Hemichorea in patients with temporal lobe infarcts: Two case reports.

BACKGROUND: Hemichorea and other hyperkinetic movement disorders are uncommon presentations of stroke and are usually secondary to deep infarctions affecting the basal ganglia and thalamus. Therefore, temporal ischemic lesions causing hemichorea are rare. We report the cases of two patients with acute ischemic temporal lobe infarct strokes that presented as hemichorea. CASE SUMMARY: Patient 1: An 82-year-old woman presented with a 1-mo history of involuntary movement of the left extremity, which was consistent with hemichorea. Her diffusion-weighted imaging (DWI) revealed an acute ischemic stroke that predominantly affected the right temporal cortex, and magnetic resonance angiography of the head showed significant stenosis of the right middle cerebral artery (MCA). Treatment with 2.5 mg of olanzapine per day was initiated. When she was discharged from the hospital, her symptoms appeared to have improved compared with those previously observed. Twenty-seven days after the first admission, she was readmitted due to acute ischemic stroke. Computed tomography perfusion showed marked hypoperfusion in the right MCA territory. An emergency transfemoral cerebral angiogram was performed and showed severe stenosis in the M1 segment of the right MCA. After percutaneous transluminal angioplasty was successfully performed, abnormal movements or other neurologic problems did not occur. Patient 2: A 76-year-old man was admitted to our hospital for a 7-d history of right-upper-sided involuntary movements. DWI showed an acute patchy ischemic stroke in the left temporal lobe without basal ganglia involvement. Subsequent diffusion tensor imaging confirmed fewer white matter fiber tracts on the left side than on the opposite side. Treatment with 2.5 mg of olanzapine per day improved his condition, and he was discharged. CONCLUSION: When acute hemichorea suddenly appears, temporal cortical ischemic stroke should be considered a possible diagnosis. In addition, hemichorea may be a sign of impending cerebral infarction with MCA stenosis.

The intervention mechanism of emodin on TLR3 pathway in the process of central nervous system injury caused by herpes virus infection.

Background and purpose: To investigate the effect of Emodin on the inflammatory response of brain tissue and the expression of the TLR3 pathway in mice with herpes virus encephalitis.Method: Twenty male BALB/c mice were randomly divided into the NS group, HSV-1 group, HSV-1 + Emodin group and HSV-1 + ACV group. The histopathological features and the effect of TLR3 expression were observed by staining and immunohistochemistry (IHC) respectively. The gene expression of TLR3, trif, TRADD, TRAF6, traf3, p38, Nemo and IRF3 was detected by polymerase chain reaction (PCR). The protein production of TLR3 and its downstream molecules was detected by Western blot. The expression of IL-6, TNF-α and IFN-ß in the brain tissues was detected by ELISA.Result: Compared to the HSV-1 group, the pathological changes (inflammatory cell infiltration, necrotic temporal lobe and massive hemorrhage) were not as obvious as those in the HSV-1+emodin and HSV-1+ACV groups. The TLR3 staining increased significantly in the HSV-1 groups and decreased in the HSV-1 + emodin group. Compared with the NS group, the mRNA expression of TLR3, TRIF, TRADD, TRAF6, traf3, p38, NEMO and IRF3 decreased by 20%-60% in the HSV-1 + emodin group and 30% in the HSV-1 + ACV group, respectively. The expression of IL-6, TNF-α and IFN-ß decreased by 30%-50% in the HSV-1 + emodin group and showed no significant change in the HSV-1 + ACV group, respectively.Conclusion: Emodin could inhibit the inflammatory response in the brain of mice with herpes virus encephalitis. The inhibition of TLR3 expression may play an important role in this process.

Inhibition of TIM-4 protects against cerebral ischaemia-reperfusion injury.

