Sarcoma, Yoshida
Sarcoma
Sarcoma, Ewing
Sarcoma, Synovial
Sarcoma, Kaposi
Avian Sarcoma Viruses
Sarcoma, Experimental
Sarcoma 180
Sarcoma Viruses, Murine
Neoplasm Transplantation
Neoplasms, Experimental
Soft Tissue Neoplasms
CHS 828, a novel pyridyl cyanoguanidine with potent antitumor activity in vitro and in vivo. (1/84)
A new class of recently discovered antineoplastic agents, the pyridyl cyanoguanidines, exert a potent antitumor activity in rodents after oral administration. Optimization in vitro and in vivo has resulted in the selection of the lead candidate CHS 828 (N-(6-chlorophenoxyhexyl)-N'cyano-N"-4-pyridylguanidine). CHS 828 was found to exert potent cytotoxic effects in human breast and lung cancer cell lines, with lesser effects on normal fibroblasts and endothelial cells. In a study using a panel of cell lines with different resistance patterns, the effects of CHS 828 showed a low correlation with the activity patterns of known anticancer agents, and no sensitivity to known mechanisms of multidrug resistance was observed. In nude mice bearing human tumor xenografts, CHS 828, at doses from 20 to 50 mg/kg/day p.o., inhibited the growth of MCF-7 breast cancer tumors and caused regression of NYH small cell lung cancer tumors. Oral administration of CHS 828 once weekly improved efficacy without increasing toxicity. CHS 828 was found to compare favorably with established chemotherapeutic agents such as cyclophosphamide, etoposide, methotrexate, and paclitaxel. In mice with NYH tumors, long-term survival (>6 months) was observed after treatment with CHS 828 was stopped. In conclusion, CHS 828 is an effective new antitumor agent, with a potentially new mechanism of action. CHS 828 is presently being tested in Phase I clinical trials in collaboration with the European Organization for Research and Treatment of Cancer. (+info)Metastasis formation of Yoshida sarcoma heterotransplanted in adult golden hamsters treated with anti-hamster thymocyte serum. (2/84)
Growth of Yoshida sarcoma cells heterotransplanted in adult golden hamsters treated with antithymocyte serum was investigated. Control animals were grafted with or without hydrocoritisone conditioning. In the antithymocyte serum-treated group, tumors were produced in cheek pouches and grew progressively in size until Day 21 with no sign of regression. Little host reaction was noticed histologically around the tumor grafts throughout the course. Distant metastases were revealed at autopsy in 9 of 12 animals from Day 14 of inoculation on, and all the experimental animals died by Day 23. Six of the 9 hamsters with metastases died of tumor. By means of the back-transplantation test, the metastatic tumor cells were shown to be consistent with Yoshida sarcoma cells. In hydrocortisone-treated and untreated groups, the tumor size reached a maximum on Day 21 and Day 5, respectively, and then regression followed. No metastasis was detected in either control group. (+info)Interleukin-15 antagonizes muscle protein waste in tumour-bearing rats. (3/84)
Tissue protein hypercatabolism (TPH) is an important feature in cancer cachexia, particularly with regard to the skeletal muscle. The Yoshida AH-130 rat ascites hepatoma is a model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle wasting, primarily due to TPH. The present study was aimed at investigating if IL-15, which is known to favour muscle fibre hypertrophy, could antagonize the enhanced muscle protein breakdown in this cancer cachexia model. Indeed, IL-15 treatment partly inhibited skeletal muscle wasting in AH-130-bearing rats by decreasing (8-fold) protein degradative rates (as measured by 14C-bicarbonate pre-loading of muscle proteins) to values even lower than those observed in non-tumour-bearing animals. These alterations in protein breakdown rates were associated with an inhibition of the ATP-ubiquitin-dependent proteolytic pathway (35% and 41% for 2.4 and 1.2 kb ubiquitin mRNA, and 57% for the C8 proteasome subunit, respectively). The cytokine did not modify the plasma levels of corticosterone and insulin in the tumour hosts. The present data give new insights into the mechanisms by which IL-15 exerts its preventive effect on muscle protein wasting and seem to warrant the implementation of experimental protocols involving the use of the cytokine in the treatment of pathological states characterized by TPH, particularly in skeletal muscle, such as in the present model of cancer cachexia. (+info)Day-night pattern of energy expenditure and body temperature in cachectic tumour-bearing rats. (4/84)
