add directory ♦ physician opportunity
Related Topics:
Infectious DiseasesMicrobial Ecology :: Ecology
Microbiology :: Biology
Microbiology :: Food Science
Today's News:
American Journal of Epidemiology - current issue
NQO1 Polymorphisms and De Novo Childhood Leukemia: A HuGE Review and Meta-Analysis
Guha, N., Chang, J. S., Chokkalingam, A. P., Wiemels, J. L., Smith, M. T., Buffler, P. A. Fri, 21 Nov 2008 00:00:00 -0000
Polymorphisms in NQO1, a gene coding for the phase II enzyme involved in the detoxification of quinone carcinogens, have been associated with childhood leukemia in some studies, although the observed direction and magnitude of effects have been inconsistent. Therefore, the authors systematically reviewed all published reports describing the effect of NQO1 in de novo childhood leukemia and conducted a meta-analysis of 7 case-control studies that examined the association between NQO1*2 and childhood leukemia. Although a family-based study previously demonstrated overtransmission of this allele among childhood acute lymphoblastic leukemia cases, the meta-analysis showed that the presence of a NQO1*2 variant allele, which reduces the activity of the enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1), had no significant effect on childhood leukemia. However, there was an increased risk associated with having at least 1 copy of the NQO1*2 allele in a subset of cases with MLL translocations (summary odds ratio = 1.39, 95% confidence interval: 0.98, 1.97). Heterogeneity between studies may be due to differences in population exposures to NQO1 substrates and small sample sizes, as well as potential population stratification in non-family-based studies. Therefore, further research is warranted on the role of NQO1 polymorphisms in the etiology of childhood leukemia, especially among MLL-positive leukemias.
Seven Lipoprotein Lipase Gene Polymorphisms, Lipid Fractions, and Coronary Disease: A HuGE Association Review and Meta-Analysis
Sagoo, G. S., Tatt, I., Salanti, G., Butterworth, A. S., Sarwar, N., van Maarle, M., Jukema, J. W., Wiman, B., Kastelein, J. J. P., Bennet, A. M., de Faire, U., Danesh, J., Higgins, J. P. T. Fri, 21 Nov 2008 00:00:00 -0000
Lipoprotein lipase (LPL) is a key enzyme in lipoprotein metabolism and a major candidate gene for coronary heart disease (CHD). The authors assessed associations between 7 LPL polymorphisms and lipid fractions and CHD risk in population-based cohort, case-control, and cross-sectional studies published by January 2007. Meta-analyses of 22,734 CHD cases and 50,177 controls in 89 association studies focused on the relations of the T-93G (rs1800590), D9N (rs1801177), G188E, N291S (rs268), PvuII (rs285), HindIII (rs320), and S447X (rs328) polymorphisms to high density lipoprotein cholesterol, triglycerides, myocardial infarction, or coronary stenosis. Carriers of 9N or 291S had modestly adverse lipid profiles. Carriers of the less common allele of HindIII or of 447X had modestly advantageous profiles. The combined odds ratio for CHD among carriers was 1.33 (95% confidence interval (CI): 1.14, 1.56) for 9N, 1.07 (95% CI: 0.96, 1.20) for 291S, 0.89 (95% CI: 0.81, 0.98) for the less common HindIII allele, and 0.84 (95% CI: 0.75, 0.94) for 447X. For T-93G (odds ratio (OR) = 1.22, 95% CI: 0.98, 1.52) and PvuII (OR = 0.96, 95% CI: 0.89, 1.04), there were null associations with lipid levels or CHD risk; information on G188E was limited (OR = 2.80, 95% CI: 0.88, 8.87). The study of LPL genotypes confirms the existence of close interrelations between high density lipoprotein cholesterol and triglyceride pathways. The influence of these genotypes on CHD risk warrants further investigation.
