The Nigerian girls education project: giving the girl child a voice

The three-year Girls’ Education Project (GEP) aims to improve the quality of life of girls by seeking to increase their enrolment, retention and completion of primary school education. The project is being implemented in six states of Northern Nigeria, under a bilateral agreement between the Federal Government of Nigeria and United Nations Children’s Fund (UNICEF) with funding support from the Department for International Development (DFID). It uses an inter-sectoral approach to provide amongst other things, WASH facilities in the targeted schools. Results in three states include construction of 323 boreholes and 688 blocks of VIP latrines; establishment of WASH school clubs; enhanced partnerships between collaborating ministries, the three tiers of government, public and private sector, communities and schools. Other outcomes include increased enrolment and retention of girls as well as improved self esteem. This paper seeks to share the human impact of the GEP project in three states of Nigeria

Improved antiretroviral treatment outcome in a rural African setting is associated with cART initiation at higher CD4 cell counts and better general health condition

Background Data on combination antiretroviral therapy (cART) in remote rural African regions is increasing. Methods We assessed prospectively initial cART in HIV-infected adults treated from 2005 to 2008 at St. Francis Designated District Hospital, Ifakara, Tanzania. Adherence was assisted by personal adherence supporters. We estimated risk factors of death or loss to follow-up by Cox regression during the first 12 months of cART. Results Overall, 1,463 individuals initiated cART, which was nevirapine-based in 84.6%. The median age was 40 years (IQR 34-47), 35.4% were males, 7.6% had proven tuberculosis. Median CD4 cell count was 131 cells/μl and 24.8% had WHO stage 4. Median CD4 cell count increased by 61 and 130 cells/μl after 6 and 12 months, respectively. 215 (14.7%) patients modified their treatment, mostly due to toxicity (56%), in particular polyneuropathy and anemia. Overall, 129 patients died (8.8%) and 189 (12.9%) were lost to follow-up. In a multivariate analysis, low CD4 cells at starting cART were associated with poorer survival and loss to follow-up (HR 1.77, 95% CI 1.15-2.75, p = 0.009; for CD4 100 cells/μl). Higher weight was strongly associated with better survival (HR 0.63, 95% CI 0.51-0.76, p < 0.001 per 10 kg increase). Conclusions cART initiation at higher CD4 cell counts and better general health condition reduces HIV related mortality in a rural African setting. Efforts must be made to promote earlier HIV diagnosis to start cART timely. More research is needed to evaluate effective strategies to follow cART at a peripheral level with limited technical possibilities

Effects of hot crude oil on concrete for offshore storage applications.

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Loss of residual cyanogens in a cassava food during storage

Residual cyanogens in gari, the most popular cassava food in West Africa, is implicated in the causation of tropical ataxic neuropathy. Gari is eaten by soaking its granules in cold water or by adding boiling water to make a food called eba. This study was conducted to determine whether loss of the residual cyanogens in gari during short-term storage and when gari is made into eba will reduce dietary cyanide load in consumers. Fifteen samples of gari, nine roasted from cassava mash fermented for at least 4 days (type A) and six roasted from cassava mash fermented for only 1 day (type B), were stored for 4 weeks. Free cyanide, linamarin, and cyanohydrin in gari and in eba made from the gari were determined at weekly intervals for 4 weeks. Free cyanide was absent in all samples of gari. Mean cyanohydrin dropped from 8.4 mg HCN Eq/kg dry weight to 4.6 mg HCN Eq/kg dry weight in type A gari, while it dropped from 3.0 mg HCN Eq/kg dry weight to 1.3 mg HCN Eq/kg dry weight in type B gari. Mean linamarin dropped from 6.6 mg HCN Eq/kg dry weight to 2.8 mg HCN Eq/kg dry weight in type A gari, while it dropped from 1.7 mg HCN Eq/kg dry weight to 0.4 mg HCN Eq/kg dry weight in type B gari. Loss of linamarin and cyanohydrin was significant at P < 0.001 for type A gari and at P < 0.002 for type B gari when the weekly levels were compared with initial values. When gari was made into eba, 36% of cyanohydrin and 47% of linamarin were lost from type A gari, while 38% of cyanohydrin and 5% of linamarin were lost from type B gari. Loss of linamarin and cyanohydrin when gari was made into eba was significant for both types of gari at P < 0.001. This study shows that the loss of cyanohydrin and linamarin in gari during short-term storage and when gari is made to eba will reduce dietary cyanide load in consumer

