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Search Results for : Stroke
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Diagnosis Therapy Rehabilitation Imaging Clinical Laboratory
Cornin ameliorates cerebral infarction in rats by antioxidant action and stabilization of mitochondrial function.
Author(s): Jiang, WL; Zhang, SP; Zhu, HB; Tian, JW
Journal: Phytother Res 2010 Jun 29; Vol. 24, Issue 4; Page(s) 547-52
[Medline ID - 20041427]

This study was conducted to investigate the efficacy of cornin, an iridoid glycoside, in an experimental cerebral ischemia induced by middle cerebral artery occlusion (MCAO) and reperfusion (I/R), and to elucidate the potential mechanism. Adult male Sprague-Dawley rats were subjected to MCAO for 1 h, then reperfusion for 23 h. Behavioral tests were used to evaluate the damage to central nervous system. The cerebral infarct volume and histopathological damage were assessed to evaluate the brain pathophysiological changes. Spectrophotometric assay methods were used to determine the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GPx). Contents of malondialdehyde (MDA), the generation of reactive oxygen species (ROS) as well as respiratory control ratio and respiratory enzymes of the brain mitochondria were also determined. The results showed th at cornin significantly decreased neurological deficit scores, and reduced cerebral infarct volume and degenerative neurons. Meanwhile, cornin significantly increased the brain ATP content, improved mitochondrial energy metabolism, inhibited the elevation of MDA content and ROS generation, and attenuated the decrease of SOD and GPx activities in brain mitochondria. These findings indicate that cornin has protective potential against cerebral ischemia injury and its protective effects may be due to amelioration of cerebral mitochondrial function and its antioxidant property.

[The difficulties in differential diagnosis of primary aldosteronism subtypes in women with strokes at a young age]
Author(s): Bohdanowicz-Pawlak, A; Szymczak, J; Jakubowska, J; Brona, A
Journal: Endokrynol Pol 2010 Apr 3; Vol. 60, Issue 6; Page(s) 492-6
[Medline ID - 20041369]

In patients with primary aldosteronism (PA), it is fundamental to distinguish between subtypes that benefit from different treatment. The authors describe difficulties in differential diagnosis in a case of 46 year old women with PA and two strokes in the past. Based on high plasma and urine aldosterone concentration, low plasma renin activity (PRA), very high aldosterone/PRA ratio and unilateral macroadenoma detected in computed tomography, aldosterone producing adenoma was diagnosed and the patient was performed unilateral adrenalectomy. Despite the surgical treatment the patient still presented with clinical and biochemical PA symptoms. Moreover, histological examination suggested adrenal hyperplasia, and laboratory tests were typ ical for glucocorticoid-remediable aldosteronism. Unfortunately, we didn't find a chimeric CYP 11beta1/CYP 11beta2 gene. Finally, bilateral adrenal hyperplasia was diagnosed and medical treatment with aldosterone antagonist was initiated.

A systematic review and meta-analysis of erythropoietin in experimental stroke.
Author(s): Jerndal, M; Forsberg, K; Sena, ES; Macleod, MR; O'Collins, VE; Linden, T; Nilsson, M; Howells, DW
Journal: J Cereb Blood Flow Metab 2010 May 28; Vol. 30, Issue 5; Page(s) 961-8
[Medline ID - 20040929]

Erythropoietin (EPO) has shown promise as a neuroprotectant in animal models of ischemic stroke. EPO is thought not only to protect neurons from cell death, but also to promote regeneration after stroke. Here, we report a systematic review and meta-analysis of the efficacy of EPO in animal models of focal cerebral ischemia. Primary outcomes were infarct size and neurobehavioral outcome. Nineteen studies involving 346 animals for infarct size and 425 animals for neurobehavioral outcome met our inclusion criteria. Erythropoietin improved infarct size by 30.0% (95% CI: 21.3 to 38.8) and neurobehavioral outcome by 39.8% (33.7 to 45.9). Studies that randomized to treatment group or that blinded assessment of outcome showed lower efficacy. Erythropoietin was tested in animals with hypertension in no studies reporting infarct size and in 7.5% of the animals reporting neurobehavioral outcome. These findings show efficacy for EPO in experimental stroke, but when the impact of common sources of bias are considered, this efficacy falls, suggesting we may be overestimating its potential benefit. As common human co-morbidities may reduce therapeutic efficacy, broader testing to delineate the range of circumstances in which EPO works best would be beneficial.