The implication of an increase in energy expenditure in cancer cachexia, which seems to be related to the type of tumour, remains unclear. We therefore investigated the energy metabolism and body temperature in anorectic and cachectic rats bearing the Yoshida sarcoma (TB), in comparison with pair-fed (PF) and ad-libitum fed (AL) control rats. The resting energy expenditure was higher in the TB than in the two control groups when corrected for the modifications of body composition. However, the total energy expenditure did not differ between the TB and the AL, presumably because of the drop of activity in TB. There was a temporal distribution of differences in energy expenditure with higher energy expenditure in TB than in AL during the diurnal phase and a lack of difference during the nocturnal phase. The TB presented a fever, which was limited to the diurnal period. Moreover, the acrophase of the body temperature rhythm was delayed in the TB. These results highlight the circadian effects of tumour development on the energy metabolism of the host and hint to the possible implication of cytokines. (+info)Tissue distribution and biotransformation of potassium oxonate after oral administration of a novel antitumor agent (drug combination of tegafur, 5-chloro-2,4-dihydroxypyridine, and potassium oxonate) to rats. (5/84)
S-1, a new oral 5-fluorouracil (5-FU)-derivative antitumor agent, is composed of tegafur, 5-chloro-2,4-dihydropyridine, and potassium oxonate (Oxo). Oxo, which inhibits the phosphorylation of 5-FU, is added to reduce the gastrointestinal (GI) toxicity of the agent. In this study, we investigated the tissue distribution and the metabolic fate of Oxo in rats after oral administration of S-1. Oxo was mainly distributed to the intracellular sites of the small intestines in a much higher concentration than 5-FU, but little distributed to other tissues, including tumorous ones in which 5-FU was observed after oral administration of S-1. Plasma concentration-time profiles of Oxo and its metabolites after i.v. and oral administration of S-1 revealed that Oxo was mainly converted to cyanuric acid in the GI tract. Furthermore, the analysis of drug-related radioactivity in GI contents and in vitro studies suggested that Oxo was converted to cyanuric acid by two routes, the first being direct conversion by the gut flora in the cecum, and the second, conversion by xanthine oxidase or perhaps by aldehyde oxidase after degradation to 5-azauracil (5-AZU) by the gastric acid. These results indicate that, although a part of the administered Oxo was degraded in the GI tract, Oxo was mainly distributed to the intracellular sites of the small intestines in a much higher concentration than 5-FU and that little was distributed to other tissues, including tumors. We conclude that this is the reason why Oxo suppresses the GI toxicity of 5-FU without affecting its antitumor activity. (+info)DNA synthesis in tumor-bearing rats. (6/84)
Thmidine (TdR) incorporation into DNA increased in the livers and spleens of rats bearing Yoshida sarcoma (solid type) or AH130 (solid type). TdR kinase and DNA polymerase activities increased in the serum, liver, and spleen of these rats, while thymidine monophosphate kinase activity increased appreciably only in the liver and spleen. On diethylaminoethyl cellulose column chromatography, 2 peaks of TdR dinase activity were separated from the serum and tumor tissues of rats bearing Yoshida sarcoma (solid type) while only 1 peak was obtained from the liver. TdR kinase activity in the serum decreased abruptly 7 hr after removal of the Yoshida sarcoma, while that in the liver decreased more slowly. (+info)D-24851, a novel synthetic microtubule inhibitor, exerts curative antitumoral activity in vivo, shows efficacy toward multidrug-resistant tumor cells, and lacks neurotoxicity. (7/84)
