Dating Violence and Self-Efficacy for Delayed Sex among Adolescents in Cape Town, South Africa

In South Africa, dating violence is known to be widespread among  adolescents, and is therefore a major public health issue because of its association with sexual risk behaviours. The objective of the study was to examine the relationship between dating violence and self-efficacy for  delayed sex among school-going adolescents in Cape Town, South Africa. The study is based on analyses of data from a school-based health  education programme targeting sexual and reproductive health issues.The study involved 3,655 school-going adolescents aged between 12 and 17 in Cape Town, South Africa. The data was collected by means of a  self-administered questionnaire composed of 153 items on sexual and reproductive health, dating violence as well as socio-demographic  characteristics. The results indicated that males showed a higher  percentage of both dating violence victimization and perpetration, as  compared to females. It was also found that adolescents from lower socio-economic backgrounds were more likely to be the victims of dating violence as compared to those from a higher socio-economic background. Female learners showed higher levels of self-efficacy for delayed sex than their male counterparts. Although the result revealed that there was a significant association between self-efficacy for delayed sex and socio-economic  status, this link decreased with age. It is concluded that educational  programmes aimed solely at improving self-efficacy for delayed sex is insufficient. Such programmes must also aim at preventing dating violence  and equipping adolescents with the skills to negotiate their way out of dating violence. Afr J Reprod Health 2014; 18[2]: 46-57).Keywords: STI, HIV, Sexual Risk Behavior, Sexual Debut, Coerced Se

From Agroforestry to Agroindustry: Smallholder Access to Benefits From Oil Palm in Ghana and the Implications for Sustainability Certification

Oil palm production in Ghana—which is primarily cultivated by smallholders (60%+)—plays an important role in local economies and rural livelihoods. As a multi-functional crop, it is embedded in the everyday life of rural and urban Ghanaians both by individual households and on an industrial level. The sector is currently experiencing a resurgence under Ghana's New Patriotic Party (NPP) rule and is being targeted by the Roundtable on Sustainable Palm Oil (RSPO) for yield intensification and increased export production. End goals of these efforts include poverty alleviation, environmentally responsible development efforts, and agricultural diversification in rural areas. We apply Ribot and Peluso's “theory of access” (2003) to assess the barriers and opportunities for smallholder oil palm farmers, and the degree to which these are addressed by RSPO interventions. Our results highlight how Ghanaian smallholders gain many benefits from palm oil production as a source of regular income, a drought-resilient crop, and a source of cooking oil for household use. However, they also report different levels of access to finance, markets, land, and technical support, along with differing views and visions of the oil palm sector's development. The focus of governmental and RSPO initiatives on international trade-based incentives overlooks this diversity and, in particular, the importance of local markets for Ghanaian livelihoods. This poses a threat to women millers and traders, poorer producers, and the local markets they supply who risk losing access to the palm oil supply chain. More generally, these findings illustrate the importance of understanding how markets interact at multiple local to international scales, in order to design interventions that will more equitably reach and benefit local communities

Experimental sheep BSE prions generate the vCJD phenotype when serially passaged in transgenic mice expressing human prion protein

The epizootic prion disease of cattle, bovine spongiform encephalopathy (BSE), causes variant Creutzfeldt-Jakob disease (vCJD) in humans following dietary exposure. While it is assumed that all cases of vCJD attributed to a dietary aetiology are related to cattle BSE, sheep and goats are susceptible to experimental oral challenge with cattle BSE prions and farmed animals in the UK were undoubtedly exposed to BSE-contaminated meat and bone meal during the late 1980s and early 1990s. Although no natural field cases of sheep BSE have been identified, it cannot be excluded that some BSE-infected sheep might have entered the European human food chain. Evaluation of the zoonotic potential of sheep BSE prions has been addressed by examining the transmission properties of experimental brain isolates in transgenic mice that express human prion protein, however to-date there have been relatively few studies. Here we report that serial passage of experimental sheep BSE prions in transgenic mice expressing human prion protein with methionine at residue 129 produces the vCJD phenotype that mirrors that seen when the same mice are challenged with vCJD prions from patient brain. These findings are congruent with those reported previously by another laboratory, and thereby strongly reinforce the view that sheep BSE prions could have acted as a causal agent of vCJD within Europe

Pesticide exposures in a malarious and predominantly farming area in Central Ghana

