The diagnosis of PD might be in difficulty, especially in the early stages. Therefore, the identification of novel biomarkers is imperative for the diagnosis and monitoring disease progression in PD. DJ-1 and α-synuclein, are two proteins that are critically involved in the pathogenesis of PD, and they have been examined as disease biomarkers in studies. However, no study exists regarding DJ-1 in plasma neural-derived exosomes. In the present study, the levels of DJ-1 and α-synuclein in plasma neural-derived exosomes were studied together in order to investigate novel biomarkers for PD. DJ-1 and α-synuclein in plasma and plasma neural-derived exosomes of the patients with PD and controls were quantified by ELISAs. The data revealed that the levels of DJ-1 and α-synuclein in plasma neural-derived exosomes and the ratio of plasma neural-derived exosomal DJ-1 to total DJ-1 were significantly higher in patients with PD, compared with controls, while levels of the two proteins in plasma exhibited no difference between the patients with PD and controls. However, no relationship was identified between biomarkers and disease progression. In addition, significant positive correlations between DJ-1 and α-synuclein in plasma neural-derived exosomes were found in the patients with PD and in healthy individuals. We hypothesize that DJ-1 in plasma neural-derived exosomes may be used as a potential biomarker as α-synuclein in PD and they might participate in the mechanism of PD together.

It is commonly considered that the morphology and interface of semiconductor-reduced graphene oxide (rGO) composite photocatalysts play a crucial role in determining their photocatalyzing performance. Herein, we report on the design and synthesis of BiVO4-rGO nanocomposites with efficient interfacial contact by self-assembly of positively charged amorphous BiVO4 powders with negatively charged graphene oxide (GO), followed by a one-step GO reduction and BiVO4 crystallization via hydrothermal treatment. The as-prepared BiVO4-rGO nanocomposites exhibit high visible light photocatalytic efficiency for the degradation of model dyes, and are significantly superior to bare crystalline BiVO4 and BiVO4-rGO-U that is hydrothermally synthesized using the mixture of GO nanosheets and BiVO4 powders without modification of surface charge. Using multiple characterization techniques, we found that the enhanced photocatalytic performance of BiVO4-rGO arises from the synergistic effects between the microscopic crystal structure of BiVO4 with smaller particle size and more sufficient interfacial interaction between BiVO4 and graphene sheets, leading to increased photocatalytic reaction sites, extended photoresponding range, enhanced photogenerated charge separation, and transportation efficiency. This work may provide a rational and convenient strategy to construct highly efficient semiconductor-rGO nanocomposite photocatalysts with well-contacted interface toward environmental purification and solar energy conversion.

BackgroundWe aimed to determine the risk conferred by metabolic syndrome (METS) and diabetes mellitus (DM) to recurrent stroke in patients with minor ischemic stroke or transient ischemic attack from the CHANCE (Clopidogrel in High‐risk patients with Acute Non‐disabling Cerebrovascular Events) trial.Methods and ResultsIn total, 3044 patients were included. Patients were stratified into 4 groups: neither, METS only, DM only, or both. METS was defined using the Chinese Diabetes Society (CDS) and International Diabetes Foundation (IDF) definitions. The primary outcome was new stroke (including ischemic and hemorrhagic) at 90 days. A multivariable Cox regression model was used to assess the relationship of METS and DM status to the risk of recurrent stroke adjusted for potential covariates. Using the CDS criteria of METS, 53.2%, 17.2%, 19.8%, and 9.8% of patients were diagnosed as neither, METS only, DM only, and both, respectively. After 90 days of follow‐up, there were 299 new strokes (293 ischemic, 6 hemorrhagic). Patients with DM only (16.1% versus 6.8%; adjusted hazard ratio 2.50, 95% CI 1.89–3.39) and both (17.1% versus 6.8%; adjusted hazard ratio 2.76, 95% CI 1.98–3.86) had significantly increased rates of recurrent stroke. No interaction effect of antiplatelet therapy by different METS or DM status for the risk of recurrent stroke (P=0.82 for interaction in the fully adjusted model of CDS) was observed. Using the METS (IDF) criteria demonstrated similar results.ConclusionsConcurrent METS and DM was associated with an increased risk of recurrent stroke in patients with minor stroke and transient ischemic attack.

