bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Typhus Group-Specific Protease Defies Reductive Evolution in Rickettsiae
Authors: Ammerman Nicole C. , Gillespie Joseph J. , Neuwald Andrew F. , Sobral Bruno W. , Azad Abdu F. 
Published: October 2009

ABSTRACT

Phylogenomics reveals extreme gene loss in typhus group (TG) rickettsiae relative to the levels for other rickettsial lineages. We report here a curious protease-encoding gene (
ppcE
) that is conserved only in TG rickettsiae. As a possible determinant of host pathogenicity,
ppcE
warrants consideration in the development of therapeutics against epidemic and murine typhus.
AlipA(yutB) Mutant, Encoding Lipoic Acid Synthase, Provides Insight into the Interplay between Branched-Chain and Unsaturated Fatty Acid Biosynthesis inBacillus subtilis
Authors: Martin Natalia , Lombardía Esteban , Altabe Silvia G. , de Mendoza Diego , Mansilla María C. 
Published: October 2009

ABSTRACTLipoic acid is an essential cofactor required for the function of key metabolic pathways in most organisms. We report the characterization of aBacillus subtilismutant obtained by disruption of thelipA(yutB) gene, which encodes lipoyl synthase (LipA), the enzyme that catalyzes the final step in the de novo biosynthesis of this cofactor. The function oflipAwas inferred from the results of genetic and physiological experiments, and this study investigated its role inB. subtilisfatty acid metabolism. Interrupting lipoate-dependent reactions strongly inhibits growth in minimal medium, impairing the generation of branched-chain fatty acids and leading to accumulation of copious amounts of straight-chain saturated fatty acids inB. subtilismembranes. Although depletion of LipA induces the expression of the Δ5 desaturase, controlled by a two-component system that senses changes in membrane properties, the synthesis of unsaturated fatty acids is insufficient to support growth in the absence of precursors for branched-chain fatty acids. However, unsaturated fatty acids generated by deregulated overexpression of the Δ5 desaturase functionally replaces lipoic acid-dependent synthesis of branched-chain fatty acids. Furthermore, we show that the cold-sensitive phenotype of aB. subtilisstrain deficient in Δ5 desaturase is suppressed by isoleucine only if LipA is present.
Draft Genome Sequences of
Yersinia pestis
Isolates from Natural Foci of Endemic Plague in China
Authors: Eppinger Mark , Guo Zhaobiao , Sebastian Yinong , Song Yajun , Lindler Luther E. , Yang Ruifu , Ravel Jacques 
Published: October 2009

ABSTRACT

To gain insights into the evolutionary origin, emergence, and pathogenicity of the etiologic agent of plague, we have sequenced the genomes of four
Yersinia pestis
strains isolated from the zoonotic rodent reservoir in foci of endemic plague in China. These resources enable in-depth studies of
Y. pestis
sequence variations and detailed whole-genome comparisons of very closely related genomes from the supposed site of the origin and the emergence of global pandemics of plague.
Complete Genome Sequence of the Probiotic
Lactobacillus rhamnosus
ATCC 53103
Authors: Morita Hidetoshi , Toh Hidehiro , Oshima Kenshiro , Murakami Masaru , Taylor Todd D. , Igimi Shizunobu , Hattori Masahira 
Published: October 2009

ABSTRACT

Lactobacillus rhamnosus
is a facultatively heterofermentative lactic acid bacterium and is frequently isolated from human gastrointestinal mucosa of healthy individuals.
L. rhamnosus
ATCC 53103, isolated from a healthy human intestinal flora, is one of the most widely used and well-documented probiotics. Here, we report the finished and annotated genome sequence of this organism.
Dengue fever and El Niño/Southern Oscillation in Queensland, Australia: a time series predictive model
Authors: Hu Wenbiao , Clements Archie , Williams Gail , Tong Shilu 
Published: October 2009

