients, the positive rates on the DLST and LMT were 6.9%. In addition, the LMT showed a higher positive rate than the DLST for many hypersensitivity symptoms such as skin eruptions and hepatic injury, and for many drug efficacy categories of the suspected drugs such as antibacterial drugs, etc. Furthermore, the positive rate of the DLST did not change when adjusted for the patients' serum and sex, while that of the LMT increased when adjusted for the patients' serum and was found to be higher in females than in males. Our findings indicate that the LMT may be more useful than the DLST in identifying the causative drug in drug allergies and that its interpretation is influenced by the patient's serum and sex. (+info)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.
Foreign-body migration refers to the movement or migration of a foreign object or material within the body over time. This can occur after a surgical procedure, injury, or other medical intervention where a foreign object is introduced into the body. The term "foreign body" includes any object or material that is not naturally present within the body, such as implants, sutures, staples, and other medical devices.
The migration of a foreign body can occur due to various factors, including:
1. Mechanical forces: Movement of the body, such as during exercise or daily activities, can cause the foreign object to shift position or migrate to another part of the body.
2. Biological forces: The body's natural healing processes and inflammatory responses can cause the foreign object to move or change shape over time.
3. Chemical forces: Corrosion or degradation of the foreign material can lead to its migration within the body.
4. Cellular forces: Cells in the body can surround and interact with the foreign object, leading to its movement or displacement.
The migration of a foreign body can have significant clinical implications, including:
1. Pain and discomfort: The movement of a foreign object within the body can cause pain, discomfort, and inflammation.
2. Infection: The migration of a foreign object can increase the risk of infection, particularly if the object is made of a material that is susceptible to bacterial growth.
3. Organ damage: If the migrated foreign object damages surrounding tissues or organs, it can lead to serious complications and long-term health problems.
4. Revision surgery: In some cases, the migration of a foreign body may require revision surgery to remove or reposition the object.
To prevent foreign-body migration, medical professionals use various techniques, such as:
1. Implant fixation: Implants can be fixed in place using bone screws, sutures, or other fixation devices to minimize their movement.
2. Biocompatible materials: Using biocompatible materials for implants and other medical devices can reduce the risk of foreign-body reaction and migration.
3. Proper surgical technique: Surgeons must use proper surgical techniques when inserting foreign objects into the body, such as using a sterile environment and appropriate insertion angles.
4. Postoperative care: Proper postoperative care, including antibiotics and pain management, can help prevent complications and promote healing.
Overall, preventing the migration of foreign bodies is essential to ensure successful medical outcomes and minimize the risk of complications.
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.
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.
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.
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 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.
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.
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.
Proteases in angiogenesis
Chemotaxis
SULF1
List of MeSH codes (E01)
EMR2
Gelatinase B
MMP9
Microfluidic cell culture
TAAR1
Thrombin
Slit-Robo
Angiostrongylus cantonensis
MYH9
LSP1
Edgar Pick
Neurofibromin 1
Anaplastic lymphoma kinase
Allergy
GRB2
Matrix metalloproteinase
Specialized pro-resolving mediators
12-Hydroxyheptadecatrienoic acid
Cell polarity
Arachidonate 5-lipoxygenase
DDX3X
CD44
Phagocyte
Computational immunology
Cytokine
Septic arthritis
Sperm chemotaxis
High-density lipoprotein
Murine respirovirus
Eugene C. Butcher
Signal transduction
Degradomics
13-Hydroxyoctadecadienoic acid
Broad-spectrum chemokine inhibitor
Lipoxin
CXCL1
