Injury-related South African mortality in children, 1981 - 1985

Data on all registered deaths in children < 15 years in the RSA (excluding Transkei, Bophuthatswana, Venda and Ciskei) were analysed for 1981 - 1985. Variations in age, sex and population group pattern for different causes of injury were evaluated. Injury accounted for 8% of deaths in children < 15 years and was the leading cause of death between the ages of 5 years and 14 years (accounting for 43% of deaths). Motor vehicle accidents were the most important cause of injury deaths in all age groups except < 1 year, when accidental choking and suffocation resulted in more deaths. Drowning accounted for 19% of injury deaths and burns for 11%. In 14% of injury deaths it was not determined if the injury was accidental or purposefuUy inflicted. In all age and population groups deaths among boys outnumbered girls. The impact and pattern of injury varied considerably between age and population groups and reasons for these findings are discussed

Carriage of Haemophilus influenzae in Cape Town children

Little is known about the epideIDiology of Haemophilus influenzae infections in South Africa. This study was designed to determine the prevalence, serotype distribution, antimicrobial susceptibility pattern and effect of age and hospitalisation on the carriage of H. influenzae in 322 Cape Town children.The overall and type b specific carriage rates in normal children (N =107) were 45,8% and 4,7% respectively. The yield following nasopharyngeal culture was twice that following throat culture (P < 0,001). Children hospitalised with tuberculosis (N =62) had significantly greater carriage rates, 66,1% and 37,1% respectively (P =0,02). Institutionalised mentally handicapped children (N =77) and children with tuberculosis attending an outpatient clinic (N =76) had lower carriage rates (P < 0,02). Antimicrobial resistance was a major problem only in children hospitalised with tuberculosis (rifampicin 100%, penicillin 43,9%, erythromycin 85,4%, co-trimoxazole 82,9%). This universal resistance to rifampicin has not been reported previously. There was no difference in the mean age of children with positive or negative cultures, with the exception of those hospitalised with tuberculosis. In this group children infected with type b were much younger (mean 19,7 months) than those with other and non-typeableinfections (32,1 months) and the non-infected(50,1 months) (P =0,04). Duration of hospitalisation or outpatient therapy in the patients with tuberculosis did not influence carriage rates.We conclude that carriage of H. influenzae in normal children is similar to that reported from other countries and that carriage, particularly of type b, in children hospitalised with tuberculosis was of significance and probably contributed to an outbreak of multi-resistant invasive H. influenzae disease in this group

Efficacy of a novel shark bycatch mitigation device in a tuna longline fishery

This is the final version. Available on open access from Cell Press via the DOI in this recordElasmobranchs (sharks, rays, and skates) are caught throughout fisheries globally, leading to over one-third of species being threatened with extinction1. Oceanic shark populations have undergone an average 71% decline over the last half century, owing to an 18-fold increase in relative fishing pressure2. Incidental capture or 'bycatch' is a primary driver of population declines, and poses an important challenge for species conservation3. This threat necessitates mitigation strategies that exist for sharks but are often focussed on haul-back and post-capture effects for longline fishing. We trialled a novel shark bycatch mitigation device ("SharkGuard") in a commercial longline fishery targeting bluefin tuna (Thunnus thynnus), where bycatch consists largely of blue sharks (Prionace glauca) and pelagic stingrays (Pteroplatytrygon violacea).Innovate U

The Possibility of Emersion of the Outer Layers in a Massive Star Simultaneously with Iron-Core Collapse: A Hydrodynamic Model

We analyze the behavior of the outer envelope in a massive star during and after the collapse of its iron core into a protoneutron star (PNS) in terms of the equations of one-dimensional spherically symmetric ideal hydrodynamics. The profiles obtained in the studies of the evolution of massive stars up to the final stages of their existence, immediately before a supernova explosion (Boyes et al. 1999), are used as the initial data for the distribution of thermodynamic quantities in the envelope.We use a complex equation of state for matter with allowances made for arbitrary electron degeneracy and relativity, the appearance of electron-positron pairs, the presence of radiation, and the possibility of iron nuclei dissociating into free nucleons and helium nuclei. We performed calculations with the help of a numerical scheme based on Godunov's method. These calculations allowed us to ascertain whether the emersion of the outer envelope in a massive star is possible through the following two mechanisms: first, the decrease in the gravitational mass of the central PNS through neutrino-signal emission and, second, the effect of hot nucleon bubbles, which are most likely formed in the PNS corona, on the envelope emersion. We show that the second mechanism is highly efficient in the range of acceptable masses of the nucleon bubbles ($\leq 0.01M_\odot$) simulated in our hydrodynamic calculations in a rough, spherically symmetric approximation.Comment: 14 pages, 11 figure