BackgroundIt remains unclear over whether it is possible to develop an epidemic forecasting model for transmission of dengue fever in Queensland, Australia.ObjectivesTo examine the potential impact of El Niño/Southern Oscillation on the transmission of dengue fever in Queensland, Australia and explore the possibility of developing a forecast model of dengue fever.MethodsData on the Southern Oscillation Index (SOI), an indicator of El Niño/Southern Oscillation activity, were obtained from the Australian Bureau of Meteorology. Numbers of dengue fever cases notified and the numbers of postcode areas with dengue fever cases between January 1993 and December 2005 were obtained from the Queensland Health and relevant population data were obtained from the Australia Bureau of Statistics. A multivariate Seasonal Auto-regressive Integrated Moving Average model was developed and validated by dividing the data file into two datasets: the data from January 1993 to December 2003 were used to construct a model and those from January 2004 to December 2005 were used to validate it.ResultsA decrease in the average SOI (ie, warmer conditions) during the preceding 3–12 months was significantly associated with an increase in the monthly numbers of postcode areas with dengue fever cases (β=−0.038; p = 0.019). Predicted values from the Seasonal Auto-regressive Integrated Moving Average model were consistent with the observed values in the validation dataset (root-mean-square percentage error: 1.93%).ConclusionsClimate variability is directly and/or indirectly associated with dengue transmission and the development of an SOI-based epidemic forecasting system is possible for dengue fever in Queensland, Australia.
Ambient air pollution and risk of congenital anomalies in England, 1991–1999
Authors: Dolk H , Armstrong B , Lachowycz K , Vrijheid M , Rankin J , Abramsky L , Boyd P A , Wellesley D 
Published: October 2009

ObjectivesTo investigate whether there is an association between risk of congenital anomaly and annual ward level exposure to air pollution in England during the 1990s.MethodsA geographical study was conducted across four regions of England using population-based congenital anomaly registers, 1991–1999. Exposure was measured as 1996 annual mean background sulphur dioxide (SO2), nitrogen dioxide (NO2) and particulate matter (PM10) concentrations at census ward level (n=1474). Poisson regression, controlling for maternal age, area socioeconomic deprivation and hospital catchment area, was used to estimate relative risk for an increase in pollution from the 10th to the 90th centile.ResultsFor non-chromosomal anomalies combined, relative risks were 0.99 (95% CI 0.93 to 1.05) for SO2, 0.97 (95% CI 0.84 to 1.11) for NO2and 0.89 (95% CI 0.75 to 1.07) for PM10. For chromosomal anomalies, relative risks were 1.06 (95% CI 0.98 to 1.15) for SO2, 1.11 (95% CI 0.95 to 1.30) for NO2and 1.18 (95% CI 0.97 to 1.42) for PM10. Raised risks were found for tetralogy of Fallot and SO2(RR=1.38, 95% CI 1.07 to 1.79), NO2(RR=1.44, 95% CI 0.71 to 2.93) and PM10(RR=1.48, 95% CI 0.57 to 3.84), which is of interest in light of previously reported associations between this cardiac anomaly and other air pollutants.ConclusionsWhile air pollution in the 1990s did not lead to sustained geographical differences in the overall congenital anomaly rate in England, further research regarding specific anomalies is indicated.
Cause-specific mortality in British coal workers and exposure to respirable dust and quartz
Authors: Miller Brian G , MacCalman Laura 
Published: October 2009

ObjectivesIn the 1950s the Pneumoconiosis Field Research (PFR) programme was set up to study the health of British coal workers. Studies included regular health surveys, an intensive characterisation of workers' individual exposures, and entry to a cohort followed up to the present for cause-specific mortality. This study reports on analyses of cause-specific mortality in a cohort of almost 18 000 men from 10 British collieries.MethodsExternal analyses used standardised mortality ratios (SMRs), comparing observed mortality with reference rates from the regions in which the collieries were situated. Causes investigated include lung and stomach cancers, chronic obstructive pulmonary disease and cardiovascular endpoints. Internal analyses used Cox regression models with time-dependent exposures adjusting for the confounding effects of age, smoking, cohort entry date and regional differences in population mortality rates.ResultsSeveral causes showed evidence of a healthy worker effect early in the follow-up, with a deficit in the SMR diminishing over time. For most of the causes there was a significant excess in the latter part of follow-up.Internal analyses found evidence of an association between increased risks of lung cancer and increased quartz exposure, particularly at a lag of 15 years.Risks of mortality from non-malignant respiratory disease showed increases with increased exposure to respirable dust.ConclusionsThis paper adds to the evidence on the long-term effects of exposure to coalmine dust on mortality from respiratory diseases.
Particulate matter and out-of-hospital coronary deaths in eight Italian cities
Authors: Serinelli Maria , Vigotti Maria Angela , Stafoggia Massimo , Berti Giovanna , Bisanti Luigi , Mallone Sandra , Pacelli Barbara , Tessari Roberta , Forastiere Francesco 
Published: October 2009

