222 research outputs found

    Private Sector Participation and Health System Performance in Sub-Saharan Africa

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    BACKGROUND: The role of the private health sector in developing countries remains a much-debated and contentious issue. Critics argue that the high prices charged in the private sector limits the use of health care among the poorest, consequently reducing access and equity in the use of health care. Supporters argue that increased private sector participation might improve access and equity by bringing in much needed resources for health care and by allowing governments to increase focus on underserved populations. However, little empirical exists for or against either side of this debate. METHODOLOGY/PRINCIPAL FINDINGS: We examine the association between private sector participation and self-reported measures of utilization and equity in deliveries and treatment of childhood respiratory disease using regression analysis, across a sample of nationally-representative Demographic and Health Surveys from 34 SSA economies. We also examine the correlation between private sector participation and key background factors (socioeconomic development, business environment and governance) and use multivariate regression to control for potential confounders. Private sector participation is positively associated with greater overall access and reduced disparities between rich and poor as well as urban and rural populations. The positive association between private sector participation and improved health system performance is robust to controlling for confounders including per capita income and maternal education. Private sector participation is positively correlated with measures of socio-economic development and favorable business environment. CONCLUSIONS/SIGNIFICANCE: Greater participation is associated with favorable intermediate outcomes in terms of access and equity. While these results do not establish a causal link between private sector participation and health system performance, they suggest that there is no deleterious link between private sector participation and health system performance in SSA

    Healthy Firms: Constraints to Growth among Private Health Sector Facilities in Ghana and Kenya

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    Background: Health outcomes in developing countries continue to lag the developed world, and many countries are not on target to meet the Millennium Development Goals. The private health sector provides much of the care in many developing countries (e.g., approximately 50 percent in Sub-Saharan Africa), but private providers are often poorly integrated into the health system. Efforts to improve health systems performance will need to include the private sector and increase its contributions to national health goals. However, the literature on constraints private health care providers face is limited. Methodology/Principal Findings: We analyze data from a survey of private health facilities in Kenya and Ghana to evaluate growth constraints facing private providers. A significant portion of facilities (Ghana: 62 percent; Kenya: 40 percent) report limited access to finance as the most significant barrier they face; only a small minority of facilities report using formal credit institutions to finance day to day operations (Ghana: 6 percent; Kenya: 11 percent). Other important barriers include corruption, crime, limited demand for goods and services, and poor public infrastructure. Most facilities have paper-based rather than electronic systems for patient records (Ghana: 30 percent; Kenya: 22 percent), accounting (Ghana: 45 percent; Kenya: 27 percent), and inventory control (Ghana: 41 percent; Kenya: 24 percent). A majority of clinics in both countries report undertaking activities to improve provider skills and to monitor the level and quality of care they provide. However, only a minority of pharmacies report undertaking such activities

    Investigating determinants of out-of-pocket spending and strategies for coping with payments for healthcare in southeast Nigeria

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    <p>Abstract</p> <p>Background</p> <p>Out-of-pocket spending (OOPS) is the major payment strategy for healthcare in Nigeria. Hence, the paper assessed the determinants socio-economic status (SES) of OOPS and strategies for coping with payments for healthcare in urban, semi-urban and rural areas of southeast Nigeria. This paper provides information that would be required to improve financial accessibility and equity in financing within the public health care system.</p> <p>Methods</p> <p>The study areas were three rural and three urban areas from Ebonyi and Enugu states in South-east Nigeria. Cross-sectional survey using interviewer-administered questionnaires to randomly selected householders was the study tool. A socio-economic status (SES) index that was developed using principal components analysis was used to examine levels of inequity in OOPS and regression analysis was used to examine the determinants of use of OOPS.</p> <p>Results</p> <p>All the SES groups equally sought healthcare when they needed to. However, the poorest households were most likely to use low level and informal providers such as traditional healers, whilst the least poor households were more likely to use the services of higher level and formal providers such as health centres and hospitals. The better-off SES more than worse-off SES groups used OOPS to pay for healthcare. The use of own money was the commonest payment-coping mechanism in the three communities. The sales of movable household assets or land were not commonly used as payment-coping mechanisms. Decreasing SES was associated with increased sale of household assets to cope with payment for healthcare in one of the communities. Fee exemptions and subsidies were almost non-existent as coping mechanisms in this study</p> <p>Conclusions</p> <p>There is the need to reduce OOPS and channel and improve equity in healthcare financing by designing and implementing payment strategies that will assure financial risk protection of the poor such pre-payment mechanisms with government paying for the poor.</p

    The P-Loop Domain of Yeast Clp1 Mediates Interactions Between CF IA and CPF Factors in Pre-mRNA 3′ End Formation

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    Cleavage factor IA (CF IA), cleavage and polyadenylation factor (CPF), constitute major protein complexes required for pre-mRNA 3′ end formation in yeast. The Clp1 protein associates with Pcf11, Rna15 and Rna14 in CF IA but its functional role remained unclear. Clp1 carries an evolutionarily conserved P-loop motif that was previously shown to bind ATP. Interestingly, human and archaean Clp1 homologues, but not the yeast protein, carry 5′ RNA kinase activity. We show that depletion of Clp1 in yeast promoted defective 3′ end formation and RNA polymerase II termination; however, cells expressing Clp1 with mutant P-loops displayed only minor defects in gene expression. Similarly, purified and reconstituted mutant CF IA factors that interfered with ATP binding complemented CF IA depleted extracts in coupled in vitro transcription/3′ end processing reactions. We found that Clp1 was required to assemble recombinant CF IA and that certain P-loop mutants failed to interact with the CF IA subunit Pcf11. In contrast, mutations in Clp1 enhanced binding to the 3′ endonuclease Ysh1 that is a component of CPF. Our results support a structural role for the Clp1 P-loop motif. ATP binding by Clp1 likely contributes to CF IA formation and cross-factor interactions during the dynamic process of 3′ end formation

