Relationship between remnant cholesterol and short-term prognosis in acute ischemic stroke patients.

OBJECTIVE: Several studies have illustrated that elevated RC levels are related to a heightened risk of acute ischemic stroke (AIS). Our research aimed to explore the correlation between RC levels and poor prognosis after a 90-day interval in AIS patients. METHODS: A total of 287 individuals were enrolled in the study, the primary outcome was defined as poor prognosis. RC was derived by the exclusion of low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) from total cholesterol (TC). RESULTS: Following the screening process, 253 AIS patients were included in the study, presenting a median age of 66[57, 75] years. Upon stratifying RC levels into quartiles, those in the top quartile faced a greater likelihood of diabetes diagnosis (42.86%, p = .014) and experienced a higher rate of unfavorable outcomes after 90 days (36.51%, p = .001). After accounting for confounding factors, the correlation between the fourth quartile of RC levels and the amplified likelihood of poor prognosis remained significant (odds ratio (OR) 8.471, 95% confidence interval (CI) (1.841, 38.985); p = .006). Analysis of subgroups unveiled a notable correlation between higher RC levels and poor 90-day prognosis, particularly in individuals with elevated NIHSS scores (p = .044). A progressively increasing 90-day risk of poor prognosis after an RC greater than 0.38 mmol/L was visualized by restricted cubic spline plots (p-overall = .011). CONCLUSIONS: Including RC as a contributing element may refine the prediction of poor 90-day prognosis for AIS patients. Integrating RC with traditional risk factors can potentially enhance the predictive value for cerebrovascular disease.

Left ventricular systolic dysfunction predicts clinical prognosis in patients with acute ischemic stroke after intravenous thrombolysis.

BACKGROUND: Although intravenous recombinant tissue plasminogen activator (rt-PA) thrombolysis is the most effective early treatment for acute ischemic stroke (AIS), outcomes vary greatly among patients. Left ventricular systolic dysfunction (LVSD) is prone to distant organ ischemia and may be a predictor for poor prognosis in AIS patients undergoing intravenous thrombolysis (IVT). Our aim was to investigate the predictivity of LVSD diagnosis (as measured by left ventricular ejection fraction (LVEF)) on 90-day clinical outcomes in AIS patients undergoing thrombolysis. METHODS: The current prospective cohort study continuously enrolled 273 AIS patients from the National Stroke Prevention and Treatment Engineering Management Special Database who underwent IVT and completed echocardiography within 24 h of admission between 2021 and 2023. LVSD was examined by evaluation of the echocardiographic LVEF values using Simpson's biplane method of discs in line with international guidelines, and defined as a LVEF value < 50%. Multivariable ordinal logistic regression model was performed to analyze the association between LVEF and functional outcome at 3 months. Restricted cubic spline (RCS) was used to examine the shape of the dose-response association between reduced LVEF and poor functional outcomes. Subgroup analysis was also employed to further verify the reliability and practicability of the results. RESULTS: Baseline data analysis showed LVSD patients had more comorbidities including on multivariate analyses, LVSD (OR 2.78, 95% CI 1.23 to 6.24, P=0.014), pre-existing diabetes mellitus (OR 2.08, 95% CI 1.11 to 3.90, P=0.023) and NIHSS on arrival (OR 1.31, 95% CI 1.21 to 1.49, P<0.001) were independent predictors of poor functional outcomes (mRS ≥ 3) at 3 months. Multivariable-adjusted spline regression indicated a linear dose-response association between LVEF after IVT and poor functional outcomes (p for linearity < 0.001), with the optimal cutoff values of LVEF being 0.48. CONCLUSIONS: Our finding indicated that AIS patients with LVSD after IVT had poorer outcomes, suggesting the need to monitor and optimize LVEF in stroke management.

Diagnostic Value of Carotid Plaque Assessment with AIS Based on Quantitative Parameters of Dual-Layer Detector Spectral CT.