N-(pyridin-4-yl)-[1-(4-chlorbenzyl)-indol-3-yl]-glyoxyl-amid (D-24851) is a novel synthetic compound that was identified in a cell-based screening assay to discover cytotoxic drugs. D-24851 destabilizes microtubules and blocks cell cycle transition specifically at G2-M phase. The binding site of D-24851 does not overlap with the tubulin binding sites of known microtubule-destabilizing agents like vincristine or colchicine. In vitro, D-24851 has potent cytotoxic activity toward a panel of established human tumor cell lines including SKOV3 ovarian cancer, U87 glioblastoma, and ASPC-1 pancreatic cancer cells. In vivo, oral D-24851 treatment induced complete tumor regressions (cures) in rats bearing Yoshida AH13 sarcomas. Of importance is that the administration of curative doses of D-24851 to the animals revealed no systemic toxicity in terms of body weight loss and neurotoxicity in contrast to the administration of paclitaxel or vincristine. Interestingly, multidrug-resistant cell lines generated by vincristine-driven selection or transfection with the Mr 170,000 P-glycoprotein encoding cDNA were rendered resistant toward paclitaxel, vincristine, or doxorubicin but not towards D-24851 when compared with the parental cells. Because of its synthetic nature, its oral applicability, its potent in vitro and in vivo antitumoral activity, its efficacy against multidrug-resistant tumors, and the lack of neurotoxicity, D-24851 may have significant potential for the treatment of various malignancies. (+info)Intracellular distribution of various enzymes concerned with DNA synthesis from normal and regenerating rat liver, and Yoshida sarcoma. (8/84)
During the fractionation of various enzymes concerned with DNA synthesis from the postmicrosomal supernatant fraction of various tissues, DNA polymerace [EC 2.7.7.7], thymidine kinase [EC 2.7.1.75], dTMP kinase [EC 2.7.4.9], deoxycytidine kinase [EC 2.7.1.74], and deoxycytidine monophosphokinase (dCMP kinase) [EC 2.7.4.14] were found in the pellet fraction of postmicrosomal supernatant. Further, the uridine kinase [EC 2.7.1.48] and aspartate transcarbamylase [EC 2.1.3.2] activities of postmicrosomal supernatant from various tissues were also present in this pellet fraction. The activities of DNA polymerase, thymidine kinase, uridine kinase, and aspartate transcarbamylase from normal and regenerating rat liver, and Yoshida sarcoma were higher in the pellet fraction than in the supernatant. On the other hand, the activities of dTMP kinase, dCMP kinase, and orotidine-5'-phosphate decarboxylase [EC 4.1.1.23] were lower in the pellet fraction than in the supernatant. The pellet fractions of regenerating rat liver and Yoshida sarcoma showed a remarkable incorporation of various precursors (thymidine, dTMP, deoxycytidine, and dCMP) into DNA in the presence of a suitable DNA template, ATP and all four deoxynucleoside 5'-triphosphates for DNA synthesis. Normal adult rat liver catalyzed a much smaller incorporation of all these precursors, except for dCMP. (+info)I'm sorry for the confusion, but "Sarcoma, Yoshida" is not a recognized medical term or a specific type of sarcoma in any major oncology reference or database. It appears that "Yoshida" might be referring to a person who described or studied a particular type of sarcoma. However, I cannot find any relevant information related to this exact term.
Sarcomas are cancers that develop from connective tissues such as bones, muscles, tendons, cartilages, nerves, and blood vessels. They can be categorized into two main groups: bone sarcomas and soft tissue sarcomas. There are many subtypes of sarcoma, each with its unique features, diagnostic criteria, and treatment approaches.
If you have more context or information about "Sarcoma, Yoshida," I would be happy to help you further research the topic. However, based on the available data, it is not possible to provide a medical definition for this term.
Sarcoma is a type of cancer that develops from certain types of connective tissue (such as muscle, fat, fibrous tissue, blood vessels, or nerves) found throughout the body. It can occur in any part of the body, but it most commonly occurs in the arms, legs, chest, and abdomen.
Sarcomas are classified into two main groups: bone sarcomas and soft tissue sarcomas. Bone sarcomas develop in the bones, while soft tissue sarcomas develop in the soft tissues of the body, such as muscles, tendons, ligaments, fat, blood vessels, and nerves.
Sarcomas can be further classified into many subtypes based on their specific characteristics, such as the type of tissue they originate from, their genetic makeup, and their appearance under a microscope. The different subtypes of sarcoma have varying symptoms, prognoses, and treatment options.
Overall, sarcomas are relatively rare cancers, accounting for less than 1% of all cancer diagnoses in the United States each year. However, they can be aggressive and may require intensive treatment, such as surgery, radiation therapy, and chemotherapy.