    The interaction of Pcf11 and Clp1 is needed for mRNA 3′-end formation and is modulated by amino acids in the ATP-binding site

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    Polyadenylation of eukaryotic mRNAs contributes to stability, transport and translation, and is catalyzed by a large complex of conserved proteins. The Pcf11 subunit of the yeast CF IA factor functions as a scaffold for the processing machinery during the termination and polyadenylation of transcripts. Its partner, Clp1, is needed for mRNA processing, but its precise molecular role has remained enigmatic. We show that Clp1 interacts with the Cleavage–Polyadenylation Factor (CPF) through its N-terminal and central domains, and thus provides cross-factor connections within the processing complex. Clp1 is known to bind ATP, consistent with the reported RNA kinase activity of human Clp1. However, substitution of conserved amino acids in the ATP-binding site did not affect cell growth, suggesting that the essential function of yeast Clp1 does not involve ATP hydrolysis. Surprisingly, non-viable mutations predicted to displace ATP did not affect ATP binding but disturbed the Clp1–Pcf11 interaction. In support of the importance of this interaction, a mutation in Pcf11 that disrupts the Clp1 contact caused defects in growth, 3′-end processing and transcription termination. These results define Clp1 as a bridge between CF IA and CPF and indicate that the Clp1–Pcf11 interaction is modulated by amino acids in the conserved ATP-binding site of Clp1

    RNA deep sequencing reveals differential MicroRNA expression during development of sea urchin and sea star

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    microRNAs (miRNAs) are small (20-23 nt), non-coding single stranded RNA molecules that act as post-transcriptional regulators of mRNA gene expression. They have been implicated in regulation of developmental processes in diverse organisms. The echinoderms, Strongylocentrotus purpuratus (sea urchin) and Patiria miniata (sea star) are excellent model organisms for studying development with well-characterized transcriptional networks. However, to date, nothing is known about the role of miRNAs during development in these organisms, except that the genes that are involved in the miRNA biogenesis pathway are expressed during their developmental stages. In this paper, we used Illumina Genome Analyzer (Illumina, Inc.) to sequence small RNA libraries in mixed stage population of embryos from one to three days after fertilization of sea urchin and sea star (total of 22,670,000 reads). Analysis of these data revealed the miRNA populations in these two species. We found that 47 and 38 known miRNAs are expressed in sea urchin and sea star, respectively, during early development (32 in common). We also found 13 potentially novel miRNAs in the sea urchin embryonic library. miRNA expression is generally conserved between the two species during development, but 7 miRNAs are highly expressed in only one species. We expect that our two datasets will be a valuable resource for everyone working in the field of developmental biology and the regulatory networks that affect it. The computational pipeline to analyze Illumina reads is available at http://www.benoslab.pitt.edu/services.html. © 2011 Kadri et al

    Genome-wide search for breast cancer linkage in large Icelandic non-BRCA1/2 families

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    Abstract Introduction: A significant proportion of high-risk breast cancer families are not explained by mutations in known genes. Recent genome-wide searches (GWS) have not revealed any single major locus reminiscent of BRCA1 and BRCA2, indicating that still unidentified genes may explain relatively few families each or interact in a way obscure to linkage analyses. This has drawn attention to possible benefits of studying populations where genetic heterogeneity might be reduced. We thus performed a GWS for linkage on nine Icelandic multiple-case non-BRCA1/2 families of desirable size for mapping highly penetrant loci. To follow up suggestive loci, an additional 13 families from other Nordic countries were genotyped for selected markers. Methods: GWS was performed using 811 microsatellite markers providing about five centiMorgan (cM) resolution. Multipoint logarithm of odds (LOD) scores were calculated using parametric and nonparametric methods. For selected markers and cases, tumour tissue was compared to normal tissue to look for allelic loss indicative of a tumour suppressor gene. Results: The three highest signals were located at chromosomes 6q, 2p and 14q. One family contributed suggestive LOD scores (LOD 2.63 to 3.03, dominant model) at all these regions, without consistent evidence of a tumour suppressor gene. Haplotypes in nine affected family members mapped the loci to 2p23.2 to p21, 6q14.2 to q23.2 and 14q21.3 to q24.3. No evidence of a highly penetrant locus was found among the remaining families. The heterogeneity LOD (HLOD) at the 6q, 2p and 14q loci in all families was 3.27, 1.66 and 1.24, respectively. The subset of 13 Nordic families showed supportive HLODs at chromosome 6q (ranging from 0.34 to 1.37 by country subset). The 2p and 14q loci overlap with regions indicated by large families in previous GWS studies of breast cancer. Conclusions: Chromosomes 2p, 6q and 14q are candidate sites for genes contributing together to high breast cancer risk. A polygenic model is supported, suggesting the joint effect of genes in contributing to breast cancer risk to be rather common in non-BRCA1/2 families. For genetic counselling it would seem important to resolve the mode of genetic interaction
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