The Effect of Racial Residential Segregation on Black Infant Mortality
Hearst, M. O., Oakes, J. M., Johnson, P. J. Fri, 21 Nov 2008 00:00:00 -0000
Economic differences and proximal risk factors do not fully explain the persistent high infant mortality rates of African Americans (blacks). The authors hypothesized that racial residential segregation plays an independent role in high black infant mortality rates. Segregation restricts social and economic advantage and imposes negative environmental exposures that black women and infants experience. The study sample was obtained from the 2000–2002 US Linked Birth/Infant Death records and included 677,777 black infants residing in 64 cities with 250,000 or more residents. Outcomes were rates of all-cause infant mortality, postneonatal mortality, and external causes of death. Segregation was measured by using the isolation index (dichotomized at 0.60) from the 2000 US Census Housing Patterns. Propensity score matching methods were used. After matching on propensity scores, no independent effect of segregation on black infant mortality rates was found. Results show little statistical evidence that segregation plays an independent role in black infant mortality. However, a key finding is that it is difficult to disentangle contextual effects from the characteristics of individuals.
Invited Commentary: Residential Segregation and Health--The Complexity of Modeling Separate Social Contexts
Acevedo-Garcia, D., Osypuk, T. L. Fri, 21 Nov 2008 00:00:00 -0000
When researching racial disparities in health, residential segregation cannot be ignored. Because of segregation, contextual differences by race are so pronounced that ignoring them may lead to misestimating the effect of individual-level factors. However, given the stark racial separation of social contexts, researching how residential segregation and neighborhood inequality contribute to racial health disparities remains methodologically challenging. Estimating the contribution of neighborhood effects to health disparities would require overlap in the racial distributions of neighborhood environment, for example, in the distributions of neighborhood poverty. Because of segregation, though, the extent of such overlap is extremely restricted. Previous analyses of the 2000 US Census found, on average, only a 24% overlap between the distribution of neighborhood poverty for black children and that for white children in metropolitan areas. Propensity score methods may be 1 useful tool for addressing limited overlap or exchangeability. However, as shown by their application to the segregation and health relation, their use should be informed by a sound conceptualization of the scale of the social exposure of interest, the hypothesized pathways between the exposure and the health outcome, and possible unmeasured confounders.
Maternal Body Mass Index and Lifestyle Exposures and the Risk of Bilateral Renal Agenesis or Hypoplasia: The National Birth Defects Prevention Study
Slickers, J. E., Olshan, A. F., Siega-Riz, A. M., Honein, M. A., Aylsworth, A. S., for the National Birth Defects Prevention Study Fri, 21 Nov 2008 00:00:00 -0000
Increased maternal body mass index, maternal smoking, and alcohol exposure during pregnancy have been inconsistently reported as potential risk factors for renal birth defects. The low incidence of the most severe renal anomaly, bilateral renal agenesis or hypoplasia (RA/H), has limited the ability to study this fatal defect. Using data from the National Birth Defects Prevention Study, a multicenter case-control study, the authors explored potential relations between RA/H and maternal body mass index, smoking, alcohol, and caffeine exposures. Data available for 75 infants with RA/H born between 1997 and 2003 and for randomly selected control infants without known birth defects (n = 868) were assessed by a model adjusted for folic acid use, all four exposures of interest, and study center. Bilateral RA/H was associated with a body mass index of greater than 30 kg/m2 prior to pregnancy (adjusted odds ratio (aOR) = 1.92, 95% confidence interval (CI): 1.00, 3.67), smoking during the periconceptional period (aOR = 2.09, 95% CI: 1.08, 4.03), and binge drinking during the second month of pregnancy (aOR = 3.64, 95% CI: 1.19, 11.1). These results support the need for further exploration into the potential mechanisms by which such exposures could interfere with early fetal kidney formation resulting in RA/H.
Advanced Parental Age and the Risk of Autism Spectrum Disorder
Durkin, M. S., Maenner, M. J., Newschaffer, C. J., Lee, L.-C., Cunniff, C. M., Daniels, J. L., Kirby, R. S., Leavitt, L., Miller, L., Zahorodny, W., Schieve, L. A. Fri, 21 Nov 2008 00:00:00 -0000
This study evaluated independent effects of maternal and paternal age on risk of autism spectrum disorder. A case-cohort design was implemented using data from 10 US study sites participating in the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network. The 1994 birth cohort included 253,347 study-site births with complete parental age information. Cases included 1,251 children aged 8 years with complete parental age information from the same birth cohort and identified as having an autism spectrum disorder based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision criteria. After adjustment for the other parent's age, birth order, maternal education, and other covariates, both maternal and paternal age were independently associated with autism (adjusted odds ratio for maternal age ≥35 vs. 25–29 years = 1.3, 95% confidence interval: 1.1, 1.6; adjusted odds ratio for paternal age ≥40 years vs. 25–29 years = 1.4, 95% confidence interval: 1.1, 1.8). Firstborn offspring of 2 older parents were 3 times more likely to develop autism than were third- or later-born offspring of mothers aged 20–34 years and fathers aged <40 years (odds ratio = 3.1, 95% confidence interval: 2.0, 4.7). The increase in autism risk with both maternal and paternal age has potential implications for public health planning and investigations of autism etiology.
