The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
David W. Stahle - One of the best experts on this subject based on the ideXlab platform.
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drought and epidemic typhus central mexico 1655 1918
Emerging Infectious Diseases, 2014Co-Authors: Jordan N. Burns, Rodolfo Acunasoto, David W. StahleAbstract:Epidemic typhus is a serious infectious disease caused by the obligate, intracellular, gram-negative bacterium Rickettsia prowazekii and transmitted by body lice (Pediculus Humanus Corporis). This disease is recognized for its high mortality rate throughout human history, particularly before modern sanitary practices and the availability of antimicrobial drugs (1). Typhus spreads where conditions are crowded and unsanitary. Historical epidemics often followed war, climate extremes, famine, and social upheaval. Zinsser (2) noted that throughout history, epidemic typhus might have claimed more human lives during war than combat. Epidemic typhus could reemerge as a serious infectious disease in areas of the world where social strife and underdeveloped public health programs persist (3). Typhus was first recorded in Mexico in 1655, and the most recent major epidemic began in 1915 during the Mexican revolution. Mexico’s rich historical record of epidemic disease is documented in archives of demographic data that include census records, health records, death certificates, and accounts of physicians. Mexico City and the high, densely populated valleys of central Mexico were particularly susceptible to smallpox, cholera, and typhus epidemics because of crowding and poor sanitation (4). Numerous epidemics, some identified as typhus, occurred during the colonial and early modern eras. We have compiled a record of 22 typhus epidemics in Mexico during 1655–1918. We compared the timing of these typhus epidemics with tree-ring reconstructions of growing-season moisture conditions to assess the relationship between climate and typhus during this period.
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Drought and Epidemic Typhus, Central Mexico, 1655–1918
Centers for Disease Control and Prevention, 2014Co-Authors: Jordan N. Burns, Rodolfo Acuna-soto, David W. StahleAbstract:Epidemic typhus is an infectious disease caused by the bacterium Rickettsia prowazekii and transmitted by body lice (Pediculus Humanus Corporis). This disease occurs where conditions are crowded and unsanitary. This disease accompanied war, famine, and poverty for centuries. Historical and proxy climate data indicate that drought was a major factor in the development of typhus epidemics in Mexico during 1655–1918. Evidence was found for 22 large typhus epidemics in central Mexico, and tree-ring chronologies were used to reconstruct moisture levels over central Mexico for the past 500 years. Below-average tree growth, reconstructed drought, and low crop yields occurred during 19 of these 22 typhus epidemics. Historical documents describe how drought created large numbers of environmental refugees that fled the famine-stricken countryside for food relief in towns. These refugees often ended up in improvised shelters in which crowding encouraged conditions necessary for spread of typhus
Miratul M K Muqit - One of the best experts on this subject based on the ideXlab platform.
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discovery of catalytically active orthologues of the parkinson s disease kinase pink1 analysis of substrate specificity and impact of mutations
Open Biology, 2011Co-Authors: Helen I Woodroof, Joe H Pogson, Mike Begley, Alexander J Whitworth, Dario R Alessi, Maria Deak, Daan M F Van Aalten, Lewis C Cantley, David G. Campbell, Miratul M K MuqitAbstract:Missense mutations of the phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1) gene cause autosomal-recessive Parkinson's disease. To date, little is known about the intrinsic catalytic properties of PINK1 since the human enzyme displays such low kinase activity in vitro. We have discovered that, in contrast to mammalian PINK1, insect orthologues of PINK1 we have investigated—namely Drosophila melanogaster (dPINK1), Tribolium castaneum (TcPINK1) and Pediculus Humanus Corporis (PhcPINK1)—are active as judged by their ability to phosphorylate the generic substrate myelin basic protein. We have exploited the most active orthologue, TcPINK1, to assess its substrate specificity and elaborated a peptide substrate (PINKtide, KKWIpYRRSPRRR) that can be employed to quantify PINK1 kinase activity. Analysis of PINKtide variants reveal that PINK1 phosphorylates serine or threonine, but not tyrosine, and we show that PINK1 exhibits a preference for a proline at the +1 position relative to the phosphorylation site. We have also, for the first time, been able to investigate the effect of Parkinson's disease-associated PINK1 missense mutations, and found that nearly all those located within the kinase domain, as well as the C-terminal non-catalytic region, markedly suppress kinase activity. This emphasizes the crucial importance of PINK1 kinase activity in preventing the development of Parkinson's disease. Our findings will aid future studies aimed at understanding how the activity of PINK1 is regulated and the identification of physiological substrates.
