Journal of Stroke & Cerebrovascular Diseases最新文献

Objective: This study aimed to explore the neuroprotective effects of Melatonin (Mel) administration on cerebral ischemia-reperfusion injury (CIRI) and elucidate its underlying mechanism in vivo to provide a theoretical foundation for the clinical application of Mel.

Materials and methods: CIRI models were established in male adult Sprague Dawley rats by middle cerebral artery occlusion (MCAO) for 2 hours in male adult Sprague Dawley rats. Water content of brain tissue was assessed using both dry/wet weight method and T2-weighted Imaging (T2WI). The infarct volume of the brain was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Cell morphology changes and brain damage were detected through hematoxylin & eosin (H&E) staining and NeuN immunofluorescence staining. The integrity of blood-brain barrier (BBB) was examined using transmission electron microscopy (TEM). The expression of aquaporin 4 (AQP4) protein was quantified through western blots analysis and immunofluorescence staining. The expression of p-PI3K, p-AKT and Nrf2 were detected by immunohistochemistry staining and western blots analysis.

Results: Compared with the CIRI group, Mel administration significantly reduced the infarct volume and ameliorated the morphology alterations, accompanied by an increase in the number of neurons. The water content of brain tissue decreased significantly, and the value of relative average diffusion coefficient (rADC) of injured brain increased in the CIRI + Mel group as compared with the CIRI group. Compared with the CIRI group, Mel administration improved the damage to the tight junctions of endothelial cells in the cerebral cortex. The expression of AQP4 protein decreased, and that of p-PI3K, p-AKT and Nrf2 proteins increased in the CIRI + Mel group compared with the CIRI group. After administration of p-PI3K inhibitor LY294002, the expression of AQP4 was upregulated, and that of the p-PI3K, p-AKT and Nrf2 protein decreased compared with the CIRI + Mel group.

Conclusions: Mel administration exerts neuroprotective effects against CIRI by mitigating brain edema through upregulating the PI3K/AKT/Nrf2 signaling pathway, and then attenuating brain damage in CIRI rats.

Objectives: The objectives of the present study were 1) to describe changes in fatigue from 3 to 12 months post-stroke and compare different patterns of fatigue changes with respect to concurrent changes in physical fitness, body composition, and activity levels, and 2) to explore whether changes in fatigue are associated with changes in physical fitness, body composition, and physical activity levels in patients recovering from first-ever ischemic stroke.

Materials and methods: In this longitudinal observational study, we assessed 72 patients (mean age 62 years, 36% females) at 3 and 12 months after first-ever ischemic stroke. Fatigue was measured with the 7-item Fatigue Severity Scale. Physical fitness, body composition and physical activity were assessed using cardiopulmonary exercise testing, physical function tests, Dual-energy X-ray Absorptiometry, and accelerometers.

Results: Fatigue levels was stable between 3 and 12 months post-stroke in 44 (61%) patients, decreased in 14 (19%), and increased in another 14 (19%). Patients with increased fatigue levels showed a greater decrease in cardiorespiratory fitness, as measured directly by peak oxygen uptake, compared to those with decreased fatigue. Robust regression analysis, adjusted for age and sex, indicated that each kilogram of lean body mass gained from 3 to 12 months post-stroke was significantly associated with a 0.3-point reduction in fatigue during the same timeframe (B= -0.32; 95%CI [-0.51, -0.12]).

Conclusion: There was considerable individual variation in changes to fatigue, physical fitness, body composition, and physical activity levels between 3 and 12 months following a first-ever ischemic stroke. Increased fatigue was linked to a greater concurrent decline in cardiorespiratory fitness, while lean body mass was associated with decreases in fatigue.

Background: Mucosal-associated invariant T (MAIT) cells are innate-like T cells that rapidly produce cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-17 (IL-17) upon activation. The immune response is crucial in stroke-related injury. However, few studies have investigated the role of MAIT cells in ischemic brain injury. This study assessed the predictive value of circulating MAIT cells in acute ischemic stroke (AIS) and early neurological deterioration (END).

Methods: We prospectively and continuously enrolled AIS patients within 72 h of stroke onset and included controls. END was defined as a ≥2-point increase in the National Institutes of Health Stroke Scale score within the first 72 h. Receiver operating characteristic curves were used to evaluate the predictive value of MAIT cells for END.

Results: This study included 188 AIS patients and 135 controls, with 50 (26.6%) AIS patients experiencing END. After adjusting for all potential confounders, circulating MAIT cell frequencies were lower in AIS patients than in controls (odds ratio [OR]: 0.83, 95% confidence interval [CI]: 0.70-0.97, P = 0.02). IL-17 and TNF-α levels were significantly higher in AIS patients and negatively correlated with MAIT cell frequencies (R = -0.26, P < 0.05; R = -0.19, P < 0.05). Multivariate logistic regression analysis revealed that MAIT cell frequencies were lower in patients with END compared to those without END (OR: 0.74, 95% CI: 0.55-0.96, P = 0.03). The area under the curve for MAIT cells in END prediction was 0.641 (95% CI: 0.548-0.725, P < 0.05).

Conclusions: MAIT cell frequency was reduced in AIS patients and may serve as a predictive marker for END. Modulating these cells could be a novel AIS treatment strategy.

Background and purpose: The National Institutes of Health Stroke Scale (NIHSS) is the standard for assessing neurological deficits in acute ischemic stroke patients undergoing thrombectomy. However, data on NIHSS scores in patients undergoing thrombectomy at national-level studies in the United States are lacking.

Methods: Acute ischemic stroke patients admitted between 2018 and 2021 were identified using ICD-10-CM codes from the Nationwide In-patient Sample, with NIHSS scores categorized into specific strata (0-9, 10-19, 20-29, 30-42). We analyzed the effect of NIHSS scores on in-hospital mortality, routine discharge without palliative care (based on discharge disposition), poor outcome defined by NIS SAH outcome measure, and length and costs of hospitalization after adjusting for potential confounders.

Results: The NIHSS score strata among 108,990 acute ischemic stroke patients undergoing thrombectomy were: NIHSS score 0-9 (29.6%), 10-19 (40.6%), 20-29 (26.4%), and 30-42 (3.4%). Patients in the Midwest and West regions (adjusted odds ratio [adjusted OR] = 1.51, p=0.002 and adjusted OR = 1.63, p<0.001, respectively), those treated in rural hospitals (adjusted OR = 1.35, p=0.009) and those who were self-pay (adjusted OR = 1.51, p=0.048) had higher odds of being in higher NIHSS score strata. Patients in higher NIHSS score strata (NIHSS score 10-19, 20-29, and 30-42 had significantly lower odds of discharge home without palliative care (adjusted OR= 0.50, 0.32, and 0.22 respectively, all p<0.001) and higher odds of in-hospital mortality (adjusted OR = 1.51, 2.30, and 3.80 respectively, all p<0.001) compared to those in NIHSS score strata of 0-9. Patients in higher NIHSS score strata had significantly higher hospital stays and higher hospitalization costs.

Conclusions: We provide a comprehensive national-level analysis of NIHSS scores in acute ischemic stroke patients undergoing thrombectomy which may assist in understanding variations in outcomes and resource utilizations in United States.