Purpose: To investigate the quantitative assessment of carotid plaque by each parameter of dual-layer detector spectral CT and its diagnostic value in patients with acute cerebral infarction. Patients and Methods: Eighty-three patients with carotid atherosclerotic plaques who underwent spectral CT scanning were retrospectively included. Forty-two patients with acute ischaemic stroke (AIS) were included in the study group, and 41 patients without AIS were included in the control group. We compared the detection of carotid plaques in the two groups and the differences in the spectral quantitative parameters of the plaques in the two groups, and their diagnostic efficacy was obtained. Results: The detection rate of carotid plaques in the AIS group was higher than that in the non-AIS group (p<0.05); the carotid plaques in the AIS group mainly consisted of non-calcified plaques, while those in the non-AIS group mainly consisted of calcified plaques. The effective atomic number (Zeff), slope of the energy spectrum curve (λH), electron density (ED), and iodine-no-water value of the carotid plaques in the AIS group were lower than those in the non-AIS (p<0.05). For the differentiation of the carotid plaques in the AIS group from those in the non-AIS group, the area under the curve (AUC) of Zeff amounted to 0.637 (cut-off value: 11.865; sensitivity: 72.5%; specificity: 56.2%), the AUC of λH amounted to 0.628 (cut-off value: 19.56; sensitivity: 76.3%; specificity: 51.6%), and that for ED amounted to 0.624 (cut-off value: 110.45; sensitivity: 60.0%; specificity: 64.1%), AUC of iodine-no-water value amounted to 0.645 (cut-off value: 9.125; sensitivity: 61.3%; specificity: 65.6%). Conclusion: In summary, the quantitative parameters of dual-layer detector spectral CT can be used to assess plaque stability and have certain value in the diagnosis of AIS. The quantitative parameters can effectively differentiate carotid plaques in AIS and non-AIS patients.

Bidirectional relationship between late-onset epilepsy (LOE) and dementia: A systematic review and meta-analysis of cohort studies.

OBJECTIVE: To explore the bidirectional relationship of late-onset epilepsy (LOE) with dementia and Alzheimer's disease (AD). METHODS: Using the common electronic databases, including PubMed, Cochrane Library databases and EMBASE, we systematically reviewed published cohort studies that assessed the risk of LOE in individuals comorbid with dementia or AD, and those with dementia or AD comorbid with LOE that had been published up to 31 March 2023. The data extraction process was carried out independently by two authors. The summary adjusted relative ratio (aRR) was calculated by employing Rev Man 5.3 for the inclusion of studies. To investigate the origins of heterogeneity, we conducted both subgroup and sensitivity analyses. In the presence of heterogeneity, a random-effects model was employed. To evaluate potential publication bias, we utilized the funnel plot and conducted Begg's and Egger's tests. RESULTS: We included 20 eligible studies in the final analysis after a rigorous screening process. Pooled results indicated that LOE was association with an increased risk of all-cause dementia (aRR: 1.34, 95% confidence interval [CI]: 1.13-1.59) and AD (aRR: 2.49, 95% CI: 1.16-5.32). In addition, the pooled effect size for LOE associated with baseline AD and all-cause dementia were 3.51 (95% CI: 3.47-3.56) and 2.53 (95% CI: 2.39-2.67), respectively. Both sensitivity and subgroup analyses showed that these positive correlations persisted. According to the results of the Egger's and Begg's tests, as well as visual inspection of funnel plots, none of the studies appeared to be biased by publication. CONCLUSION: The findings suggested that LOE is a potential risk factor for dementia and AD, and vice versa, dementia and AD are both potential risk indicators for LOE. Since there is substantial heterogeneity among the cohorts analyzed and more cohort studies should be conducted to confirm the correlations found in the current study.

Prognostic Significance of Uric Acid Levels in Intracerebral Hemorrhage Patients.