TIM-4 plays an important role in ischaemia-reperfusion injury of liver and kidney; however, the effects of TIM-4 on cerebral ischaemia-reperfusion injury (IRI) are unknown. The purpose of the present study was to investigate the potential role of TIM-4 in experimental brain ischaemia-reperfusion injury. In this study, cerebral ischaemia reperfusion was induced by transient middle cerebral artery occlusion (MCAO) for 1 hour in C57/BL6 mice. The TIM-4 expression was detected in vivo or vitro by real-time quantitative polymerase chain reaction, Western blot and flow cytometric analysis. In vivo, the administration of anti-TIM-4 antibodies significantly suppressed apoptosis, inhibited inflammatory cells and enhanced anti-inflammatory responses. In vitro, activated microglia exhibited reduced cellular proliferation and induced IRI injury when co-cultured with neurons; these effects were inhibited by anti-TIM-4 antibody treatment. Similarly, microglia transfected with TIM-4 siRNA and stimulated by LPS + IFN-γ alleviated the TIM-4-mediated damage to neurons. Collectively, our data indicate that the inhibition of TIM-4 can improve the inflammatory response and exerts a protective effect in cerebral ischaemia-reperfusion injury.

Development and validation of a novel and robust blood small nuclear RNA signature in diagnosing autism spectrum disorder.

Reliable molecular signatures are needed to improve the early and accurate diagnosis of autism spectrum disorder (ASD), and indicate physicians to provide timely intervention. This study aimed to identify a robust blood small nuclear RNA (snRNA) signature in diagnosing ASD. 186 blood samples in the microarray dataset were randomly divided into the training set (n = 112) and validation set (n = 72). Then, the microarray probe expression profiles were re-annotated into the expression profiles of 1253 snRNAs though probe sequence mapping. In the training set, least absolute shrinkage and selection operator (LASSO) penalized generalized linear model was adopted to identify the 9-snRNA signature (RNU1-16P, RNU6-1031P, RNU6-258P, RNU6-335P, RNU6-485P, RNU6-549P, RNU6-98P, RNU6ATAC26P, and RNVU1-15), and a diagnostic score was calculated for each sample according to the snRNA expression levels and the model coefficients. The score demonstrated a good diagnostic ability for ASD in the training set (area under receiver operating characteristic curve (AUC) = 0.90), validation set (AUC = 0.87), and the overall (AUC = 0.88). Moreover, the blood samples of 23 ASD patients and 23 age- and gender-matched controls were collected as the external validation set, in which the signature also showed a good diagnostic ability for ASD (AUC = 0.88). In subgroup analysis, the signature was robust when considering the confounders of gender, age, and disease subtypes, and displayed a significantly better performance among the female and younger cases (P = .039; P = .002). In comparison with a 55-gene signature deriving from the same dataset, the snRNA signature showed a better diagnostic ability (AUC: 0.88 vs 0.80, P = .049). In conclusion, this study identified a novel and robust blood snRNA signature in diagnosing ASD, which might help improve the diagnostic accuracy for ASD in clinical practice. Nevertheless, a large-scale prospective study was needed to validate our results.

Overexpression of MicroRNA-145 Ameliorates Astrocyte Injury by Targeting Aquaporin 4 in Cerebral Ischemic Stroke.

Cerebral ischemic stroke, which affects the global population, is a major disease with high incidence, mortality, and disability. Accumulating evidence has indicated that abnormal microRNA (miRNA) expression plays essential roles in the pathologies of ischemic stroke. Yet, the underlying regulatory mechanism of miRNAs in cerebral ischemic stroke remains unclear. We investigated the role of miR-145 in cerebral ischemic stroke and its potential mechanism in a model using primary cultured astrocytes. We detected the expression levels of miR-145 and its target gene AQP4 and assessed the role of miR-145 in cell death and apoptosis caused by oxygen-glucose deprivation (OGD). Bioinformatics analysis was used to explore the targets of miR-145. miR-145 expression levels were significantly decreased in primary astrocytes subjected to OGD. miR-145 overexpression promoted astrocyte health and inhibited OGD-induced apoptosis. AQP4 was a direct target of miR-145, and miR-145 suppressed AQP4 expression. Moreover, AQP4 enhanced astrocyte injury in ischemic stroke, and AQP4 knockdown diminished the miR-145-mediated protective effect on ischemic injury. Taken together, our results show that miR-145 plays an important role in protecting astrocytes from ischemic injury by downregulating AQP4 expression. These findings may highlight a novel therapeutic target in cerebral ischemic stroke.