Neuromyelitis optica spectrum disorder
Leukocyte extravasation
Tetherin
Pasteurella multocida
KLF2
IL1β induces mesenchymal stem cells migration and leucocyte chemotaxis through NF-κB - PubMed
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Breast Cancer: subgroups specific blood-biomarkers for early / predictive diagnosis and personalized treatment
MESH TREE NUMBER CHANGES - 2012 MeSH. August 19, 2011
NEW (2008) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 11/05/2007
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Endothelial cells11
- Murine and human endothelial cells (ECs) were infected with R. prowazekii, including the virulent Breinl strain and the attenuated Madrid E strain. (nih.gov)
- Simple Modifications to Methimazole that Enhance its Inhibitory Effect on Tumor Necrosis Factor-alpha-Induced Vascular Cell Adhesion Molecule-1 Expression by Human Endothelial Cells. (ohio.edu)
- Attachment of tumor cells to endothelial cells is crucial for migration of Tubastatin A HCl tumor cells from the vascular program to determine metastases. (hiv-proteases.com)
- The activation of XO and reduced Tetrahydrobiopterin (BH 4 ) levels in endothelial cells leads to increased reactive oxygen species (ROS) formation, which in turn leads to endothelial nitric oxide synthase (eNOS) uncoupling and further production of superoxide (Thomas, et al 2010). (justia.com)
- The Sickled-shaped erythrocytes together with endothelial cells, activated leukocytes, platelets and plasma proteins participate in the multistep vaso-occlusion process (Frenette 2002). (justia.com)
- In endothelial cells arginase can constrain eNOS activity by limiting the availability of L-arginine functionally. (opioid-receptors.com)
- Although KG-WE can induce NO creation in endothelial cells the root molecular systems and proteins involved with this pathway possess yet to become elucidated. (opioid-receptors.com)
- However, very little is known about the regulation of CARD8 in endothelial cells and atherosclerosis. (nature.com)
- The aim of this study was to investigate CARD8 in the regulation of cytokine and chemokine expression in endothelial cells. (nature.com)
- The CARD8 mRNA was knocked-down in human umbilical vein endothelial cells (HUVECs) in vitro, followed by quantitative RT-PCR analysis and OLINK Proteomics. (nature.com)
- The present study suggest that CARD8 regulate the expression of cytokines and chemokines in endothelial cells and atherosclerotic lesions, suggesting that CARD8 plays a significant role in endothelial activation. (nature.com)
Vitro10
- 3. [Determination of the tuberculin hypersensitivity by in vitro method of leukocyte migration inhibition from the capillary micro-hematocrit]. (nih.gov)
- 6. [Cellular immunity: in vitro leukocyte migration inhibition does not correlate with the tuberculin skin test]. (nih.gov)
- 14. Correlation of in vitro and in vivo tests for cell-mediated immunity in the dog. (nih.gov)
- 15. A comparison of the inhibition of leucocyte migration and monocyte spreading as in vitro assays for tuberculin hypersensitivity in man. (nih.gov)
- Finally, we examined the direct effects of ethanol on endothelial cell activation and leukocyte-endothelial cell interactions in vitro. (nih.gov)
- Ethanol, at concentrations within the range found in human blood after acute exposure and below the levels that induce cytotoxicity (0.1-0.5%), did not induce endothelial cell activation, but significantly inhibited TNF-mediated endothelial cell activation, as measured by adhesion molecule (E-selectin, ICAM-1, VCAM-1) expression and chemokine (IL-8, MCP-1, RANTES) production and leukocyte adhesion in vitro. (nih.gov)
- NIH/3T3 cell lysates (500 µl at 1 mg/ml) were treated in vitro with GTPγS or GDP to activate or inactivate Rap1 (refer to optional step C in protocol). (cellsignal.com)
- In addition, effector function and CNS migration of T cells using a human in vitro blood-brain barrier (BBB) assay were analyzed. (regionh.dk)
- The injection of HT29 cells, exposed to platelets in vitro , into the tail vein of humanized immunodeficient mice led to higher incidence of lung metastasis compared to the injection of untreated HT29 cells. (oncotarget.com)
- Platelet COX-1 inhibition by aspirin administration to mice prevented the increased rate of metastasis as well as the enhanced production of TXA 2 and PGE 2 induced by the in vitro priming of HT29 cells by platelets. (oncotarget.com)
