arginase/hemoragie

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Involvement of accumulated NOS inhibitors and endothelin-1, enhanced arginase, and impaired DDAH activities in pulmonary dysfunction following subarachnoid hemorrhage in the rabbit.

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We designed the present experiments to investigate the involvement of endogenous nitric oxide synthase (NOS) inhibitors, dimethylarginine dimethylaminohydrolase (DDAH) as a hydrolyzing enzyme of the NOS inhibitors, NOS, arginase which shares l-arginine as a common substrate with NOS, and

Vascular arginase contributes to arteriolar endothelial dysfunction in a rat model of hemorrhagic shock.

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BACKGROUND Hemorrhagic shock causes hypoperfusion of peripheral tissues and promotes endothelial dysfunction, which may lead to further tissue injury. Trauma increases extrahepatic activity of arginase, an enzyme which competes for l-arginine with nitric oxide synthase, and plays a key role in the

[Activity of serum arginase in liver cirrhosis. Its special study in the hemorrhagic syndrome and cirrhogenic encephalopathies].

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Hypertonic saline resuscitation contributes to early accumulation of circulating myeloid-derived suppressor cells in a rat model of hemorrhagic shock.

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BACKGROUND Hemorrhagic shock is usually associated with complicated immune and inflammatory responses, which are sometimes crucial for the prognosis. As regulators of the immune and inflammatory system; proliferation, migration, distribution and activation of myeloid-derived suppressor cells (MDSCs)

Arginase I suppresses IL-12/IL-23p40-driven intestinal inflammation during acute schistosomiasis.

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Alternatively activated macrophages prevent lethal intestinal pathology caused by worm ova in mice infected with the human parasite Schistosoma mansoni through mechanisms that are currently unclear. This study demonstrates that arginase I (Arg I), a major product of IL-4- and IL-13-induced

Nitric oxide and arginase levels in peri-implant tissues after delayed loading.

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OBJECTIVE Nitric oxide (NO) is synthesized from the conversion of L-arginine to L-citrulline by NO synthase (NOS). Arginase can compete with NOS for the common substrate L-arginine, and thus inhibit NO production. NO levels and arginase ezyme might affect the bone remodeling cycle around implants.

Melatonin ameliorates cerebral vasospasm after experimental subarachnoidal haemorrhage correcting imbalance of nitric oxide levels in rats.

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In the present study, we investigated the in vivo effects of melatonin on SAH-induced cerebral vasospasm and oxidative stress, resulting from SAH in an experimental rat model. Twenty-eight rats (225-250 g) were divided into four groups equally: group 1; control, group 2; SAH, group 3; SAH plus

Mannitol and Hypertonic Saline Reduce Swelling and Modulate Inflammatory Markers in a Rat Model of Intracerebral Hemorrhage.

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BACKGROUND Spontaneous intracerebral hemorrhage (ICH) leaves most survivors dependent at follow-up. The importance of promoting M2-like microglial responses is increasingly recognized as a key element to ameliorate brain injury following ICH. The osmotherapeutic agents, mannitol and hypertonic

A Virus-Derived Immune Modulating Serpin Accelerates Wound Closure with Improved Collagen Remodeling.

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Numerous treatments have been developed to promote wound healing based on current understandings of the healing process. Hemorrhaging, clotting, and associated inflammation regulate early wound healing. We investigated treatment with a virus-derived immune modulating serine protease inhibitor

Microcystin-LR decreases hepatic and renal perfusion, and causes circulatory shock, severe hypoglycemia, and terminal hyperkalemia in intravascularly dosed swine.

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Cross-bred, anesthetized female swine were given intravascularly a lethal (72 microg/kg; n = 6) or toxic-sublethal (25 microg/kg; n = 6) dose of microcystin-LR (MCLR), from Microcystis aeruginosa, or the vehicle (n = 4). At the high dose, from 12 to 18 min after administration, central venous

CD137-CD137L signaling affects angiogenesis by mediating phenotypic conversion of macrophages.

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Angiogenesis in atherosclerotic plaque is an important factor causing plaque hemorrhage, vulnerability and rupture and different phenotypes of macrophages have different effects on angiogenesis. Our previous study has demonstrated CD137-CD137L signaling, a pair of inflammatory

[Clinical and biochemical alterations in rats treated with high doses of vitamin A].

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In the present work the effect of intramuscular administration of 30.000, 50.000 and 100.000 IU of vitamin A palmitate daily for seven days, respectively, on the liver enzyme activity in 45 white male Wistar rats, aged 12 weeks and weighing 180-200 g, have been studied. The group control was

Uterine Carcinosarcoma with Alpha-Fetoprotein-Producing Hepatoid Component: A Case Report and Literature Review.

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A 67-year-old woman presented with postmenopausal vaginal bleeding. Full body imaging demonstrated an intrauterine mass with deep myometrial invasion but no nodal or other metastatic disease. Uterine curettage was performed. Histologically, the tumor was an endometrioid adenocarcinoma with

Health Effects of Trimellitic Anhydride Occupational Exposure: Insights from Animal Models and Immunosurveillance Programs

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Acid anhydrides are used by chemical industries as plasticizers. Trimellitic acid (TMA) is an acid anhydride widely utilized in factories to produce paints, varnishes, and plastics. In addition to causing direct irritant effects, TMA can augment antibody responses in exposed factory workers leading

Extensive macrophage accumulation in young and old Niemann-Pick C1 model mice involves the alternative, M2, activation pathway and inhibition of macrophage apoptosis.

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We have studied the pathophysiology of lung disease which occurs in two mouse models of Niemann-Pick C1 disease. We utilized Npc1(-/-) mice transgenic for normal gene expression in glia or neurons and glia at ages several fold the usual and a mouse model of the juvenile form of NPC1, a point

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