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Andreas N Mbah,1,2 Ousman Mahmud,1 Omotayo R Awofolu,2 Raphael D Isokpehi11Center for Bioinformatics and Computational Biology, Department of Biology, Jackson State University, Jackson, MS, USA; 2Department of Environmental Sciences, College of Agriculture and Environmental Sciences, University of South Africa, Pretoria, South AfricaBackground: Human schistosomiasis is a freshwater snail-transmitted disease caused by parasitic flatworms of the Schistosoma genus. Schistosoma haematobium, Schistosoma mansoni, and Schistosoma japonicum are the three major species infecting humans. These parasites undergo a complex developmental life cycle, in which they encounter a plethora of environmental signals. The presence of genes encoding the universal stress protein (USP) domain in the genomes of Schistosoma spp. suggests these flatworms are equipped to respond to unfavorable conditions. Though data on gene expression is available for USP genes, their biochemical and environmental regulation are incompletely understood. The identification of additional regulatory molecules for Schistosoma. USPs, which may be present in the human, snail, or water environments, could also be useful for schistosomiasis interventions.Methods: We developed a protocol that includes a visual analytics stage to facilitate integration, visualization, and decision making, from the results of sequence analyses and data collection on a set of 13 USPs from S. mansoni and S. japonicum.Results: Multiple sequence alignment identified conserved sites that could be key residues regulating the function of USPs of the Schistosoma spp. Based on the consistency and completeness of sequence annotation, we prioritized for further research the gene for a 184-amino-acid-long USP that is present in the genomes of the three human-infecting Schistosoma spp. Calcium, zinc, and magnesium ions were predicted to interact with the protein product of the gene.Conclusion: Given that the initial effects of praziquantel on schisto

The draft genome sequence of the parasitic flatworm Schistosoma mansoni (S. mansoni), a cause of schistosomiasis, encodes a predicted guanosine triphosphate (GTP) binding protein tagged Smp_059340.1. Smp_059340.1 is predicted to be a member of the G protein alpha-s subunit responsible for regulating adenylyl cyclase activity in S. mansoni and a possible drug target against the parasite. Our structural bioinformatics analyses identified key amino acid residues (Ser53, Thr188, Asp207 and Gly210) in the two molecular switches responsible for cycling the protein between active (GTP bound) and inactive (GDP bound) states. Residue Thr188 is located on Switch I region while Gly210 is located on Switch II region with Switch II longer than Switch I. The Asp207 is located on the G3 box motif and Ser53 is the binding residue for magnesium ion. These findings offer new insights into the dynamic and functional determinants of the Smp_059340.1 protein in regulating the S. mansoni life cycle. The binding interfaces and their residues could be used as starting points for selective modulations of interactions within the pathway using small molecules, peptides or mutagenesis., non disponibile

The draft genome sequence of the parasitic flatworm Schistosoma mansoni (S. mansoni), a cause of schistosomiasis, encodes a predicted guanosine triphosphate (GTP) binding protein tagged Smp_059340.1. Smp_059340.1 is predicted to be a member of the G protein alpha-s subunit responsible for regulating adenylyl cyclase activity in S. mansoni and a possible drug target against the parasite. Our structural bioinformatics analyses identified key amino acid residues (Ser53, Thr188, Asp207 and Gly210) in the two molecular switches responsible for cycling the protein between active (GTP bound) and inactive (GDP bound) states. Residue Thr188 is located on Switch I region while Gly210 is located on Switch II region with Switch II longer than Switch I. The Asp207 is located on the G3 box motif and Ser53 is the binding residue for magnesium ion. These findings offer new insights into the dynamic and functional determinants of the Smp_059340.1 protein in regulating the S. mansoni life cycle. The binding interfaces and their residues could be used as starting points for selective modulations of interactions within the pathway using small molecules, peptides or mutagenesis., non disponibile

The draft genome sequence of the parasitic flatworm Schistosoma mansoni (S. mansoni), a cause of schistosomiasis, encodes a predicted guanosine triphosphate (GTP) binding protein tagged Smp_059340.1. Smp_059340.1 is predicted to be a member of the G protein alpha-s subunit responsible for regulating adenylyl cyclase activity in S. mansoni and a possible drug target against the parasite. Our structural bioinformatics analyses identified key amino acid residues (Ser53, Thr188, Asp207 and Gly210) in the two molecular switches responsible for cycling the protein between active (GTP bound) and inactive (GDP bound) states. Residue Thr188 is located on Switch I region while Gly210 is located on Switch II region with Switch II longer than Switch I. The Asp207 is located on the G3 box motif and Ser53 is the binding residue for magnesium ion. These findings offer new insights into the dynamic and functional determinants of the Smp_059340.1 protein in regulating the S. mansoni life cycle. The binding interfaces and their residues could be used as starting points for selective modulations of interactions within the pathway using small molecules, peptides or mutagenesis., non disponibile

Studies into social inequalities in health tend to focus more on parental socio-economic status (SES) as it affects the children. We aimed to test the hypothesis that socio-economic inequalities would not affect the casual blood pressure among Nigerian adults. Resting blood pressure (BP) and pulse rate of 1067 sedentary adults were measured. Rate pressure product and pulse pressure were later calculated. Second, a structured questionnaire, which objectively assessed the SES of the subjects, was administered. Subsequently, a self-rating SES ladder was employed to classify the subjects into different socio-economic groups. This was used as a check for the structured questionnaire. A Pearson product correlation coefficient comparing the two outcome measures revealed a high correlation (r=0.951, P<0.01). Socio-economic status was found to have an inverse significant (P<0.05) effect on systolic pressure, heart rate and pulse pressure. The 95th centile blood pressure obtained was 154/91 mmHg. Low SES is associated with development of hypertension among the Nigerian adults.

Studies into social inequalities in health tend to focus more on parental socio-economic status (SES) as it affects the children. We aimed to test the hypothesis that socio-economic inequalities would not affect the casual blood pressure among Nigerian adults. Resting blood pressure (BP) and pulse rate of 1067 sedentary adults were measured. Rate pressure product and pulse pressure were later calculated. Second, a structured questionnaire, which objectively assessed the SES of the subjects, was administered. Subsequently, a self-rating SES ladder was employed to classify the subjects into different socio-economic groups. This was used as a check for the structured questionnaire. A Pearson product correlation coefficient comparing the two outcome measures revealed a high correlation (r=0.951, P<0.01). Socio-economic status was found to have an inverse significant (P<0.05) effect on systolic pressure, heart rate and pulse pressure. The 95th centile blood pressure obtained was 154/91 mmHg. Low SES is associated with development of hypertension among the Nigerian adults.