Financial Intermediation by Microfinance Banks in Rural Sub-Saharan Africa: Financial Intermediation Theoretical Approach

Premised on Meta analysis of financial intermediation theory by Gurley and Shaw (1960), Leland and Pyle (1977), Diamond and Dybvig (1983), Allen and Santomero (1996), Scholtens and van Wensveen (2000), the main purpose of this study is to test for the predictive power of each of the dimensions of financial intermediation of market penetration and quality of financial services on financial inclusion of the poor by microfinance banks in rural sub-Saharan Africa grounded on the financial intermediation theory. This study adopted a cross-sectional research design and data were collected from 400 poor households located in rural Uganda. The data were analyzed using ordinary least square hierarchical regression (OLS) in SPSS (statistical packages for social sciences) to generate the explanatory power of each of the dimensions of financial intermediation on financial inclusion based on coefficient of determination (R²). In addition, results from analysis of variances (ANOVA) were also generated to establish the differences in the perceptions of the poor towards being financially included through financial intermediation. The results revealed that market penetration and quality of financial services as dimensions of financial intermediation significantly explains 22 percent of the variation in financial inclusion of the poor in rural Uganda. Additionally, when individual effects were considered, both market penetration and quality of financial services had significant and positive effects on financial inclusion of the poor in rural Uganda. Accordingly, our study contributes and recommends specific policies toward the role of financial intermediaries in financial deepening, especially in rural sub-Saharan Africa where there are limited presence of traditional banking structures to serve the unbanked rural poor households

Prevalence and factors associated with hypertension among people living with HIV/AIDS on antiretroviral therapy in Uganda.

INTRODUCTION: antiretroviral therapy (ART) has improved survival of People Living with HIV (PLWH); however, this has resulted in an increasingly high prevalence of non-communicable diseases (NCD) like hypertension. Hypertension is a major risk factor for cardiovascular and cerebral vascular disease, which are both associated with high morbidity and mortality rates. We studied the prevalence and factors associated with hypertension among PLWH on ART. METHODS: we conducted a retrospective data analysis of PLWH on ART enrolled between 2011 and 2014 into a randomized double-blinded placebo-controlled trial investigating the safety of discontinuing cotrimoxazole prophylaxis (COSTOP) among PLWH in Central Uganda. We used the mean blood pressure (BP) measurements of the first four monthly clinic visits to define hypertension. Patients were categorised as: having normal BP (?120/80mmHg), elevated BP (systolic >120-129, and diastolic ?80), Stage 1 hypertension (systolic 130-139, or diastolic >80-89) and Stage 2 hypertension (systolic ?140 or diastolic ?90). Multiple logistic regression was used to evaluate factors associated with hypertension. RESULTS: data from 2026 COSTOP trial study participants were analysed, 74.1% were women and 77.2% were aged 35 years and above. The overall prevalence of hypertension was 29%, of whom 19.5% had Stage 1 hypertension and 9.5% had Stage 2 hypertension. About 21.4% were overweight or obese. Factors independently associated with hypertension among PLWH on ART included increasing age (p?0.001) and high body mass index (p?0.001). Efavirenz (p?0.001) and lopinavir/ritonavir (p=0.036) based regimen had lower odds of hypertension than Nevirapine based regimens. CONCLUSION: PLWH on ART have a high prevalence of hypertension, which rises with increasing age and body mass index (BMI) and among those on nevirapine-based ART. Implementation of hypertension prevention measures among PLWH on ART and integration of NCD and HIV care to improve patients' management outcomes are required

Incidence and Factors Associated with Postpartum Anemia at Mbarara Regional Referral Hospital

Background: The World Health organization defines postpartum anemia as hemoglobin <11g/dl at 1 week postpartum and <12g/dl at 8 weeks postpartum. Postpartum anemia can also be defined as less than 11.8 g/dl for women aged 12–15 years and less than 12g/dl for women at least age 15 years. In Uganda, 23% of women age 15-49 are anemic, with 18 percent having mild anemia, 5 percent having moderate anemia, and less than 1 percent having severe anemia. Objective: To determine the incidence and factors associated with the new cases of post natal anemia in Mbarara Regional Referral Hospital. Methods:  A prospective cohort study of 271 postpartum mothers without anemia enrolled on discharge after delivery. Participants were followed up to determine development of anemia at 10 weeks postpartum and associated factors on the subsequent postnatal visits. Incidence of postpartum anemia in MRRH was 29.9%, 95% CI (24 - 35). Helminthes infestations AOR95%CI; 12.88(5.25- 31.64, P<0.000), malaria infections AOR95%CI 4.74(1.50-14.94, P=0.008), poor hematinic adherence AOR95%CI, 6.81(3.17-14.62, P<0.000), high parity AOR95%CI, 2.48(1.11- 5.54, P=0.026), and husband unemployment AOR 3.92(1.14 – 13.39, P=0.030) were found to be statistically associated with post-partum anemia. Conclusion: The incidence of postpartum anemia in Mbarara Regional Referral Hospital is very high. Hematinics non adherence, husband unemployment, increased parity; malaria infection and helminthes infestation were found to be associated with post-partum anemia at MRRH