ObjectivesWe evaluated the association between PM10concentration and out-of-hospital coronary deaths in eight Italian cities during 1997–2004.Methods16 989 subjects aged >35 years who died out-of-hospital from coronary causes were studied and hospital admissions in the previous 2 years identified. We studied the effect of the mean of current and previous day PM10values (lag 0–1). A city-specific case-crossover analysis was applied using a time-stratified approach considering as confounders weather, holidays, influenza epidemics, and summer decrease in population. The pooled percentage increase (95% CI) in mortality per 10 μg/m3increase in PM10was estimated.ResultsA statistically significant increase in out-of-hospital coronary deaths was related to a 10 μg/m3increase in PM10: 1.46% (95% CI 0.50 to 2.43). Although no statistically significant effect modification by age was found, the effect was stronger among subjects aged >65 years (1.60%, 0.59 to 2.63), particularly those aged 65–74 (3.01%, 0.74 to 5.34). People in the lowest socio-economic category (3.34%, 1.28 to 5.45) had a stronger effect than those in the highest category. No clear effect modification was seen for gender, season or any specific comorbidity. An indication of negative effect modification was seen for previous admission for cardiac dysrhythmias. Subjects without hospital admissions in the previous 2 years were slightly more affected by PM10effects (1.91%, 0.28 to 3.47) than those with at least one previous hospital admission (1.44%, 0.09 to 2.82).ConclusionsOur results show that short term exposure to PM10is associated with coronary mortality especially among the elderly and socio-economically disadvantaged. No clear effect modification by previous hospitalisations was detected except for cardiac dysrhythmias, possibly due to protective treatment.
The bibliographic impact of epidemiological studies: what can be learnt from citations?: Table 1
Authors: Leclerc Annette , Chastang Jean-François , Kaniewski Nadine , Cyr Diane , Ozguler Anna , Descatha Alexis 
Published: October 2009

ObjectiveTo document one dimension of the impact of an epidemiological study through citations in scientific journals.MethodsTwo sets of articles from studies performed in France were considered. They presented original results on occupational risk factors for low back pain and upper limb disorders. Citations of these articles were retrieved through the Web of Science and Google Scholar, and selected according to several criteria. Most citations present in the Web of Science were also retrieved from Google Scholar, except for the most recent articles. In the Web of Science, after exclusion of self-citations and duplicates, the total number of citations was 109 from 23 different countries for the low back pain articles, with 96 citations from 18 countries for upper limb disorders. A relatively large number of the citations belonged to clinical journals outside the fields of occupational health, ergonomics and public health.ConclusionThis study suggests that results dealing with occupational health disseminate into various fields of clinical research. However, this is only one dimension of the impact of a study.
Mortality from myocardial infarction in relation to exposure to vibration and dust among a cohort of iron-ore miners in Sweden
Authors: Björ Bodil , Burström Lage , Eriksson Kåre , Jonsson Håkan , Nathanaelsson Lena , Nilsson Tohr 
Published: October 2009

ObjectivesThe aim of this study was to investigate myocardial infarction (MI) mortality in relation to exposure to hand/arm vibration (HAV) and whole body vibration (WBV) as well as exposure to dust among men employed in two Swedish iron-ore mines.MethodsThis study comprised employed men at two iron-ore mines in Sweden who had been employed for at least 1 year from 1923 up to 1996. The causes of death were obtained from the national cause of death register from 1952 to 2001. Myocardial infarction mortality was obtained by linking personal identification numbers to the national cause of death register. Poisson regression was used for risk estimations on exposure–response relation, and analyses were made on the two age groups ≤60 years and >60 years.ResultsRelative risks for MI mortality in relation to exposure were significantly increased for exposure (0/>0) to WBV (RR 1.18, 95% CI 1.06 to 1.31) and dust (RR 1.15, 95% CI 1.02 to 1.31), and the results indicated an exposure–response relation for WBV and dust separately. For 60 years and younger, exposure to HAV (0/>0) (RR 1.34, 95% CI 1.03 to 1.74) and WBV (0/>0) (RR 1.39, 95% CI 1.13 to 1.72) increased the risk of MI mortality. An exposure–response was found for HAV and WBV, as the medium and high exposed categories showed significantly increased risk estimates. None of the exposures significantly increased the risk in the group above 60 years. The increased risk estimates for exposure to WBV remained when adjusting for exposure to dust.ConclusionsThe results for the working age (≤60 years) group showed significantly increased MI mortality for univariate exposure to HAV, WBV and dust. We found an association between increased mortality from MI and occupational exposure to WBV, and the risk remained after adjustment for dust exposure.
Fatal occupational injuries in Taiwan, 1994–2005
Authors: Ho Shu-Chen , Wang Li-Yu , Ho Chi-Kung , Yang Chun-Yuh 
Published: October 2009

