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Stroke is the loss of brain function due to a disturbance in the blood supply to the brain resulting from either ischemia or hemorrhage. Previous studies have evaluated the clinical importance of nutritional interventions such as vitamin B supplementation in the management of acute strokes. However, it is still inconclusive whether or not vitamin B supplementation will benefit patients with acute strokes. Therefore, a meta-analysis was performed to assess the efficacy of vitamin B supplementation in the treatment of stroke patients. Medline, Embase, Scopus, and Cochrane Library databases were searched (from 1960 to June 2015) and forest plots were generated to illustrate the treatment effects. A systemic review of the electronic databases yielded 12 eligible studies consisting of 7474 patients. Forest plots from the meta-analyses of the included studies illustrated that vitamin B supplementation significantly lowered the plasma concentration of total homocysteine (SMD = -0.82; 95% CI: -0.77; Z = -29.06, p < 0.0001) and resulted in significant reduction in stroke recurrence (OR = 0.86%; 95% CI: 0.76, 0.97; Z = -2.41; p = 0.016) as well as a combined incidence of vascular events, including recurrent strokes, myocardial infarctions and vascular deaths (OR = 0.87%; 95% CI: 0.79, 0.96; Z= -2.73; p = 0.0063). Additionally, the nearly-symmetrical funnel plot (Egger’s test, t = −1.705, p = 0.1224) indicated the absence of publication bias regarding the meta-analysis that examined the effect of vitamin B supplementation on the plasma levels of homocysteine in acute stroke patients. These findings suggested that vitamin B supplementation presents a potential addition to the armamentarium for the management of acute stroke patients.

Gastric cancer (GC) remains to be a familiar malignant tumor with poor prognosis and daunting impacts on global health. We planned to grab the latent impacts of microRNA-183 in regulating cell autophagy, thus to clarify its possible regulatory principle in GC. The miR-183 level in GC tissues and cell lines was investigated. The impacts of miR-183 dysregulation on cell biological performances including viability, apoptosis and autophagy of GC cell lines including SGC-7901 were detected. Also, cells were disposed with 3-methyladenine (3-MA, an autophagy inhibition) before dysregulation of miR-183 to further investigate the correlation between cell autophagy and viability or apoptosis. Furthermore, the regulatory mechanisms between miR-183 and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), silent mating type information regulation 1 (SIRT1) or PI3K/AKT/mTOR pathway were explored. miR-183 was under-expressed both in GC tissues and in cell lines. miR-183 mimic alone depressed SGC-7901 cell viability and enhanced cell apoptosis and autophagy, whereas miR-183 inhibitor exhibited opposite effects. Moreover, the impacts of miR-183 on SGC-7901 cell viability and apoptosis were mediated by affecting the activation of autophagy. Our results indicate that miR-183 is under-expressed in GC cells and depression of miR-183 may enhance GC cell viability and inhibit cell apoptosis by affecting the activation of cell autophagy. MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR pathway may be mechanisms to mediate autophagy in GC. miR-183 may serve as a towardly therapeutic target for GC. [ABSTRACT FROM AUTHOR]

Byline: Jia. Fu, Guangxian. Nan Sir, Computed tomography (CT) and magnetic resonance imaging (MRI) are very helpful imaging modalities for the diagnosis of brain abscess. Here, we report the imaging [...]

The present case report described a patient with thrombotic thrombocytopenic purpura (TTP), who presented to the China-Japan Union Hospital of Jilin University (Changchun, China), and the changes in plasma von Willebrand factor (vWF) and vWF cleaving protease (vWF-cp) observed during treatment. Computed tomography and diffusion-weighted magnetic resonance (MR) imaging of the brain, cerebral MR angiography and other experimental tests were performed and the patient was subsequently diagnosed with TTP. The patient underwent treatment with plasma exchange, glucocorticoids and supportive care. Hematologic and biochemical parameters began to gradually improve over the 12 days after admission; platelet count, serum creatinine and serum lactate dehydrogenase concentrations returned to their normal ranges, plasma vWF concentration decreased to normal levels over the 30 days after admission, and vWF-cp activity increased compared with the levels detected in healthy volunteers. Monthly rituximab treatment was administered 4 times following patient discharge to prevent relapse, and no recurrence was detected at the 20-month follow-up. Plasma exchange therapy is effective in patients with TTP. After low-dose rituximab treatment, recurrent TTP has not been detected found till now. In the present case, vWF concentration and vWF-cp activity were measured at 8, 10, 23 and 32 days after admission; compared with the control group, patient's vWF concentration gradually decreased and vWF-cp activity slowly increased, suggesting that the patient had a favorable prognosis and a low risk of recurrence. [ABSTRACT FROM AUTHOR]

