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ribonuclease/وذمة

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مقالاتالتجارب السريريةبراءات الاختراع
15 النتائج

Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice.

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الدخول التسجيل فى الموقع
BACKGROUND Following myocardial infarction (MI), peri-infarct myocardial edema formation further impairs cardiac function. Extracellular RNA (eRNA) released from injured cells strongly increases vascular permeability. This study aimed to assess the role of eRNA in MI-induced cardiac edema formation,

Ribonuclease (RNase) Prolongs Survival of Grafts in Experimental Heart Transplantation.

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Cell damage, tissue and vascular injury are associated with the exposure and release of intracellular components such as RNA, which promote inflammatory reactions and thrombosis. Based on the counteracting anti-inflammatory and cardioprotective functions of ribonuclease A (RNase A) in this context,

[Activity of lysosomal enzymes in rabbit brain during the development of edema].

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Liberation and consequent activation of lysosomal enzymes seems to play significant role in the development of brain edema. In the present experiment with adult rabbits, anesthetized with urethane we investigated in the brain tissue homogenates the activity of four lysosomal enzymes, such as

Ex Vivo Functionality of 3D Bioprinted Corneal Endothelium Engineered with Ribonuclease 5-Overexpressing Human Corneal Endothelial Cells.

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Human corneal endothelial cells (HCECs) are scarcely proliferative in vivo. The cultured HCECs engineered to overexpress ribonuclease (RNase) 5 (R5-HCECs) are prepared after transient transfection with RNase 5 plasmid vector. As candidate targets of R5-HCECs for enhancement of cellular proliferation

Ribonucleases as a novel pro-apoptotic anticancer strategy: review of the preclinical and clinical data for ranpirnase.

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Cytotoxic ribonucleases (RNases), such as ranpiranase, represent a novel mechanism-based approach to anticancer therapy. These relatively small proteins selectively attack malignant cells, triggering apoptotic response and inhibiting protein synthesis. Ranpirnase, originally isolated from oocytes of

RNase therapy assessed by magnetic resonance imaging reduces cerebral edema and infarction size in acute stroke.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
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Ischemic stroke causes cell necrosis with the exposure of extracellular ribonucleic acid (RNA) and other intracellular material. As shown recently, extracellular RNA impaired the blood-brain-barrier and contributed to vasogenic edema-formation. Application of ribonuclease 1 (RNase 1) diminished

Induction of aquaporin-1 mRNA following cardiopulmonary bypass and reperfusion.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
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BACKGROUND Cardiopulmonary bypass (CPB) and hypothermic circulatory arrest (HCA) are important components of congenital cardiac surgery. Ischemia/reperfusion injury and inflammatory cascade activation result in endothelial damage and vascular leak which are clinically manifested as pulmonary edema

Altered pulmonary response to hyperoxia in Clara cell secretory protein deficient mice.

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Clara cell secretory protein (CCSP) is an abundant component of the extracellular lining fluid of airways. Even though the in vivo function of CCSP is unknown, in vitro studies support a potential role of CCSP in the control of inflammatory responses. CCSP-deficient mice (CCSP -/-) were generated to

Interstitial nephritis in a patient with atypical Sjögren's syndrome.

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A patient was observed with interstitial nephritis which resulted in renal tubular acidosis (distal type), tubular proteinuria and defective urinary concentrating ability in the absence of edema, elevated arterial blood pressure, glomerular proteinuria or abnormal urinary sediment. The presence of

Extracellular RNAs as a chemical initiator for postoperative cognitive dysfunction.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
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Postoperative cognitive dysfunction (POCD) is a common complication that presents in the postoperative stage, especially in elderly patients. Despite years of considerable progress, the detailed molecular mechanisms of POCD remain largely unknown. Neuroinflammation has been increasingly pointed out

Extracellular RNA, a Potential Drug Target for Alleviating Atherosclerosis, Ischemia/Reperfusion Injury and Organ Transplantation.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
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Extracellular RNA (eRNA), composed of mainly rRNA e.g. released upon cell injury, has previously been shown to have three main detrimental functions in the context of cardiovascular disease: (1) to promote tissue edema by activating the VEGF signal transduction cascade, disrupting endothelial tight

Properties of the Hemolytic Activities of Escherichia coli.

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Some properties of the cell-free and cell-associated hemolysins of Escherichia coli were studied. Several strains of E. coli that were isolated from intestines of pigs with edema disease produce large quantities of cell-free hemolysin when grown in the presence of an extract of meat. The component

Cannabinoids in acute gastric damage and pancreatitis.

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Recent studies have shown that stimulation of cannabinoid 1 (CB1) receptor reduces the area of ischemic myocardial necrosis and affects activity of the digestive tract. The aim of the present study was to check whether the administration of CB1 receptor agonist or antagonist affects the

Hippocampal neurokinin-1 receptor and brain-derived neurotrophic factor gene expression is decreased in rat models of pain and stress.

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Acute or chronic stress can alter hippocampal structure, cause neuronal damage, and decrease hippocampal levels of the neurotrophin brain-derived neurotrophic factor (BDNF). The tachykinin substance P and its neurokinin-1 (NK-1) receptor may play a critical role in neuronal systems that process

Interferon-gamma and interleukin-10 reciprocally regulate endothelial junction integrity and barrier function.

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Inflammatory bowel disease (IBD) is associated with Th1/Th2 cytokine dysregulation, leukocyte extravasation, and tissue edema, but the mechanisms for cytokine-mediated vascular dysfunction are not understood. To investigate how cytokines might control edema in IBD, we determined vascular
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