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Background: Serum levels of C-reactive protein (CRP) were measured in patients with deficit schizophrenia (DS) to confirm the association between CRP level and cognitive performance and to determine whether CRP was a new biological indicator with the potential clinical applications in DS patients. Methods: Three independent samples [41 DS and 50 non-deficit schizophrenia (NDS) and 30 sex- and age-matched healthy controls (HCs)] were recruited in our study. Serum CRP levels were measured by immunofluorescence. The Positive and Negative Syndrome Scale (PANSS) and alternative forms of the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) were also assessed. And the relationships between serum CRP levels and both PANSS and RBANS scores were finally analyzed. Results: The results of serum CRP level were showed significantly different among the three groups and increased from the HCs to NDS patients to DS patients. There were also significant differences in the cognitive subdomain analyses among the three groups. Serum CRP levels were found positively correlated with total and negative PANSS scores, and showed negatively correlated with overall cognitive test scores in the DS samples. Conclusion: Serum C-reactive protein levels and their association with cognitive performance were different between deficit schizophrenia and non-deficit schizophrenia samples, and higher serum CRP level was associated with worse cognitive performance in the DS patients. The results indicated that CRP could be a potential biomarker, and DS could be a distinct subset of schizophrenia. [ABSTRACT FROM AUTHOR]

In this work, the crystal structure, thermal conductivity, as well as dielectric and electrical properties of poly(vinylidene fluoride-co-chlorotrifluoroethylene) [P(VDF-CTFE)] filled with two different carbon nanofillers including exfoliated graphite nanoplates (xGNPs) and multi-walled carbon nanotubes (MWCNTs) have been compared. The xGNPs and the MWCNTs were well dispersed in the P(VDF-CTFE) matrix using a simple solution-blending process. The xGNPs have the ability to induce the large amount of useful polar β and γ crystal phases for P(VDF-CTFE) via the relatively strong interfacial interaction between their functional groups and the dipoles of P(VDF-CTFE), while the MWCNTs only produce the relatively low amount of β crystal phases for P(VDF-CTFE) due to their weak π-dipole interactions with P(VDF-CTFE). It was found that both the electrical conductivity and dielectric properties of xGNPs/P(VDF-CTFE) composite were better than those of MWCNTs/P(VDF-CTFE) composite. The thermal conductivities of xGNPs/P(VDF-CTFE) composites were much higher when compared with those of MWCNTs/P(VDF-CTFE) composites at the same filler content, which is probably owing to the better compatibility between xGNPs and P(VDF-CTFE). For example, the thermal conductivities of xGNPs (5 wt%)/P(VDF-CTFE) composite and MWCNTs (5 wt%)/P(VDF-CTFE) composite were 0.83 W/mK and 0.43 W/mK, respectively. [ABSTRACT FROM AUTHOR]

Presents information on a study wherein the exact solutions for fully three-dimensional electrostatic quantities due to a free charge in a nanoscale tip/base junction, such as the scanning-tunneling microscope, are given for the problem as modeled in the prolate-spheroidal coordinate system. Methods; Results; Discussion.

Nosocomial infections caused by carbapenemase-producing Enterobacteriaceae have emerged as an important challenge worldwide and represent a great limitation for antimicrobial therapy. Detection of carbapenemase in Enterobacteriaceae species also remains challenging. Although the modified Hodge test is recommended, it lacks specificity and is unable to distinguish between carbapenemase types. Here, we demonstrated a screening strategy for the phenotypic detection of carbapenemases among Enterobacteriaceae isolates in the clinical laboratory by using ethylenediaminetetraacetic acid and phenylboronic acid. This strategy displayed an overall 100% sensitivity and 98.6% specificity for carbapenemase detection in Enterobacteriaceae, which was superior to that of the modified Hodge test (98.0% sensitivity and 84.3% specificity), and it also discriminated the carbapenemase phenotypes of KPC-2, VIM-1, and OXA-48. [ABSTRACT FROM AUTHOR]