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In this study, we aimed to evaluate the safety and feasibility of simultaneous bilateral carotid artery stenting (BCAS) compared with staged BCAS in patients with bilateral atherosclerotic carotid stenosis (BCS). From January 2004 to March 2012, 68 patients who underwent BCAS were identified from the Nanjing Stroke Registry Program. Of these patients, 42 (61.8 %) underwent simultaneous BCAS (simultaneous group), and 26 (38.2 %) underwent staged BCAS (staged group). We compared demographic data, major vascular risk factors, procedural parameters, and 30 day outcomes between the simultaneous and staged groups. No significant differences were detected in baseline data between the groups. Patients in the simultaneous group had a lower post-operative systolic pressure compared with the staged group (119.1 ± 16.1 vs. 130.2 ± 17.5 mmHg, P = 0.009). Technical success was 100 % of patients in the simultaneous group and 98.1 % in the staged group. Hemodynamic depression was observed in 57.4 % of procedures, with no significant difference between groups in the rate of HD. Four (5.9 %) patients had neurological complications within 30 days, including two cases of hyperperfusion syndrome in the simultaneous group, and two ischemic events in the staged group. There was no significant difference in the 30 day complication rate between the simultaneous and staged groups (4.8 vs. 7.7 %, P = 0.633). Simultaneous BCAS may be safe and feasible for most patients with BCS, with a similar 30 day complication rate to staged BCAS. Multicenter randomized control studies with larger sample sizes are warranted to further explore the safety and efficacy of simultaneous BCAS.

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Background Disruption of the blood–brain barrier (BBB) after a stroke can lead to brain injury and neurological impairment. Previous work confirmed the involvement of the immunoproteasome subunit of low molecular mass peptide 2 (LMP2) in the pathophysiology of ischemia stroke. However, the relationship between the immunoproteasome LMP2 and the BBB remains unclear. Methods Adult male Sprague–Dawley rats were subjected to transient middle cerebral artery occlusion/reperfusion (MCAO/R). Three days before MCAO, the rats were treated with lentivirus-mediated LMP2 shRNA preparations by stereotactical injection into the ipsilateral hemispheric region. The rat brain microvascular endothelial cell (RBMVEC) line was exposed to oxygen–glucose deprivation/reperfusion (OGD/R) to mimic ischemic conditions in vitro. The RNA interference-mediated knockdown of LMP2 or β-catenin was analysed in vivo and in vitro. Analysis of the quantity of extravasated Evans blue (EB) and cerebral fluorescent angiography were performed to evaluate the integrity of the BBB. Immunofluorescence and Western blotting were employed to detect the expression of target proteins. Cell migration was evaluated using a scratch migration assay. The results of immunofluorescence, Western blotting and cell migration were quantified using the software ImageJ (Version 1.53m). Parametric data from different groups were compared using one-way ANOVA followed by the least significant difference (LSD) test. Results Cerebral ischemia led to lower levels of structural components of the BBB such as tight junction proteins (occludin, claudin-1 and ZO-1) in the MCAO/R group compared with the sham group (P < 0.001). However, inhibition of the immunoproteasome LMP2 restored the expression of these proteins, resulting in higher levels of occludin, claudin-1 and ZO-1 in the LMP2-shRNA group compared with the control-shRNA group (P < 0.001). In addition, inhibition of the immunoproteasome LMP2 contributed to higher microvascular density and decreased BBB permeability [e.g., the quantity of extravasated EB: LMP2-shRNA group (58.54 ± 7.37) µg/g vs. control-shRNA group (103.74 ± 4.32) µg/g, P < 0.001], and promoted the upregulation of Wnt-3a and β-catenin proteins in rats following MCAO/R. In vitro experiments, OGD/R induced marked upregulation of LMP2, proapoptotic protein Bax and cleaved caspase-3, and downregulation of occludin, claudin-1, ZO-1 and Bcl-2, as well as inhibition of the Wnt/β-catenin pathway Wnt-3a and β-catenin proteins in RBMVECs, compared with the control group under normal culture conditions (P < 0.001). However, silencing of LMP2 gene expression reversed these protein changes and promoted proliferation and migration of RBMVECs following OGD/R. Silencing of β-catenin by transfection of RBMVECs with β-catenin-siRNA aggravated the downregulation of tight junction proteins, and reduced the proliferation and migration of RBMVECs following OGD/R, compared with the control-siRNA group (P < 0.001). LMP2-siRNA and β-catenin-siRNA co-transfection partly counteracted the beneficial effects of silencing LMP2-siRNA on the levels of tight junction proteins in RBMVECs exposed to OGD/R. Conclusion This study suggests that inhibition of the immunoproteasome LMP2 ameliorates ischemia/hypoxia-induced BBB injury, and that the molecular mechanism involves the immunoproteasome-regulated activation of the Wnt/β-catenin signalling pathway under ischemic conditions.