American Journal of Epidemiology - recent issues
NQO1 Polymorphisms and De Novo Childhood Leukemia: A HuGE Review and Meta-Analysis
Guha, N., Chang, J. S., Chokkalingam, A. P., Wiemels, J. L., Smith, M. T., Buffler, P. A. Fri, 21 Nov 2008 00:00:00 -0000
Polymorphisms in NQO1, a gene coding for the phase II enzyme involved in the detoxification of quinone carcinogens, have been associated with childhood leukemia in some studies, although the observed direction and magnitude of effects have been inconsistent. Therefore, the authors systematically reviewed all published reports describing the effect of NQO1 in de novo childhood leukemia and conducted a meta-analysis of 7 case-control studies that examined the association between NQO1*2 and childhood leukemia. Although a family-based study previously demonstrated overtransmission of this allele among childhood acute lymphoblastic leukemia cases, the meta-analysis showed that the presence of a NQO1*2 variant allele, which reduces the activity of the enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1), had no significant effect on childhood leukemia. However, there was an increased risk associated with having at least 1 copy of the NQO1*2 allele in a subset of cases with MLL translocations (summary odds ratio = 1.39, 95% confidence interval: 0.98, 1.97). Heterogeneity between studies may be due to differences in population exposures to NQO1 substrates and small sample sizes, as well as potential population stratification in non-family-based studies. Therefore, further research is warranted on the role of NQO1 polymorphisms in the etiology of childhood leukemia, especially among MLL-positive leukemias.
Seven Lipoprotein Lipase Gene Polymorphisms, Lipid Fractions, and Coronary Disease: A HuGE Association Review and Meta-Analysis
Sagoo, G. S., Tatt, I., Salanti, G., Butterworth, A. S., Sarwar, N., van Maarle, M., Jukema, J. W., Wiman, B., Kastelein, J. J. P., Bennet, A. M., de Faire, U., Danesh, J., Higgins, J. P. T. Fri, 21 Nov 2008 00:00:00 -0000
Lipoprotein lipase (LPL) is a key enzyme in lipoprotein metabolism and a major candidate gene for coronary heart disease (CHD). The authors assessed associations between 7 LPL polymorphisms and lipid fractions and CHD risk in population-based cohort, case-control, and cross-sectional studies published by January 2007. Meta-analyses of 22,734 CHD cases and 50,177 controls in 89 association studies focused on the relations of the T-93G (rs1800590), D9N (rs1801177), G188E, N291S (rs268), PvuII (rs285), HindIII (rs320), and S447X (rs328) polymorphisms to high density lipoprotein cholesterol, triglycerides, myocardial infarction, or coronary stenosis. Carriers of 9N or 291S had modestly adverse lipid profiles. Carriers of the less common allele of HindIII or of 447X had modestly advantageous profiles. The combined odds ratio for CHD among carriers was 1.33 (95% confidence interval (CI): 1.14, 1.56) for 9N, 1.07 (95% CI: 0.96, 1.20) for 291S, 0.89 (95% CI: 0.81, 0.98) for the less common HindIII allele, and 0.84 (95% CI: 0.75, 0.94) for 447X. For T-93G (odds ratio (OR) = 1.22, 95% CI: 0.98, 1.52) and PvuII (OR = 0.96, 95% CI: 0.89, 1.04), there were null associations with lipid levels or CHD risk; information on G188E was limited (OR = 2.80, 95% CI: 0.88, 8.87). The study of LPL genotypes confirms the existence of close interrelations between high density lipoprotein cholesterol and triglyceride pathways. The influence of these genotypes on CHD risk warrants further investigation.
