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Highly dispersed copper nanowire (CuNW) is an essential prerequisite for its practical application in various electronic devices. At present, the dispersion of CuNW is almost realized through the steric hindrance effect of polymers. However, the high post-treatment temperature of polymers makes this dispersion mechanism impractical for many actual applications. Here, after investigating the relationship between the electrostatic dispersion force and influence factors, an electrostatic dispersion mechanism is refined by us. Under the guidance of this mechanism, high dispersion of CuNW and a record low post-treatment temperature (80 °C) are realized simultaneously. The high dispersity endows CuNW with good stability (-45.66 mV) in water-based ink, high uniformity (65.7 ± 2.5 Ω sq-1) in the prepared transparent conducting film (TCF) (23 cm × 23 cm), and industrial film preparation process, which are the issues that hinder the widespread application of CuNW-based TCF at present. The low post-treatment temperature makes the application of CuNW possible on any substrate. In addition, the charge modifier, 2-mercaptoethanol, enables CuNW to resist oxidation well. Finally, flexible optoelectronic devices employing the CuNW film as the electrode are fabricated and show efficiencies comparable to those of optoelectronic devices on indium tin oxide/glass.

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Emerging evidence shows that obesity induces renal injury and is an independent risk factor for the development of chronic kidney disease (CKD), even without diabetes or hyperglycemia. Although multiple metabolic factors have been suggested to account for obesity-associated renal injury, the precious underlying mechanisms are not completely understood. Recent study shows that increased trimethylamine N-Oxide (TMAO), a gut microbiota-generated metabolite, directly contributes to renal interstitial fibrosis and dysfunction. Circulating TMAO is elevated in high-fat diets (HFD)-induced obese animals. Here we tested the hypothesis that elevated TMAO might play a contributory role in the development of renal dysfunction in a mouse model of HFD-induced obesity that mimics human obesity syndrome. Male C57BL/6 mice received either a low-fat diet (LFD) or a HFD, without or with 3,3-Dimethyl-1-butanol (DMB, a trimethylamine formation inhibitor) for 16 weeks. Compared with mice fed a LFD, mice fed a HFD developed obesity and metabolic disorders, and exhibited significantly elevated plasma TMAO levels at the end of the experiment. Molecular and morphological studies revealed that renal interstitial fibrosis, phosphorylation of SMAD3 (a key regulator of renal fibrosis), expression of kidney injury molecule-1 and plasma cystatin C were significantly increased in mice fed a HFD, compared with mice fed a LFD. Additionally, expression of NADPH oxidase-4 and pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1 ß was also augmented in mice fed a HFD as compared to mice fed a LFD. These molecular and morphological alterations observed in mice fed a HFD were prevented by concomitant treatment with DMB, which reduced plasma TMAO levels. Furthermore, elevated circulating TMAO levels were positively correlated with increased renal interstitial fibrosis and expression of kidney injury molecule-1. Notable, there was no difference in blood pressure among groups, and DMB treatment had no effects on body weight and metabolic parameters. These data suggest that HFD-induced obesity leads to elevations in gut microbiota-generated metabolite TMAO in the circulation, which contributes to renal interstitial fibrosis and dysfunction by promoting renal oxidative stress and inflammation. These findings may provide new insights into the mechanisms underlying obesity-associated CKD. Targeting TMAO may be a novel strategy for prevention and treatment of CKD in patients with obesity.