Ewing sarcoma is a type of cancer that originates in bones or the soft tissues surrounding them, such as muscles and tendons. It primarily affects children and adolescents, although it can occur in adults as well. The disease is characterized by small, round tumor cells that typically grow quickly and are prone to metastasize (spread) to other parts of the body, most commonly the lungs, bones, and bone marrow.
Ewing sarcoma is caused by a genetic abnormality, specifically a chromosomal translocation that results in the fusion of two genes, EWSR1 and FLI1. This gene fusion leads to the formation of an abnormal protein that disrupts normal cell growth and division processes, ultimately resulting in cancer.
Symptoms of Ewing sarcoma can vary depending on the location and size of the tumor but may include pain or swelling in the affected area, fever, fatigue, and weight loss. Diagnosis typically involves imaging studies such as X-rays, CT scans, or MRI scans to locate the tumor, followed by a biopsy to confirm the presence of cancer cells. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these approaches, depending on the stage and location of the disease.
Synovial sarcoma is a rare type of cancer that typically develops in the soft tissues surrounding the joints, such as the synovial membrane, which lines the joint capsules. Despite its name, synovial sarcoma does not necessarily arise from the synovium. It is called so due to its resemblance to this tissue under a microscope.
This form of sarcoma primarily affects young adults and can be found in various parts of the body, but it most commonly occurs in the extremities, particularly near the knees. Synovial sarcoma is characterized by specific genetic changes that result in the formation of fusion proteins, which contribute to uncontrolled cell growth and tumor development.
There are two main subtypes of synovial sarcoma: monophasic and biphasic. Monophasic synovial sarcoma is composed of either spindle-shaped (spaghetti-like) cells or epithelioid (roundish) cells, while biphasic synovial sarcoma contains both types of cells. A third subtype, called poorly differentiated synovial sarcoma, has a more aggressive behavior and is composed of small round cells that do not resemble the typical spindle or epithelioid cells.
Treatment for synovial sarcoma usually involves surgical removal of the tumor, often followed by radiation therapy and/or chemotherapy to reduce the risk of recurrence and metastasis. The prognosis varies depending on factors such as the size and location of the tumor, the patient's age, and the presence of metastases at diagnosis.
Kaposi sarcoma (KS) is a type of cancer that causes abnormal growths in the skin, lymph nodes, or other organs. It is caused by the Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8). There are several forms of KS, including:
1. Classic KS: This form primarily affects older men of Mediterranean, Middle Eastern, or Ashkenazi Jewish descent. It tends to progress slowly and mainly involves the skin.
2. Endemic KS: Found in parts of Africa, this form predominantly affects children and young adults, regardless of their HIV status.
3. Immunosuppression-associated KS: This form is more aggressive and occurs in people with weakened immune systems due to organ transplantation or other causes.
4. Epidemic KS (AIDS-related KS): This is the most common form of KS, seen primarily in people with HIV/AIDS. The widespread use of antiretroviral therapy (ART) has significantly reduced its incidence.
KS lesions can appear as red, purple, or brown spots on the skin and may also affect internal organs such as the lungs, lymph nodes, or gastrointestinal tract. Symptoms vary depending on the location of the lesions but often include fever, fatigue, weight loss, and swelling in the legs or abdomen. Treatment options depend on the extent and severity of the disease and may involve local therapies (e.g., radiation, topical treatments), systemic therapies (e.g., chemotherapy, immunotherapy), or a combination of these approaches.
Experimental liver neoplasms refer to abnormal growths or tumors in the liver that are intentionally created or manipulated in a laboratory setting for the purpose of studying their development, progression, and potential treatment options. These experimental models can be established using various methods such as chemical induction, genetic modification, or transplantation of cancerous cells or tissues. The goal of this research is to advance our understanding of liver cancer biology and develop novel therapies for liver neoplasms in humans. It's important to note that these experiments are conducted under strict ethical guidelines and regulations to minimize harm and ensure the humane treatment of animals involved in such studies.
Avian sarcoma viruses (ASVs) are a group of retroviruses that primarily infect birds and cause various types of tumors, particularly sarcomas. These viruses contain an oncogene, which is a gene that has the ability to transform normal cells into cancerous ones. The oncogene in ASVs is often derived from cellular genes called proto-oncogenes, which are normally involved in regulating cell growth and division.
