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Pagina 1 a partire dal 2236 risultati
[Fatalities after injuries by wild animals].
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The article summarises three fatalities after attacks by wild animals. The first case describes a 90-year-old woman who died as a result of pneumonia after a bear fell on her and caused multiple chest fractures. The second case deals with a 76-year-old woman who was hit in the middle face by the
Cardiac Sympathetic Denervation in Wild-Type Transthyretin Amyloidosis
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Background: Tissue accumulation of misfolded transthyretin (TTR) may occur because of TTR gene mutations (variant amyloid TTR amyloidosis, ATTRv), or as an age-related phenomenon (wild-type ATTR, ATTRwt). Cardiac sympathetic denervation has been reported in ATTRv, but has never been
Wild-type p53-induced Phosphatase 1 Deficiency Exacerbates Myocardial Infarction-induced Ischemic Injury.
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BACKGROUND
Myocardial infarction (MI) is a major disease burden. Wild-type p53-induced phosphatase 1 (Wip1) has been studied extensively in the context of cancer and the regulation of different types of stem cells, but the role of Wip1 in cardiac adaptation to MI is unknown. We investigated the
Coronary vasospasm causing acute myocardial infarction: an unusual result of wild mushroom poisoning.
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Aeromonas hydrophila isolated from wild freshwater fish in Croatia.
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Aeromonas hydrophila was recovered from fish living in lake Vrana on the Croatian island of Cres. The occurrence of the bacterium in the fish was assessed and related to gross signs of disease and findings at necropsy as a potential health hazard for fish. Isolated bacteria were subjected to
Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths.
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UNASSIGNED
Wild-type transthyretin amyloidosis (ATTRwt) is mostly considered a disease predominantly of elderly male, characterized by concentric LV hypertrophy, preserved LVEF, and low QRS voltages. We sought to describe the characteristics of a large cohort of ATTRwt patients to better define the
Modulation of apoptosis-related microRNAs following myocardial infarction in fat-1 transgenic mice vs wild-type mice.
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Microfilarial granulomas in the spleens of wild-caught cynomolgus monkeys (Macaca fascicularis).
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Splenic nodules from 38 cynomolgus monkeys (Macaca fascicularis) which were captured in Malaysia and Indonesia were studied histologically. The lesions were characterized by well-circumscribed focal fibrosis, accumulation of eosinophils and histiocytes, hemorrhage or hemosiderosis, and loss of
Hydrogen Sulfide Treatment Improves Post-Infarct Remodeling and Long-Term Cardiac Function in CSE Knockout and Wild-Type Mice
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Hydrogen sulfide (H2S) is recognized as an endogenous gaseous signaling molecule generated by cystathionine γ-lyase (CSE) in cardiovascular tissues. H2S up-regulation has been shown to reduce ischemic injury, and H2S donors are cardioprotective in rodent models when
Novel Neuroprotective Loci Modulating Ischemic Stroke Volume in Wild-Derived Inbred Mouse Strains.
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To identify genes involved in cerebral infarction we have employed a forward genetic approach in inbred mouse strains, using quantitative trait locus (QTL) mapping for cerebral infarct volume after middle cerebral artery occlusion. We had previously observed that infarct volume is inversely
Melatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice.
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Cyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24
Melatonin reduced volume of cerebral infarct induced by photothrombosis in wild-type mice, not in Cyclooxygenase-1 gene knockout mice.
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Cyclooxygenase (COX) is crucial in inflammation and plays important role in cerebral ischemia. Antiinflammatory effects of melatonin have been verified in previous studies. In this study, cerebral blood flow (CBF) was monitored during operation, infarct volume (IFV) was determined with
Regional CBF in apolipoprotein E-deficient and wild type mice during focal cerebral ischemia.
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Apolipoprotein E-(apoE) deficient mice exhibit hypercholesterolemia, accelerated atherosclerosis and increased infarct size after middle cerebral artery occlusion (MCAO). This study examined whether worsened ischemic outcome is attributable to effects of apoE deficiency on cerebral circulation. Wild
L-Arginine increases ischemic injury in wild-type mice but not in iNOS-deficient mice.
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Delayed administration of the nitric oxide precursor L-arginine increases brain injury in models of focal cerebral ischemia. We tested the hypothesis that L-arginine worsens the damage by acting as a substrate for inducible nitric oxide synthase (iNOS) and increasing the output of this enzyme.
Minocycline protects against permanent cerebral ischemia in wild type but not in matrix metalloprotease-9-deficient mice.
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Minocycline is protective in models of transient middle cerebral artery occlusion (MCAO). We studied whether minocycline and doxycycline, another tetracycline derivative, provide protection in permanent MCAO. Because minocycline inhibits matrix metalloprotease-9 (MMP-9), we also compared
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