In areas where malaria is endemic, pesticides are widely deployed for vector control, which has contributed to reductions in malaria deaths. Pesticide use for agrarian purposes reduces pest populations, thus improving crop production and post-harvest losses. However, adverse health effects have been associated with pesticide exposure, ranging from skin irritation to neurotoxicity and carcinogenicity. Though misuse of these pesticides can lead to widespread potential dangers, the debilitating effects are usually underappreciated in many developing countries. To evaluate the pattern of pesticide usage among rural communities in the Kintampo area of Ghana, a cross-sectional survey was conducted among 1455 heads of households randomly sampled from among 29,073 households in the Kintampo Health and Demographic Surveillance System area of Ghana to estimate the prevalence of pesticide use and indications for use among this rural populace. Seventy-one percent (1040/1455) of household heads reported having used pesticides on either their farms or homes, most commonly for control of weeds (96.4%, 1003/1040) or insects (85.4%, 888/1040). Dichlorodiphenyltrichloroethane (DDT) was used by 22.9% (238/1040) of respondents. The majority of households who reported use of pesticides said women in their households assisted in the spraying efforts (69.3%, 721/1040); of these women, 50.8% (366/721) did so while carrying their babies on their backs. Only 28.9% (301/1040) of the study participants wore protective devices during pesticide applications. Frequent symptoms that were reported after spraying, included cough (32.3%; 336/1040), difficulty in breathing (26.7%; 278/1040) and skin irritation (39.0%; 406/1040). Pesticide use among community members in the Kintampo area of Ghana is common and its potential health impacts warrant further investigation.Key words: Pesticide, malaria, prevalence, Kintampo, dichlorodiphenyltrichloroethane

Frontotemporal dementia caused by CHMP2B mutation is characterised by neuronal lysosomal storage pathology

Mutations in the charged multivesicular body protein 2B (CHMP2B) cause frontotemporal dementia (FTD). We report that mice which express FTD-causative mutant CHMP2B at physiological levels develop a novel lysosomal storage pathology characterised by large neuronal autofluorescent aggregates. The aggregates are an early and progressive pathology that occur at 3 months of age and increase in both size and number over time. These autofluorescent aggregates are not observed in mice expressing wild-type CHMP2B, or in non-transgenic controls, indicating that they are a specific pathology caused by mutant CHMP2B. Ultrastructural analysis and immuno- gold labelling confirmed that they are derived from the endolysosomal system. Consistent with these findings, CHMP2B mutation patient brains contain morphologically similar autofluorescent aggregates. These aggregates occur significantly more frequently in human CHMP2B mutation brain than in neurodegenerative disease or age-matched control brains. These data suggest that lysosomal storage pathology is the major neuronal pathology in FTD caused by CHMP2B mutation. Recent evidence suggests that two other genes associated with FTD, GRN and TMEM106B are important for lysosomal function. Our identification of lysosomal storage pathology in FTD caused by CHMP2B mutation now provides evidence that endolysosomal dysfunction is a major degenerative pathway in FTD

Humanised transgenic mice are resistant to chronic wasting disease prions from Norwegian reindeer and moose

Chronic wasting disease (CWD) is the transmissible spongiform encephalopathy or prion disease affecting cervids. In 2016 the first cases of CWD were reported in Europe in Norwegian wild reindeer and moose. The origin and zoonotic potential of these new prion isolates remain unknown. In this study to investigate zoonotic potential we inoculated brain tissue from CWD-infected Norwegian reindeer and moose into transgenic mice overexpressing human prion protein. After prolonged post-inoculation survival periods no evidence for prion transmission was seen suggesting that the zoonotic potential of these isolates is low

Transmission characteristics of heterozygous cases of Creutzfeldt-Jakob disease with variable abnormal prion protein allotypes

In the human prion disease Creutzfeldt-Jakob disease (CJD), different CJD neuropathological subtypes are defined by the presence in normal prion protein (PrPC) of a methionine or valine at residue 129, by the molecular mass of the infectious prion protein PrPSc, by the pattern of PrPSc deposition, and by the distribution of spongiform change in the brain. Heterozygous cases of CJD potentially add another layer of complexity to defining CJD subtypes since PrPSc can have either a methionine (PrPSc-M129) or valine (PrPSc-V129) at residue 129. We have recently demonstrated that the relative amount of PrPSc-M129 versus PrPSc-V129, i.e. the PrPSc allotype ratio, varies between heterozygous CJD cases. In order to determine if differences in PrPSc allotype correlated with different disease phenotypes, we have inoculated 10 cases of heterozygous CJD (7 sporadic and 3 iatrogenic) into two transgenic mouse lines overexpressing PrPC with a methionine at codon 129. In one case, brain-region specific differences in PrPSc allotype appeared to correlate with differences in prion disease transmission and phenotype. In the other 9 cases inoculated, the presence of PrPSc-V129 was associated with plaque formation but differences in PrPSc allotype did not consistently correlate with disease incubation time or neuropathology. Thus, while the PrPSc allotype ratio may contribute to diverse prion phenotypes within a single brain, it does not appear to be a primary determinative factor of disease phenotype