ASVs can be divided into two main types: non-defective and defective. Non-defective ASVs contain a complete set of viral genes that allow them to replicate independently, while defective ASVs lack some of the necessary viral genes and require assistance from other viruses to replicate.
One well-known example of an avian sarcoma virus is the Rous sarcoma virus (RSV), which was first discovered in chickens by Peyton Rous in 1910. RSV causes a highly malignant form of sarcoma in chickens and has been extensively studied as a model system for cancer research. The oncogene in RSV is called v-src, which is derived from the normal cellular gene c-src.
Avian sarcoma viruses have contributed significantly to our understanding of the molecular mechanisms underlying cancer development and have provided valuable insights into the role of oncogenes in tumorigenesis.
I'm sorry for any confusion, but "Sarcoma, Experimental" is not a recognized medical term or definition. Sarcomas are a type of cancer that develop in the body's connective tissues, such as bones, muscles, tendons, cartilage, and fat. There are many different types of sarcomas, classified based on the specific type of tissue they originate from.
Experimental, on the other hand, refers to something that is being tested or tried out for the first time, typically as part of a scientific experiment or clinical trial. In the context of cancer treatment, an experimental therapy might refer to a new drug, procedure, or device that is still being studied in clinical trials to determine its safety and effectiveness.
Therefore, "Sarcoma, Experimental" could potentially refer to a clinical trial or research study involving a new treatment for sarcoma, but it would not be a medical definition in and of itself. If you have any specific questions about sarcomas or experimental treatments, I would recommend consulting with a healthcare professional or medical researcher for more accurate information.
I'm sorry for any confusion, but "Sarcoma 180" is not a recognized medical term or an official classification of sarcomas in humans. It appears to be a term used primarily in research involving mice. Sarcoma 180 is a transplantable tumor that was first isolated from a mouse and has been used as a model for cancer research, particularly in studies involving immunotherapy and cancer treatment.
In general, sarcomas are cancers that develop from connective tissues such as bones, muscles, tendons, cartilages, nerves, and blood vessels. They can be further classified into various subtypes based on the specific type of tissue they originate from and their genetic characteristics. If you have any concerns about a specific medical condition or term, I would recommend consulting with a healthcare professional for accurate information.
Sarcoma viruses, murine, are a group of RNA viruses that primarily affect mice and other rodents. They are classified as type C retroviruses, which means they contain an envelope, have reverse transcriptase enzyme activity, and replicate through a DNA intermediate.
The murine sarcoma viruses (MSVs) are associated with the development of various types of tumors in mice, particularly fibrosarcomas, which are malignant tumors that originate from fibroblasts, the cells that produce collagen and other fibers in connective tissue.
The MSVs are closely related to the murine leukemia viruses (MLVs), and together they form a complex called the murine leukemia virus-related viruses (MLVRVs). The MLVRVs can undergo recombination events, leading to the generation of new viral variants with altered biological properties.
The MSVs are important tools in cancer research because they can transform normal cells into tumor cells in vitro and in vivo. The study of these viruses has contributed significantly to our understanding of the molecular mechanisms underlying cancer development and progression.
Cachexia is a complex metabolic disorder characterized by severe weight loss, muscle wasting, and weakness. It is often associated with chronic diseases such as cancer, HIV/AIDS, heart failure, kidney disease, and chronic obstructive pulmonary disease (COPD). Cachexia differs from simple malnutrition or starvation in that it involves a significant loss of muscle mass and an imbalance in energy metabolism, even when adequate calories are consumed.
The hallmark features of cachexia include:
1. Weight loss: Unintentional loss of more than 5% of body weight over 12 months or less, or more than 2% in individuals already underweight.
2. Muscle wasting: Reduction in skeletal muscle mass and strength, leading to weakness and functional impairment.
3. Fatigue and anorexia: Decreased appetite and reduced food intake due to various factors such as inflammation, hormonal imbalances, and psychological distress.
4. Inflammation: Elevated levels of pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) that contribute to metabolic dysregulation and muscle wasting.
5. Insulin resistance: Impaired glucose uptake and utilization by cells, leading to increased blood glucose levels and altered energy metabolism.
6. Altered protein metabolism: Increased protein breakdown and decreased protein synthesis in skeletal muscles, contributing to muscle wasting.