Background: Hyperlipidemia is a risk factor for neurodegenerative diseases. Proprotein convertase subtilisin / Kexin type 9 (PCSK9) degrades hepatic low-density lipoprotein receptor (LDLR) to regulate lipid metabolism. It is unclear if PCSK9 plays a role in neurodegenerative diseases.Objective: This study was designed to determine whether PCSK9 is crucial between hyperlipidemia and Alzheimer's disease. The interrelationship between PCSK9 and neuronal apoptosis was explored in PC12 cells in response to treatment with oxidized low-density lipoprotein (oxLDL).Methods: Cultured PC12 cells were serum-starved and incubated with different concentrations of oxLDL for 24 h. Intracytoplasmic lipid droplets were observed by oil red O staining. Morphological assessment of apoptotic cells was performed using Hoechst 33258 staining and flow cytometry analysis. The expression of mRNA and protein was detected by reverse-transcription polymerase chain reaction (RT-PCR) and western blot analyses, respectively. Transfection of small interfering RNA (siRNA) into PC12 cells was conducted using HiperFect Transfection Reagent. Concentrations of Aβ40 and Aβ42 were detected by enzyme-linked immunosorbent assay (ELISA) kit.Results: Intracellular lipid content, the number of apoptotic cells, and PCSK9 expression were increased in PC12 cells after oxLDL treatment. Transfection with PCSK9 siRNA reduced the oxLDL-induced apoptosis of PC12 cells. We further confirmed the involvement of Bcl-2/Bax-Caspase (9, 3) signaling pathway in the regulation of PC12 cells apoptosis.β-Secretase 1, another target gene of PCSK9, was downregulated in PC12 cells in response to oxLDL treatment. Aβ40 and Aβ42 contents were also decreased.Conclusion: PCSK9 promotes oxLDL-induced PC12 cell apoptosis through the Bcl-2/Bax-Caspase 9/3 signaling pathway. [ABSTRACT FROM AUTHOR]

Transistor mismatch data and analysis from poly/SiON and high-k/metal-gate (HKMG) bulk CMOS technologies are presented. It is found that the traditional mismatch figure of merit from the Pelgrom plot (AVT) continuously scales down as technology advances. Furthermore, the AVT values for both nFET and pFET in the HKMG technology are significantly reduced from poly/SiON technologies. By normalizing the mismatch data against electrical oxide thickness (TINV), threshold voltage (VTH), and effective work function, a direct comparison of the mismatch data from various technologies is made. The differences in nFET and pFET mismatch behaviors in both poly/SiON and HKMG technologies are discussed in detail. Correlation between transistor VTH mismatch and flicker noise variation is observed in both poly/SiON and HKMG technologies. Finally, it is quantitatively demonstrated that effective work function variation does not generate significant VTH variability in the present HKMG technology. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (AMI) is an acute heart disease. Cycloastragenol, as a natural product, inhibits inflammation and protects cardiomyocytes. Cycloastragenol (Y006) modulates inflammation in AMI is not known. To explore the function of Cycloastragenol in AMI, this study investigated the effect of Y006 and its mechanisms both in vitro and in vivo. Y006 influences the concentration of 11 proteins, as shown by a proteomics analysis, immunohistochemistry and western blotting. Among these 11 proteins, Erk1/2, PLCG1, IKBKG, and ZEB1 are related to inflammatory regulation. BAX, COX2, and GSK3β are involved in modulating cardiomyocyte apoptosis, and RhoA and DSC2 are directly associated with myocardial function. However, the functions of ARHGAP17 and Rit2 in heart are less well established. Additionally, Y006 suppressed TNF-α, IFN-γ and IL-17 production in PBMCs (peripheral blood monocytes) from patients with acute myocardial infarction and enhanced IL-10 and IL-4 expression. Similar results were obtained in a rat model of AMI by flow cytometry detection and ELISA. Our findings indicate that Y006 protects rats from AMI through direct or indirect inhibition of inflammation and cardiomyocyte apoptosis. However, the specific mechanism of Y006's protective function requires further study. Nonetheless, this research revealed a novel aspect for the treatment of myocardial infarction. In the present study, we undertook the first proteomic evaluation of Cycloastragenol (Y006) function in acute myocardial infarction (AMI). Y006 significantly improved myocardial function in vivo by regulating multiple molecular expressions. Hypoxia is a direct reason for AMI. And our data support a role of Y006 in gene expression, cell apoptosis under hypoxia. The conclusions of this research assist to explain the potential molecular mechanism in Cycloastragenol treating AMI and supply a new method for ameliorating AMI. Unlabelled Image • A new small molecule Y006 on acute myocardial infarction rat model is identified. • Y006 affects 11 proteins by a proteomics assay, including inflammation and apoptosis proteins. • Y006 exerts myocardial protection effects via blocking PLCG1, RhoA, and PI3K pathways. [ABSTRACT FROM AUTHOR]