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An increasing number of circulating micro-ribonucleic acids (microRNAs, miRNAs) have been discovered its potential as biomarkers to diagnose neurodegenerative diseases (NDs) by many researchers. However, there were obvious inconsistencies among previous studies, and thus we performed this meta-analysis to evaluate whether miRNA is an effective biomarker with high accuracy to diagnose the NDs. PubMed, MEDLINE, EMBASE, the Cochrane Library, and other related databases were used to search eligible articles. The data of sensitivity and specificity were employed to plot the summary receiver operator characteristic (SROC) curve and calculate the area under the SROC curve (AUC). I (2) test were used to estimate the heterogeneity among different studies. In addition, the possible sources of heterogeneity were further explored by subgroup analyses and meta-regression. All analyses were performed by STATA 12.0 software. In this meta-analysis, eight publications with 459 NDs patients and 340 healthy controls were included to investigate the diagnostic performance of circulating miRNAs for NDs. The overall sensitivity and specificity, positive likelihood ratio (PLR), negative likelihood ration (NLR), and diagnostic odds ratio (DOR) were 0.83 (95% confidence interval (CI) 0.77-0.88), 0.87 (95% CI 0.83-0.89), 6.2 (95% CI 4.9-7.9), 0.19 (95% CI 0.14-0.27), 33 (95% CI 20-52), and 0.91 (95% CI: 0.88-0.93), respectively. The overall SROC curve was plotted with AUC of 0.91 (95% CI 0.88-0.93), which indicated an excellent diagnostic performance of circulating miRNA for NDs. Subgroup analysis based on miRNA profile demonstrated that multiple-miRNA assay had higher diagnostic accuracy for NDs when compared with single-miRNA assay. In conclusion, the circulating miRNAs may be the potential biomarkers in the clinical diagnosis of NDs, and the diagnostic accuracy would be better by using multiple-miRNA assay. However, large-scale studies are still needed to explore the relation between the circulating miRNA dysregulation and the pathological mechanism of NDs.

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Glioblastoma (GBM), a deadly brain tumor, is the most malignant glioma. It mainly occurs in adults and occurs significantly more in males than in females. We genotyped 19 tag single nucleotide polymorphisms (tSNPs) from 13 genes in a case-control study of the Han Chinese population to identify genetic factors contributing to the risk of GBM. These tSNPs were genotyped by Sequenom MassARRAY RS1000. Statistical analysis was performed using χ(2) test and SNPStats, a website software. Using χ(2) test, we found that the distribution of two tSNPs (rs2267130 in checkpoint kinase 2 (CHEK2), p = 0.040; rs1695 in GSTP1, p = 0.023) allelic frequencies had significant difference between cases and controls. When we analyzed all of the tSNPs using the SNPStats software, we found that rs1695 in GSTP1 decreased the risk of GBM in log-additive model (OR = 0.56, 95% CI, 0.34-0.94, p = 0.022). Besides, we found that there is an interaction between rs3212986 in excision repair cross-complementing group 1 (ERCC1) and gender under codominant and recessive models. The gene polymorphisms in CHEK2, GSTP1, and ERCC1 may be involved in GBM in the Han Chinese population. Since our sample size is small, further investigation needs to be performed.

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Quercetin has been demonstrated to play an important role in altering the progression of ischemic brain injuries and neurodegenerative diseases by protecting against oxidative stress. The effects of quercetin on brain damage after subarachnoid hemorrhage (SAH), however, have not been investigated. This study was designed to explore the effects of quercetin on oxidative stress and brain edema after experimental SAH using four equal groups (n = 16) of adult male Sprague-Dawley (SD) rats, including a sham group, an SAH + vehicle group, an SAH + quercetin10 group, and an SAH + quercetin50 group. The rat SAH model was induced by injection of 0.3 ml of non-heparinised arterial blood into the prechiasmatic cistern. In the SAH + quercetin10 and SAH + quercetin50 groups, doses of 10 mg/kg and 50 mg/kg quercetin, respectively, were directly administered by intraperitoneal injection at 30 min, 12 h, and 24 h after SAH induction. Cerebral tissue samples were extracted for enzymatic antioxidant determination, lipid peroxidation assay, caspase-3 activity and water content testing 48 h after SAH. Treatment with a high dose (50 mg/kg) of quercetin markedly enhanced the activities of copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px), and treatment with this dose significantly reduced the level of malondialdehyde (MDA). Caspase-3 and brain edema was ameliorated and neurobehavioral deficits improved in rats that received the high dose of quercetin. The findings suggest that the early administration of optimal dose of quercetin may ameliorate brain damage and provide neuroprotection in the SAH model, potentially by enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation.

