Increased serum SGLT2 and its potential diagnostic and prognostic value in patients with acute ischemic stroke.

BACKGROUND: Recently acquired data suggests that sodium-glucose cotransporter-2 (SGLT2) may be a therapeutic target for cerebral ischemia. The specific impact of SGLT2 in acute ischemic stroke (AIS) remains unknown. We aimed to explore the levels of SGLT2 in AIS patients and its association with functional prognosis. METHODS: In this study, 132 AIS patients and 44 healthy controls were recruited prospectively to determine serum SGLT2 levels. Logistic regression analysis was employed to assess the association between serum SGLT2 level and stroke risk as well as 3-month outcome. Receiver operating characteristic (ROC) curves were utilized to evaluate predictive values for blood biomarkers. RESULTS: Serum SGLT2 levels were significantly higher (P =.000) in AIS patients (47.1 (interquartile range [IQR]: 42.4-50.9) ng/mL) than healthy controls (35.7 (IQR: 28.6-39.5) ng/mL). The optimal SGLT2 cutoff point for diagnosing AIS was 39.55 ng/mL, with a sensitivity of 90.2 % and specificity of 77.3 %. Serum levels of SGLT2 were negatively correlated with the onset time of AIS (linear fit R2 = 0.056, P =.006), but were not associated with National Institutes of Health Stroke Scale (NIHSS) scores (r = 0.007, P >.05) and lesion volume (r = -0.151, P >.05). SGLT2 was not remarkably different between patients with unfavorable and favorable outcomes (46.7 (IQR: 41.9-49.6) ng/mL vs 47.6 (IQR: 42.5-51.9) ng/mL; P =.321). CONCLUSIONS: The serum SGLT2 concentration may be a potential biomarker for the diagnosis of AIS. However, it does not exhibit any association with disease severity or functional prognosis.

Wernicke encephalopathy induced by glucose infusion: A case report and literature review.

Introduction: Wernicke encephalopathy (WE) is a potentially fatal condition caused by thiamine (vitamin B1) deficiency. Chronic alcoholism is the most common cause of WE; however, other conditions responsible for thiamine deficiency should also be considered. Case Report: We report the case of a 64-year-old woman with a history of diabetes who presented with confusion and apathy. Magnetic resonance imaging of the brain showed T2 hyperintensities involving dorsolateral medulla oblongata, tegmentum of the pons, vermis of the cerebellum, periaqueductal region, and the bilateral mammillary bodies. She had a history of intravenous glucose administration before her mental symptoms developed. On suspicion of WE, she was treated with a high dose of thiamine empirically. Her clinical condition improved rapidly in 2 weeks. Conclusion: Endogenous thiamine stores can be rapidly depleted in the case of enhanced glucose oxidation. Patients who receive glucose should also be prescribed thiamine to avoid inducing or exacerbating WE.

Revealing the link between gut microbiota and brain tumor risk: a new perspective from Mendelian randomization.

Background: Recent studies have shown that gut microbiota may be related to the occurrence of brain tumors, but direct evidence is lacking. This study used the Mendelian randomization study (MR) method to explore the potential causal link between gut microbiota and brain tumors. Method: We analyzed the genome-wide association data between 211 gut microbiota taxa and brain tumors, using the largest existing gut microbiota Genome-Wide Association Studies meta-analysis data (n=13266) and combining it with brain tumor data in the IEU OpenGWAS database. We use inverse-variance weighted analysis, supplemented by methods such as Mendelian randomization-Egger regression, weighted median estimator, simple mode, and weighted mode, to assess causality. In addition, we also conducted the Mendelian randomization-Egger intercept test, Cochran's Q test, and Mendelian randomization Steiger directionality test to ensure the accuracy of the analysis. Quality control includes sensitivity analysis, horizontal gene pleiotropy test, heterogeneity test, and MR Steiger directionality test. Result: Our study found that specific gut microbial taxa, such as order Lactobacillales and family Clostridiaceae1, were positively correlated with the occurrence of brain tumors, while genus Defluviitaleaceae UCG011 and genus Flavonifractor were negatively correlated with the occurrence of brain tumors. The Mendelian randomization-Egger intercept test showed that our analysis was not affected by pleiotropy (P>0.05). Conclusion: This study reveals for the first time the potential causal relationship between gut microbiota and brain tumors, providing a new perspective for the prevention and treatment of early brain tumors. These findings may help develop new clinical intervention strategies and point the way for future research.

Correlation Between Oncostatin M and Acute Ischemic Stroke: A Case-Control Study.

BACKGROUND: The expression of oncostatin M (OSM) has been studied in various diseases related to inflammatory response, but its implementation in acute ischemic stroke (AIS) remains to be explored.  Objective: The objective of this study is to assess the correlation between serum OSM expression and various aspects of AIS in a clinical setting. MATERIALS AND METHOD: A single-centered case-control study was performed in the First Affiliate Hospital of Chongqing Medical University from October 2020 to March 2021. A total of 134 patients were enrolled in the AIS group and 34 healthy individuals were enrolled in the control group. Physical examinations were performed and venous blood samples were collected. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum OSM. Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, National Institutes of Health Stroke Scale (NIHSS) score, magnetic resonance imaging (MRI) scan, and modified Rankin scale (mRS) were used to assess the classification, etiology, severity, and prognosis of the AIS group. Assessments were done to analyze serum OSM expression based on sensitivity, etiology, severity, prognosis, and several risk factors of AIS. Regression models, correlation, and sensitivity tests were performed to explore the correlation of OSM expression with various aspects of AIS. RESULTS: There was a statistically significant elevation of serum OSM expression in the AIS group (P<0.001). All AIS subgroups showed elevation in OSM level and statistically significant results were reflected in three subgroups. The area under the curve to differentiate AIS patients and control by serum OSM level was 0.747 (P<0.001), with the optimal cut-off value showing sensitivity at 58.82% and specificity at 75.37%. The elevation of serum OSM expression was proportional with severity, not proportional to the volume of infarct, and less elevated in the favorable outcome group. Serum OSM correlation with several risk factors of AIS was statistically significant in age, low-density lipoprotein, non-high-density lipoprotein, prothrombin time, and systolic blood pressure. CONCLUSION: Serum OSM was expressed differently in correlation with various aspects of AIS. Our findings supported the initial hypothesis that OSM is correlated with various aspects of AIS in humans.