7. Altered lipid metabolism: Increased lipolysis (breakdown of fat) and impaired lipogenesis (formation of fat), leading to loss of adipose tissue and altered energy storage.
Cachexia significantly impacts patients' quality of life, treatment outcomes, and overall survival. Currently, there is no single effective treatment for cachexia, and management typically involves addressing the underlying disease, nutritional support, exercise interventions, and pharmacological therapies to target specific aspects of the metabolic dysregulation associated with this condition.
Neoplasm transplantation is not a recognized or established medical procedure in the field of oncology. The term "neoplasm" refers to an abnormal growth of cells, which can be benign or malignant (cancerous). "Transplantation" typically refers to the surgical transfer of living cells, tissues, or organs from one part of the body to another or between individuals.
The concept of neoplasm transplantation may imply the transfer of cancerous cells or tissues from a donor to a recipient, which is not a standard practice due to ethical considerations and the potential harm it could cause to the recipient. In some rare instances, researchers might use laboratory animals to study the transmission and growth of human cancer cells, but this is done for scientific research purposes only and under strict regulatory guidelines.
In summary, there is no medical definition for 'Neoplasm Transplantation' as it does not represent a standard or ethical medical practice.
Experimental neoplasms refer to abnormal growths or tumors that are induced and studied in a controlled laboratory setting, typically in animals or cell cultures. These studies are conducted to understand the fundamental mechanisms of cancer development, progression, and potential treatment strategies. By manipulating various factors such as genetic mutations, environmental exposures, and pharmacological interventions, researchers can gain valuable insights into the complex processes underlying neoplasm formation and identify novel targets for cancer therapy. It is important to note that experimental neoplasms may not always accurately represent human cancers, and further research is needed to translate these findings into clinically relevant applications.
Ascites is an abnormal accumulation of fluid in the peritoneal cavity, which is the space between the lining of the abdominal wall and the organs within it. This buildup of fluid can cause the belly to swell and become distended. Ascites can be caused by various medical conditions, including liver cirrhosis, cancer, heart failure, and kidney disease. The accumulation of fluid in the peritoneal cavity can lead to complications such as infection, reduced mobility, and difficulty breathing. Treatment for ascites depends on the underlying cause and may include diuretics, paracentesis (a procedure to remove excess fluid from the abdomen), or treatment of the underlying medical condition.
Soft tissue neoplasms refer to abnormal growths or tumors that develop in the soft tissues of the body. Soft tissues include muscles, tendons, ligaments, fascia, nerves, blood vessels, fat, and synovial membranes (the thin layer of cells that line joints and tendons). Neoplasms can be benign (non-cancerous) or malignant (cancerous), and their behavior and potential for spread depend on the specific type of neoplasm.
Benign soft tissue neoplasms are typically slow-growing, well-circumscribed, and rarely spread to other parts of the body. They can often be removed surgically with a low risk of recurrence. Examples of benign soft tissue neoplasms include lipomas (fat tumors), schwannomas (nerve sheath tumors), and hemangiomas (blood vessel tumors).
Malignant soft tissue neoplasms, on the other hand, can grow rapidly, invade surrounding tissues, and may metastasize (spread) to distant parts of the body. They are often more difficult to treat than benign neoplasms and require a multidisciplinary approach, including surgery, radiation therapy, and chemotherapy. Examples of malignant soft tissue neoplasms include sarcomas, such as rhabdomyosarcoma (arising from skeletal muscle), leiomyosarcoma (arising from smooth muscle), and angiosarcoma (arising from blood vessels).
It is important to note that soft tissue neoplasms can occur in any part of the body, and their diagnosis and treatment require a thorough evaluation by a healthcare professional with expertise in this area.
I'm sorry for any confusion, but "Avian Sarcoma" is not a widely recognized medical term. The term "sarcoma" is used in pathology to describe a type of cancer that develops from certain types of connective tissue (such as bone, cartilage, muscle, or blood vessels).
On the other hand, "avian" refers to birds or related to birds. In medical literature, avian sarcomas are sometimes used to describe sarcomas that occur in birds. However, specific types of avian sarcomas would be defined by the type of cell from which they originate (like a fibrosarcoma, osteosarcoma, etc.).
If you're asking about a specific medical condition or context, could you please provide more details? I'm here to help!