Staphylococcus aureus is a common pathogen that causes a wide range of infectious diseases. The function of TLRs, specifically TLR2, during S. aureus infection is still debated. In this study, we investigated the extent to which TLR2 contributes to the host innate response against the bacterial infection using TLR2-deficient mice. Intravenous inoculation with S. aureus resulted in all TLR2-deficient mice dying within 4 d, along with a high bacterial burden in the livers. However, histological examination showed the same degree of macrophage and neutrophil accumulation in the livers of infected TLR2-deficient mice as that in infected wild-type (WT) mice. TLR2-deficient mouse macrophages also showed normal phagocytic activity, although they failed to express CD36 that appeared on the surface of WT mouse cells upon challenge with heat-killed S. aureus. These data indicate that TLR2, as well as CD36, does not directly affect S. aureus clearance and that CD36 expression on macrophages depends on the presence of TLR2. In vivo infection with S. aureus caused significantly elevated production of TNF-α and IL-6 in the livers and blood of TLR2-deficient mice compared with those in WT mice, while the hepatic and serum levels of IL-10 decreased in these mice. In contrast, lower expression of IL-6 and IL-10, but not of TNF-α, at both the gene and protein levels was found in TLR2-deficient mouse macrophages compared to that in WT mouse cells, in response to challenge with heat-killed S. aureus. These findings suggest that the S. aureus-induced pro-inflammatory cytokine response is not dependent on macrophages and that TLR2 deficiency results in decreased IL-10 release by macrophages, which contributes to dysregulated cytokine balance, impaired bacterial clearance, and mouse death. Therefore, TLR2 possesses a protective function during S. aureus infection by regulating pro- and anti-inflammatory cytokine responses. [ABSTRACT FROM AUTHOR]

Purpose: Small dense low-density lipoprotein cholesterol (S-LDL-C) has been suggested as a particularly atherogenic factor for ischemic stroke (IS) in observational studies, but the causality regarding the etiological subtype remains unclear. This study aims to explore the causal effects of small dense low-density lipoprotein cholesterol (S-LDL-C), medium (M-LDL-C) and large (L-LDL-C) subfractions on the lifetime risk of ischemic stroke (IS) and main subtypes using two-sample Mendelian randomization (TSMR) design., Methods: We identified genetic instruments for S-LDL-C, M-LDL-C and L-LDL-C from a genome-wide association study of 115 082 UK Biobank participants. Summary-level data for genetic association of any ischemic stroke (AIS), large artery stroke (LAS), small vessel stroke (SVS) and cardioembolic stroke (CES) were obtained from MEGASTROKE consortium. Accounting for the pleiotropic effects of triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C), we conducted multivariable TSMR analysis., Results: In univariable TSMR, we found a causal association between genetically predicted S-LDL-C and LAS (IVW-FE: odds ratio (OR) = 1.481, 95% confidence interval (CI): 1.117-1.963, P = 0.006, q = 0.076) but not AIS, SVS or CES. No causal effects were observed for M-LDL-C or L-LDL-C in terms of AIS and IS subtype. In multivariable analysis, the causal association between S-LDL-C and LAS remained significant (IVE-MRE: OR = 1.329, 95% CI: 1.106-1.597, P = 0.002)., Conclusions: Findings supported a causal association between S-LDL-C and LAS. Further studies are warranted to elucidate the underlying mechanism and clinical benefit of targeting S-LDL-C., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer Y-XC declared a shared affiliation with the author PL to the handling editor at the time of the review., (Copyright © 2024 Yu, Shen, Zhang, Cui, Zha, Li, Li, Wang and Nan.)

Introduction: A recent clinical study revealed that Ninjin'yoeito (NYT) may potentially improve cognitive outcome. However, the mechanism by which NYT exerts its effect on elderly patients remains unclear. The aim of this study is to evaluate the effect of Ninjin'yoeito on regional brain glucose metabolism by 18 F-FDG autoradiography with insulin loading in aged wild-type mice. Materials and Methods: After 12 weeks of feeding NYT, mice were assigned to the control and insulin-loaded groups and received an intraperitoneal injection of human insulin (2 U/kg body weight) 30 min prior to 18 F-FDG injection. Ninety minutes after the injection, brain autoradiography was performed. Results: After insulin loading, the 18 F-FDG accumulation showed negative changes in the cortex, striatum, thalamus, and hippocampus in the control group, whereas positive changes were observed in the NYT-treated group. Conclusions: Ninjin'yoeito may potentially reduce insulin resistance in the brain regions in aged mice, thereby preventing age-related brain diseases., Competing Interests: RI and YO were employed by the company Tsumura & Co. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Zhao, Imai, Ukon, Shimoyama, Tan, Maejima, Omiya, Takahashi, Nan, Zhao, Ito and Shimomura.)

Bilateral medial medullary infarction is a rare stroke subtype, and its diagnosis has become possible by brain magnetic resonance imaging. In this report, we describe a case in which acute bilateral medial medullary infarction accompanied by cerebral watershed infarction was clearly identified by diffusion-weighted imaging, and we discuss the mechanisms of bilateral medial medullary infarction accompanied by cerebral watershed infarction., (Copyright Journal of Radiology Case Reports.)