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discovery of catalytically active orthologues of the parkinson s disease kinase pink1 analysis of substrate specificity and impact of mutations
Open Biology, 2011Co-Authors: Helen I Woodroof, Joe H Pogson, Mike Begley, Alexander J Whitworth, Dario R Alessi, Maria Deak, Daan M F Van Aalten, Lewis C Cantley, David G. Campbell, Miratul M K MuqitAbstract:Missense mutations of the phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1) gene cause autosomal-recessive Parkinson's disease. To date, little is known about the intrinsic catalytic properties of PINK1 since the human enzyme displays such low kinase activity in vitro. We have discovered that, in contrast to mammalian PINK1, insect orthologues of PINK1 we have investigated—namely Drosophila melanogaster (dPINK1), Tribolium castaneum (TcPINK1) and Pediculus Humanus Corporis (PhcPINK1)—are active as judged by their ability to phosphorylate the generic substrate myelin basic protein. We have exploited the most active orthologue, TcPINK1, to assess its substrate specificity and elaborated a peptide substrate (PINKtide, KKWIpYRRSPRRR) that can be employed to quantify PINK1 kinase activity. Analysis of PINKtide variants reveal that PINK1 phosphorylates serine or threonine, but not tyrosine, and we show that PINK1 exhibits a preference for a proline at the +1 position relative to the phosphorylation site. We have also, for the first time, been able to investigate the effect of Parkinson's disease-associated PINK1 missense mutations, and found that nearly all those located within the kinase domain, as well as the C-terminal non-catalytic region, markedly suppress kinase activity. This emphasizes the crucial importance of PINK1 kinase activity in preventing the development of Parkinson's disease. Our findings will aid future studies aimed at understanding how the activity of PINK1 is regulated and the identification of physiological substrates.
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Author for correspondence:
2011Co-Authors: Miratul M K MuqitAbstract:active orthologues of the Parkinson’s disease kinase PINK1: analysis of substrate specificity1. Summary Missense mutations of the phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1) gene cause autosomal-recessive Parkinson’s disease. To date, little is known about the intrinsic catalytic properties of PINK1 since the human enzyme displays such low kinase activity in vitro. We have discovered that, in contrast to mammalian PINK1, insect orthologues of PINK1 we have investigated—namely Drosophila melanogaster (dPINK1), Tribolium castaneum (TcPINK1) and Pediculus Humanus Corporis (PhcPINK1)—are active as judged by their ability to phosphorylate the generic substrate myelin basic protein. We have exploited the most active orthologue, TcPINK1, to assess its substrate speci-ficity and elaborated a peptide substrate (PINKtide, KKWIpYRRSPRRR) that can be employed to quantify PINK1 kinase activity. Analysis of PINKtide variants reveal that PINK1 phosphorylates serine or threonine, but not tyrosine, and we show that PINK1 exhibits a preference for a proline at the þ1 position relativ
Jordan N. Burns - One of the best experts on this subject based on the ideXlab platform.
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drought and epidemic typhus central mexico 1655 1918
Emerging Infectious Diseases, 2014Co-Authors: Jordan N. Burns, Rodolfo Acunasoto, David W. StahleAbstract:Epidemic typhus is a serious infectious disease caused by the obligate, intracellular, gram-negative bacterium Rickettsia prowazekii and transmitted by body lice (Pediculus Humanus Corporis). This disease is recognized for its high mortality rate throughout human history, particularly before modern sanitary practices and the availability of antimicrobial drugs (1). Typhus spreads where conditions are crowded and unsanitary. Historical epidemics often followed war, climate extremes, famine, and social upheaval. Zinsser (2) noted that throughout history, epidemic typhus might have claimed more human lives during war than combat. Epidemic typhus could reemerge as a serious infectious disease in areas of the world where social strife and underdeveloped public health programs persist (3). Typhus was first recorded in Mexico in 1655, and the most recent major epidemic began in 1915 during the Mexican revolution. Mexico’s rich historical record of epidemic disease is documented in archives of demographic data that include census records, health records, death certificates, and accounts of physicians. Mexico City and the high, densely populated valleys of central Mexico were particularly susceptible to smallpox, cholera, and typhus epidemics because of crowding and poor sanitation (4). Numerous epidemics, some identified as typhus, occurred during the colonial and early modern eras. We have compiled a record of 22 typhus epidemics in Mexico during 1655–1918. We compared the timing of these typhus epidemics with tree-ring reconstructions of growing-season moisture conditions to assess the relationship between climate and typhus during this period.
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Drought and Epidemic Typhus, Central Mexico, 1655–1918
Centers for Disease Control and Prevention, 2014Co-Authors: Jordan N. Burns, Rodolfo Acuna-soto, David W. StahleAbstract:Epidemic typhus is an infectious disease caused by the bacterium Rickettsia prowazekii and transmitted by body lice (Pediculus Humanus Corporis). This disease occurs where conditions are crowded and unsanitary. This disease accompanied war, famine, and poverty for centuries. Historical and proxy climate data indicate that drought was a major factor in the development of typhus epidemics in Mexico during 1655–1918. Evidence was found for 22 large typhus epidemics in central Mexico, and tree-ring chronologies were used to reconstruct moisture levels over central Mexico for the past 500 years. Below-average tree growth, reconstructed drought, and low crop yields occurred during 19 of these 22 typhus epidemics. Historical documents describe how drought created large numbers of environmental refugees that fled the famine-stricken countryside for food relief in towns. These refugees often ended up in improvised shelters in which crowding encouraged conditions necessary for spread of typhus
Philippe Brouqui - One of the best experts on this subject based on the ideXlab platform.