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PURPOSE: Mesial temporal lobe epilepsy (MTLE) is one of the most common forms of epilepsies in adults. The calcium homeostasis modulator 1 gene (CALHM1) has been considered one of the candidate genes that play a role in epileptogenesis due to its function in calcium homeostasis and amyloid ß (Aß) regulation. Recently, the association of a single nucleotide polymorphism (rs11191692) of CALHM1 has been reported to be associated with MTLE in Han Chinese, but independent replication is needed. In the present study, rs11191692 and rs2986017 of CALHM1 were determined in 512 MTLE patients and 412 control subjects to investigate the possible involvement of CALHM1 in the etiology of MTLE. METHOD: Genotyping was determined by polymerase chain reaction-restriction fragment length polymorphism method. Major statistical analyses were performed by SAS. RESULTS: No significant differences in the genotypic or allelic frequencies of both single-nucleotide polymorphisms were revealed between subjects with and without MTLE (rs11191692: P=0.890 and 0.230; rs2986017: P=0.581 and 0.072). Further stratification analysis by gender and age, and analysis of clinical features in relation to MTLE also yielded negative results. CONCLUSION: rs11191692 and rs2986017 of CALHM1 do not contribute substantially to MTLE in Han Chinese.

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Hypoxia-inducible factor 1α (HIF-1α) is a master regulator of cellular adaptation to hypoxia and has been proposed as a potent therapeutic target for cerebral ischemia. However, research on the expression and effects of HIF-1α in subarachnoid hemorrhage (SAH) is limited. The aim of the present study was to investigate the expression of HIF-1α in the hippocampus and its possible protective effect against hippocampal apoptosis and cognitive dysfunction in a rat model of SAH. Seventy-two Sprague-Dawley (SD) rats were randomly divided into the sham group, the SAH+vehicle group, and the SAH+YC-1 group. Immunohistochemical staining and western blotting analyses revealed that the expression of HIF-1α and its downstream effectors, vascular endothelial growth factor (VEGF), erythropoietin (EPO), and glucose transporter 1 (GLUT1), increased in the hippocampus 48h after the induction of SAH. YC-1 blocked this upregulation. The number of active caspase-3-positive cells and the expression of active caspase-3 in the hippocampus significantly increased in the YC-1 group relative to the vehicle group. A cell death assay further revealed that DNA fragmentation was significantly increased at 48h in the YC-1 group compared with the vehicle group. In Morris water maze (MWM) tests, the YC-1 group showed increased escape latency times and distances as well as reduced time spent and distance traveled in the target quadrant. These results indicate that hippocampal apoptosis increased and cognitive function deteriorated when HIF-1α was inhibited, suggesting that HIF-1α has a neuroprotective effect in SAH and may represent an effective therapeutic target.

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Hindlimb ischemia is a major complication of diabetic patients due to poor neovascularization. Therapy with pulsed electromagnetic fields (PEMF) can promote angiogenesis in ischemic lesions. However, the efficacy and therapeutic mechanisms of PEMF in diabetes-related hindlimb ischemia are unclear. Sprague-Dawley rats were injected with streptozocin to induce diabetes, and 10 weeks later diabetic rats were subjected to surgical induction of acute hindlimb ischemia. The rats were randomized and treated with PEMF, and the blood perfusion of individual rats was determined longitudinally by laser Doppler perfusion imaging (LDPI). The neovascular density was examined using immunofluorescent analysis of CD31 expression and alkaline phosphatase (AP) staining. The levels of VEGF, VEGFR, FGF-2, and FGFR1 expression, and ERK 1/2 and P38 phosphorylation in the muscles were characterized using enzyme-linked immunosorbent assay (ELISA) and Western blot assays. The values of LDPI in the PEMF-treated rats at 14 and 28 days post surgery were significantly greater than those in the controls, accompanied by significantly elevated levels of anti-CD31 and AP staining. The relative levels of FGF-2 and FGFR1, but not VEGF and VEGFR expression, and ERK1/2, but not P38 phosphorylation, in the muscles of the PEMF-treated rats were significantly higher than those in the controls. Our data indicated that PEMF enhanced acute hindlimb ischemia-related perfusion and angiogenesis, associated with up-regulating FGF-2 expression and activating the ERK1/2 pathway in diabetic rats. Therefore, PEMF may be valuable for the treatment of diabetic patients with ischemic injury.

