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gamma linolenic acid/hypoxia

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Introduction: Gastric cancer is one of the most common malignancies in China and the fifth most common cancer in the world. Gamma linolenic acid (GLA) was reported to have anti-inflammatory and anti-cancer effects. The purpose of this

Gamma linolenic acid suppresses hypoxia-induced proliferation and invasion of non-small cell lung cancer cells by inhibition of HIF1α

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Background: The main therapies for cancer often results in many side effects and drug resistance. Gamma linolenic acid (GLA) is a kind of natural reagent with negligible cytotoxicity. Objective:
Gamma linolenic acid is a polyunsaturated fatty acid having selective anti-tumour properties with negligible systemic toxicity. In the present study, the anti-cancer potential of gamma linolenic acid and its effects on mitochondrial as well as hypoxia-associated marker was evaluated. The effect of

Gamma linolenic acid regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DEN induced hepatocellular carcinoma.

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Hepatocellular carcinoma (HCC) is one of the known major health problems across the globe, and is sixth ranked among all cancer, due to its high mortality rate. Polyunsaturated fatty acids (PUFAs) play an important role in the formation of a cell membrane, along with the fluidity of
OBJECTIVE The aim was to show differences between the effects of various dietary long chain fatty acids (palmitic, oleic, linoleic, alpha and gamma linolenic acids) perfused in isolated rat hearts subjected to a sequence of high flow anoxia and subsequent reoxygenation. METHODS Isolated working rat

The use of gamma linolenic acid in the prevention and treatment of diabetic neuropathy.

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A substantial disturbance of the metabolism of the n-6 essential fatty acids (EFAs) exists in both human and experimental diabetes mellitus. The process of conversion of dietary linoleic acid to gammalinolenic, dihomogammalinolenic and arachidonic acids, and other polyunsaturates is inadequate in

GLA supplementation regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DMBA induced mammary gland carcinoma.

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The aim of the present study is to evaluate the effect of gamma linolenic acid (GLA) on mitochondrial mediated death apoptosis, hypoxic microenvironment and cholinergic anti-inflammatory pathway against 7, 12-dimethylbenz (a) anthracene (DMBA) induced mammary gland carcinoma. The effects of GLA were

[Diabetic somatic polyneuropathy. Pathogenesis, clinical manifestations and therapeutic concepts].

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Diabetic polyneuropathy is the most frequent neuropathy in western countries. In Germany, there are 3.5 to 4 million diabetic patients. Diagnosis should rule out other polyneuropathies and assess two out of the five diagnostic criteria: neuropathic symptoms, neuropathic deficits, pathological nerve

Effects of antioxidants on nerve and vascular dysfunction in experimental diabetes.

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Reactive oxygen species (ROS) are elevated by metabolic changes in diabetes, including autoxidation and increased advanced glycation. Endogenous protection by the glutathione redox cycle is also compromised by the competing NADPH requirement of elevated polyol pathway flux. Antioxidant treatment

Sudden infant death syndrome (SIDS): T-cell immunodeficiency--Part 1.

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It is hypothesized that SIDS mimics AIDS and atopic eczema in that defective T lymphocytes and overactive B cells overstimulate pro-inflammatory cytokines in the mucosal immune system. Virally infected cells are unable to convert linoleic acid (LA) into gamma-linolenic acid (GLA) which eventually

Omega-3 polyunsaturated fatty acids in critically ill patients with acute respiratory distress syndrome: A systematic review and meta-analysis.

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Acute respiratory distress syndrome (ARDS) is characterized by an acute inflammatory response in the lung parenchyma leading to severe hypoxemia. Because of its anti-inflammatory and immunomodulatory properties, omega-3 polyunsaturated fatty acids (ω-3 PUFA) have been administered to

Keloids in rural black South Africans. Part 3: a lipid model for the prevention and treatment of keloid formations.

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In the third part of this study a basic lipid model (regarding phospholipids, triglycerides, cholesterol esters and free fatty acids) for keloids (n=20), compared with normal skin of keloid prone and non-keloid prone patients (n=20 of each), was constructed according to standard methods, to serve as
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