HIV/AIDS in Nigeria: a bibliometric analysis

Background  

Nigeria is home to more people living with HIV than any other country in the world, except South Africa and India-where an estimated 2.9 million [1.7 million – 4.2 million] people were living with the virus in 2005. A systematic assessment of recent HIV/AIDS research output from Nigeria is not available. Without objective information about the current deficiencies and strengths in the HIV research output from Nigeria, it is difficult to plan substantial improvements in HIV/AIDS research that could enhance population health. The aim of this study was to analyse the trends in Nigeria's SCI publications in HIV/AIDS from 1980 to 2006. Special attention was paid to internationally collaborated works that were identified based on the countries of the authors' affiliation.     

Individual and contextual factors associated with childhood stunting in Nigeria: a multilevel analysis

Stunting, a form of undernutrition, is the best measure of child health inequalities as it captures multiple dimensions of children's health, development and the environment where they live. The aim of this study was to quantify the predictors of childhood stunting in Nigeria. This study used data obtained from the 2008 Nigeria Demographic and Health Survey (NDHS). A total of 28 647 children aged 0–59 months included in NDHS in 2008 were analysed in this study. We applied multilevel multivariate logistic regression analysis in which individual‐level factors were at the first level and community‐level factors at the second level. The percentage change in variance of the full model accounted for about 46% in odds of stunting across the communities. The present study found that the following predictors increased the odds of childhood stunting: male gender, age above 11 months, multiple birth, low birthweight, low maternal education, low maternal body mass index, poor maternal health‐seeking behaviour, poor household wealth and short birth interval. The community‐level predictors found to have significant association with childhood stunting were: child residing in community with high illiteracy rate and North West and North East regions of the country. In conclusion, this study revealed that both individual‐ and community‐level factors are significant determinants of childhood stunting in Nigeria.     

Adverse relationships of adiposity and gait parameters: A survey of stroke patients undergoing rehabilitation

Poor adiposities are risk factors for major morbidities, but reports on how these relate with gait function of stroke patients undergoing rehabilitation is sparse and need further investigation. A convenience sample of 94 ambulatory stroke survivors and 94 matched apparently healthy individuals were assessed for adiposity markers (body mass index, waist circumference, thigh girth, waist-hip ratio, and percent body fat) and gait parameters (cadence, step length, stride length, stride width, gait velocity, and cycle). Mean age of the stroke and apparently healthy participants were 57 ± 5.2 years and 56.9 ± 4.8 years, respectively. We found significant (p < 0.05) relationships between waist circumference and each of gait cycle (r = 0.67) namely, cadence (r = −0.68), stride length (−0.62), step length (−0.61), and gait velocity (−0.75). Fairly similar correlations existed between body mass index, waist-hip ratio, percent body fat, thigh girth, and each of gait parameters, with only the thigh girth significantly correlating with stride width (r = 0.79). Obesity more than triples the odds of low gait velocities (odds ratio: 3.28; 95% confidence interval: 1.60–6.74). Findings provide clinicians with likely influence of adiposities on gait parameters of stroke patients. This may inform treatment decision and help to prioritize interventions through adiposity management for stroke patients undergoing rehabilitation.     

Association of high-sensitivity C-reactive protein and odds of breast cancer by molecular subtype: analysis of the MEND study

Breast cancer (BC) in Nigeria is characterized by disproportionately aggressive molecular subtypes. C-reactive protein (CRP) is associated with risk and aggressiveness for several types of cancer. We examined the association of high-sensitivity CRP (hsCRP) with odds of BC by molecular subtype among Nigerian women. Among 296 newly diagnosed BC cases and 259 healthy controls, multivariable logistic regression models were used to estimate adjusted odds ratios (aOR) and 95% confidence intervals (CI) for the association between hsCRP and odds of BC overall and by molecular subtype (luminal A, luminal B, HER2-enriched and triple-negative or TNBC). High hsCRP (> 3 mg/L) was observed in 57% of cases and 31% of controls and was associated with 4 times the odds of BC (aOR: 4.43; 95% CI: 2.56, 7.66) after adjusting for socio-demographic, reproductive, and clinical variables. This association persisted regardless of menopausal status and body mass index (BMI) category. High hsCRP was associated with increased odds of TNBC (aOR: 3.32; 95% CI: 1.07, 10.35), luminal A BC (aOR: 4.03; 95% CI: 1.29, 12.64), and HER2-enriched BC (aOR: 6.27; 95% CI: 1.69, 23.25). Future studies are necessary in this population to further evaluate a potential role for CRP as a predictive biomarker for BC.     

