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uridine diphosphate/التهاب
يتم حفظ الارتباط في الحافظة
الصفحة 1 من عند 57 النتائج
Enhancement by Uridine Diphosphate of Macrophage Inflammatory Protein-1 Alpha Production in Microglia Derived from Sandhoff Disease Model Mice.
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Sandhoff disease (SD) is a lysosomal β-hexosaminidase (Hex) deficiency involving excessive accumulation of undegraded substrates, including GM2 ganglioside, and progressive neurodegeneration. Macrophage inflammatory protein-1α (MIP-1α) is a crucial factor for microglia-mediated neuroinflammation in
Characterization of autoantibodies against uridine-diphosphate glucuronosyltransferase in patients with inflammatory liver diseases.
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Uridine diphosphate glucuronosyltransferase (UGT) was identified as an antigenic target in a subgroup of liver-kidney microsomal autoantibodies and was termed LKM-3. To evaluate the nature of LKM-3 antibodies, we screened sera from 80 untreated patients with autoimmune hepatitis (AIH) type 1 and 2,
HISTOCHEMICAL STUDIES OF LEUKOCYTES FROM AN INFLAMMATORY EXUDATE. IV. URIDINE DIPHOSPHATE GLUCOSE-GLYCOGEN TRANSGLYCOSYLASE.
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[INTERVENTION OF ANTI-INFLAMMATORY AGENTS IN THE TRANSGLUCOSIDATION PHENOMENA LINKED TO URIDINE DIPHOSPHATE GLUCOSE].
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Regulation of uridine diphosphate glucuronosyltransferase during the acute-phase response.
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The acute-phase response is associated with profound effects on oxidative drug metabolism. However, the effects on glucuronidation are poorly characterized. The aim of the present study was to determine the role of mediators of the acute-phase response in the regulation of hepatic uridine
Cysteinyl leukotrienes and uridine diphosphate induce cytokine generation by human mast cells through an interleukin 4-regulated pathway that is inhibited by leukotriene receptor antagonists.
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We previously reported that interleukin (IL)-4 upregulates the expression of leukotriene C(4) synthase (LTC(4)S) by human cord blood--derived mast cells (hMCs), augments their high-affinity Fc receptor for IgE (Fc(epsilon)RI)-dependent generation of eicosanoids and cytokines, and induces a calcium
Expression of the P2Y6 purinergic receptor in human T cells infiltrating inflammatory bowel disease.
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The human P2Y6 receptor is a member of the G-protein-coupled P2Y purinergic receptor family that responds to extracellular uridine diphosphate (UDP). In previous work, we cloned the human P2Y6 receptor from an activated T-cell library, and others have shown that it is expressed as a 1.9-kb
Label-free LC-MS/MS shotgun proteomics to investigate the anti-inflammatory effect of rCC16.
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Clara cell protein (CC16) is an anti-inflammatory protein, which is expressed in the airway epithelium. It is involved in the development of airway inflammatory diseases, including chronic obstructive pulmonary disease and asthma. However, the exact molecular mechanism underlying its
Interactions between CYP2C9 and UGT1A6 polymorphisms and nonsteroidal anti-inflammatory drugs in colorectal cancer prevention.
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OBJECTIVE
Variant genotypes of uridine diphosphate glucuronsyltransferase isoenzyme 1A6 (UGT1A6) associated with decreased metabolic activity have been associated with an enhanced protective effect of aspirin on the development of colorectal adenomas. However, interactions between UGT1A6 variants or
Study of biochemical behavior of some exported and nonexported hepatic proteins during an acute inflammatory reaction in the rat.
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Haptoglobin, albumin, glucose-6-phosphatase, p-nitrophenol uridine diphosphate (UDP)-glucuronosyltransferase and cytochrome P-450 were measured in liver microsomes from normal rats and from rats undergoing an acute inflammatory reaction (AIR) induced either by subcutaneous administration of
No association between cyclooxygenase-2 and uridine diphosphate glucuronosyltransferase 1A6 genetic polymorphisms and colon cancer risk.
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OBJECTIVE
To investigate the association of variations in the cyclooxygenase-2 (COX2) and uridine diphosphate glucuronosyltransferase 1A6 (UGT1A6) genes and non-steroidal anti-inflammatory drugs (NSAIDs) use with risk of colon cancer.
METHODS
NSAIDs, which are known to reduce the risk of colon
Prediction by pharmacogenetics of safety and efficacy of non-steroidal anti- inflammatory drugs: a review.
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Non-steroidal anti-inflammatory drugs (NSAIDs) are the most frequently used drugs, either on prescription or over-thecounter (OTC). Their daily dosage is based on randomised controlled trials and an empirical clinical assessment of their efficacy and toxicity that allows dose adjustment. The
Pro-inflammatory P2Y14 receptor inhibition protects against ischemic acute kidney injury in mice.
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Ischemic acute kidney injury (AKI), a complication that frequently occurs in hospital settings, is often associated with hemodynamic compromise, sepsis, cardiac surgery or exposure to nephrotoxicants. Here, using a murine renal ischemia-reperfusion injury (IRI) model we show that intercalated cells
Intestinal alkaline phosphatase inhibits the proinflammatory nucleotide uridine diphosphate.
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Uridine diphosphate (UDP) is a proinflammatory nucleotide implicated in inflammatory bowel disease. Intestinal alkaline phosphatase (IAP) is a gut mucosal defense factor capable of inhibiting intestinal inflammation. We used the malachite green assay to show that IAP dephosphorylates UDP. To study
Glutamine metabolism in adipocytes: a bona fide epigenetic modulator of inflammation
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A chronic low-grade inflammation of white adipose tissue (WAT) is one of the hallmarks of obesity and is proposed to contribute to insulin resistance and type 2 diabetes. Despite this, the causal mechanisms underlying WAT inflammation remain unclear. Based on metabolomic analyses of human WAT,
قاعدة بيانات الأعشاب الطبية الأكثر اكتمالا التي يدعمها العلم
- يعمل في 55 لغة
- العلاجات العشبية مدعومة بالعلم
- التعرف على الأعشاب بالصورة
- خريطة GPS تفاعلية - ضع علامة على الأعشاب في الموقع (قريبًا)
- اقرأ المنشورات العلمية المتعلقة ببحثك
- البحث عن الأعشاب الطبية من آثارها
- نظّم اهتماماتك وابقَ على اطلاع دائم بأبحاث الأخبار والتجارب السريرية وبراءات الاختراع
اكتب أحد الأعراض أو المرض واقرأ عن الأعشاب التي قد تساعد ، واكتب عشبًا واطلع على الأمراض والأعراض التي تستخدم ضدها.
* تستند جميع المعلومات إلى البحوث العلمية المنشورة