Background and Purpose: The role of serum uric acid (UA) level in patients suffering from stroke remains controversial. Our aim was to investigate the effect of UA level on clinical outcomes in patients with intracerebral hemorrhage (ICH). Methods: In the retrospective cohort study, we analyzed data from 250 patients with intracerebral hemorrhage (85 women and 165 men) to investigate the difference in UA levels between patients with a good prognosis and those with a poor prognosis. Additionally, we analyzed the impact of UA levels on the risk of short-time prognosis of ICH patients. Results: Patients with a good prognosis presented with significantly lower levels of UA (348.71 ± 84.97 µmol/L) than those with poor prognosis (393.06 ± 148.46 µmol/L). Furthermore, multivariate logistic regression model demonstrated that a high UA level was a likely risk factor for worse prognosis among patients suffering in ICH (odds ratio [95% confidence interval], 1.006 [1.0012, 1.0108]; P = 0.015). Additionally, UA has a threshold effect value of 363.9 µmol/L and was presented in levels that were in a nonlinear relationship with incidence rate of short-time prognosis outcome of ICH patients. Conclusion: Our findings indicate that higher UA levels can increase the risk of poor clinical prognosis in patients with ICH and high UA levels are not conductive to the clinical prognosis of patients with ICH. These findings provide a new perspective on the treatment and prevention of ICH.

Gout/hyperuricemia reduces the risk of Alzheimer's disease: A meta-analysis based on latest evidence.

OBJECTIVE: Previous studies have found the potential role of gout or hyperuricemia in subsequent development of Alzheimer's disease (AD) but reported inconsistent results. We conducted the current meta-analysis to evaluate whether an association exists between gout/ hyperuricemia and AD. METHODS: We systematically searched PubMed and EMBASE for the published cohort studies that measured the risk of AD in subject with gout/ hyperuricemia up to May 20, 2023. Data extraction was employed by two authors independently. Rev Man 5.3 and Stata 15.0 software were used to calculate the relative ratio (RR) or hazard ratio (HR) for including studies. Subgroup analysis was performed to assess the sources of heterogeneity. A random-effects model was adopted when heterogeneity was present. The funnel plot, Begg's test, and and Egger's test were used to assess publication bias. RESULTS: After rigorous screening, seven eligible studies were included in the final analyses. Pooled results indicated that gout or hyperuricemia decreases the risk of AD (RR: 0.69, 95% CI: 0.64∼0.72), with a high heterogeneity of 93%. Subgroup analyses showed that regional distribution was the source of heterogeneity. Egger's and Begg's tests as well as visual inspection of funnel plot suggested no publication bias in the studies. CONCLUSION: The findings suggested that gout or hyperuricemia might have a protective effect against AD. This negative correlation should be verified by more cohort studies due to the existence of substantial heterogeneity.

The Relationship Between Sarcopenia, Cognitive Impairment, and Cerebral White Matter Hyperintensity in the Elderly.

Purpose: To explore the relationship between sarcopenia-related indices, cognitive impairment and cerebral white matter hyperintensities. Patients and methods: Ninety-five hospitalized older adults aged 60 years and older were used in this study. Three sarcopenia-related indicators were measured: hand grip strength (Measured with a spring-type dynamometer), gait speed (6m step speed method), and appendicular skeletal muscle mass (ASM, bioelectrical impedance). Sarcopenia was defined according to the Asian Working Group for Sarcopenia (AWGS) criteria. Cognitive function was assessed using Montreal Cognitive Assessment (MoCA). Cerebral white matter hyperintensity was assessed using 3.0T superconducting magnetic resonance imaging. Results: In both men and women, these three indices of sarcopenia were significantly and negatively correlated with WMH grades, except for appendicular skeletal muscle mass and WMH grades in women. Scores on the MoCA scale were significantly positive correlated with grip strength, and ASM, both in men and women. After adjusting for confounders and WMHs, regression analyses showed an increased incidence of cognitive impairment in patients with sarcopenia relative to those without sarcopenia. Conclusion: Lower sarcopenia-related indices were significantly associated with cognitive impairment. WMHs may be one of the factors linking sarcopenia and cognitive function.

Serum ß2-microglobulin is closely associated with 3-month outcome of acute intracerebral hemorrhage: a retrospective cohort study.