Adhesion molecule3
- In this model, ethanol markedly suppressed leukocyte accumulation and endothelial cell adhesion molecule expression in a dose-dependent manner. (nih.gov)
- Enables cell adhesion molecule binding activity. (nih.gov)
- It counts epithelial cancer cells from whole blood using magnetic immunotargeting of the epithelial cell adhesion molecule (EpCAM), and subsequently identifies CTCs with fluorescently labelled antibodies against cyto-keratin7. (cadworks3d.com)
Chemokine4
- Chemokine-directed leukocyte migration is crucial for effective immune and inflammatory responses. (nih.gov)
- Fluorescent chemokine uptake assays were instrumental in providing these novel insights into CCL2 receptor biology, and the sensitivity, specificity, and versatility of these assays are discussed. (nih.gov)
- Reduction of chemokine levels and leukocyte traffic to joints by tumor necrosis factor alpha blockade in patients with rheumatoid arthritis. (ox.ac.uk)
- OBJECTIVE: To verify the hypothesis that in rheumatoid arthritis (RA), tumor necrosis factor alpha (TNFalpha) plays a critical role in regulating leukocyte trafficking and chemokine levels. (ox.ac.uk)
Comet Assay5
- E. Comet Assay Slide Scoring. (nih.gov)
- F. Statistical Methods Used in the Evaluation of Comet Assay Data. (nih.gov)
- 3. NTP Evaluation of the Comet Assay Results in Mice and Rats. (nih.gov)
- 4. Summary Data Tables for the Comet Assay. (nih.gov)
- Comet Assay analysis The "Comet assay" provides a simple and effective method for evaluation of DNA damage and DNA-repair capacity in single cells such as leukocytes. (nih.gov)
Platelet7
- Platelet activation has been associated with an epithelial to mesenchymal transition (EMT), while Tissue Factor (TF) protein expression by cancer cells has been shown to correlate with hypercoagulable state and metastasis. (biomedcentral.com)
- The aim of this work was to determine the effect of platelet-cancer cell interaction on TF and "Metastasis Initiating Cell (MIC)" marker levels and migration in ovarian cancer cell lines and cancer cells isolated from the ascetic fluid of ovarian cancer patients. (biomedcentral.com)
- Our results suggest that platelet-cancer cell interaction plays a role in the formation of metastatic foci. (biomedcentral.com)
- We investigated whether platelets prime colon cancer cells for metastasis and whether pharmacological inhibition of platelet function may prevent it. (oncotarget.com)
- In conclusion, targeting platelet COX-1 with low-dose aspirin exerts an antimetastatic action by averting the stem cell mimicry of cancer cells associated with enhanced proaggregatory effects induced by platelet-tumor cell interactions. (oncotarget.com)
- The regenerative potential of two types of platelet-rich plasma (PRP), prepared in the presence of EDTA (EPRP) and citrate (CPRP) and an alternative blood product-hyperacute serum (hypACT) was evaluated using a 3D osteoarthritic chondrocyte pellet model by assessing the metabolic cell activity, cartilage-related gene expression and extracellular matrix deposition within the pellets. (mdpi.com)
- The endothelium plays a central role in overall vascular homeostasis by regulating vasoreactivity oxidation of low-density lipoprotein platelet activation leukocyte adhesion and smooth muscle cell proliferation and migration. (opioid-receptors.com)
Chemotactic5
- CytoSelect Cell Migration Assays are ideal for determining the chemotactic properties of cells. (bionotatki.com)
- No functional effects on phagocytic (changes in enzyme secretions not altered, chemotactic migration of granulocytes, macrophage migration, carbon clearance in vivo ) or tumor cells (growth rate, metastasis) can be detected in animals. (nih.gov)
- Some chemotactic elements including ECM substances have been proven to stimulate the intrinsic motility of tumor cells (7 8 These elements are thought to influence both extent as well as the path of tumor cell motion to specific focus on organs. (hiv-proteases.com)
- Tumor cells display an amoeboid motion similar compared to that of individual polymorphonuclear (PMN) leukocytes seen as a pseudopod protrusion on the leading edge from the cell accompanied by directional locomotion toward a chemotactic supply derived from the mark tissues. (hiv-proteases.com)
