EVALUATION OF THE PARENTERAL NUTRITION SERVICES IN HOSPITAL PULAU PINANG

Parenteral nutrition (PN

A framework for the successful implementation of food traceability systems in China

Implementation of food traceability systems in China faces many challenges due to the scale, diversity and complexity of China’s food supply chains. This study aims to identify critical success factors specific to the implementation of traceability systems in China. Twenty-seven critical success factors were identified in the literature. Interviews with managers at four food enterprises in a pre-study helped identify success criteria and five additional critical success factors. These critical success factors were tested through a survey of managers in eighty-three food companies. This study identifies six dimensions for critical success factors: laws, regulations and standards; government support; consumer knowledge and support; effective management and communication; top management and vendor support; and information and system quality

Distinct genetic architectures for syndromic and nonsyndromic congenital heart defects identified by exome sequencing.

Congenital heart defects (CHDs) have a neonatal incidence of 0.8-1% (refs. 1,2). Despite abundant examples of monogenic CHD in humans and mice, CHD has a low absolute sibling recurrence risk (∼2.7%), suggesting a considerable role for de novo mutations (DNMs) and/or incomplete penetrance. De novo protein-truncating variants (PTVs) have been shown to be enriched among the 10% of 'syndromic' patients with extra-cardiac manifestations. We exome sequenced 1,891 probands, including both syndromic CHD (S-CHD, n = 610) and nonsyndromic CHD (NS-CHD, n = 1,281). In S-CHD, we confirmed a significant enrichment of de novo PTVs but not inherited PTVs in known CHD-associated genes, consistent with recent findings. Conversely, in NS-CHD we observed significant enrichment of PTVs inherited from unaffected parents in CHD-associated genes. We identified three genome-wide significant S-CHD disorders caused by DNMs in CHD4, CDK13 and PRKD1. Our study finds evidence for distinct genetic architectures underlying the low sibling recurrence risk in S-CHD and NS-CHD

Sex Differences in Civilian Injury in Baghdad From 2003 to 2014: Results of a Randomized Household Cluster Survey.

OBJECTIVE: To examine sex differences in injury mechanisms, injury-related death, injury-related disability, and associated financial consequences in Baghdad since the 2003 invasion of Iraq to inform prevention initiatives, health policy, and relief planning. BACKGROUND: Reliable estimates of injury burden among civilians during conflict are lacking, particularly among vulnerable subpopulations, such as women. METHODS: A 2-stage, cluster randomized, community-based household survey was conducted in May 2014 to determine the civilian burden of injury in Baghdad since 2003. Households were surveyed regarding injury mechanisms, healthcare required, disability, deaths, connection to conflict, and resultant financial hardship. RESULTS: We surveyed 900 households (5148 individuals), reporting 553 injuries, 162 (29%) of which were injuries among women. The mean age of injury was higher among women compared with men (34 ± 21.3 vs 27 ± 16.5 years; P \u3c 0.001). More women than men were injured while in the home [104 (64%) vs 82 (21%); P \u3c 0.001]. Fewer women than men died from injuries [11 (6.8%) vs 77 (20%); P \u3c 0.001]; however, women were more likely than men to live with reduced function [101 (63%) vs 192 (49%); P = 0.005]. Of intentional injuries, women had higher rates of injury by shell fragments (41% vs 26%); more men were injured by gunshots [76 (41%) vs 6 (17.6%); P = .011). CONCLUSIONS: Women experienced fewer injuries than men in postinvasion Baghdad, but were more likely to suffer disability after injury. Efforts to improve conditions for injured women should focus on mitigating financial and provisional hardships, providing counseling services, and ensuring access to rehabilitation services

Germline Chd8 haploinsufficiency alters brain development in mouse

The chromatin remodeling gene CHD8 represents a central node in neurodevelopmental gene networks implicated in autism. We examined the impact of germline heterozygous frameshift Chd8 mutation on neurodevelopment in mice. Chd8+/del5 mice displayed normal social interactions with no repetitive behaviors but exhibited cognitive impairment correlated with increased regional brain volume, validating that phenotypes of Chd8+/del5 mice overlap pathology reported in humans with CHD8 mutations. We applied network analysis to characterize neurodevelopmental gene expression, revealing widespread transcriptional changes in Chd8+/del5 mice across pathways disrupted in neurodevelopmental disorders, including neurogenesis, synaptic processes and neuroimmune signaling. We identified a co-expression module with peak expression in early brain development featuring dysregulation of RNA processing, chromatin remodeling and cell-cycle genes enriched for promoter binding by Chd8, and we validated increased neuronal proliferation and developmental splicing perturbation in Chd8+/del5 mice. This integrative analysis offers an initial picture of the consequences of Chd8 haploinsufficiency for brain development

Germline Chd8 haploinsufficiency alters brain development in mouse.

The chromatin remodeling gene CHD8 represents a central node in neurodevelopmental gene networks implicated in autism. We examined the impact of germline heterozygous frameshift Chd8 mutation on neurodevelopment in mice. Chd8+/del5 mice displayed normal social interactions with no repetitive behaviors but exhibited cognitive impairment correlated with increased regional brain volume, validating that phenotypes of Chd8+/del5 mice overlap pathology reported in humans with CHD8 mutations. We applied network analysis to characterize neurodevelopmental gene expression, revealing widespread transcriptional changes in Chd8+/del5 mice across pathways disrupted in neurodevelopmental disorders, including neurogenesis, synaptic processes and neuroimmune signaling. We identified a co-expression module with peak expression in early brain development featuring dysregulation of RNA processing, chromatin remodeling and cell-cycle genes enriched for promoter binding by Chd8, and we validated increased neuronal proliferation and developmental splicing perturbation in Chd8+/del5 mice. This integrative analysis offers an initial picture of the consequences of Chd8 haploinsufficiency for brain development