BACKGROUND: Intracerebral hemorrhage (ICH) is a frequent type of hemorrhagic stroke. Numerous studies have suggested that inflammation plays an important role in the injury and recovery of ICH. ß2-microglobulin (ß2M) is an inflammatory indicator with an unclear association with ICH development. This study aimed to explore the role of ß2M in the outcome of patients with ICH after 3 months of ICH onset. METHODS: The ß2M and other baseline information of 231 patients with ICH were assessed (83 females and 148 males). We followed up with all patients 3 months after ICH onset, and severe disability or a worse outcome was our main focus. We collected the serum ß2M levels, National Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) scores, and other relevant baseline information of each patient. We used multiple regression analysis to explore the association between ß2M levels and follow-up outcomes. RESULTS: Our results indicated that the ß2M level of the good outcome (2.35 ± 0.84 mg/l) group was significantly lower than that of the poor outcome group (3.06 ± 1.71 mg/l) (P < 0.001). Further multiple regression analysis showed that ß2M was regarded as a risk factor that was closely associated with the poor outcome 3 months after ICH onset (odds ratio = 2.26, 95% confidence interval = 1.22-4.19, P = 0.009). Further correlation analysis revealed that ß2M was significantly correlated with NIHSS scores (r = 0.187, P = 0.004) and follow-up mRS scores (r = 0.25, P < 0.001). CONCLUSION: ß2M was a risk factor for early outcome after ICH onset, and high ß2M level was associated with short-time poor prognosis of ICH patients.

ß2-Microglobulin is a Novel and Reliable Biomarker for Predicting Ischemic Stroke Recurrence: A Prospective Cohort Study.

Immune and inflammatory mechanisms play key roles in the development and outcome of acute ischemic stroke (AIS). ß2-Microglobulin (ß2M) is the light chain of major histocompatibility complex-1 (MHC-1), which can directly and quickly reflect the immune and inflammatory state of the body. Previous studies have shown a close relationship between ß2M and AIS, but its relationship with the recurrence of AIS has not been reported. This study attempted to explore the relationship between ß2M and the recurrence of AIS. A single-center AIS cohort involving 135 patients was followed for approximately 26-46 months. Clinical and laboratory data from the patients were collected when hospitalized. The endpoint was the occurrence of recurrent AIS after patients were discharged. Propensity score matching was used to match cohort groups. Cox regression analysis was used to predict risk factors for recurrent AIS, and receiver operating characteristic curve (ROC) analysis was used to calculate the optimal cutoff value for discriminating recurrence in patients with AIS. The rate of recurrence was 29.6% [95% CI, 21.8%-37.3%] in the follow-up group. Patients with higher levels of serum ß2M had a higher risk of AIS recurrence than patients with lower levels of ß2M (adjusted hazard ratio, 3.214 [95% CI, 1.557-6.633]; adjusted hazard ratio after matching, 5.831, [95% CI, 2.052-16.572]). A ß2M value of 2.31 mg/L was calculated by ROC analysis as the optimal cutoff value for AIS recurrence (area under the curve 0.770, [95% CI, 0.687-0.853]). As a quick responder to the body's immune and inflammatory states, ß2M may be a novel and reliable biomarker in predicting AIS recurrence.

Overexpression of BDNF in the ventrolateral periaqueductal gray regulates the behavior of epilepsy-migraine comorbid rats.

OBJECTIVE: To investigate the effects of brain-derived neurotrophic factor (BDNF) overexpression in the ventrolateral periaqueductal gray (vlPAG) on behavioral changes in epilepsy-migraine comorbid rats. METHOD: We used an adeno-associated virus (AAV)-mediated vector to supplement BDNF in the vlPAG area prior to the establishment of a pilocarpine-nitroglycerin (Pilo-NTG) combination-induced comorbid model of epilepsy and migraine. Seizure- and migraine-related behaviors were analyzed. Cell loss and apoptosis in vlPAG were detected through hematoxylin-eosin (HE) and TUNEL staining. Immunofluorescence staining analyses were employed to detect expressions of BDNF and its receptor, tyrosine kinase B (TrkB), in vlPAG. Immunohistochemical staining was conducted to detect expressions of c-Fos and calcitonin gene-related peptide (CGRP) in the trigeminal nucleus caudalis (TNC) and trigeminal ganglion (TG). RESULTS: Comparing to control group, AAV-BDNF injected comorbid group showed lower pain sensitivity, scratching head, and spontaneous seizures accompanied by the downregulation of c-Fos labeling neurons and CGRP immunoreactivity in the TNC and TG. However, these changes were still significantly higher in the comorbid group than those in both epilepsy and migraine groups under the same intervention. CONCLUSION: These data demonstrated that supplying BDNF to vlPAG may protect structural and functional abnormalities in vlPAG and provide an antiepileptic and analgesic therapy.

