Cross Cultural Study About College Adjustment Study of China & Indonesian College Students: "How Coping Strategies Help Social Adjustment"

Many studies indicate that study in university bring a big experience for emerging adult, because of the transition. Many factors contributes to the qualityof adjustment, it could came from the internal and external. Abdullah, etl. (2010) found that coping strategies had significant and positive correlations with overall university adjustment. According to the preliminary survey, social adjustment usually became the most difficult one. So, the aim of this study is to investigate the correlation between coping strategies and students college adjusment (social adjustment) and the differences of cross cultural conditions between Indonesian and Chinese students This study is quantitative methods using two instruments, which are Student Adaptation to College Questionnaire (SACQ, Baker & Syrik, 1984,1989) and The Ways of Coping Questionnaire (WCQ)adapted from Folkman and Lazarus, 1988). Subjects in this study are 20 Indonesian students and 20 Chinese students. The study found only Engagement Coping Strategies have significant correlation with Social Adjustment. Problem Focused, Emotional Focused and Disengagement Coping Strategies have no significant correlation with Social Adjustment. Indonesian and Chinese students were different significantly in Problem and Emotional Focused Coping Strategy, and Engagement Coping Strategies. Some cultural differences in relationship and entry programme in each university assumed to play role in these difference

CROSS CULTURAL STUDY ABOUT COLLEGE ADJUSTMENT STUDY OF CHINA & INDONESIAN COLLEGE STUDENTS: "HOW QUALITIES OF FAMILY CONTRIBUTE SOCIAL ADJUSTMENT"

Many studies indicate that study in university bring a big experience for emerging adult, because of the transition. Many factors contributes to the quality of adjustment, it could came from the internal and external. Aspinwall (1992, in Abdullah, Elias, Uli & Mahyuddin, 2010) mentioned that students with family support will be predicted more success in adjustment. Balk (1995, in Wodka) asserting that higher family support may hinder identity exploration and achievement. According to the preliminary survey, social adjustment usually became the most difficult one. So, the aim of this study is to investigate the correlation between Family Function and Students Social Adjustment, and the differences of cross cultural conditions in Family Function between Indonesian and Chinese students. This study is quantitative methods using two instruments, which are Student Adaptation to College Questionnaire (SACQ, Baker & Syrik, 1984,1989) and ICPS Family Functioning Scales (ICPS-FFS, P. Noller, in Perlmutter ,2001). Subjects in this study are 20 Indonesian students and 20 Chinese students. There is significant differences in Family function between Indonesian students and Chinese students ( t : -3.121, p < .05). There is significant correlation between Students Social Adjustment and Family Function in the aspect of Intimacy, but not in the aspect of Parenting Styles (r ; 0.32, p < 0.05)

Fast generation of Schr\uf6dinger cat states using a Kerr-tunable superconducting resonator

Schr\uf6dinger cat states, quantum superpositions of macroscopically distinct classical states, are an important resource for quantum communication, quantum metrology and quantum computation. Especially, cat states in a phase space protected against phase-flip errors can be used as a logical qubit. However, cat states, normally generated in three-dimensional cavities and/or strong multi-photon drives, are facing the challenges of scalability and controllability. Here, we present a strategy to generate and preserve cat states in a coplanar superconducting circuit by the fast modulation of Kerr nonlinearity. At the Kerr-free work point, our cat states are passively preserved due to the vanishing Kerr effect. We are able to prepare a 2-component cat state in our chip-based device with a fidelity reaching 89.1% under a 96 ns gate time. Our scheme shows an excellent route to constructing a chip-based bosonic quantum processor

A Comparative Study of Workers Conditions in Football Manufacturing in China, India and Pakistan

A critical challenge facing developing country producers is to meet international labour standards and codes of conduct in order to engage in global production networks. Evidence of gains for workers from compliance with such standards and codes remains limited and patchy. This paper focuses on the global football industry, a sector dominated by leading global brands who manage dispersed global production networks. It assesses the work conditions for football stitchers engaged in different forms of work organisation, factories, stitching centres, and home-based settings, in Pakistan, India, and China. It draws on detailed qualitative primary field research with football stitching workers and producers in these three countries. The paper explains how, and why, work conditions of football stitchers differ across these locations through an analytical framework that interweaves both global and local production contexts that influence work condition. In doing so, it argues that current debates on the role of labour in global production networks have to go beyond a narrow focus on labour standards and CSR compliance and engage with economic, technological and social upgrading as factors that could generate sustained improvements in real wages and workers conditions

Nuclear Smooth Muscle α-actin Participates in Vascular Smooth Muscle Cell Differentiation

Missense variants throughout ACTA2, encoding smooth muscle α-actin (αSMA), predispose to adult-onset thoracic aortic disease, but variants disrupting arginine 179 (R179) lead to Smooth Muscle Dysfunction Syndrome (SMDS) characterized by diverse childhood-onset vascular diseases. Here we show that αSMA localizes to the nucleus in wildtype (WT) smooth muscle cells (SMCs), enriches in the nucleus with SMC differentiation, and associates with chromatin remodeling complexes and SMC contractile gene promotors. The ACTA2 p.R179 αSMA variant shows decreased nuclear localization. Primary SMCs from Acta2SMC-R179C/+ mice are less differentiated than WT SMCs in vitro and in vivo and have global changes in chromatin accessibility. Induced pluripotent stem cells from patients with ACTA2 p.R179 variants fail to fully differentiate from neuroectodermal progenitor cells to SMCs, and single-cell transcriptomic analyses of an ACTA2 p.R179H patient’s aortic tissue show increased SMC plasticity. Thus, nuclear αSMA participates in SMC differentiation, and loss of this nuclear activity occurs with ACTA2 p.R179 pathogenic variants