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Primer and probe alignments with partial Phum_PHUM540560 gene sequences from body and head lice [35].
2013Co-Authors: Rezak Drali, Didier Raoult, Jean-marc Rolain, Amina Boutellis, Philippe BrouquiAbstract:A portion of the Phum_PHUM540560 gene sequences from body and head lice were aligned with the primers and probes designed for the multiplex RT-PCR assay. Part of the first exon spanings nucleotides 1 to 64 was analyzed. The forward and reverse primer sequences are boxed in black. The FAM- and VIC-labeled probe sequences are boxed in purple and green, respectively. The nucleotides in blue represent single-nucleotide polymorphisms that are specific to head lice. The nucleotides in black represent single-nucleotide polymorphisms that are specific to body lice. BL: body louse; HL: head louse; NW_002987859.1: Pediculus Humanus Corporis strain USDA 1103172108290 Phum_PHUM540560 (gene sequence available in GenBank).
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Detection of a Knockdown Resistance Mutation Associated with Permethrin Resistance in the Body Louse Pediculus Humanus Corporis by Use of Melting Curve Analysis Genotyping
Journal of clinical microbiology, 2012Co-Authors: Rezak Drali, Samir Benkouiten, Sékéné Badiaga, Idir Bitam, Jean-marc Rolain, Philippe BrouquiAbstract:Louse-borne diseases are prevalent in the homeless, and body louse eradication has thus far been unsuccessful in this population. We aim to develop a rapid and robust genotyping method usable in large field-based clinical studies to monitor permethrin resistance in the human body louse Pediculus Humanus Corporis. We assessed a melting curve analysis genotyping method based on real-time PCR using hybridization probes to detect the M815I-T917I-L920F knockdown resistance (kdr) mutation in the paraorthologous voltage-sensitive sodium channel (VSSC) α subunit gene, which is associated with permethrin resistance. The 908-bp DNA fragment of the VSSC gene, encoding the α subunit of the sodium channel and encompassing the three mutation sites, was PCR sequenced from 65 lice collected from a homeless population. We noted a high prevalence of the 3 indicated mutations in the body lice collected from homeless people (100% for the M815I and L920F mutations and 56.73% for the T917I mutation). These results were confirmed by melting curve analysis genotyping, which had a calculated sensitivity of 100% for the M815I and T917I mutations and of 98% for the L920F mutation. The specificity was 100% for M815I and L920F and 96% for T917I. Melting curve analysis genotyping is a fast, sensitive, and specific tool that is fully compatible with the analysis of a large number of samples in epidemiological surveys, allowing the simultaneous genotyping of 96 samples in just over an hour (75 min). Thus, it is perfectly suited for the epidemiological monitoring of permethrin resistance in human body lice in large-scale clinical studies.
Subba Reddy Palli - One of the best experts on this subject based on the ideXlab platform.
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rna interference of nadph cytochrome p450 reductase results in reduced insecticide resistance in the bed bug cimex lectularius
PLOS ONE, 2012Co-Authors: Fang Zhu, Sarah Sams, Tim Moural, Kenneth F Haynes, Michael F Potter, Subba Reddy PalliAbstract:Background NADPH-cytochrome P450 reductase (CPR) plays a central role in cytochrome P450 action. The genes coding for P450s are not yet fully identified in the bed bug, Cimex lectularius. Hence, we decided to clone cDNA and knockdown the expression of the gene coding for CPR which is suggested to be required for the function of all P450s to determine whether or not P450s are involved in resistance of bed bugs to insecticides. Methodology/Principal Findings The full length Cimex lectularius CPR (ClCPR) cDNA was isolated from a deltamethrin resistant bed bug population (CIN-1) using a combined PCR strategy. Bioinformatics and in silico modeling were employed to identify three conserved binding domains (FMN, FAD, NADP), a FAD binding motif, and the catalytic residues. The critical amino acids involved in FMN, FAD, NADP binding and their putative functions were also analyzed. No signal peptide but a membrane anchor domain with 21 amino acids which facilitates the localization of ClCPR on the endoplasmic reticulum was identified in ClCPR protein. Phylogenetic analysis showed that ClCPR is closer to the CPR from the body louse, Pediculus Humanus Corporis than to the CPRs from the other insect species studied. The ClCPR gene was ubiquitously expressed in all tissues tested but showed an increase in expression as immature stages develop into adults. We exploited the traumatic insemination mechanism of bed bugs to inject dsRNA and successfully knockdown the expression of the gene coding for ClCPR. Suppression of the ClCPR expression increased susceptibility to deltamethrin in resistant populations but not in the susceptible population of bed bugs. Conclusions/Significance These data suggest that P450-mediated metabolic detoxification may serve as one of the resistance mechanisms in bed bugs.