A high-sensitive and fast-fabricated glucose biosensor based on Prussian blue/topological insulator Bi(2)Se(3) hybrid film

A novel and fast-fabricated Prussian blue (PB)/topological insulator Bi(2)Se(3) hybrid film has been prepared by coelectrodeposition technique. Taking advantages of topological insulator in possessing exotic metallic surface states with bulk insulating gap, Prussian blue nanoparticles in the hybrid film have smaller size as well as more compact structure, showing excellent pH stability even in the alkalescent solution of pH 8.0. Based on the Laviron theory, the electron transfer rate constant of PB/Bi(2)Se(3) hybrid film modified electrode was calculated to be 4.05±0.49s(-1), a relatively big value which may be in favor of establishing a high-sensitive biosensor. An amperometric glucose biosensor was then fabricated by immobilizing glucose oxidase (GOD) on the hybrid film. Under the optimal conditions, a wide linear range extending over 3 orders of magnitude of glucose concentrations (1.0×10(-5)-1.1×10(-2)M) was obtained with a high sensitivity of 24.55μAmM(-1) cm(-2). The detection limit was estimated for 3.8μM defined from a signal/noise of 3. Furthermore, the resulting biosensor was applied to detect the blood sugar in human serum samples without any pretreatment, and the results were comparatively in agreement with the clinical assay.     

MicroRNA-205 affects mouse granulosa cell apoptosis and estradiol synthesis by targeting CREB1

MicroRNA-205 (miR-205) is involved in various physiological and pathological processes, but its biological function in follicular atresia remains unclear. In this study, we investigated miR-205 expression in mouse granulosa cells (mGCs) and analyzed its functions in primary mGCs by performing a series of in vitro experiments. Quantitative real-time polymerase chain reaction showed that miR-205 expression was significantly higher in early atretic follicles and progressively atretic follicles than in healthy follicles. miR-205 overexpression in mGCs significantly promoted apoptosis and caspase-3/9 activities, as well as inhibited estrogen (E2) release and cytochrome P450 family 19 subfamily A polypeptide 1 (CYP19A1, a key gene in E2 production) expression. Bioinformatics and luciferase reporter assays revealed that the gene encoding cyclic AMP response element (CRE)-binding protein 1 (CREB1) was a direct target of miR-205 in mGCs. CREB1 upregulation partially rescued the effects of miR-205 on apoptosis, caspase-3/9 activities, E2 production, and CYP19A1 expression on mGCs. These results indicate that miR-205 might play an important role in ovarian follicular development and provide new insights into follicular atresia     

The Role of HSPA12B in Regulating Neuronal Apoptosis

Heat shock protein A12B (HSPA12B) is the newest member of a recently defined subfamily of proteins distantly related to the 70-kDa family of heat shock proteins (HSP70) family. HSP70s play a crucial role in protecting cells, tissues, organs and animals from various noxious conditions. Here we studied the dynamic expression changes and localization of HSPA12B after middle cerebral artery occlusion (MCAO) with reperfusion induced ischemic insult processes in adult rats. Apoptosis, as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, was also increased in the peri-ischemic cortex compared to non-ischemic hemisphere. The expression of HSPA12B was strongly induced in the ischemic hemisphere of MCAO reperfusion rats in vivo. In vitro studies indicated that the up-regulation of HSPA12B may be involved in oxygen-glucose deprivation-induced PC12 cell death. And knockdown of HSPA12B in cultured differentiated PC12 cells by siRNA showed that HSPA12B inhibited the expression of active caspase-3. Collectively, these results suggested that HSPA12B may be required for protecting neurons from ischemic insults.     

Identification of spatial genetic boundaries using a multifractal model in human population genetics

