Son preference and intimate partner violence victimization in India: examining the role of actual and desired family composition

Son preference has been considered as a determinant of women's risk of intimate partner violence (IPV) experience in India, although quantitative evidence from large nationally representative studies testing this relationship is limited. This study examines the association between husband's son preference, sex composition of children and risk of physical and sexual IPV victimization among wives. Information was collected for 26,284 couples in the nationally representative 2005-2006 National Family Health Survey of India. The exposures were husband's son preference measured as husband's desire for one or more sons greater than the number of daughters and sex composition of the household: only sons, only daughters and mixed. Outcome included past year physical and/or sexual IPV. The results showed that husband's reported son preference (RR: 1.05; 95% CI: 0.98-1.13) and sex composition of children were not associated with risk for IPV victimization in the models adjusted for socio-demographic factors. The findings from this first population-based study of socio-cultural norms around son preference and married Indian women's risk for IPV victimization indicate that cultural preference for sons does not influence women's risk for IPV victimization.     

Perception of Neighborhood Safety and Reported Childhood Lifetime Asthma in the United States (U.S.): A Study Based on a National Survey

Background

Recent studies have emphasized the role of psychosocial stressors as a determinant of asthma, and neighborhoods can be a potential source of such stressors. We investigated the association between parental perception of neighborhood safety and reported lifetime asthma among children.

Methodology/Principal Findings

Data for the study came from the 2003–04 National Survey of Children Health (NSCH); a nationally representative cross-sectional sample of children aged 0–17 years. Demographic, socioeconomic and behavioral covariates were included in the study. Models were estimated after taking account of weighting and complex survey design. Parental report of whether the child has ever been diagnosed with asthma by a physician was used to define the outcome. Parental report of perception of neighborhood safety was the main exposure. In unadjusted models, the odds ratio (OR) for reporting asthma associated with living in neighborhoods that were perceived to be sometimes or never safe was 1.36 (95% confidence intervals [CI] 1.21, 1.53) compared to living in neighborhoods that were perceived to be always safe. Adjusting for covariates including exposure to second hand tobacco smoke, mother''s self-rated health, child''s physical activity and television viewing attenuated this association (OR 1.25, 95% CI 1.08, 1.43). In adjusted models, the increased odds ratio for reporting asthma was also higher among those who perceived neighborhoods as being usually safe (OR 1.15 95% CI 1.06, 1.26), as compared to always safe, suggestive of a dose-response relationship, with the differentials for usually safe and never safe being statistically significant (p = 0.009).

Conclusion

Psychosocial stressors may be important risk factors that may impact the pathogenesis of asthma and/or contribute to asthma morbidity by triggering exacerbations through neuroimmunologic mechanisms, as well as social mechanisms.     

Cells Lacking the Fragile X Mental Retardation Protein (FMRP) have Normal RISC Activity but Exhibit Altered Stress Granule Assembly

The fragile X mental retardation protein (FMRP) is an RNA-binding protein involved in the mRNA metabolism. The absence of FMRP in neurons leads to alterations of the synaptic plasticity, probably as a result of translation regulation defects. The exact molecular mechanisms by which FMRP plays a role in translation regulation have remained elusive. The finding of an interaction between FMRP and the RNA interference silencing complex (RISC), a master of translation regulation, has suggested that both regulators could be functionally linked. We investigated here this link, and we show that FMRP exhibits little overlap both physically and functionally with the RISC machinery, excluding a direct impact of FMRP on RISC function. Our data indicate that FMRP and RISC are associated to distinct pools of mRNAs. FMRP, unlike RISC machinery, associates with the pool of mRNAs that eventually goes into stress granules upon cellular stress. Furthermore, we show that FMRP plays a positive role in this process as the lack of FMRP or a point mutant causing a severe fragile X alter stress granule formation. Our data support the proposal that FMRP plays a role in controlling the fate of mRNAs after translation arrest.     

Analysis of DHHC Acyltransferases Implies Overlapping Substrate Specificity and a Two-Step Reaction Mechanism

Asp-His-His-Cys (DHHC) cysteine-rich domain (CRD) acyltransferases are polytopic transmembrane proteins that are found along the endomembrane system of eukaryotic cells and mediate palmitoylation of peripheral and integral membrane proteins. Here, we address the in vivo substrate specificity of five of the seven DHHC acyltransferases for peripheral membrane proteins by an overexpression approach. For all analysed DHHC proteins we detect strongly overlapping substrate specificity. In addition, we now show acyltransferase activity for Pfa5. More importantly, the DHHC protein Pfa3 is able to trap several substrates at the vacuole. For Pfa3 and its substrate Vac8, we can distinguish two consecutive steps in the acylation reaction: an initial binding that occurs independently of its central cysteine in the DHHC box, but requires myristoylation of its substrate Vac8, and a DHHC-motif dependent acylation. Our data also suggest that proteins can be palmitoylated on several organelles. Thus, the intracellular distribution of DHHC proteins provides an acyltransferase network, which may promote dynamic membrane association of substrate proteins.     