- For chemotactic assays the collagen was diluted to several concentrations in Dulbecco's improved Eagle's moderate (DMEM) (Biofluids MD) with 0.1% bovine serum albumin (BSA) (Sigma St. Louis MO) and the answer was taken to a pH of 7.4 and an osmolality of 300 mmol/kg. (hiv-proteases.com)
Agarose3
- 11. Leucocyte migration test in agarose. (nih.gov)
- They may involve a variety of techniques such as measuring the movement of leukocytes through substrates such as AGAROSE gels or the rate of exit of cells from a glass capillary. (nih.gov)
- The capacity for production of migration inhibitory factor was assessed by the agarose droplet cell migration inhibition assay, using peritoneal exudate cells and a CVB3(m) cell lysate or KCl extracted antigens from heart tissues of CVB3(m)-inoculated mice. (nih.gov)
Specificity2
- In this study, by using fluorescent CCL2 uptake to label cells bearing functional CCL2 receptors, we have defined the expression profile, scavenging activity, and ligand specificity of CCL2 receptors on mouse leukocytes. (nih.gov)
- In addition to the increased risk of tumour-spreading by invasive biopsies, a serious disadvantage of utilizing biopsy samples for molecular imaging is the mixed cell population obtained, strongly varying from case to case, and resulting in differential gene expression with limited specificity related to the pathology. (nih.gov)
Viability1
- Chondrocyte viability was determined by XTT assay and it revealed no significant difference in metabolic activity of OA chondrocyte pellets after supplementation with different blood products. (mdpi.com)
Reagents distributed2
- Human IgG antibody Laboratories manufactures the ldh cytoselecttm cell biolabs milano italia reagents distributed by Genprice. (bionotatki.com)
- Assay Biotech Omnikine Laboratories manufactures the migration assay bioteck reagents distributed by Genprice. (bioinfolab.org)
Epithelial5
- The 8 µm pore size is suitable for most cell types including epithelial cells, fibroblasts, and cancer cell lines. (bionotatki.com)
- The two-component sensor response regulator RoxS/RoxR plays a role in Pseudomonas aeruginosa interactions with airway epithelial cells. (umassmed.edu)
- Metastasis Initiating Cells (MICs) are characterized by their enhanced chemoresistance, low metabolic rate, possessing "stemness", for having undergone Epithelial-Mesenchymal Transition (EMT) and their enhanced capacity to generate metastatic foci. (biomedcentral.com)
- Here, we present a pipeline to quantify and analyse cell shapes as cells undergo the epithelial-mesenchymal transition (EMT). (mpg.de)
- We find that cell morphology is closely associated with their state: While epithelial cells display spherical shapes, mesenchymal cells undergo spreading. (mpg.de)
Mice7
- Cell-mediated immunity in ts 1 survivors was compared with that of normal mice after challenge with CVB3(m). (nih.gov)
- Migration inhibitory factor activity was not detected in cultures of splenic leukocytes from ts 1 survivors of CVB3(m)-inoculated ts 1 survivors, but it was readily detected in cultures of splenic leukocytes from CVB3(m)-inoculated normal adolescent mice. (nih.gov)
- A higher proportion of normal mice and ts 1 survivors, both inoculated with CVB3(m), contained splenic cytotoxic T lymphocytes with higher reactivity against CVB3(m)-infected neonatal skin fibroblasts than against normal skin fibroblasts, as assessed by a (51)Cr release assay. (nih.gov)
- The data are compatible with the notion that an immune deviation mechanism, thought to be controlled through a mechanism requiring suppressor cell activity which inhibits macrophage activation in ts 1 survivors, protects these mice from induction of myocarditis. (nih.gov)
- Inactive Sendai virus grown in LLC-MK(2) cells, which possessed an uncleaved precursor glycoprotein, F, and was noninfectious to tissue culture cells, neither grew nor caused pathological changes in the lung of mice. (nih.gov)
- Inside a vascular pressure assay when aortas isolated from crazy type mice had been incubated with KG-WE NO-dependent improved vasorelaxation was noticed. (opioid-receptors.com)
- and leucocyte counts, pulmonary oedema and oedema paw of mice in a dose-dependent manner. (who.int)
Boyden3
- Description: The Radius Cell Migration Assay provides a unique alternative to conventional cell migration assays using the Boyden chamber. (bioinfolab.org)