B cells expressing IFN‐γ suppress Treg‐cell differentiation and promote autoimmune experimental arthritis

Clinical efficacy in the treatment of rheumatoid arthritis with anti‐CD20 (Rituximab)‐mediated B‐cell depletion has garnered interest in the mechanisms by which B cells contribute to autoimmunity. We have reported that B‐cell depletion in a murine model of proteoglycan‐induced arthritis (PGIA) leads to an increase in Treg cells that correlate with decreased autoreactivity. Here, we demonstrate that the increase in Treg cells after B‐cell depletion is due to an increase in the differentiation of naïve CD4⁺ T cells into Treg cells. Since the development of PGIA is dependent on IFN‐γ and B cells are reported to produce IFN‐γ, we hypothesized that B‐cell‐specific IFN‐γ plays a role in the development of PGIA. Accordingly, mice with B‐cell‐specific IFN‐γ deficiency were as resistant to the induction of PGIA as mice that were completely IFN‐γ deficient. Importantly, despite a normal frequency of IFN‐γ‐producing CD4⁺ T cells, B‐cell‐specific IFN‐γ‐deficient mice exhibited a higher percentage of Treg cells compared with that in WT mice. These data indicate that B‐cell IFN‐γ production inhibits Treg‐cell differentiation and exacerbates arthritis. Thus, we have established that IFN‐γ, specifically derived from B cells, uniquely contributes to the pathogenesis of autoimmunity through prevention of immunoregulatory mechanisms.     

Effect of the experimental chemopreventative agent, glucarate, on intestinal carcinogenesis in rats

Dietary calcium glucarate was previously shown to protect effectivelyagainst chemically-induced mammary, lung, liver and skin carcinogenesisin rodents, whereas the negative dietary calcium control, calciumgluconate, had no effect. In the present study the chemopreventativeactivity of dietary calcium glucarate was evaluated in the azoxymethaneintestinal carcinogenesis model using the Fischer strain rat.The protocol limited the duration of azoxymethane treatmentto 3 weeks to permit the evaluation of the separate effectsof glucarate on the initiation and promotion phases. Controlrats, treated with azoxymethane and maintained on a low fatchow diet throughout the 32-week experiment had an intestinaladenocarcinoma incidence of 55%, with an equal incidence of27.7% in the small and large intestines. There was no significantdifference between this control group and a negative calciumcontrol group fed 128 mmol/kg chow of calcium as calcium gluconate.In contrast to these two control groups, supplementation ofthe diet of azoxymethane-treated rats with 128 mmol/kg dietof calcium glucarate during both the initiation and promotionphases significantly inhibited the overall induction of adenocarcinomasin the intestine, the incidence in the entire intestine andin the small and large intestines being 11.8, 5.8 and 5.8%,respectively. When fed only during the initiation phase, theinhibition again was statistically significant, the correspondingvalues being 11.8%, 5.8 and 5.8%. When calcium glucarate wasfed during the promotion phase, a statistically significantinhibition of adenocarcinoma induction was observed only inthe colon where the incidence was 5.5%. Weight gain was similarin all groups. These and related data indicate that dietaryglucarate exerts a significant inhibitory effect on azoxymethane-inducedintestinal and in particular colon carcinogenesis in the rat,decreasing their incidence and size and reducing their metasticpotential.