Meta-analysis of association between migraine and risk of dementia.

OBJECTIVES: The association between migraine and dementia has rarely been investigated, and available results are conflicting. Thus, the aim of this meta-analysis was to evaluate whether an association exists between migraine and dementia. MATERIALS & METHODS: We searched for cohort studies from databases including PubMed, EBSCO, Web of Science, and EMBASE database from inception to April 1, 2021, using subject and free words. RevMan 5.1 software was used to calculate the risk ratio (RR) of dementia in patients with migraine. Subgroup and sensitivity analyses were conducted to assess the source of heterogeneity. A random-effects model was used when heterogeneity was present. The Funnel plot and Egger's test were used to evaluate publication bias. RESULTS: Five published cohort studies covering a total of 249,303 individuals were identified. Pooled analysis showed that migraine was associated with increased risk of all-cause dementia (RR: 1.34, 95% CI: 1.13-1.59) and Alzheimer's disease (AD) (RR: 2.49, 95% CI: 1.16-5.32). However, we did not found any association between migraine and risk of vascular dementia (VaD) (RR: 1.51, 95% CI: 0.77-2.96). CONCLUSIONS: Our results revealed that migraine was a potential risk indicator for AD and all-cause dementia.

Effect of Vitamin D Supplementation on the Prognosis of Post-stroke Fatigue: A Retrospective Cohort Study.

Objective: We aimed to evaluate the effect of vitamin D supplementation in post-stroke fatigue (PSF) patients with vitamin D deficiency on fatigue symptoms and outcomes. Methods: Patients with primary acute ischemic stroke (AIS) were recruited consecutively from July 2016 to June 2018. Post-stroke fatigue patients were screened out with the Fatigue Severity Scale (FSS) questionnaire, serum concentrations of 25-hydroxyvitamin D [25-(OH)-D] were assessed with enzyme-linked immunosorbent assay (ELISA), and neurological function was evaluated with FSS and modified Rankin Scale (mRS) scoring criteria. Post-stroke fatigue patients with vitamin D deficiency were divided into two groups: a study group in which patients received vitamin D supplementation (cholecalciferol, 600 IU/day) along with usual care, and a control group in which patients received usual care alone. At the end of 1 and 3 months after treatment, all PSE patients accepted re-measurement of serum vitamin D and re-evaluation of fatigue and neurological function. Results: A total of 532 AIS patients were consecutively recruited to participate in this study. Patients without PSF, non-vitamin D deficiency, pre-stroke fatigue, or vitamin D supplementation were excluded from the study. In addition, patients who were lost to follow-up were also excluded. Finally, 139 out of 532 (26.1%) patients with PSF and vitamin D deficiency received vitamin D supplementation treatment. Fatigue Severity Scale score was significantly lower in the study group than in the control group at 1 month (t = -4.731, p < 0.01) and 3 months (t = -7.937, p < 0.01) after treatment. One month after treatment, mRS score in the study group was lower than that in the control group without statistical difference (t = -0.660, p > 0.05), whereas mRS was significantly higher in the study group than in the control group at 3 months after treatment (t = -4.715, p < 0.01). Conclusions: Our results indicated that vitamin D supplementation could improve fatigue symptoms and neurological outcomes in PSF patients with vitamin D deficiency. Subject to replication in other settings, a randomized controlled trial (RCT) might be undertaken to validate the potential beneficial impact of vitamin D supplementation in post-stroke patients found to be vitamin D deficient.

