Antimalarial activities of benzothiazole analogs: A systematic review.

BACKGROUND: Benzothiazole derivatives have been reported to possess a wide range of biological activities, including antimalarial activity. This systematic review aims to summarize and evaluate the antimalarial activities of benzothiazole analogs. METHODS: We conducted an electronic search using nine databases in October 2017 and subsequently updated in September 2022. We included all original in vitro and in vivo studies that documented the antimalarial activities of compounds containing benzothiazole analogs with no restriction. The risk of bias of each included study was assessed by ToxRTool. RESULTS: Twenty-eight articles were included in our study, which are in vitro, in vivo, or both. Of these, 232 substances were identified to have potent antiplasmodial activity against various strains of the malaria parasite. Benzothiazole analogs show different antimalarial mechanisms, including inhibition of Plasmodium falciparum enzymes in in vitro studies and inhibition of blood parasites in in vivo studies. CONCLUSIONS: Benzothiazole derivatives are promising substances for treating malaria. The structure-activity relationship studies suggest that the substitution pattern of the benzothiazole scaffold plays a crucial role in determining the antimalarial activity of the analog.

Bacteriological and parasitological assessment of food handlers in the Omdurman area of Sudan.

BACKGROUND/PURPOSE: Pathogenic organisms are thought to be widely distributed among food handlers. This study was designed to assess the prevalence of carriers of some pathogenic bacteria and intestinal parasites among food handlers in the city of Omdurman, Sudan. METHODS: A total of 518 nasal swabs and stool specimens were collected. Nasal swabs were cultured on bacteriological culture media. Stool specimens were examined microscopically for intestinal parasites. RESULTS: Of the total subjects examined, 30.1% were found to be carriers of pathogenic organisms. The pathogens isolated and identified were the bacteria Staphylococcus aureus, Salmonella typhi, and Shigella boydii, and the intestinal parasites, Giardia lamblia and Entamoeba histolytica/dispar. Bacteria and intestinal parasites were most prevalent among storekeepers (41%), followed by restaurant workers (24.4%), bakers (24.4%), butchers (5.1%), milk distributors (2.6%), and fruits/vegetables sellers (2.6%). S. aureus, the most abundant pathogen, was most prevalent in storekeepers (44.6%), followed by restaurant workers (25%), bakers (17.9%), butchers (5.4%), milk distributors (3.6%), and fruit/vegetable sellers (3.6%). CONCLUSION: The findings from this study indicate a key role for food handlers in the spread and transmission of food communicable diseases and reveal the need for protective measures.

The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice.

Regulation of sodium balance is a critical factor in the maintenance of euvolemia, and dysregulation of renal sodium excretion results in disorders of altered intravascular volume, such as hypertension. The amiloride-sensitive epithelial sodium channel (ENaC) is thought to be the only mechanism for sodium transport in the cortical collecting duct (CCD) of the kidney. However, it has been found that much of the sodium absorption in the CCD is actually amiloride insensitive and sensitive to thiazide diuretics, which also block the Na-Cl cotransporter (NCC) located in the distal convoluted tubule. In this study, we have demonstrated the presence of electroneutral, amiloride-resistant, thiazide-sensitive, transepithelial NaCl absorption in mouse CCDs, which persists even with genetic disruption of ENaC. Furthermore, hydrochlorothiazide (HCTZ) increased excretion of Na+ and Cl- in mice devoid of the thiazide target NCC, suggesting that an additional mechanism might account for this effect. Studies on isolated CCDs suggested that the parallel action of the Na+-driven Cl-/HCO3- exchanger (NDCBE/SLC4A8) and the Na+-independent Cl-/HCO3- exchanger (pendrin/SLC26A4) accounted for the electroneutral thiazide-sensitive sodium transport. Furthermore, genetic ablation of SLC4A8 abolished thiazide-sensitive NaCl transport in the CCD. These studies establish what we believe to be a novel role for NDCBE in mediating substantial Na+ reabsorption in the CCD and suggest a role for this transporter in the regulation of fluid homeostasis in mice.