- Unlike Boyden chamber assays which may only be analyzed at endpoint, the Radius assay uses a proprietary cell culture plate containing a carefully-defined biocompatible hydrogel (Radius gel) spot centralized at the bottom of each well. (bioinfolab.org)
- Cancer cell migration was determined by Boyden chambers and the scratch assay. (biomedcentral.com)
Concentrations4
- Numerous assays are being developed to measure blood concentrations of cyclosporine. (nih.gov)
- Comparison of concentrations in published literature to patient concentrations using current assays must be done with detailed knowledge of the assay methods employed. (nih.gov)
- Serum IL-8 and MCP-1 concentrations were measured by enzyme-linked immunosorbent assay. (ox.ac.uk)
- There was a simultaneous and significant reduction in the numbers of infiltrating synovial CD3+ T cells, CD22+ B cells, and CD68+ macrophages and in the expression of IL-8 and MCP-1, with a trend toward a reduction in serum concentrations of these chemokines. (ox.ac.uk)
Endothelium2
- Rickettsia prowazekii, the etiologic agent of epidemic typhus, infects vascular endothelium, leading to vasculitis and tissue infiltration of leukocytes. (nih.gov)
- members mediate the original moving of circulating cells over the endothelium whereas solid adhesion is normally mediated by connections between integrin receptors and immunoglobulin very family members (4). (hiv-proteases.com)
Western blot1
- Western blot analysis of cell lysate (20 µg, lane 1) or 20 µl of the eluted samples (lanes 2, 3, and 4) was performed using a Rap1 Rabbit Antibody. (cellsignal.com)
Toxicity1
- These studies were conducted to obtain additional information and clarification regarding the in vivo genotoxicity of cumene to help in interpretation of the sporadic positive responses that were reported in the literature for some genetic toxicity assays. (nih.gov)
Vascular2
- Conventional stream chambers can be used to research cell connections with different surface area (5 6 Metastasizing tumor cells Tubastatin A HCl will probably encounter both soluble and insoluble extracellular matrix (ECM) elements because they traverse vascular wall space and cellar membranes. (hiv-proteases.com)
- This system in addition has been connected with vascular dysfunction normal of atherogenesis ageing erection dysfunction and sickle cell disease [12-20]. (opioid-receptors.com)
Lysates1
- Arginase activity assay Cells lysates had been ready using lysis buffer (50 mM Tris-HCl pH7.5 0.1 mM EDTA and protease inhibitors) by homogenization at 4℃ accompanied by centrifugation for 20 min at 14 0. (opioid-receptors.com)
Metastasis2
- In this study, cell migration, invasion and adhesion abilities as well as metastasis-associated protein and NF-B pathway signaling factor expression were analyzed after treating HT-29 cells with THSG. (ntu.edu.tw)
- Increasingly, more insight is available pertaining to the physiology of metastasis, and to the involvement of several stages in the metastatic cascade, includ-ing trans-endothelial migration and intravasation of tumour cells into the circulation, cell survival in the circulation, transport of cells through the vasculature followed by extravasation, and coloniza-tion and formation of metastatic lesions (Fig. 1)15,16. (cadworks3d.com)
Tumor cells3
- Using a peristaltic pump circulating tumor cells can then become introduced into the circulation channel inside a well-defined circulation field. (hiv-proteases.com)
- The total quantity of transmigrated tumor cells can be microscopically quantified in terms of various guidelines including shear stress chemoattractant focus and modulated cell adhesion. (hiv-proteases.com)
- Tumor cells for assays had been detached while subconfluent by short contact with 0.05% trypsin/0.02% EDTA and permitted to regenerate for 1 hr within a tissues lifestyle medium containing DMEM/10% FBS. (hiv-proteases.com)
Proliferation1
- MicroRNA-376c inhibits cell proliferation and invasion in osteosarcoma by targeting to transforming growth factor-alpha. (idrblab.net)
Laboratories1
- Monoclonal antibodies to individual Compact disc11a (LFA-1) Compact disc11b (Macintosh-1) and ICAM-1 had been bought from CalTag Laboratories (CA). 3.2 Cell Lifestyle C8161 individual melanoma cells had been cultured in DMEM-F12 supplemented with 10% FBS. (hiv-proteases.com)
Peripheral blood1