Using metagenomic analysis to assess the effectiveness of oral health promotion interventions in reducing risk for pneumonia among patients with stroke in acute phase: study protocol for a randomized controlled trial.

BACKGROUND: The prevalence of pneumonia complicating stroke in acute phase has a poor prognosis and higher risk for death. Oral opportunistic pathogens have been reported to be associated with pneumonia among people with compromised health. Oral health promotion is effective in reducing dental plaque among patients with stroke, which is considered as reservoirs for oral opportunistic pathogens. This study evaluates the effectiveness of oral health promotions in reducing the prevalence of pneumonia via its effects on composition and relative abundance of oral opportunistic pathogens. METHODS/DESIGN: This study is a randomized, single-blind, parallel trial of 6 months duration. The study is being conducted at one of the largest medical teaching hospitals in Hefei, China. A total of 166 patients with stroke and free from any post-stroke complication will be recruited. After enrollment, patients will be randomized to one of the following groups: (1) oral hygiene instruction (OHI) or (2) OHI, 6-month use of powered tooth brushing, and 0.2% chlorhexidine gluconate mouth rinse (10 ml twice daily). The primary outcome is the prevalence of pneumonia complicating stroke. Patients will be monitored closely for any occurrence of pneumonia over the entire period of this trial. Oral rinse samples will be collected at baseline and multiple follow-up reviews (3, 5, 7 days, and 1, 3, 6 months after baseline). Next-generation sequencing will be employed to detect composition and relative abundances of the microorganism in the oral rinse samples. Questionnaire interviews and clinical oral examinations will be conducted at baseline and 1, 3, and 6 months after baseline. DISCUSSION: The findings of this trial will provide evidence whether oral health promotion intervention is effective in reducing the prevalence of pneumonia complicating stroke via its effect on the oral microbiome. The analysis of the outcomes of this trial is empowered by metagenomic analysis at 16S rRNA level, which is more sensitive and comprehensive to help us detect how oral health promotion inventions affect the oral microbiome in terms of its composition, relative abundance, and interactions between species, which all may contribute to the occurrence of pneumonia complicating stroke. TRIAL REGISTRATION: ClinicalTrials.gov NCT04095780 . Registered on 19 September 2019.

Genetically Confirmed CARASIL: Case Report with Novel HTRA1 Mutation and Literature Review.

BACKGROUND: Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is an extremely rare monogenic autosomal disease associated with the HtrA serine protease 1 (HTRA 1) gene mutation. Recently, a few genetically confirmed CARASIL cases with novel HTRA1 mutations have been reported in countries other than Japan. CASE DESCRIPTION: Here, we report a case of a patient presenting with worsening right hemiplegia and hemiparesthesia. Physical examination revealed that the patient had typical clinical features of CARASIL including thinning hair, cognitive impairment, emotional changes, lumbago, and gait disorder. Brain magnetic resonance imaging showed abnormal diffuse symmetric changes in white matter and hypertensive diffusion-weighted imaging signals in the left centrum ovale and right splenium of the corpus callosum, and susceptibility-weighted imaging showed multiple cerebral microbleeds. Lumbar magnetic resonance imaging showed herniated disks with degenerative changes. A genetic test showed a novel homozygous nucleotide variation of c.847G>T in the HTRA1 gene, thereby resulting in p.Gly283Ter. Thus the patient met the diagnostic criteria for CARASIL. We provide a literature review of genetically confirmed CARASIL cases reported to date. CONCLUSIONS: CARASIL is a rare autosomal recessive disease with an HTRA1 mutation. Familiarity with the early clinical and imaging features of CARASIL combined with a genetic test is key for its early diagnosis.

Gene polymorphisms and circulating levels of the TNF-alpha are associated with ischemic stroke: A meta-analysis based on 19,873 individuals.