Fine-mapping identifies multiple prostate cancer risk loci at 5p15, one of which associates with TERT expression

Associations between single nucleotide polymorphisms (SNPs) at 5p15 and multiple cancer types have been reported. We have previously shown evidence for a strong association between prostate cancer (PrCa) risk and rs2242652 at 5p15, intronic in the telomerase reverse transcriptase (TERT) gene that encodes TERT. To comprehensively evaluate the association between genetic variation across this region and PrCa, we performed a fine-mapping analysis by genotyping 134 SNPs using a custom Illumina iSelect array or Sequenom MassArray iPlex, followed by imputation of 1094 SNPs in 22 301 PrCa cases and 22 320 controls in The PRACTICAL consortium. Multiple stepwise logistic regression analysis identified four signals in the promoter or intronic regions of TERT that independently associated with PrCa risk. Gene expression analysis of normal prostate tissue showed evidence that SNPs within one of these regions also associated with TERT expression, providing a potential mechanism for predisposition to disease

Cluster effect for SNP–SNP interaction pairs for predicting complex traits

Single nucleotide polymorphism (SNP) interactions are the key to improving polygenic risk scores. Previous studies reported several significant SNP–SNP interaction pairs that shared a common SNP to form a cluster, but some identified pairs might be false positives. This study aims to identify factors associated with the cluster effect of false positivity and develop strategies to enhance the accuracy of SNP–SNP interactions. The results showed the cluster effect is a major cause of false-positive findings of SNP–SNP interactions. This cluster effect is due to high correlations between a causal pair and null pairs in a cluster. The clusters with a hub SNP with a significant main effect and a large minor allele frequency (MAF) tended to have a higher false-positive rate. In addition, peripheral null SNPs in a cluster with a small MAF tended to enhance false positivity. We also demonstrated that using the modified significance criterion based on the 3 p-value rules and the bootstrap approach (3pRule + bootstrap) can reduce false positivity and maintain high true positivity. In addition, our results also showed that a pair without a significant main effect tends to have weak or no interaction. This study identified the cluster effect and suggested using the 3pRule + bootstrap approach to enhance SNP–SNP interaction detection accuracy

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Alcohol consumption and prostate cancer incidence and progression: A Mendelian randomisation study

Prostate cancer is the most common cancer in men in developed countries, and is a target for risk reduction strategies. The effects of alcohol consumption on prostate cancer incidence and survival remain unclear, potentially due to methodological limitations of observational studies. In this study, we investigated the associations of genetic variants in alcohol-metabolising genes with prostate cancer incidence and survival. We analysed data from 23,868 men with prostate cancer and 23,051 controls from 25 studies within the international PRACTICAL Consortium. Study-specific associations of 68 single nucleotide polymorphisms (SNPs) in 8 alcohol-metabolising genes (Alcohol Dehydrogenases (ADHs) and Aldehyde Dehydrogenases (ALDHs)) with prostate cancer diagnosis and prostate cancer-specific mortality, by grade, were assessed using logistic and Cox regression models, respectively. The data across the 25 studies were meta-analysed using fixed-effect and random-effects models. We found little evidence that variants in alcohol metabolising genes were associated with prostate cancer diagnosis. Four variants in two genes exceeded the multiple testing threshold for associations with prostate cancer mortality in fixed-effect meta-analyses. SNPs within ALDH1A2 associated with prostate cancer mortality were rs1441817 (fixed effects hazard ratio, HRfixed  = 0.78; 95% confidence interval (95%CI):0.66,0.91; p values = 0.002); rs12910509, HRfixed  = 0.76; 95%CI:0.64,0.91; p values = 0.003); and rs8041922 (HRfixed  = 0.76; 95%CI:0.64,0.91; p values = 0.002). These SNPs were in linkage disequilibrium with each other. In ALDH1B1, rs10973794 (HRfixed  = 1.43; 95%CI:1.14,1.79; p values = 0.002) was associated with prostate cancer mortality in men with low-grade prostate cancer. These results suggest that alcohol consumption is unlikely to affect prostate cancer incidence, but it may influence disease progression