PRNP Haplotype Associated with Classical BSE Incidence in European Holstein Cattle

Background: Classical bovine spongiform encephalopathy (BSE) is an acquired prion disease of cattle. The bovine prion gene (PRNP) contains regions of both high and low linkage disequilibrium (LD) that appear to be conserved across Bos taurus populations. The region of high LD, which spans the promoter and part of intron 2, contains polymorphic loci that have been associated with classical BSE status. However, the complex genetic architecture of PRNP has not been systematically tested for an association with classical BSE. Methodology/Principal Findings: In this study, haplotype tagging single nucleotide polymorphisms (htSNPs) within PRNP were used to test for association between PRNP haplotypes and BSE disease. A combination of Illumina goldengate assay, sequencing and PCR amplification was used to genotype 18 htSNPs and 2 indels in 95 BSE case and 134 control animals. A haplotype within the region of high LD was found to be associated with BSE unaffected animals (p-value = 0.000114). Conclusion/Significance: A PRNP haplotype association with classical BSE incidence has been identified. This result suggests that a genetic determinant in or near PRNP may influence classical BSE incidence in cattle

Iron Regulation of the Major Virulence Factors in the AIDS-Associated Pathogen Cryptococcus neoformans

Iron overload is known to exacerbate many infectious diseases, and conversely, iron withholding is an important defense strategy for mammalian hosts. Iron is a critical cue for Cryptococcus neoformans because the fungus senses iron to regulate elaboration of the polysaccharide capsule that is the major virulence factor during infection. Excess iron exacerbates experimental cryptococcosis and the prevalence of this disease in Sub-Saharan Africa has been associated with nutritional and genetic aspects of iron loading in the background of the HIV/AIDS epidemic. We demonstrate that the iron-responsive transcription factor Cir1 in Cr. neoformans controls the regulon of genes for iron acquisition such that cir1 mutants are “blind” to changes in external iron levels. Cir1 also controls the known major virulence factors of the pathogen including the capsule, the formation of the anti-oxidant melanin in the cell wall, and the ability to grow at host body temperature. Thus, the fungus is remarkably tuned to perceive iron as part of the disease process, as confirmed by the avirulence of the cir1 mutant; this characteristic of the pathogen may provide opportunities for antifungal treatment

Identification of additional risk loci for stroke and small vessel disease: a meta-analysis of genome-wide association studies

BACKGROUND: Genetic determinants of stroke, the leading neurological cause of death and disability, are poorly understood and have seldom been explored in the general population. Our aim was to identify additional loci for stroke by doing a meta-analysis of genome-wide association studies. METHODS: For the discovery sample, we did a genome-wide analysis of common genetic variants associated with incident stroke risk in 18 population-based cohorts comprising 84 961 participants, of whom 4348 had stroke. Stroke diagnosis was ascertained and validated by the study investigators. Mean age at stroke ranged from 45·8 years to 76·4 years, and data collection in the studies took place between 1948 and 2013. We did validation analyses for variants yielding a significant association (at p<5 × 10(-6)) with all-stroke, ischaemic stroke, cardioembolic ischaemic stroke, or non-cardioembolic ischaemic stroke in the largest available cross-sectional studies (70 804 participants, of whom 19 816 had stroke). Summary-level results of discovery and follow-up stages were combined using inverse-variance weighted fixed-effects meta-analysis, and in-silico lookups were done in stroke subtypes. For genome-wide significant findings (at p<5 × 10(-8)), we explored associations with additional cerebrovascular phenotypes and did functional experiments using conditional (inducible) deletion of the probable causal gene in mice. We also studied the expression of orthologs of this probable causal gene and its effects on cerebral vasculature in zebrafish mutants. FINDINGS: We replicated seven of eight known loci associated with risk for ischaemic stroke, and identified a novel locus at chromosome 6p25 (rs12204590, near FOXF2) associated with risk of all-stroke (odds ratio [OR] 1·08, 95% CI 1·05-1·12, p=1·48 × 10(-8); minor allele frequency 21%). The rs12204590 stroke risk allele was also associated with increased MRI-defined burden of white matter hyperintensity-a marker of cerebral small vessel disease-in stroke-free adults (n=21 079; p=0·0025). Consistently, young patients (aged 2-32 years) with segmental deletions of FOXF2 showed an extensive burden of white matter hyperintensity. Deletion of Foxf2 in adult mice resulted in cerebral infarction, reactive gliosis, and microhaemorrhage. The orthologs of FOXF2 in zebrafish (foxf2b and foxf2a) are expressed in brain pericytes and mutant foxf2b(-/-) cerebral vessels show decreased smooth muscle cell and pericyte coverage. INTERPRETATION: We identified common variants near FOXF2 that are associated with increased stroke susceptibility. Epidemiological and experimental data suggest that FOXF2 mediates this association, potentially via differentiation defects of cerebral vascular mural cells. Further expression studies in appropriate human tissues, and further functional experiments with long follow-up periods are needed to fully understand the underlying mechanisms

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development