Myxinidin, A Novel Antimicrobial Peptide from the Epidermal Mucus of Hagfish, Myxine glutinosa L.

Fish epidermal mucus contains innate immune components that provide a first line of defense against various infectious pathogens. This study reports the bioassay-guided fractionation and characterization of a novel antimicrobial peptide, myxinidin, from the acidic epidermal mucus extract of hagfish (Myxine glutinosa L.). Edman sequencing and mass spectrometry revealed that myxinidin consists of 12 amino acids and has a molecular mass of 1,327.68 Da. Myxinidin showed activity against a broad range of bacteria and yeast pathogens at minimum bactericidal concentration (MBC) ranging from 1.0 to 10.0 μg/mL. Screened pathogens, Salmonella enterica serovar Typhimurium C610, Escherichia coli D31, Aeromonas salmonicida A449, Yersinia ruckeri 96-4, and Listonella anguillarum 02-11 were found to be highly sensitive to myxinidin at the MBC of 1.0–2.5 μg/mL; Staphylococcus epidermis C621 and yeast (Candida albicans C627) had an MBC of 10.0 μg/mL. The antimicrobial activity of myxinidin was found to be two to 16 times more active than a potent fish-derived antimicrobial peptide, pleurocidin (NRC-17), against most of the screened pathogens. The microbicidal activity of myxinidin was retained in the presence of sodium chloride (NaCl) at concentrations up to 0.3 M and had no hemolytic activity against mammalian red blood cells. These results suggest that myxinidin may have potential applications in fish and human therapeutics.     

Novel neutral network approach to call admission control in high-speed networks

This paper presents a novel Call Admission Control (CAC) scheme which adopts the neural network approach, namely Minimal Resource Allocation Network (MRAN) and its extended version EMRAN. Though the current focus is on the Call Admission Control (CAC) for Asynchronous Transfer Mode (ATM) networks, the scheme is applicable to most high-speed networks. As there is a need for accurate estimation of the required bandwidth for different services, the proposed scheme can offer a simple design procedure and provide a better control in fulfilling the Quality of Service (QoS) requirements. MRAN and EMRAN are on-line learning algorithms to facilitate efficient admission control in different traffic environments. Simulation results show that the proposed CAC schemes are more efficient than the two conventional CAC approaches, the Peak Bandwidth Allocation scheme and the Cell Loss Ratio (CLR) upperbound formula scheme. The prediction precision and computational time of MRAN and EMRAN algorithms are also investigated. Both MRAN and EMRAN algorithms yield similar performance results, but the EMRAN algorithm has less computational load.     

Transfer of severe experimental autoimmune encephalomyelitis by IL-12- and IL-18-potentiated T cells is estrogen sensitive

The aim of this study was to evaluate the roles of IL-18 and IL-12 in potentiating the encephalitogenic activity of T cell lines specific for myelin oligodendrocyte glycoprotein (MOG(35-55)). MOG-specific T cells stimulated with anti-CD3 and anti-CD28 in the presence of IL-12 or IL-18 alone transferred only mild experimental autoimmune encephalomyelitis (EAE) into a low percentage of recipients. However, T cells cocultured with both cytokines transferred aggressive clinical and histological EAE into all recipients. Coculture of T cells with IL-12 enhanced the secretion of IFN-gamma, but not TNF-alpha, whereas coculture with IL-18 enhanced the secretion of TNF-alpha, but not INF-gamma. However, coculture with both IL-18 and IL-12 induced high levels of both TNF-alpha and IFN-gamma. Additionally, IL-12 selectively enhanced mRNA expression of CCR5, whereas IL-18 selectively enhanced the expression of CCR4 and CCR7, and CCR4 and CCR5 were coexpressed on the surface of T cells cocultured with IL-12 and IL-18. Finally, estrogen treatment, previously found to inhibit both TNF-alpha and IFN-gamma production, completely abrogated all signs of passive EAE. These data demonstrate that optimal potentiation of encephalitogenic activity can be achieved by conditioning MOG-specific T cells with the combination of IL-12 and IL-18, which, respectively, induce the secretion of IFN-gamma/CCR5 and TNF-alpha/CCR4/CCR7, and that estrogen treatment, which is known to inhibit both proinflammatory cytokines, can completely ablate this aggressive form of passive EAE.     

Multiple sulfatase deficiency is caused by mutations in the gene encoding the human C(alpha)-formylglycine generating enzyme

C(alpha)-formylglycine (FGly) is the catalytic residue in the active site of eukaryotic sulfatases. It is posttranslationally generated from a cysteine in the endoplasmic reticulum. The genetic defect of FGly formation causes multiple sulfatase deficiency (MSD), a lysosomal storage disorder. We purified the FGly generating enzyme (FGE) and identified its gene and nine mutations in seven MSD patients. In patient fibroblasts, the activity of sulfatases is partially restored by transduction of FGE encoding cDNA, but not by cDNA carrying an MSD mutation. The gene encoding FGE is highly conserved among pro- and eukaryotes and has a paralog of unknown function in vertebrates. FGE is localized in the endoplasmic reticulum and is predicted to have a tripartite domain structure.