Sympathoinhibition induced by centrally administered atorvastatin is associated with alteration of NAD(P)H and Mn superoxide dismutase activity in rostral ventrolateral medulla of stroke-prone spontaneously hypertensive rats.
Author(s): Kishi, T; Hirooka, Y; Konno, S; Sunagawa, K
Journal: J Cardiovasc Pharmacol 2009 Dec 31; Vol. 55, Issue 2; Page(s) 184-90
[Medline ID - 20040888]

Oxidative stress in the rostral ventrolateral medulla (RVLM) increases sympathetic nervous system activity (SNA). Oral treatment with atorvastatin decreases SNA through antioxidant effects in the RVLM of stroke-prone spontaneously hypertensive rats (SHRSP). We aimed to examine whether centrally administered atorvastain reduces SNA in SHRSP and, if so, to determine whether it is associated with the reduction of oxidative stress induced by alteration of activities of nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase and superoxide dismutase (SOD) in the RVLM of SHRSP. SHRSP received atorvastatin (S-ATOR) or vehicle (S-VEH) by continuous intracerebroventricular infusion for 14 days. Mean blood pressure, heart rate, and SNA were significantly lower in S-ATOR than in S-VEH. Oxidative stress, Rac1 activity, NAD(P)H oxidase activity, Rac1, gp91(phox) and p22(phox) expression in the membrane fraction, and p47(phox) and p40(phox) expression in the cytosolic fraction in the RVLM were significantly lower in S-ATOR than in S-VEH. Rac1 expression in the cytosolic fraction and Mn-SOD activity, however, were significantly higher in S-ATOR than in S-VEH. Our findings suggest that centrally administered atorvastatin decreases SNA and is associated with decreasing NAD(P)H oxidase activity and upregulation of Mn-SOD activity in the RVLM of SHRSP, leading to suppressing oxidative stress.

Simvastatin enhances hippocampal long-term potentiation in C57BL/6 mice.
Author(s): Mans, RA; Chowdhury, N; Cao, D; McMahon, LL; Li, L
Journal: Neuroscience 2011 Mar 17; Vol. 166, Issue 2; Page(s) 435-44
[Medline ID - 20040368]

Statins inhibit 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme in the cholesterol biosynthetic pathway, and they are widely used to control plasma cholesterol levels and prevent cardiovascular disease. However, emerging evidence indicates that the beneficial effects of statins extend to t he CNS. Statins have been shown to improve the outcome of stroke and traumatic brain injury, and statin use has been associated with a reduced prevalence of Alzheimer's disease (AD) and dementia. However, prospective studies with statins in AD have produced mixed results. Recently, we reported that simvastatin, a widely used statin in humans, enhances learning and memory in non-transgenic mice as well as in transgenic mice with AD-like pathology on a mixed genetic background. However, the cellular and molecular mechanisms underlying the beneficial effects of simvastatin on learning and memory remain elusive. The present study was undertaken to investigate the effect of acute simvastatin treatment on hippocampal long-term potentiation (LTP), a cellular model of learning and memory, in brain slices from C57BL/6 mice. Our results demonstrate that a prolonged in vitro simvastatin treatment for 2-4 h, but not a short-term 20-min exposure, significantly increases the magnitude of LTP at CA3-CA1 synapses without altering basal synaptic transmission or the paired-pulse facilitation ratio in hippocampal slices. Furthermore, we show that phosphorylation of Akt (protein kinase B) is increased significantly in the CA1 region following 2-hour treatment with simvastatin, and that inhibition of Akt phosphorylation suppresses the simvastatin-induced enhancement of LTP. These findings suggest activation of Akt as a molecular pathway for augmented hippocampal LTP by simvastatin treatment, and implicate enhancement of hippocampal LTP as a potential cellular mechanism underlying the beneficial effects of simvastatin on cognitive function.

Resveratrol preconditioning induces cellular stress proteins and is mediated via NMDA and estrogen receptors.
Author(s): Saleh, MC; Connell, BJ; Saleh, TM
Journal: Neuroscience 2010 May 4; Vol. 166, Issue 2; Page(s) 445-54
[Medline ID - 20040366]

Resveratrol pretreatment has been shown to provide neuroprotection in models of cerebral ischemia. This phenomenon, commonly termed preconditioning, promotes ischemic tolerance and may involve mild activation of endoplasmic reticulum stress pathways in the affected tissue. Systemic injection of resveratrol (2 x 10(-3), 2 x 10(-4), 1 x 10(-4) mg/kg) 30 min prior to a 4 h period of right middle cerebral artery occlusion significantly reduced infarct area in the insular region of rat prefrontal cortex. This affect was blocked when resveratrol treatment was combined with a non-selective estrogen receptor antagonist, or preceded by intracortical injection of an NMDA receptor antagonist. The neuroprotective effect of resveratrol was associated with reduced renal sympathetic nerve activity as well as induction of resident endoplasmic reticulum chaperone proteins, glucose-regulated proteins 78 and 94. The calcium-sensitive chaperone heat shock protein 70 and the cysteine protease m calpain did not respond to resveratrol pretreatment. However, a significant induction of heat shock protein 70 was observed in the contralateral cortex of resveratrol pretreated rats following 4 h of right middle cerebral artery occlusion. These data suggest that resveratrol preconditioning promotes ischemic tolerance in the short term, in part via effects mediated through activation of estrogen and NMDA receptors, as well as through mild activation of cellular stress proteins.

