Transmission of methicillin-resistant staphylococcus aureus in the long term care facilities in Hong Kong

Background The relative contribution of long term care facilities (LTCFs) and hospitals in the transmission of methicillin-resistant Staphylococcus aureus (MRSA) is unknown. Methods Concurrent MRSA screening and spa type analysis was performed in LTCFs and their network hospitals to estimate the rate of MRSA acquisition among residents during their stay in LTCFs and hospitals, by colonization pressure and MRSA transmission calculations. Results In 40 LTCFs, 436 (21.6%) of 2020 residents were identified as ‘MRSA-positive’. The incidence of MRSA transmission per 1000-colonization-days among the residents during their stay in LTCFs and hospitals were 309 and 113 respectively, while the colonization pressure in LTCFs and hospitals were 210 and 185 per 1000-patient-days respectively. MRSA spa type t1081 was the most commonly isolated linage in both LTCF residents (76/121, 62.8%) and hospitalized patients (51/87, 58.6%), while type t4677 was significantly associated with LTCF residents (24/121, 19.8%) compared with hospitalized patients (3/87, 3.4%) (p < 0.001). This suggested continuous transmission of MRSA t4677 among LTCF residents. Also, an inverse linear relationship between MRSA prevalence in LTCFs and the average living area per LTCF resident was observed (Pearson correlation −0.443, p = 0.004), with the odds of patients acquiring MRSA reduced by a factor of 0.90 for each 10 square feet increase in living area. Conclusions Our data suggest that MRSA transmission was more serious in LTCFs than in hospitals. Infection control should be focused on LTCFs in order to reduce the burden of MRSA carriers in healthcare settings.published_or_final_versio

Religion and HIV in Tanzania: Influence of Religious Beliefs on HIV stigma, Disclosure, and Treatment Attitudes.

Religion shapes everyday beliefs and activities, but few studies have examined its associations with attitudes about HIV. This exploratory study in Tanzania probed associations between religious beliefs and HIV stigma, disclosure, and attitudes toward antiretroviral (ARV) treatment. A self-administered survey was distributed to a convenience sample of parishioners (n = 438) attending Catholic, Lutheran, and Pentecostal churches in both urban and rural areas. The survey included questions about religious beliefs, opinions about HIV, and knowledge and attitudes about ARVs. Multivariate logistic regression analysis was performed to assess how religion was associated with perceptions about HIV, HIV treatment, and people living with HIV/AIDS. Results indicate that shame-related HIV stigma is strongly associated with religious beliefs such as the belief that HIV is a punishment from God (p < 0.01) or that people living with HIV/AIDS (PLWHA) have not followed the Word of God (p < 0.001). Most participants (84.2%) said that they would disclose their HIV status to their pastor or congregation if they became infected. Although the majority of respondents (80.8%) believed that prayer could cure HIV, almost all (93.7%) said that they would begin ARV treatment if they became HIV-infected. The multivariate analysis found that respondents' hypothetical willingness to begin ARV treatme was not significantly associated with the belief that prayer could cure HIV or with other religious factors. Refusal of ARV treatment was instead correlated with lack of secondary schooling and lack of knowledge about ARVs. The decision to start ARVs hinged primarily on education-level and knowledge about ARVs rather than on religious factors. Research results highlight the influence of religious beliefs on HIV-related stigma and willingness to disclose, and should help to inform HIV-education outreach for religious groups

A saturated map of common genetic variants associated with human height

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes(1). Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel(2)) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries.A large genome-wide association study of more than 5 million individuals reveals that 12,111 single-nucleotide polymorphisms account for nearly all the heritability of height attributable to common genetic variants

A saturated map of common genetic variants associated with human height.

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes1. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel2) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

Greater infarct size and more severe neurological deficit in transgenic mice overexpressing endothelin-1 in astrocytes after transient focal cerebral ischemia

Oral Presentatio

Transgenic mice overexpressing endothelin-1 in astrocytes display greater infarct size and more severe neurological deficit after transient focal cerebral ischemia

Poster PresentationOur preliminary studies demonstrated that endothelin-1 (ET-1) mRNA expression is increased in astrocyte-like and endothelial cells in experimentally induced hypoxia/ischemia. Therefore, we developed a transgenic mouse model to study the role of astrocytic ET-1 in cerebral injury by microinjection of a modified GFAP genomic cassette containing the mouse ET-1 cDNA. A total of 5 lines were generated. All embryos appeared to develop to full term since the number of animals being born followed Mendelian distribution. Two lines of mice, 3804 and 3808, show brain-specific transgene expression as revealed by both rt-PCR and Northern analyses. In line 3804, the brain ET-1 peptide level was increased by two folds. No obvious abnormalities were observed in the gross anatomy of the brain and cerebrovasculature of these transgenic mice. GFAP ICC also revealed no differences in the number of positively-stained astrocytes and their cellular distribution. Therefore, it appears that over-expression of ET-1 in the brain did not affect the development of the mouse embryo and the brain. However, upon focal cerebral ischemia induced by transient filament occlusion of the middle cerebral artery, transgenic mouse brains displayed an increase in infarct area and infarct volume percentages. A higher number of transgenic mice showed more severe neurological deficit when compared to their wildtype littermates. The present data suggested that overexpression of ET-1 in astrocytes may have adverse effects on the brain during cerebral ischemic injury. Supported by Research Grants Council Hong Kon

Endothelin-1 leads to increased necrotic cell density in the brain after transient focal cerebral ischemia

Presentation no. 206.12A transgenic (Tg) mouse model was developed to study the role of astrocytic endothelin-1 (ET-1) in cerebral injury. We have previously shown that this over-expression of ET-1 in the brain did not affect the development of the mouse embryo and the brain since no gross abnormalities were observed in Tg mouse brains. However, Tg mice displayed an increase in cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) as reported previously. By quantitative PCR analyses, we observed that wildtype (WT) animals displayed a 2.5 fold increase in ET-1 mRNA levels in the ipsilateral brain after MCAO as we expected whereas Tg mice showed a 17.5 fold increase in ET-1 mRNA levels when compared to WT animals under both sham-operation and MCAO. Interestingly, when we examined the brain sections of the MCAO animals, we observed that there were fewer apoptotic cells but more necrotic cells in the lesion core of cerebral infarct regions in Tg mice when compared to their WT littermates. Our data suggested that ET-1 overexpression resulted in larger infarct size with more severe neurological deficits and increased cell death after MCAO. Yet, the relatively higher density of necrotic vs. apoptotic cells in the lesion core suggested that ET-1 may contribute to increased necrotic cell density in the brain after transient focal cerebral ischemia. Supported by Research Grants Council (Hong Kong