ObjectivesThis study examines the trends in rates of fatal occupational injuries in Taiwan by demographic group and occupation for 1994–2005.MethodsData on deaths due to injuries at work from 1994 through 2005 were obtained from the Department of Health which is responsible for the death registration system in Taiwan. Employment data, which were used as the denominators of fatality rates in this study, were retrieved from the Directorate-General of Budget and Accounting Statistics ‘Employment and Earnings’ database. A Poisson regression model was used to examine the trends in rates of fatal occupational injuries in various occupations while controlling for demographic characteristics.ResultsOverall fatal occupational injury rates declined during the study period among all demographic groups and occupations. Adjusted annual changes in rates of fatal injuries ranged from a decrease of 13.6% a year in machine operators/related workers to a decrease of 35.9% in clerks. The annual decrement was faster for males than for females and for older workers compared to young workers.ConclusionsDespite declining rates, the number of fatal occupational injuries in Taiwan remains significant because of the growing work force. Future research should focus on the disparities in fatal injury trends.
Do pre-employment influences explain the association between psychosocial factors at work and coronary heart disease? The Whitehall II study
Authors: Hintsa Taina , Shipley Martin J , Gimeno David , Elovainio Marko , Chandola Tarani , Jokela Markus , Keltikangas-Järvinen Liisa , Vahtera Jussi , Marmot Michael G , Kivimäki Mika 
Published: October 2009

ObjectivesTo examine whether the association between psychosocial factors at work and incident coronary heart disease (CHD) is explained by pre-employment factors, such as family history of CHD, education, paternal education and social class, number of siblings and height.MethodsA prospective cohort study of 6435 British men aged 35–55 years at phase 1 (1985–1988) and free from prevalent CHD at phase 2 (1989–1990) was conducted. Psychosocial factors at work were assessed at phases 1 and 2 and mean scores across the two phases were used to determine long-term exposure. Selected pre-employment factors were assessed at phase 1. Follow-up for coronary death, first non-fatal myocardial infarction or definite angina between phase 2 and 1999 was based on clinical records (250 events, follow-up 8.7 years).ResultsThe selected pre-employment factors were associated with risk for CHD: HRs (95% CI) were 1.33 (1.03 to 1.73) for family history of CHD, 1.18 (1.05 to 1.32) for each quartile decrease in height and 1.16 (0.99 to 1.35) for each category increase in number of siblings. Psychosocial work factors also predicted CHD: 1.72 (1.08 to 2.74) for low job control and 1.72 (1.10 to 2.67) for low organisational justice. Adjustment for pre-employment factors changed these associations by 4.1% or less.ConclusionsIn this occupational cohort of British men, the association between psychosocial factors at work and CHD was largely independent of family history of CHD, education, paternal educational attainment and social class, number of siblings and height.
Cathepsin D Is the Primary Protease for the Generation of Adenohypophyseal Vasoinhibins: Cleavage Occurs within the Prolactin Secretory Granules
Authors: Cruz-Soto Martha E. , Cosío Gabriela , Jeziorski Michael C. , Vargas-Barroso Víctor , Aguilar Manuel B. , Cárabez Alfonso , Berger Peter , Saftig Paul , Arnold Edith , Thebault Stéphanie , Martínez de la Escalera Gonzalo , Clapp Carmen 
Published: October 2009

AbstractVasoinhibins are a family of N-terminal prolactin (PRL) fragments that inhibit blood vessel growth, dilation, permeability, and survival. The aspartyl endoprotease cathepsin D is active at acidic pH and can cleave rat PRL to generate vasoinhibins. We investigated whether and where vasoinhibins could be generated by cathepsin D in the adenohypophysis of rats and mice and whether their production could be gender dependent. Vasoinhibins were detected in primary cultures of rat adenohypophyseal cells by Western blot with antibodies directed against the N terminus of PRL but not the C terminus. Ovariectomized, estrogen-treated females show greater levels of adenohypophyseal vasoinhibins than males. Peptide sequencing analysis revealed that the cleaved form of PRL in rat adenohypophyseal extracts contains the PRL N terminus and a second N terminus starting at Ser149, the reported cleavage site of cathepsin D in rat PRL. In addition, cathepsin D inhibition by pepstatin A reduced vasoinhibin levels in rat adenohypophyseal cell cultures. Confocal and electron microscopy showed the colocalization of cathepsin D and PRL within rat adenohypophyseal cells and secretory granules, and a subcellular fraction of rat adenohypophysis enriched in secretory granules contained cathepsin D activity able to generate vasoinhibins from PRL. Of note, vasoinhibins were absent in the adenohypophysis of mice lacking the cathepsin D gene but not in wild-type mice. These findings show that cathepsin D is the main protease responsible for the generation of adenohypophyseal vasoinhibins and that its action can take place within the secretory granules of lactotrophs.
Local Secretion of Urocortin 1 Promotes Microvascular Permeability during Lipopolysaccharide-Induced Inflammation
Authors: Cureton Elizabeth L. , Ereso Alexander Q. , Victorino Gregory P. , Curran Brian , Poole Daniel P. , Liao Min , Harken Alden H. , Bhargava Aditi 
Published: October 2009