B-type natriuretic peptide and severe heart failure at baseline predict overall mortality in incident dialysis patients.
Author(s): Koch, M; Trapp, R; Kohnle, M; Aker, S; Haastert, B; Rump, LC
Journal: Clin Nephrol 2010 Mar 10; Vol. 73, Issue 1; Page(s) 21-9
[Medline ID - 20040348]

AIMS: The B-type natriuretic peptide (BNP) has become increasingly important as a diagnostic and prognostic method for cardiovascular disease or death. To our knowledge no prospective studies exist to evaluate the value of baseline BNP and baseline heart failure as predictors of overall death in incident rather than prevalent hemodialysis patients with end-stage renal disease (ESRD). METHODS: 255 ESRD patients were included in our observational study with a median observation period of 1.11 years. A Kaplan-Meier survival curve was stratified by BNP concentration ( < 340 pg/ml and > or = 340 pg/ml) to estimate the impact on the overall mortality rate. Univariate and multiple Cox regression models were fitted for a variety of covariables including severe heart failure (graded according to the New York Heart Association) to evaluate the independent predictors of death. Association between BNP and four explanatory variables was described in a multiple linear regression model. RESULTS: Survival analysis demonstrated a significantly higher mortality rate in patients with higher BNP values at baseline. The independent predictive value of high BNP concentration at baseline could be statistically confirmed by multiple Cox regression analysis. However, when including the covariates hemoglobin and severe heart failure, significantly associated with BNP, in the same model, severe heart failure rather than BNP becomes a significant predictor of overall death. CONCLUSIONS: A higher BNP level at baseline may be confirmed as an independent predictor of death in the incident dialysis population. However, severe heart failure may affect the impact of BNP on the overall survival rate and thus be a stronger predictor of death than BNP.

Oral anticoagulation with Factor Xa and thrombin inhibitors: Is there an alternative to warfarin?
Author(s): Zikria, J; Ansell, J
Journal: Discov Med 2010 May 21; Vol. 8, Issue 43; Page(s) 196-203
[Medline ID - 20040270]

Vitamin K antagonists (VKA), such as warfarin, have been the only available oral anticoagulants despite their many limitations. The greatest medical need is to find a replacement for warfarin for long-term therapy, particularly for stroke prevention in atrial fibrillation (AF) patients. Emerging oral anticoagulants are free from many of warfarin's drawbacks and may offer a convenient alternative. Drugs in advanced development target factor Xa (rivaroxaban, apixaban) or thrombin (dabigatran etexilate). Recently, the RE-LY phase III study found dabigatran etexilate was an effective and convenient alternative to warfarin in stroke prevention for AF patients. Within the next two years, similar studies comparing rivaroxaban and apixaban versus warfarin in AF patients will become available. This paper reviews warfarin's limitations, discusses the pharmacokinetics of emerging anticoagulants in advanced development, and summarizes trials with an emphasis on head-to-head studies comparing novel anticoagulants to warfarin.

Familial risk for chronic disease and intent to share family history with a health care provider among urban Appalachian women, southwestern Ohio, 2007.
Author(s): Au, MG; Cornett, SJ; Nick, TG; Wallace, J; Wang, Y; Warren, NS; Myers, MF
Journal: Prev Chronic Dis 2010 Mar 11; Vol. 7, Issue 1; Page(s) A07
[Medline ID - 20040222]

INTRODUCTION: Family history of certain chronic diseases is a risk factor for those diseases. We assessed demographic characteristics associated with familial risk for common diseases and whether familial risk was associated with intent to share family history with a health care provider among urban Appalachian women. METHODS: Urban Appalachian women (N = 88) with less than a college education participated in education sessions about family history in health promotion in southwest Ohio. Participants used My Family Health Portrait, electronically or on paper, to document their level of familial risk. Evaluations completed after each session gauged intent to share family history with a health care provider. RESULTS: Participants who used the paper version of My Family Health Portrait had lower odds of high familial risk for diabetes, heart disease, and stroke. Most participants (n = 62, 77%) reported that they intended to share their family history with a health care provider. Factors associated with intent to share family history included younger age, use of the electronic family history tool, and high familial risk of heart disease. CONCLUSION: The large proportion of women who intended to share family history with a health care provider may reflect the success of the educational component. Since familial risk for chronic disease is high among these urban Appalachian women, the need to share family history should continue to be promoted.

Does higher usage of low-cost statins correlate with a poorer achievement in cholesterol quality markers for secondary prevention?
Author(s): Hickman, J
Journal: Br J Gen Pract 2011 Jan 1; Vol. 60, Issue 570; Page(s) 50-2
[Medline ID - 20040169]

There is pressure on primary care trusts, and therefore on GPs, to reach specific levels of use of low-cost statins as a proportion of total statin prescribing. This simple study looks at some markers of the quality of the results achieved. A correlation is found between a higher proportion of low-cost statin prescribing and lower achievement raising questions as to whether financial savings may be offset by poorer results.
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