Anti-Paraflagellar Rodc Antibodies Inhibit the In-Vitro Growth of Trypanosoma Brucei Brucei

Paraflagellar rod (PFR), a conserved structure expressed in all lifecycle stages of the order kinetoplasida except in the amastigotes is vital for the parasites survival. In T.b.brucei, the PFR protein has two major components, PFRc and PFRa with molecular mass 73kDa and 68kDa respectively. Experimental evidences implicate the PFR protein as a highly immunogenic and protective antigen. However, its immunogenic properties underlying its suitability as vaccine candidate has not been adequately investigated in-vitro. This study aimed to demonstrate the growth inhibitory potential of PFR protein against T.b.brucei parasites in–vitro. Antibodies against a recombinant form of the PFRc protein were produced and used to generate immune response. A deoxyribonucleotide (DNA) segment of approximate 672bp encoding the PFRc protein component was amplified using polymerase chain reaction (PCR), cloned and expressed in E.coli (BL21) cells. A 200 µg portion of the purified PFRc protein mixed with 100µl Freund's complete adjuvant (FCA) was used to immunize rabbits. An antibody titre of 2.5 x 104 reciprocal dilutions was obtained following three immunisation boosts, spaced two weeks apart. Western blot analysis showed that rabbit anti-PFRc antibodies recognised specifically a 25kDa protein corresponding to the estimated size of the expressed PFRc protein. 25% of purified anti-rabbit IgG antibodies were able to inhibit ~70% T.b.brucei parasite in vitro. This confirmed that the PFRc protein is immunogenic in rabbits and can elicit specific growth inhibitory antibodies. However, we recommend invivo studies in humans and domestic animals infected by trypanosomes to ascertain the vaccine potential of this candidate protein for trypanosomiasis

Acute kidney injury in hospitalized children with sickle cell anemia

Background: Children with sickle cell anemia (SCA) are at increased risk of acute kidney injury (AKI) that may lead to death or chronic kidney disease. This study evaluated AKI prevalence and risk factors in children with SCA hospitalized with a vaso-occlusive crisis (VOC) in a low-resource setting. Further, we evaluated whether modifcations to the Kidney Disease: Improving Global Outcomes (KDIGO) defnition would infuence clinical outcomes of AKI in children with SCA hospitalized with a VOC. Methods: We prospectively enrolled 185 children from 2 – 18 years of age with SCA (Hemoglobin SS) hospitalized with a VOC at a tertiary hospital in Uganda. Kidney function was assessed on admission, 24–48 h of hospitalization, and day 7 or discharge. Creatinine was measured enzymatically using an isotype-dilution mass spectrometry traceable method. AKI was defned using the original-KDIGO defnition as≥1.5-fold change in creatinine within seven days or an absolute change of≥0.3 mg/dl within 48 h. The SCA modifed-KDIGO (sKDIGO) defnition excluded children with a 1.5-fold change in creatinine from 0.2 mg/dL to 0.3 mg/dL. Results: Using KDIGO, 90/185 (48.7%) children had AKI with 61/185 (33.0%) AKI cases present on admission, and 29/124 (23.4%) cases of incident AKI. Overall, 23 children with AKI had a 1.5-fold increase in creatinine from 0.2 mg/ dL to 0.3 m/dL. Using the sKDIGO-defnition, 67/185 (36.2%) children had AKI with 43/185 (23.2%) cases on admission, and 24/142 (16.9%) cases of incident AKI. The sKDIGO defnition, but not the original-KDIGO defnition, was associated with increased mortality (0.9% vs. 7.5%, p=0.024). Using logistic regression, AKI risk factors included age (aOR, 1.10, 95% CI 1.10, 1.20), hypovolemia (aOR, 2.98, 95% CI 1.08, 8.23), tender hepatomegaly (aOR, 2.46, 95% CI 1.05, 5.81), and infection (aOR, 2.63, 95% CI 1.19, 5.81) (p\u3c0.05). Conclusion: These results demonstrate that AKI is a common complication in children with SCA admitted with VOC. The sKDIGO defnition of AKI in children with SCA was a better predictor of clinical outcomes in children. There is need for promotion of targeted interventions to ensure early identifcation and treatment of AKI in children with SCA

T-helper 1 versus T-helper 2 lymphocyte immunodysregulation is the central factor in genesis of Burkitt lymphoma: hypothesis