AbstractUrocortin 1 (Ucn1) is a neuropeptide that regulates vascular tone and is implicated in both the vascular and immune cell-mediated responses to inflammation. The role of Ucn1 in regulating microvascular permeability has not been determined. We hypothesized that local Ucn1 release promotes microvascular permeability and that this effect augments the local gastrointestinal vascular response to lipopolysaccharide (LPS)-induced systemic inflammation. We measured hydraulic (Lp) and macromolecule permeability in mesenteric venules. We show that a continuous infusion of 10−7m Ucn1 in a postcapillary venule increased Lp 2-fold over baseline, as did LPS-induced inflammation. However, simultaneous infusion of Ucn1 and LPS markedly increased Lp by 7-fold. After local knockdown of Ucn1 using RNA interference, infusion of Ucn1 with LPS resulted in return to 2-fold increase, confirming that Ucn1 synergistically augments hydraulic permeability during inflammation. LPS and Ucn1 treatment also resulted in increased numbers of interstitial microspheres, which colocalized with CD31+ immune cells. Ucn1 activity is mediated through two receptor subtypes, CRH-R1 and CRH-R2. CRH-R1 receptor blockade exacerbated, whereas CRH-R2 receptor blockade decreased the LPS-induced increase in Lp. Finally, treatment with the c-JUN N-terminal kinase (JNK) antagonist SP600125 during infusion of LPS, but not Ucn1, decreased Lp. These findings suggest that Ucn1 increases microvascular permeability and acts synergistically with LPS to increase fluid and macromolecule losses during inflammation. Knockdown of endogenous Ucn1 during inflammation attenuates synergistic increases in Lp. Ucn1’s effect on Lp is partially mediated by the CRH-R2 receptor and acts independently of the c-JUN N-terminal kinase signal transduction pathway.
The Rho Guanosine 5′-Triphosphatase, Cell Division Cycle 42, Is Required for Insulin-Induced Actin Remodeling and Glucagon-Like Peptide-1 Secretion in the Intestinal Endocrine L Cell
Authors: Lim Gareth E. , Xu Molie , Sun Jane , Jin Tianru , Brubaker Patricia L. 
Published: October 2009

AbstractRho GTPases, such as cell division cycle 42 (Cdc42) and ras-related C3 botulinum toxin substrate 1 (Rac1), have been identified as regulators of F-actin dynamics and hormone release from endocrine cells; however, their role in secretion of the incretin hormone, glucagon-like peptide-1 (GLP-1), from the enteroendocrine L cell is unknown. Insulin induced a 1.4-fold increase in L cell GLP-1 release; however, secretion was potentiated to 2.1-fold in the presence of the F-actin depolymerizing agent, latrunculin B, suggesting that F-actin functions as a permissive barrier. In murine GLUTag L cells, insulin stimulated F-actin depolymerization and Cdc42 activation simultaneously, and these events occurred prior to detectable increases in insulin-induced GLP-1 release. After insulin treatment, Cdc42-dependent p21-activated kinase-1 (PAK1) activation was also detected, and transfection of small-interfering RNA against Cdc42 or of dominant-negative Cdc42(T17N) impaired insulin-stimulated PAK1 activation, actin remodeling, and GLP-1 secretion. Overexpression of kinase-dead PAK1(K299R) or PAK1 small interfering RNA similarly attenuated insulin-induced GLP-1 secretion. Knockdown or inhibition of Cdc42 and PAK1 activities also prevented activation of MAPK/ERK (MEK)-1/2-ERK1/2 by insulin, which was previously identified as a critical pathway for insulin-regulated GLP-1 release. Taken together, these data identify a novel signaling pathway in the endocrine L cell, whereby Cdc42 regulates actin remodeling, activation of the cannonical 1/2-ERK1/2 pathway and PAK1, and GLP-1 secretion in response to insulin.