Mycobacterium africanum, first described in Senegal in 1968, causes up to half of the smear-positive pulmonary tuberculosis cases in West Africa, but it has not been found in other geographical areas except among recent West African migrants. The reasons for the geographic restriction of M. africanum are unknown. We used molecular tools to determine the population structure of the Mycobacterium tuberculosis complex in a cohort study of consecutive smear-positive tuberculosis cases in The Gambia. We collected and genotyped 386 clinical isolates using spoligotype analysis and PCRs for large sequence polymorphisms (LSPs) and compared the genotype patterns to the patterns in an international database. The results of spoligotyping and LSP analysis for the study population were also compared to determine the correlation between them. The main lineages within the Mycobacterium tuberculosis complex identified in The Gambia included M. africanum type I (38.4%), characterized by an LSP in region of difference 702 (RD702; West African type 2). Among the M. tuberculosis sensu stricto isolates, lineages characterized by RD182 and by RD174 were the most common. We also detected a gradient in the prevalence of M. africanum that extended from neighboring Guinea-Bissau. The genotypic diversity of the spoligotype patterns was greater among the isolates of M. africanum than among the isolates of M. tuberculosis. We postulate that M. africanum became endemic in West Africa first, before the introduction of different lineages within M. tuberculosis sensu stricto.Molecular epidemiologic techniques have been used to compare isolates within the Mycobacterium tuberculosis complex and have clarified many aspects of tuberculosis (TB) transmission, such as the importance of ongoing transmission in lowincidence countries (21) and the limited importance of withinhousehold transmission in high-incidence settings (26). In recent years, genotyping techniques have also been applied to infer the phylogenetic relationships between lineages within the M. tuberculosis complex (2, 17). Different genetic markers have different rates of evolutionary change. Genetic markers such as large sequence polymorphisms (LSPs) that change slowly are essentially limited to analysis by phylogenetic studies (11,24). On the other hand, spoligotyping, which is based on the polymorphism of the direct repeat region and which has the ability to detect changes with a faster molecular clock, has been used for both phylogeny and molecular epidemiological studies of M. tuberculosis (10).The population structure of the M. tuberculosis complex in The Gambia or Senegal has not been described since biochemical methods were used to demonstrate that M. africanum caused approximately 20% of the TB cases in Senegal during the 1970s (9). Since the advent of molecular methods, the strains previously classified as East African M. africanum type II have been reclassified as M. tuberculosis sensu stricto (22). West African M. africanum type I is now subdivided into West African M. africa...

<p class="abstract"><strong>Background:</strong> This study was carried out to determine the growth performance of rats fed graded levels of chitosan supplemented High fat diet.  </p><p class="abstract"><strong>Methods:</strong> Thirty male wistar rats weighing between 70 g and 90 g were purchased and randomly allotted into three (3) treatment groups with graded levels of chitosan in High fat diet (1%, 3% and 5%) and three (3) control groups namely: normal diet, High fat diet and normal diet +5% chitosan. The feed intakes as well as weight change of the experimental rats were monitored for six (6) weeks.</p><p class="abstract"><strong>Results:</strong> The results obtained showed that the highest level of feed intake and feed efficiency were recorded for animals in group fed 5% level of chitosan supplementation when compared to other treatment groups. Similar result was observed for the weight change (as there was significant reduction in the weight gain with increase chitosan supplementation in HFD) which can be attributed to the efficient utilization of feed consumption.</p><p class="abstract"><strong>Conclusions:</strong> It can be concluded that dietary chitosan prevents excess weight gain in hyperlipidemia and improves the overall nutritional attributes of the experimental diets by improving their feed efficiencies as compared to the control.</p>

Hepato-renal dysfunctions associated with hyperlipidemia necessitates a continuous search for natural remedies. This study thus evaluated the effect of dietary chitosan on diet-induced hyperlipidemia in rats. A total of 30 male Wistar rats (90 ± 10) g were randomly allotted into six (6) groups (n = 5): Normal diet, High-fat diet (HFD), and Normal diet + 5% chitosan. The three other groups received HFD, supplemented with 1%, 3%, and 5% of chitosan. The feeding lasted for 6 weeks, after which the rats were sacrificed. The liver and kidneys were harvested for analyses. He-patic alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activity, and renal biomarkers (ALT, AST, urea, and creatinine) were assayed spectrophoto-metrically. Additionally, expression of hepatic and renal CD43 and p53 was estimated immuno-histochemically. The HFD group had elevated bodyweight compared to normal which was reversed in the chitosan-supplemented groups. Hyperlipidemia caused a significant (p < 0.05) decrease in the hepatic (AST, ALT, and ALP) and renal (AST and ALT) activities, while renal urea and creatinine increased. Furthermore, the HFD group showed an elevated level of hepatic and renal CD43 while p53 expression decreased. However, groups supplemented with chitosan showed improved hepatic and renal biomarkers, as well as corrected the aberrations in the expressions of p53 and CD43. Con-clusively, dietary chitosan inclusion in the diet (between 3% and 5%) could effectively improve kid-ney and liver functionality via abatement of inflammatory responses.

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Hepato-renal dysfunctions associated with hyperlipidemia necessitates continuous search for natural remedies. This study thus, evaluated the effect of dietary chitosan on diet-induced hyperlipidemic rats. Thirty male Wistar rats (90 ± 5.2) g were randomly allotted into six (6) groups (n=5): Normal diet, High-fat diet (HFD), Normal diet + 5% chitosan. The three other groups received HFD, supplemented with 1%-, 3%-, and 5% of chitosan. The feeding lasted for 8 weeks, after which the rats were sacrificed. The liver and kidneys were harvested for Analyses. Hepatic alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activity, and renal biomarkers (ALT, AST, urea, and creatinine) were assayed spectrophotometrically. Additionally, expression of hepatic and renal CD43 and p53 was estimated immunohistochemically. Hyperlipidemia caused a significant (p&lt;0.05) decrease in the hepatic (AST, ALT, and ALP) and renal (AST and ALT) activities, while renal urea and creatinine increased. Furthermore, the HFD group showed an elevated level of hepatic and renal CD43 while p53 expression decreased. However, groups supplemented with chitosan showed improved hepatic and renal biomarkers, as well as corrected the aberrations in the expressions of p53 and CD43. Conclusively, dietary chitosan could effectively improve kidney and liver functionality via abatement of inflammatory responses.