- The transendothelial migration (TM) of murine and human peripheral blood mononuclear cells (PBMCs) across ECs infected with Breinl organisms was significantly increased compared with that for uninfected ECs or for ECs infected with attenuated organisms, demonstrating that increased TM was related to R. prowazekii virulence. (nih.gov)
Immune6
- Because endothelial cell activation and immune cell-endothelial cell interactions are critical regulators of leukocyte recruitment, we analyzed the effect of acute ethanol exposure on endothelial cell activation in vivo using the localized Shwartzman reaction model. (nih.gov)
- The results suggest two mechanisms by which ts 1 survivors exhibit resistance to CVB3(m) induction of myocarditis, namely, the rapid production of high-titered anti-CVB3(m) neutralizing antibody in response to CVB3(m) inoculation and altered cell-mediated immune responses against CVB3(m) induced viral or novel cellular antigens. (nih.gov)
- The purpose of this study was to examine the derivative effects of B cell depletion on the peripheral immune system and a direct treatment effect on T cells expressing CD20. (regionh.dk)
- Metastatic inefficiency offers largely been regarded as the result of a massive damage of malignancy cells within the dynamic blood circulation due to the immune system and/or hemodynamic shear causes. (hiv-proteases.com)
- Frequently observed immunologic features include depression of cutaneous delayed-type hypersensitivity and a heightened helper T-cell type 1 (Th1) immune response at sites of disease. (medscape.com)
- Circulating immune complexes, along with signs of B-cell hyperactivity, may also be found. (medscape.com)
Tissues2
- The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
- Surprisingly, tissue surface tension in such confluent tissues can induce unique interfacial behaviour like- cell shape elongation and topological pinning- that can make perhaps make cells extrusion much costlier, possibly resulting in a delayed onset of differentiation. (mpg.de)
Inhibits1
- Cyclosporine also inhibits lymphokine production and release including interleukin-2 or T-cell growth factor (TCGF). (nih.gov)
Receptor2
- Flow cytometry identifies RET by the presence of an active transferrin (CD71) cell surface receptor. (nih.gov)
- We show that qualitative and quantitative differences in the expression of CCR2 and ACKR2 endow individual leukocyte subsets with distinctive CCL2 receptor profiles and CCL2-scavenging capacities. (nih.gov)
Flow cytometry3
- METHODS: Frequency and absolute numbers of peripheral leukocytes of treatment-naive patients with relapsing-remitting MS (RRMS) and patients treated with ofatumumab for a mean of 482 days were assessed in this observational study by flow cytometry. (regionh.dk)
- Finally, our study pointed out a bias in the measurement of CD20+ cells due to a steric hindrance between the treatment antibody and the flow cytometry antibody. (regionh.dk)
- TF, EMT and stem cell marker levels were determined by Western blotting, flow cytometry and RT-PCR. (biomedcentral.com)
Sickle cell di4
- The present invention includes embodiments for treatment and/or prevention of sickle cell disease that employ Hydroxyfasudil or Isocoronarin D alone or either in conjunction with each other or an inducer of HbF production. (justia.com)
- In particular aspects, the field of the present invention includes treatment and/or prevention of a blood disorder, such as sickle cell disease. (justia.com)
- Sickle cell disease (SCD) is the most common life-threatening monogenic disorder in the world with statistics indicating that approximately 80% (230,000) of children affected globally are born in sub-Saharan Africa (Modell and Darlison 2008). (justia.com)
- Sickle cell disease (SCD) can arise from a single point mutation that causes erythrocyte deformation or sickle-shaped erythrocytes (Ingram 1957). (justia.com)
Methods3
- 5. [Blood leukocyte migration in agar in tuberculin hypersensitivity: comparison with other methods and review of the literature]. (nih.gov)
- Tubastatin A HCl Many methods such as micropipette (9) and migration chamber (10 11 have been used regularly to characterize cellular chemotaxis - the directional migration of cells along a gradient of soluble attractant activation. (hiv-proteases.com)
- We will present how the morphological features of a cell can be quantified and analysed with the help of dimensional reduction methods. (mpg.de)
Murine2
Acute2