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Accumulated understanding of epigenetic modifications during ischemia-reperfusion (IR) injury suggests that additional targeted approaches and novel mechanisms that have not been explored in the reproductive system underlie the pathogenesis. Here we show, with a standard murine model of testicular IR, ischemia-induced histone deacetylase (HDAC) activity in the testis with concomitant reduction in histone acetyl transferase activity in vivo. Pretreatment with chemical HDAC inhibitors significantly induced apoptosis in tetraploid pachytene spermatocytes during ischemic insult and thereafter resulted in attenuated meiotic differentiation. We also identified the distinct HDACs involved in primary spermatocytes upon hypoxic stress. In vitro, elevated expression of HDAC2 was physiologically associated with p53, a master regulator believed to be a guardian of genome integrity during spermatogenesis. p53-mediated apoptosis was inhibited by deacetylation of p53 in differentiating pachytene spermatocytes in response to ischemic stress. Overall, the current data suggest that hypoxia-induced deacetylation may operate as an indispensible defensive mechanism for meiotic differentiation during the ischemic period of IR testis, thus pointing to a novel therapeutic target for future medical intervention.

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OBJECTIVE: To identify global research trends in the use of stem cell transplantation to treat epilepsy. DATA RETRIEVAL: We performed a bibliometric analysis of studies on the use of stem cell transplantation to treat epilepsy during 2002-2011, retrieved from Web of Science, using the key words epilepsy or epileptic or epilepticus or seizure and "stem cell". INCLUSION CRITERIA: (a) peer-reviewed published articles on the use of stem cell transplantation to treat epilepsy indexed in Web of Science; (b) original research articles, reviews, meeting abstracts, proceedings papers, book chapters, editorial material, and news items. MAIN OUTCOME MEASURES: (a) Annual publication output; (b) type of publication; (c) publication by research field; (d) publication by journal; (e) publication by author; (f) publication by country and institution; (g) publications by institution in China; (h) most-cited papers; and (i) papers published by Chinese authors or institutions. RESULTS: A total of 460 publications on the use of stem cell transplantation to treat epilepsy were retrieved from Web of Science, 2002-2011. The number of publications gradually increased over the 10-year study period. Articles and reviews constituted the major types of publications. More than half of the studies were in the field of neuroscience/neurology. The most prolific journals for this topic were Epilepsia, Bone Marrow Transplantation, and Journal of Neuroscience. Of the 460 publications, almost half came from American authors and institutions; relatively few papers were published by Chinese authors or institutions. CONCLUSION: Literature on stem cell transplantation for epilepsy includes many reports of basic research, but few of clinical trials or treatments. Exact effects are not yet evaluated. Epilepsy rehabilitation is a long-term, complex, and comprehensive system engineering. With advances in medical development, some effective medical, social and educational measures are needed to facilitate patient's treatment and training and accelerate the recovery of life ability, learning ability and social adaptability to the largest extent to improve patient's quality of life.

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Functional magnetic resonance imaging was used during emotion recognition to identify changes in functional brain activation in 21 first-episode, treatment-naive major depressive disorder patients before and after antidepressant treatment. Following escitalopram oxalate treatment, patients exhibited decreased activation in bilateral precentral gyrus, bilateral middle frontal gyrus, left middle temporal gyrus, bilateral postcentral gyrus, left cingulate and right parahippocampal gyrus, and increased activation in right superior frontal gyrus, bilateral superior parietal lobule and left occipital gyrus during sad facial expression recognition. After antidepressant treatment, patients also exhibited decreased activation in the bilateral middle frontal gyrus, bilateral cingulate and right parahippocampal gyrus, and increased activation in the right inferior frontal gyrus, left fusiform gyrus and right precuneus during happy facial expression recognition. Our experimental findings indicate that the limbic-cortical network might be a key target region for antidepressant treatment in major depressive disorder.

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OBJECTIVE: To explore the efficacy and complication of bilateral multi-target radiofrequency lesion operation in patients with affective disorder. METHODS: One hundred and eighty-two cases with affective disorder were treated with unstaged bilateral multi-target radiofrequency thermocoagulation. The efficacy was evaluated with the method established in 1990 by the National Psychosurgery Cooperative Group. RESULTS: After 2 weeks of operation, 86 cases with remarkable improvements, 81 cases with improvements, 15 case with no improvements, no case with progression, total efficient ratio was 91.76%. With 6-54 months of follow-up to all of 166 cases, 38 cases with recovery, 59 cases with remarkable improvements, 52 cases with improvements, 17 cases with no improvements, no case with progression, total efficient ratio was 89.76%. Except for early temporal complication of stereotaxic operation, the long-term complication ratio was less than 1%. CONCLUSION: CT-guided bilateral multi-target operation is prominent in treatment of affective disorder with high efficacy and safety.

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