Staff perspectives of barriers to women accessing birthing services in Nepal: A qualitative study

Background: Nepal has made significant progress with regard to reducing the maternal mortality ratio but a major challenge remains the under-utilisation of skilled birth attendants who are predominantly facility based. Studies have explored women's views of the barriers to facility birth; however the voices of staff who offer services have not been studied in detail. This research explores the views of staff as to the key reasons why pregnant women do not give birth in a maternity-care facility. Methods: This mixed methods study comprised qualitative interviews and non-participant observation. The study was conducted in two small non-governmental hospitals, one semi-rural and one urban, in Kathmandu Valley. Twenty interviews were conducted with health care providers and other staff in these hospitals. The interviews were undertaken with the aid of a Nepali translator, with some interviews being held in English. Twenty-five hours of non-participant observation was conducted in both maternity hospitals . Both observation and interview data were analysed thematically. Ethical approval was granted by the Nepal Research Health Council and Bournemouth University's Ethics Committee. Results: Key themes that emerged from the analysis reflected barriers that women experience in accessing services at different conceptual levels and resembled the three phases of delay model by Thaddeus and Maine. This framework is used to present the barriers. First Phase Delays are: 1) lack of awareness that the facility/services exist; 2) women being too busy to attend; 3) poor services; 4) embarrassment; and 5) financial issues. Themes for the second Phase of Delay are: 1) birthing on the way; and 2) by-passing the facility in favour of one further away. The final Phase involved: 1) absence of an enabling environment; and 2) disrespectful care. Conclusion: This study highlights a multitude of barriers, not all of the same importance or occuring at the same time in the pregnancy journey. It is clear that staff are aware of many of the barriers for women in reaching the facility to give birth, and these fit with previous literature of women's views. However, staff had limited insight into barriers occuring within the facility itself and were more likely to suggest that this was a problem for other institutions and not theirs

Protective Role of Taurine against Arsenic-Induced Mitochondria-Dependent Hepatic Apoptosis via the Inhibition of PKCδ-JNK Pathway

BACKGROUND: Oxidative stress-mediated hepatotoxic effect of arsenic (As) is mainly due to the depletion of glutathione (GSH) in liver. Taurine, on the other hand, enhances intracellular production of GSH. Little is known about the mechanism of the beneficial role of taurine in As-induced hepatic pathophysiology. Therefore, in the present study we investigated its beneficial role in As-induced hepatic cell death via mitochondria-mediated pathway. METHODOLOGY/PRINCIPAL FINDINGS: Rats were exposed to NaAsO(2) (2 mg/kg body weight for 6 months) and the hepatic tissue was used for oxidative stress measurements. In addition, the pathophysiologic effect of NaAsO(2) (10 microM) on hepatocytes was evaluated by determining cell viability, mitochondrial membrane potential and ROS generation. As caused mitochondrial injury by increased oxidative stress and reciprocal regulation of Bcl-2, Bcl-xL/Bad, Bax, Bim in association with increased level of Apaf-1, activation of caspase 9/3, cleavage of PARP protein and ultimately led to apoptotic cell death. In addition, As markedly increased JNK and p38 phosphorylation with minimal disturbance of ERK. Pre-exposure of hepatocytes to a JNK inhibitor SP600125 prevented As-induced caspase-3 activation, ROS production and loss in cell viability. Pre-exposure of hepatocytes to a p38 inhibitor SB2035, on the other hand, had practically no effect on these events. Besides, As activated PKCdelta and pre-treatment of hepatocytes with its inhibitor, rottlerin, suppressed the activation of JNK indicating that PKCdelta is involved in As-induced JNK activation and mitochondrial dependent apoptosis. Oral administration of taurine (50 mg/kg body weight for 2 weeks) both pre and post to NaAsO(2) exposure or incubation of the hepatocytes with taurine (25 mM) were found to be effective in counteracting As-induced oxidative stress and apoptosis. CONCLUSIONS/SIGNIFICANCE: Results indicate that taurine treatment improved As-induced hepatic damages by inhibiting PKCdelta-JNK signalling pathways. Therefore taurine supplementation could provide a new approach for the reduction of hepatic complication due to arsenic poisoning

Berberine enhances inhibition of glioma tumor cell migration and invasiveness mediated by arsenic trioxide

<p>Abstract</p> <p>Background</p> <p>Arsenic trioxide (As₂O₃) exhibits promising anticarcinogenic activity in acute promyelocytic leukemic patients and induces apoptosis in various tumor cells <it>in vitro</it>. Here, we investigated the effect of the natural alkaloid berberine on As₂O₃-mediated inhibition of cancer cell migration using rat and human glioma cell lines.</p> <p>Methods</p> <p>The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to determine the viability of rat C6 and human U-87 glioma cells after treatment with As₂O₃or berberine, and after co-treatment with As₂O₃and berberine. The wound scratch and Boyden chamber assays were applied to determine the effect of As₂O₃and berberine on the migration capacity and invasiveness of glioma cancer cells. Zymography and Western blot analyses provided information on the effect of As₂O₃and berberine on the intracellular translocation and activation of protein kinase C (PKC), and some PKC-related downstream factors. Most assays were performed three times, independently, and data were analyzed using ANOVA.</p> <p>Results</p> <p>The cell viability studies demonstrated that berberine enhances As₂O₃-mediated inhibition of glioma cell growth after 24 h incubation. Untreated control cells formed a confluent layer, the formation of which was inhibited upon incubation with 5 μM As₂O₃. The latter effect was even more pronounced in the presence of 10 μM berberine. The As₂O₃-mediated reduction in motility and invasion of glioma cells was enhanced upon co-treatment with berberine. Furthermore, it has been reported that PKC isoforms influence the morphology of the actin cytoskeleton, as well as the activation of metalloproteases MT1-MMP and MMP-2, reported to be involved in cancer cell migration. Treatment of glioma cells with As₂O₃and berberine significantly decreased the activation of PKC α and ε and led to actin cytoskeleton rearrangements. The levels of two downstream transcription factors, myc and jun, and MT1-MMP and MMP-2 were also significantly reduced.</p> <p>Conclusion</p> <p>Upon co-treatment of glioma cells with As₂O₃and berberine, cancer cell metastasis can be significantly inhibited, most likely by blocking the PKC-mediated signaling pathway involved in cancer cell migration. This study is potentially interesting for the development of novel chemotherapeutic approaches in the treatment of malignant gliomas and cancer development in general.</p

A case study of physical and social barriers to hygiene and child growth in remote Australian Aboriginal communities

Background\ud Despite Australia's wealth, poor growth is common among Aboriginal children living in remote communities. An important underlying factor for poor growth is the unhygienic state of the living environment in these communities. This study explores the physical and social barriers to achieving safe levels of hygiene for these children.\ud \ud Methods\ud A mixed qualitative and quantitative approach included a community level cross-sectional housing infrastructure survey, focus groups, case studies and key informant interviews in one community.\ud \ud Results\ud We found that a combination of crowding, non-functioning essential housing infrastructure and poor standards of personal and domestic hygiene underlie the high burden of infection experienced by children in this remote community.\ud \ud Conclusion\ud There is a need to address policy and the management of infrastructure, as well as key parenting and childcare practices that allow the high burden of infection among children to persist. The common characteristics of many remote Aboriginal communities in Australia suggest that these findings may be more widely applicable