There are two purposes in displaying spatial genetic structure. One is that a visual representation of the variation of the genetic variable should be provided in the contour map. The other is that spatial genetic structure should be reflected by the patterns or the gradients with genetic boundaries in the map. Nevertheless, most conventional interpolation methods, such as Cavalli-Sforza's method in genography, inverse distance-weighted methods, and the Kriging technique, focus only on the first primary purpose because of their arbitrary thresholds marked on the maps. In this paper we present an application of the contour area multifractal model (CAMM) to human population genetics. The method enables the analysis of the geographic distribution of a genetic marker and provides an insight into the spatial and geometric properties of obtained patterns. Furthermore, the CAMM may overcome some of the limitations of other interpolation techniques because no arbitrary thresholds are necessary in the computation of genetic boundaries. The CAMM is built by establishing power law relationships between the area A (> or =rho) in the contour map and the value p itself after plotting these values on a log-log graph. A series of straight-line segments can be fitted to the points on the log-log graph, each representing a power law relationship between the area A (> or =rho) and the cutoff genetic variable value for rho in a particular range. These straight-line segments can yield a group of cutoff values, which can be identified as the genetic boundaries that can classify the map of genetic variable into discrete genetic zones. These genetic zones usually correspond to spatial genetic structure on the landscape. To provide a better understanding of the interest in the CAMM approach, we analyze the spatial genetic structures of three loci (ABO, HLA-A, and TPOX) in China using the CAMM. Each synthetic principal component (SPC) contour map of the three loci is created by using both Han and minority groups data together. These contour maps all present an obvious geographic diversity, which gradually increases from north to south, and show that the genetic differences among populations in different districts of the same nationality are greater than those among different nationalities of the same district. It is surprising to find that both the value of p and the fractal dimension alpha have a clear north to south gradient for each locus, and the same clear boundary between southern and northern Asians in each contour map is still seen in the zone of the Yangtze River, although substantial population migrations have occurred because of war or famine in the last 2,000 or 3,000 years. A clear genetic boundary between Europeans and Asians in each contour map is still seen in northwestern China with a small value of alpha, although the genetic gradient caused by gene flow between Europeans and Asians has tended to show expansion from northwestern China. From the three contour maps another interesting result can be found: The values of alpha north of the Yangtze River are generally less than those south of the Yangtze River. This indicates that the genetic differences among the populations north of the Yangtze River are generally smaller than those in populations south of the Yangtze River.     

Ataxin-10 is involved in Golgi membrane dynamics

<正>Cytokinesis is the final stage of cell division that generates two daughter cells(Fededa and Gerlich,2012).The textbook version di-vides the plant and animal cell cytokinesis into two categories.Plant cells form a mid-zone phragmoplast via vesicle delivering and fusion,and cell wall materials are thus deposited.Animal cells form actomyosin contractile rings,which are the sole force that drives abscission.However,recent evidence has been mounting and pinpointing a pivotal role of membrane transport and subse-     

Coexistence of Anhedonia and anxiety-independent increased novelty-seeking behavior in the chronic mild stress model of depression

Previous research demonstrated excessive decreases in reward sensitivity and increases in harm avoidance in depressed individuals. These results straightly lead to a hypothesis that depressed patients should avoid novelty or express reduced novelty-seeking behavior. Nevertheless, literature in this regard is inconsistent. Furthermore, whether the potentially altered novelty-associated behavior is dependent on changed anxiety/fear or related to altered goal-directed approaching tendency is unclear. Here, we tested novel object-approaching behavior in a free-exploration paradigm in chronic mild stress (CMS)-induced anhedonic and stress-resistant rats respectively. Other CMS-induced, emotional behaviors were also examined in a battery of behavioral tests including novel cage, exploration, locomotor activity and elevated plus maze (EPM). We found that compared with controls, stress-resistant rats who consistently showed lower anxiety level in EPM (time in open arms) and, open-field (OF) test (time in central area) showed no sign of enhanced novel object approaching behavior. To the contrary, the anhedonic ones who did not express any sign of reduced anxiety showed paradoxically intensified novelty-approaching behavior. We concluded that reduced anxiety would not necessarily lead to enhanced novelty-seeking behavior; anhedonia coexists with anxiety-independent, increased novelty-seeking behavior. The salient paradox of coexistence of anhedonia and increased novelty-seeking behavior was critically discussed.     

Identification of a Novel Universal Potential Epitope on the Cytoplasmic Tail of H7N9 Virus Hemagglutinin

<正>Dear Editor,H7 N9 is a recently identified subtype of influenza A virus that caused a major outbreak in humans in China in 2013.According to the latest data provided by the Chinese Center for Disease Control and Prevention(http://www.moh.gov.cn/zwgk/yqbb3/ejlist.shtml, updated on October 31, 2018),the mortality rate of H7 N9 infections in China amounts to     

IQGAP1 is necessary for pulmonary vascular barrier protection in murine acute lung injury and pneumonia

We recently reported that integrin α(v)β(3) is necessary for vascular barrier protection in mouse models of acute lung injury and peritonitis. Here, we used mass spectrometric sequencing of integrin complexes to isolate the novel β(3)-integrin binding partner IQGAP1. Like integrin β(3), IQGAP1 localized to the endothelial cell-cell junction after sphingosine-1-phosphate (S1P) treatment, and IQGAP1 knockdown prevented cortical actin formation and barrier enhancement in response to S1P. Furthermore, knockdown of IQGAP1 prevented localization of integrin α(v)β(3) to the cell-cell junction. Similar to β(3)-null animals, IQGAP1-null mice had increased pulmonary vascular leak compared with wild-type controls 3 days after intratracheal LPS. In an Escherichia coli pneumonia model, IQGAP1 knockout mice had increased lung weights, lung water, and lung extravascular plasma equivalents of (125)I-labeled albumin compared with wild-type controls. Taken together, these experiments indicate that IQGAP1 is necessary for S1P-mediated vascular barrier protection during acute lung injury and is required for junctional localization of the barrier-protective integrin α(v)β(3).