- 12. Cell-mediated immunity to hepatitis-associated antigen (HAA) demonstrated by leucocyte migration test during and after acute B hepatitis. (nih.gov)
- We hypothesized that acute ethanol administration would inhibit leukocyte recruitment and endothelial cell activation during inflammation and infection. (nih.gov)
Inflammatory2
- CONCLUSION: TNFalpha blockade reduces synovial expression of the chemokines IL-8 and MCP-1 and diminishes inflammatory cell migration into RA joints. (ox.ac.uk)
- Endothelial and smooth muscle cells in arterial tissue expressed CARD8 and CARD8 correlated with vWF , CD163 and the expression of inflammatory genes, such as CXCL1 , CXCL6 and PDGF-A in plaque. (nature.com)
Progression4
- These small G proteins have both GDP/GTP-binding and GTPase activities and function as binary switches in diverse cellular and developmental events that include cell cycle progression, cell survival, actin cytoskeletal organization, cell polarity and movement, and vesicular and nuclear transport (1). (cellsignal.com)
- Cell chemotaxis plays a pivotal role in the progression of cancer and other diseases. (bionotatki.com)
- The current theory of cancer progression proposes that from the total population of cancer cells within a primary tumor, only a small sub-population has the capacity to migrate, survive in isolation and establish secondary tumors within distant organs [ 3 ]. (biomedcentral.com)
- During cancer progression, many tumours shed circulating tumour cells (CTCs) and other biomarkers into the bloodstream. (cadworks3d.com)
Samples4
- Description: A competitive ELISA for quantitative measurement of Human Anti centriole and centrosome antibody IgG in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (bionotatki.com)
- The Ldh Cytoselecttm Cell Biolabs Milano Italia reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (bionotatki.com)
- In this Review, we discuss progress towards the isolation and recovery of bulk CTCs from whole blood samples for the identification of cells with high metastatic potential. (cadworks3d.com)
- At the same sequential time points, synovial biopsy samples were assessed for infiltrating CD3+ T cells, CD22+ B cells, and CD68+ macrophages. (ox.ac.uk)
Hypersensitivity3
- 1. [Comparison between results of leukocyte migration inhibition test and skin hypersensitivity of tuberculin in man]. (nih.gov)
- 16. [Delayed hypersensitivity in thyroid diseases studied by means of the leukocyte migration test with human thyroglobulin]. (nih.gov)
- Cyclosporine has been demonstrated to suppress some humoral immunity and to a greater extent, cell-mediated reactions such as allograft rejection, delayed hypersensitivity, experimental allergic encephalomyelitis, Freund's adjuvant arthritis, and graft vs. host disease in many animal species for a variety of organs. (nih.gov)
Capillary1
- 10. Sealed capillary leucocyte migration test. (nih.gov)
Significantly2
- The luciferase activity of miR-376c transfected cells was significantly reduced and miR-376c-mediated repression of luciferase activity was abolished by the mutant putative binding site. (idrblab.net)
- RESULTS: Anti-TNFalpha therapy in RA significantly reduced 111In-labeled granulocyte migration into affected joints. (ox.ac.uk)
Stem cells1
- In adult skin tissue, stem cells - which are responsible for repair and renewal - are confined to the bottom-most basal layer (attached to a basement membrane with high rigidity) and loose their 'stemness' irreversibly when it extrudes/leaves the basal layer into the supra-basal layer above. (mpg.de)
Chemotaxis1
- Description: Chemotaxis describes the movement of cells toward or away from a chemical stimulus in their environment. (bionotatki.com)
Mediated cell adhesion2
Rats1
- 7. Tinelli M, Pantosti A, Lusardi C, Vim- international migration of rats and also negative. (cdc.gov)
Neutrophils1
- The 3 µm pore size is best for the smallest cells including neutrophils and other leukocytes. (bionotatki.com)
Blood4
- 2. [Leukocyte migration inhibition test in blood microcultures in the assessment of cellular immunity in tuberculosis]. (nih.gov)
- All experiments performed on red cell lysed bovine blood gated on lymphocytes in the presence of 10% bovine serum. (bio-rad-antibodies.com)
- Circulating tumour cells (CTCs) and other cancer-related biomarkers are present in the blood of many patients with cancer. (cadworks3d.com)