Interaction between prion protein and toxic amyloid beta assemblies can be therapeutically targeted at multiple sites

A role for PrP in the toxic effect of oligomeric forms of A beta, implicated in Alzheimer's disease (AD), has been suggested but remains controversial. Here we show that PrP is required for the plasticity-impairing effects of ex vivo material from human AD brain and that standardized A beta-derived diffusible ligand (ADDL) preparations disrupt hippocampal synaptic plasticity in a PrP-dependent manner. We screened a panel of anti-PrP antibodies for their ability to disrupt the ADDL-PrP interaction. Antibodies directed to the principal PrP/A beta-binding site and to PrP helix-1, were able to block A beta binding to PrP suggesting that the toxic A beta species are of relatively high molecular mass and/or may bind multiple PrP molecules. Two representative and extensively characterized monoclonal antibodies directed to these regions, ICSM-35 and ICSM-18, were shown to block the A beta-mediated disruption of synaptic plasticity validating these antibodies as candidate therapeutics for AD either individually or in combination

A naturally occurring variant of the human prion protein completely prevents prion disease

Mammalian prions, transmissible agents causing lethal neurodegenerative diseases, are composed of assemblies of misfolded cellular prion protein (PrP)1. A novel PrP variant, G127V, was under positive evolutionary selection during the epidemic of kuru—an acquired prion disease epidemic of the Fore population in Papua New Guinea—and appeared to provide strong protection against disease in the heterozygous state2. Here we have investigated the protective role of this variant and its interaction with the common, worldwide M129V PrP polymorphism. V127 was seen exclusively on a M129 PRNP allele. We demonstrate that transgenic mice expressing both variant and wild-type human PrP are completely resistant to both kuru and classical Creutzfeldt–Jakob disease (CJD) prions (which are closely similar) but can be infected with variant CJD prions, a human prion strain resulting from exposure to bovine spongiform encephalopathy prions to which the Fore were not exposed. Notably, mice expressing only PrP V127 were completely resistant to all prion strains, demonstrating a different molecular mechanism to M129V, which provides its relative protection against classical CJD and kuru in the heterozygous state. Indeed, this single amino acid substitution (G→V) at a residue invariant in vertebrate evolution is as protective as deletion of the protein. Further study in transgenic mice expressing different ratios of variant and wild-type PrP indicates that not only is PrP V127 completely refractory to prion conversion but acts as a potent dose-dependent inhibitor of wild-type prion propagation

De Novo Generation of Infectious Prions In Vitro Produces a New Disease Phenotype

Prions are the proteinaceous infectious agents responsible for Transmissible Spongiform Encephalopathies. Compelling evidence supports the hypothesis that prions are composed exclusively of a misfolded version of the prion protein (PrPSc) that replicates in the body in the absence of nucleic acids by inducing the misfolding of the cellular prion protein (PrPC). The most common form of human prion disease is sporadic, which appears to have its origin in a low frequency event of spontaneous misfolding to generate the first PrPSc particle that then propagates as in the infectious form of the disease. The main goal of this study was to mimic an early event in the etiology of sporadic disease by attempting de novo generation of infectious PrPSc in vitro. For this purpose we analyzed in detail the possibility of spontaneous generation of PrPSc by the protein misfolding cyclic amplification (PMCA) procedure. Under standard PMCA conditions, and taking precautions to avoid cross-contamination, de novo generation of PrPSc was never observed, supporting the use of the technology for diagnostic applications. However, we report that PMCA can be modified to generate PrPSc in the absence of pre-existing PrPSc in different animal species at a low and variable rate. De novo generated PrPSc was infectious when inoculated into wild type hamsters, producing a new disease phenotype with unique clinical, neuropathological and biochemical features. Our results represent additional evidence in support of the prion hypothesis and provide a simple model to study the mechanism of sporadic prion disease. The findings also suggest that prion diversity is not restricted to those currently known, and that likely new forms of infectious protein foldings may be produced, resulting in novel disease phenotypes