Exposure to cyanide following a meal of cassava food

Exposure to cyanide from gari, a popular cassava food in West Africa, is implicated in the causation of ataxic polyneuropathy and amblyopia, but this has been questioned because cyanide was not detected in gari in a study. This study was carried out to determine if gari is a source of exposure to cyanide. Gari (150 g) containing cyanohydrin, from which 128 μmol of cyanide ions could be released, was dissolved in 500 ml of cold water for each of the 12 healthy subjects to drink. Concentrations of cyanide in plasma and erythrocytes were determined at baseline and following the meal at 30 min, 1 h, hourly for 4 h and two hourly for 12 h. The mean concentrations of cyanide in the plasma were 6 μmol/l (95% CI 2–10) at baseline, 12 μmol/l (95% CI 6–17) at peak and 6 μmol/l (95% CI 2–10) on return to baseline. The mean amount of cyanide absorbed into the plasma was 13 μmol (S.D. 12), while the transit time of absorbed cyanide was 7.3 h (S.D. 2.1). This study shows that exposure to cyanide follows consumption of gari, but the amount of cyanide absorbed into the plasma from a single meal is small and unlikely to cause acute intoxication. The long transit time of absorbed cyanide in the plasma suggests that frequent intake of gari could cause cyanide to accumulate in the plasma

Incidence of endemic ataxic polyneuropathy and its relation to exposure to cyanide in a Nigerian community

Background The occurrence of ataxic polyneuropathy in an endemic area in south west Nigeria has been attributed to exposure to cyanide from cassava foods. However, it has been shown that the prevalence of ataxic polyneuropathy is not high in several communities in the tropics where exposure to cyanide from cassava foods is high. Objectives To determine the incidence of ataxic polyneuropathy in an endemic community, and to compare the intake of cassava foods, exposure to cyanide, and levels of thiols in cases and controls. Methods A cohort of 3167 healthy subjects aged 10 years and over in Ososa, Nigeria, was followed for two years, screened, and examined neurologically. Ataxic polyneuropathy was diagnosed if sensory polyneuropathy and sensory gait ataxia were both present. Controls were selected randomly within 10 year age groups of subjects who screened negative. Intake of cassava foods, exposure to cyanide, concentrations of thiols (glutathione, cysteine, and γ glutamylcysteine) in plasma, and visual evoked potentials were measured. Results Person–years of follow up were 6246 for 1469 male and 1698 female subjects in the cohort. The incidence of ataxic polyneuropathy was 64 per 10 000 person–years (31 for male and 93 for female subjects). Multivariate odd ratios were 0.78 (95% CI 0.23 to 2.61) for intake of the commonest cassava food, and 1.64 (0.56 to 5.09) for concentration of thiocyanate in plasma. The concentration of thiols was less than the reference limits in two controls, but in none of the cases. The latency of P100 was prolonged in 20 cases (69%) compared with 14 controls (42%) (p<0.05). Conclusions The incidence of ataxic polyneuropathy is high in Ososa, Nigeria, but the intake of cassava foods, exposure to cyanide, and levels of thiols, are not related to the occurrence. These findings do not suggest that cyanide is the cause of endemic ataxic polyneuropathy

Persistence of tropical ataxic neuropathy in a Nigerian community

OBJECTIVES—The term tropical ataxic neuropathy (TAN) is currently used to describe several neurological syndromes attributed to toxiconutritional causes. However, TAN was initially proposed to describe a specific neurological syndrome seen predominantly among the Ijebu speaking Yorubas in south western Nigeria. In this study, the prevalence of TAN was determined in Ososa, a semiurban community in south western Nigeria described as endemic for TAN in 1969, and its neurological features were compared with Strachan's syndrome, prisoners of war neuropathy, the epidemic neuropathy in Cuba, and konzo.
METHODS—A census of Ososa was followed by door to door screening of all subjects aged 10 years and above with a newly designed screening instrument. Subjects who screened positive had a neurological examination, and the diagnosis of TAN was made if any two or more of bilateral optic atrophy, bilateral neurosensory deafness, sensory gait ataxia, or distal symmetric sensory polyneuropathy were present.
RESULTS—A total of 4583 inhabitants were registered in the census. Of these, 3428 subjects aged 10 years and above were screened. The diagnosis of TAN was made in 206 of 323 subjects who screened positive for TAN. The prevalence of TAN was 6.0%, 3.9% in males and 7.7% in females. The highest age specific prevalence was 24% in the 60-69 years age group in women.
CONCLUSION—The occurrence of TAN in Ososa continues at a higher prevalence than was reported 30 years ago. Its neurological features and natural history do not resemble those described for Strachan syndrome, epidemic neuropathy in Cuba, or konzo. The increasing consumption of cassava foods linked to its causation makes TAN of public health importance in Nigeria, the most populous African country.