OBJECTIVE: Numerous studies have investigated associations of gene polymorphisms and circulating levels of TNF-α with ischemic stroke (IS), but the results were controversial. The aims of this study were to systematically evaluate these associations. METHODS: Relevant publications were retrieved by searching databases. Odds ratios (ORs) and standard mean differences (SMDs) with 95% confidence intervals (95% CIs) were used to assess the association of the TNF-α gene and cytokine with IS, respectively. The Cochrane Q test and I2 statistic were used to test heterogeneity. Subgroup analysis and publication bias were performed. RESULTS: 25 and 9 articles examined the association of polymorphisms and levels of the TNF-α with IS risk, respectively. Rs1800629 polymorphism was associated with IS susceptibility (OR (95% CI) =0.82 (0.72, 0.95)), especially in Asians (OR (95% CI) =0.75 (0.63, 0.89)); and rs1800610 was associated with IS susceptibility in Asians patients (OR (95% CI) =1.54 (1.31, 1.80)). While rs361525, rs1799964 and rs1799724 polymorphisms were not associated with IS susceptibility. The TNF-α level was elevated in IS patients (SMD (95% CI) =0.65 (0.29, 1.01)) including Asians (SMD (95% CI) =1.26 (0.49, 2.03)) and Caucasians (SMD (95% CI) =0.26 (0.03, 0.49)). In addition, increased level occurred in patients' serum (SMD (95% CI) =0.54 (0.08, 1.01)). CONCLUSIONS: Rs1800629 and rs1800610 polymorphisms were elucidated to be a protective factor for IS (especially in Asians) and a risk factor for Asians patients, respectively. The TNF-α level was elevated in IS, indicating that TNF-α plays an important role in the pathogenesis of IS and is a promising therapeutic target for IS.

Serum beta2-microglobulin levels are highly associated with the risk of acute ischemic stroke.

Inflammation is considered an important mechanism of cell death or survival after ischemic stroke. As an important marker of inflammation, the role of ß2-microglobulin (ß2M) in acute ischemic stroke is unclear. We investigated the relationship between serum ß2M and the risk of acute ischemic stroke (AIS). Patients with AIS (202 cases), intracerebral hemorrhage (ICH, 41 cases), and healthy controls (253 cases) were recruited. Clinical and biochemical characteristics were collected. We used three binary logistic regression models to evaluate the correlation of ß2M with the risk of AIS. Furthermore, we investigated the relationship between serum ß2M and the National Institute of Health Stroke Scale (NIHSS) score, the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) subtypes, and the Essen Stroke Risk Score (ESRS) in patients with AIS. Our results showed that serum ß2M levels in patients with AIS were much higher than those in patients with ICH and in the control subjects. Individuals with higher levels of ß2M had higher odds of AIS. Moreover, serum ß2M levels were significantly and positively correlated with ESRS. In addition, the levels of ß2M were varied with different subgroups of AIS (TOAST classification). Serum ß2M is highly associated with the risk of AIS.

Serum ß2-Microglobulin Is Closely Associated With the Recurrence Risk and 3-Month Outcome of Acute Ischemic Stroke.

Background and Purpose: Inflammation plays a significant role in the pathogenesis of acute ischemic stroke (AIS). The role of ß2-microglobulin (ß2M) as a potential initiator of the inflammatory response in AIS is unclear. The purpose of this study was to analyze the relationship of serum ß2M with the recurrence risk and 3-month outcome of AIS. Methods: A total of 205 patients with AIS were recruited, and their clinical and biochemical characteristics were collected. All patients were followed up for 3 months after stroke onset, and the occurrence of death or major disability at 3 months after onset was the outcome of interest in this study. We evaluated the association of serum ß2M levels with the National Institute of Health Stroke Scale (NIHSS) scores, modified Rankin Scale (mRS) scores, and Essen Stroke Risk Score (ESRS) values in patients with AIS. Then, we used receiver operating curve analysis to calculate the optimal cutoff value for discriminating outcomes in patients with AIS and a binary logistic regression model to evaluate the risk factors for a poor outcome after AIS. Results: Our results showed that serum ß2M levels were significantly and positively correlated with ESRS values (r = 0.176, P < 0.001) and mRS scores (r = 0.402, P < 0.001), but the levels of ß2M were not correlated with NIHSS scores (r = 0.080, P = 0.255) or with infarct volume (r = 0.013, P = 0.859). In a further study, we found that 121 patients (59.02%) had poor outcomes. The optimal ß2M cutoff to predict the 3-month outcome of AIS in this study was 1.865 mg/l, and ß2M was independently associated with a poor outcome at 3 months (OR = 3.325, 95% confidence interval: 1.089~10.148). Conclusions: In conclusion, we inferred that serum ß2M was positively associated with the recurrence risk and 3-month outcome of AIS, but it did not appear to be directly related to the severity of AIS or the size of the infarct at admission.

