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Страница 1 от 26 резултата
Argyria resulting from chronic use of colloidal silver in a patient presenting for colonoscopy.
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An elderly male with a history of argyria caused by chronic ingestion of colloidal silver presented for elective colonoscopy. The patient's skin was a profound blue-gray color that caused concern among staff until his condition was identified through his medical and medication history. Colonoscopy
L-deprenyl reduces brain damage in rats exposed to transient hypoxia-ischemia.
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OBJECTIVE
L-Deprenyl (Selegiline) protects animal brains against toxic substances such as 1-methyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine. Experiments were conducted to test whether L-deprenyl prevents or reduces cerebral damage in a transient hypoxia/ischemia rat model.
METHODS
Rats were
GSK-3β/mTORC1 Couples Synaptogenesis and Axonal Repair to Reduce Hypoxia Ischemia-Mediated Brain Injury in Neonatal Rats.
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Glycogen synthase kinase 3 beta (GSK-3β) plays an important role in neurological outcomes after brain injury. However, its roles and mechanisms in hypoxia-ischemia (HI) are unclear. Activation of mTOR complex 1 (mTORC1) has been proven to induce the synthesis of proteins associated with
Extracellular ATP promotes breast cancer invasion and epithelial-mesenchymal transition via hypoxia-inducible factor 2α signaling.
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Extracellular ATP has been shown to play an important role in invasion and the epithelial-mesenchymal transition (EMT) process in breast cancer; however, the mechanism is unclear. Here, by using a cDNA microarray, we demonstrated that extracellular ATP could stimulate hypoxia-inducible factor (HIF)
Naringenin and quercetin reverse the effect of hypobaric hypoxia and elicit neuroprotective response in the murine model.
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Exposure to high-altitude results in hypobaric hypoxia which is considered as an acute physiological stress. This condition often leads to high-altitude illnesses such as high-altitude cerebral edema, high altitude pulmonary edema and hypoxic muscle weakness. Hypoxic injuries can be prevented by
Primary sensory and forebrain motor systems in the newborn brain are preferentially damaged by hypoxia-ischemia.
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Cerebral hypoxia-ischemia causes encephalopathy and neurologic disabilities in newborns by unclear mechanisms. We tested the hypothesis that hypoxia-ischemia causes brain damage in newborns that is system-preferential and related to regional oxidative metabolism. One-week-old piglets were subjected
Serum from patients undergoing remote ischemic preconditioning protects cultured human intestinal cells from hypoxia-induced damage: involvement of matrixmetalloproteinase-2 and -9.
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Remote ischemic preconditioning (RIPC) can be induced by transient occlusion of blood flow to a limb with a blood pressure cuff and exerts multiorgan protection from ischemia/reperfusion injury. Ischemia/reperfusion injury in the intestinal tract leads to intestinal barrier dysfunction and can
A genetic study of the depressive respiratory responses to hypoxia in chronic obstructive pulmonary disease patients with type II respiratory failure.
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OBJECTIVE
The depression of the ventilatory and P(0.1 )responses to hypoxia and hypercapnia may play an important role in the development of CO(2) retention in the patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate if there is any linkage
Early Neurodegeneration after Hypoxia-Ischemia in Neonatal Rat Is Necrosis while Delayed Neuronal Death Is Apoptosis.
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We used silver staining to demonstrate neuronal cell body, axonal, and terminal degeneration in brains from p7 rat pups recovered for 0, 1.5, 3, 6, 24, 48, 72 h, and 6 days following hypoxia-ischemia. We found that initial injury is evident in ipsilateral forebrain by 3 h following hypoxia-ischemia,
Use of an amino-cupric-silver technique for the detection of early and semiacute neuronal degeneration caused by neurotoxicants, hypoxia, and physical trauma.
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A new amino-cupric silver protocol is described for detection of neuronal degeneration. We describe its selectivity in visualizing both early and semiacute degeneration after intracerebral or systemic administration of a variety of neurotoxicants in rats, and after transient ischemic episodes in
Microwave bioeffects in the erythrocyte are temperature and pO2 dependent: cation permeability and protein shedding occur at the membrane phase transition.
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Microwave exposure (2450 MHz, 60 mW/g, CW) of rabbit erythrocytes increases Na passive transport only at membrane phase transition temperatures (Tc) of 17-19 degrees C. This permeability effect is enhanced for relative hypoxia which is characteristic of intracellular oxygen tension (pO2 less than or
Topography of hypoxic injury proved by argyrophilia in postnatal rat brain.
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The argyrophil III method, a new esterification-silver staining approach, was used to elucidate regional differences in the susceptibility of developing brain to hypoxic-ischemic (H-I) injury. We created a unilateral common carotid artery-ligation model with hypoxia (8% oxygen) in postnatal day (P)
[Formation and repression of neuromuscular endplates in neurogenic and muscular lesions].
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The motor endplates and intramuscular nerves of rat and rabbit masticatory muscle were preferentially demonstrated using an acetylcholinesterase reaction followed by silver staining. The regeneration of the neuromuscular unit was followed serially at the site of an earlier biopsy. Using observations
Functional link between ferroxidase activity of ceruloplasmin and protective effect of apo-lactoferrin: studying rats kept on a silver chloride diet.
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Strongly pronounced argyrosis caused by adding AgCl to the feed of laboratory rats efficiently mimics the deficiency of ceruloplasmin (CP) ferroxidase activity. Bringing the concentration of AgCl in the feedstuff of lactating rats to 250 mg % and keeping their progeny (Ag-rats) for 3 months on the
Ischemia of the dog heart induces the appearance of a cardiac mRNA coding for a protein with migration characteristics similar to heat-shock/stress protein 71.
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Recent evidence indicates that different forms of stress, including hypoxia, can induce specific proteins called heat-shock or stress proteins in various types of mammalian cells. These studies examined whether myocardial ischemia can result in increased levels of proteins with molecular weight and
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