<p>Abstract</p> <p>Background</p> <p>The HIV epidemic has challenged our previous understanding of endemic Burkitt's lymphoma. Despite the strong association of Burkitt's lymphoma and HIV infection in the Developed world, and against previous postulations that the cancer is due to immunosupression among African children, the HIV epidemic in the Malaria belt has not been associated with a corresponding increase in incidence of childhood Burkitt's lymphoma. Even outside the context of HIV infection, there is substantial evidence for a strong but skewed immune response towards a TH2 response in genesis of Burkitt lymphoma.</p> <p>Presentation of the hypothesis</p> <p>Rather than a global and/or profound immunosupression, the final common pathway in genesis of Burkitt's lymphoma is the dysregulation of the immune response towards a TH2 response dominated by B-lymphocytes, and the concomitant suppression of the TH1 cell-mediated immune surveillance, driven by various viral/parasitic/bacterial infections.</p> <p>Testing the hypothesis</p> <p>Case control studies comparing TH2 and TH1 immune responses in Burkitt lymphoma of different etiological types (sporadic, HIV-related, endemic and post-transplant) to demonstrate significant dominance of TH2 immune response in presence of poor CMI response as a common factor. Immunological profiling to evaluate differences between immune states that are associated (such as recurrent Malaria infection) and those that are not associated (such as severe protein-energy malnutrition) with Burkitt lymphoma. Prospective cohorts profiling chronology of immunological events leading to Burkitt lymphoma in children with EBV infection.</p> <p>Implications of the hypothesis</p> <p>The dysregulation of the immune response may be the missing link in our understanding of Burkitt lymphomagenesis. This will provide possibilities for determination of risk and for control of development of malignancy in individuals/populations exposed to the relevant infections.</p

Genetic errors of immunity distinguish pediatric non-malignant lymphoproliferative disorders

Background Pediatric non-malignant lymphoproliferative disorders (PLPD) are clinically and genetically heterogeneous. Long-standing immune dysregulation and lymphoproliferation in children may be life-threatening, and a paucity of data exists to guide evaluation and treatment of children with PLPD. Objective The primary objective of this study was to ascertain the spectrum of genomic immunologic defects in PLPD. Secondary objectives included characterization of clinical outcomes and associations between genetic diagnoses and those outcomes. Methods PLPD was defined by persistent lymphadenopathy, lymph organ involvement, or lymphocytic infiltration for more than 3 months, with or without chronic or significant EBV infection. Fifty-one subjects from 47 different families with PLPD were analyzed using whole exome sequencing (WES). Results WES identified likely genetic errors of immunity in 51% to 62% of families (53% to 65% of affected children). Presence of a genetic etiology was associated with younger age and hemophagocytic lymphohistiocytosis. Ten-year survival for the cohort was 72.4%, and patients with viable genetic diagnoses had a higher survival rate (82%) compared to children without a genetic explanation (48%, p = 0.03). Survival outcomes for individuals with EBV-associated disease and no genetic explanation were particularly worse than outcomes for subjects with EBV-associated disease and a genetic explanation (17% vs. 90%; p = 0.002). Ascertainment of a molecular diagnosis provided targetable treatment options for up to 18 individuals and led to active management changes for 12 patients. Conclusion PLPD therefore defines children with high risk for mortality, and WES informs clinical risks and therapeutic opportunities for this diagnosis

Association of population mixing and incidence of acute lymphocytic leukemia in children and young adults in the State of Texas

Although accelerated population mixing (PM) has been associated with increased incidence of acute lymphocytic leukemia (ALL), the most common cancer in children, the mechanisms underlying this association are not known. To determine whether genetic mixing or environmentally transmitted factors are responsible for the association of PM and ALL, we conducted an ecological study of incidence of ALL in children & young adults (0–21 years old) among 253 of 254 counties in the State of Texas (USA) and with leukemia and surrogate indicators of genetic and environmental population mixing. The study used ALL incidence data from the Texas Cancer Registry for 2000 and 2009, and county population statistics from the US Census Bureau for 2000 and 2010. Surrogates of genetic mixing included proportion of multiracial households, ratio of Hispanics to non-Hispanics, and racial diversity index. Surrogates for environmental population mixing included total population density, ratio of foreign to native-born residents, and proportion of households with ≥5 persons. We assessed confounding or interaction with median income of households in the county (as a marker for socio-economic status) and with proportion of urban population in the county. Poisson multivariable regression was used to compare incidence rates of ALL with categorized PM indicators. The regression model included time change, the raw PM variable, and a PM-by-time interaction term. Incidence rate ratios, 95% confidence intervals, and p-values were calculated. We found a widely variable degree of on-going population mixing among the counties of Texas. A higher proportion of multiracial households and higher ratio of Hispanics to non-Hispanics in a county were associated with 52%–81% higher incidence rate of ALL after adjusting for time change. This association was not confounded or modified by median income. Interestingly, the “risk” of ALL associated with multiracial households waned over time—suggesting that the risk of ALL is affected by dynamic population mixing rather than static genetic heterogeneity. None of the surrogates of environmental mixing were associated with incidence of ALL. There was no association of ALL incidence with urbanization. These results are consistent with our hypothesis that the leukemogenic agent implicated in population mixing is probably genetically transmitted rather than an exogenous infection. The results also explain why cosmopolitan urban populations that do not have significant ongoing PM may not have higher ALL incidence. To follow up on these findings, we are currently testing whether transmission of endogenous retroviruses may account for PM and ALL incidence in children