Long-term outcomes of a patient with late-onset multiple acyl-CoA dehydrogenase deficiency caused by novel mutations in ETFDH: A case report.

RATIONALE: Late-onset multiple acyl-coenzyme A dehydrogenase deficiency (MADD) mainly affects the neck extensor muscle group, which has been confirmed by novel mutations in electron-transferring-flavoprotein dehydrogenase (ETFDH). So far, a few cases have been reported with long-term follow-up. Here we report a case of late-onset MADD where the patient was followed up for 8 years during which time he underwent 2 muscle biopsies and 2 pathological examinations and his symptoms were significantly alleviated after appropriate treatments. PATIENT CONCERNS: In September 2009, a 16-year-old male patient was hospitalized due to gradually increasing difficulty in raising his head and weakness in limb muscles over a 6-month period. During the physical examination, the patient's neck extensor muscle strength was grade III-IV. His proximal limb muscle strength was grade IV, and his distal muscle strength was normal. His blood creatine kinase (CK) was 783 U/L. DIAGNOSIS: Muscle biopsy revealed a large number of vacuolar fibers, which were mainly type I fibers. These findings were consistent with the diagnosis of lipid storage myopathy (LSM). ETFDH gene test detected C.736G > A at exon 7 and C.920C > G at exon 8. INTERVENTIONS: Coenzyme Q10 treatment was administered. The first coenzyme Q10 40 mg tid was treated for three months, with the change of coenzyme Q10 20 mg tid for 6 months, followed by the change of coenzyme Q10 10 mg tid for long-term use. OUTCOMES: The patient's condition significantly improved after 3 months. At 7th year follow-up the patient's blood CK was normal, and a second muscle biopsy revealed no muscle vacuolar fibers and no increase in lipid droplets. Subsequently, the patient was withdrawn from the coenzyme Q10 treatment, and the condition of the patient remained normal. LESSONS: Muscle biopsy was the main method used to determine LSM. Treatment with riboflavin should be started when the diagnosis of LSM is definitive. Furthermore, ETFDH gene tests should be performed for further classification. Moreover, coenzyme Q10 may be another effective drug for MADD.

Neutrophil-To-Lymphocyte Ratio Predicts 3-Month Outcome of Acute Ischemic Stroke.

Increasing evidences have demonstrated that inflammation is involved in the mechanisms of acute ischemic stroke (AIS). As an important and easy-to-measure inflammatory marker, neutrophil-to-lymphocyte ratio (NLR) shows a high association with mortality in patients with stroke in recent studies. In this study, we evaluated the prognostic role of NLR in patients with AIS. One hundred forty-three patients with AIS were enrolled. Clinical data were collected and the NLR was calculated from the admission blood work. The patients were followed up for 3 months after stroke onset. The occurrence of death and the major disability at 3 months after onset were end points in this study. Modified Rankin Scale score ≥3 was considered as poor outcome. In this study, 75 patients (52%) had poor outcome. We used binary logistic regression model to evaluate risk factor for poor outcome of AIS and found that the NLR was independently associated with the poor outcome of 3 months (P < 0.001). The optimal cutoff value for NLR as a predictor for 3-month outcome was 2.995. Therefore, in our study, high NLRs inversely predicted 3-month outcome in patients with AIS.