- To further simulate tumor cell migration within the blood circulation standard circulation assay or micropipette technique will not be relevant. (hiv-proteases.com)
Cutaneous1
- 13. [Inhibition of leukocyte migration in tuberculosis and diseases with cutaneous energy]. (nih.gov)
Human platelets2
- With informed patient consent, ascitic fluid isolated ovarian cancer cells, cell lines and ovarian cancer spheres were co-cultivated with human platelets. (biomedcentral.com)
- Coculturing HT29 human colon carcinoma cells with human platelets led to the induction of mesenchymal-like cancer cells characterized by downregulation of E-cadherin and upregulation of Twist1, enhanced cell mobility and a proaggregatory action on platelets. (oncotarget.com)
Results1
- RESULTS: This study showed that ofatumumab treatment of patients with RRMS increased the control of effector T cells and decreased T cell autoreactivity. (regionh.dk)
Inflammation1
- Chronic Inflammation Contributes to Tumor Growth: Possible Role of L-Selectin-Expressing Myeloid-Derived Suppressor Cells (MDSCs). (nih.gov)
Tissue2
- While several cell-intrinsic biochemical markers have been discovered to predict stem cell potential, we explore a complementary hypothesis to this question with the help of tissue biomechanics, that can take into account the cell extrinsic mechano-chemical changes in the environment. (mpg.de)
- We use a fully 3D vertex-like model to study the differentiation propensity in terms of cell extrusion dynamics, and its dependence on global mechanical properties like- tissue fluidity and basement tension. (mpg.de)
Test3
- 19. Test of leukocyte migration inhibition. (nih.gov)
- 20. [The leukocyte migration test: possibilities of its use]. (nih.gov)
- Before each test the cells had been detached and rocked (8 rpm) for just one hour Tubastatin A HCl in lifestyle moderate at 37°C and for yet another hour in RPMI 1640 with 0.1%w/v BSA. (hiv-proteases.com)
20171
- Cell Rep, 2017 Sep 26. (nih.gov)
Invasive1
- miR-152 Controls Migration and Invasive Potentialby Targeting TGFa in Prostate Cancer Cell Lines. (idrblab.net)
Cellular4
- The development of an organism is characterized by a series of cellular fate transitions where cells become increasingly specialized. (mpg.de)
- After defining the distinct cellular shapes corresponding to cell states, we study how exactly the morphological features of a cell evolve during EMT. (mpg.de)
- To this aim, we investigate cell trajectories of morphological features in a low-dimensional space and describe the time evolution of cellular features as a stochastic process. (mpg.de)
- By integrating morphometric analysis into studies of cell fate changes, we aim to better understand the crosstalk between cellular fate and shape changes. (mpg.de)
Liver1
- Loss of L-selectin-guided CD8(+) , but not CD4(+) , cells protects against ischemia reperfusion injury in a steatotic liver. (nih.gov)
Migratory3
- Following cell seeding the Radius gel is removed, allowing migratory cells to move across the area and close the gap. (bioinfolab.org)
- It also showed that ofatumumab reduced the level of peripheral CD20+ T cells and that the observed decrease in CNS-migratory capacity of T cells was caused by the depletion of CD20+ T cells. (regionh.dk)
- DISCUSSION: The substantial ofatumumab-induced alteration in the T cell compartment including a severely decreased CNS-migratory capacity of T cells could partly be attributed to the depletion of CD20+ T cells. (regionh.dk)
Activity2
- The prognostic role of leukocyte activity in breast cancer patients has long been recognised. (nih.gov)
- The co-culture of patient-derived ovarian cancer cells with platelets causes: 1) a phenotypic change in cancer cells, 2) chemoattraction and cancer cell migration, 3) induced MIC markers (EMT/stemness), 3) increased sphere formation and 4) increased TF protein levels and activity. (biomedcentral.com)
Cancer2
- Phenylmethimazole and a Thiazole Derivative of Phenylmethimazole Inhibit IL-6 Expression by Triple Negative Breast Cancer Cells. (ohio.edu)
- We present the first evidence that platelets act as chemoattractants to cancer cells. (biomedcentral.com)
Expression2
- CD62L expression level determines the cell fate of myeloid progenitors. (nih.gov)
- Histograms were first gated on singlet, live lymphocytes and gating strategies applied to allow phenotyping of cells for expression of CD44, CD45RO and CD62L. (bio-rad-antibodies.com)