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anti inflammatory/stroke

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頁 1 從 2698 結果
BACKGROUND A recent study demonstrated that the inflammatory response accompanying necrotic brain injury played an important role in stroke. Thus, inhibition of this response may help to stop the expansion of infarcts. It has been also shown that the spleen, a major peripheral immune organ, plays a
It has been shown that remote ischemic preconditioning (RIPreC) attenuates ischemic injury after stroke in healthy rats or mice. The present study aims to examine whether RIPreC offers neuroprotection against ischemic stroke in streptozotocin-induced diabetic
Background: Hemorrhagic strokes have not declined in the United States despite a decline worldwide. Purpose: To identify hemorrhagic stroke risk associated with nonsteroidal
Atorvastatin decreases inflammation and thrombogenesis in patients with carotid artery plaque. Atorvastatin is administered to lower lipid levels, but its anti-inflammatory and anti-thrombogenic effects remain unclear. Eighty-nine patients from northeastern China with acute ischemic stroke caused by
BACKGROUND Activated protein C (APC) contributes to systemic anticoagulant and anti-inflammatory activities. APC may reduce organ damage by inhibiting thrombin generation and leukocyte activation. Neutrophils and cerebrovascular thrombosis contribute to ischemic neuronal injury, suggesting that APC
Heat stroke is characterized by hyperthermia, systemic inflammation, and multiple organ failure including arterial hypotension. This definition can be fulfilled by a rat model of heat stroke used in the present study. Anesthetized animals were exposed to heat exposure (43 °C for 70 min) and then
BACKGROUND Our recent research showed that resistin has a neuroprotective effect against stroke-induced injury through suppressing apoptosis and oxidative stress. However, the molecular mechanism of neuroprotection of resistin is unclear. This work was designed to examine the effect of mouse
OBJECTIVE Proinflammatory and anti-inflammatory cytokines may play a pivotal role in cerebral inflammation, which is implicated in the development of brain injury. Systemic cytokine release is mediated by the sympathetic nervous system and catecholamines. The aim of this study was to investigate
BACKGROUND This study investigated the potential for bias introduction when selecting controls for secondary analysis of case-control study data. METHODS We used a data set previously collected for an acute brain bleeding analysis (ABBA) study, which was designed to investigate the risk of
There are still debates on the association of increased cardiovascular risk with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis (RA) because of inconsistent results. Therefore, our study aims to evaluate the transient effects of selective and
BACKGROUND The genetic basis of complex diseases like ischemic stroke probably consists of several predisposing risk factors, such as genes involved in inflammation and thrombotic pathways. On this basis the aim of our study was to evaluate the role of SNPs (single nucleotide polymorphisms) of some
OBJECTIVE Studies on the risk of stroke in users of non-steroidal anti-inflammatory drugs (NSAIDs) have provided conflicting results. We studied the association between the use of non-selective ns-NSAIDs, selective COX-2 inhibitors, or either of these NSAIDs, and the incidence of stroke-related
Recent professional statements from established bodies, i.e. American Heart Association, European Medicines Agency, and Medicines and Healthcare products Regulatory Agency, have cautioned on the use of non-steroidal anti-inflammatory drugs (NSAIDs) given the potential increase in atherothrombotic
A number of prominent studies have been conducted using anti-inflammatory therapies to reduce reperfusion injury in myocardial infarction and stroke. Unfortunately, most strategies have failed. This review summarizes in detail the human studies of anti-inflammatory therapy that have been conducted

Proinflammatory and Anti-inflammatory genes in stroke pathogenesis

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The brain's response to ischemic injury is an acute and long-term inflammatory process. This process involves activation of resident cells (mainly microglia, hematogenous macrophages), production of proinflammatory mediators and infiltration of various proinflammatory cells (mainly neutrophils and
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