The Effect of Racial Residential Segregation on Black Infant Mortality
Hearst, M. O., Oakes, J. M., Johnson, P. J. Fri, 21 Nov 2008 00:00:00 -0000
Economic differences and proximal risk factors do not fully explain the persistent high infant mortality rates of African Americans (blacks). The authors hypothesized that racial residential segregation plays an independent role in high black infant mortality rates. Segregation restricts social and economic advantage and imposes negative environmental exposures that black women and infants experience. The study sample was obtained from the 2000–2002 US Linked Birth/Infant Death records and included 677,777 black infants residing in 64 cities with 250,000 or more residents. Outcomes were rates of all-cause infant mortality, postneonatal mortality, and external causes of death. Segregation was measured by using the isolation index (dichotomized at 0.60) from the 2000 US Census Housing Patterns. Propensity score matching methods were used. After matching on propensity scores, no independent effect of segregation on black infant mortality rates was found. Results show little statistical evidence that segregation plays an independent role in black infant mortality. However, a key finding is that it is difficult to disentangle contextual effects from the characteristics of individuals.
Invited Commentary: Residential Segregation and Health--The Complexity of Modeling Separate Social Contexts
Acevedo-Garcia, D., Osypuk, T. L. Fri, 21 Nov 2008 00:00:00 -0000
When researching racial disparities in health, residential segregation cannot be ignored. Because of segregation, contextual differences by race are so pronounced that ignoring them may lead to misestimating the effect of individual-level factors. However, given the stark racial separation of social contexts, researching how residential segregation and neighborhood inequality contribute to racial health disparities remains methodologically challenging. Estimating the contribution of neighborhood effects to health disparities would require overlap in the racial distributions of neighborhood environment, for example, in the distributions of neighborhood poverty. Because of segregation, though, the extent of such overlap is extremely restricted. Previous analyses of the 2000 US Census found, on average, only a 24% overlap between the distribution of neighborhood poverty for black children and that for white children in metropolitan areas. Propensity score methods may be 1 useful tool for addressing limited overlap or exchangeability. However, as shown by their application to the segregation and health relation, their use should be informed by a sound conceptualization of the scale of the social exposure of interest, the hypothesized pathways between the exposure and the health outcome, and possible unmeasured confounders.
Maternal Body Mass Index and Lifestyle Exposures and the Risk of Bilateral Renal Agenesis or Hypoplasia: The National Birth Defects Prevention Study
Slickers, J. E., Olshan, A. F., Siega-Riz, A. M., Honein, M. A., Aylsworth, A. S., for the National Birth Defects Prevention Study Fri, 21 Nov 2008 00:00:00 -0000
Increased maternal body mass index, maternal smoking, and alcohol exposure during pregnancy have been inconsistently reported as potential risk factors for renal birth defects. The low incidence of the most severe renal anomaly, bilateral renal agenesis or hypoplasia (RA/H), has limited the ability to study this fatal defect. Using data from the National Birth Defects Prevention Study, a multicenter case-control study, the authors explored potential relations between RA/H and maternal body mass index, smoking, alcohol, and caffeine exposures. Data available for 75 infants with RA/H born between 1997 and 2003 and for randomly selected control infants without known birth defects (n = 868) were assessed by a model adjusted for folic acid use, all four exposures of interest, and study center. Bilateral RA/H was associated with a body mass index of greater than 30 kg/m2 prior to pregnancy (adjusted odds ratio (aOR) = 1.92, 95% confidence interval (CI): 1.00, 3.67), smoking during the periconceptional period (aOR = 2.09, 95% CI: 1.08, 4.03), and binge drinking during the second month of pregnancy (aOR = 3.64, 95% CI: 1.19, 11.1). These results support the need for further exploration into the potential mechanisms by which such exposures could interfere with early fetal kidney formation resulting in RA/H.
Advanced Parental Age and the Risk of Autism Spectrum Disorder
Durkin, M. S., Maenner, M. J., Newschaffer, C. J., Lee, L.-C., Cunniff, C. M., Daniels, J. L., Kirby, R. S., Leavitt, L., Miller, L., Zahorodny, W., Schieve, L. A. Fri, 21 Nov 2008 00:00:00 -0000
This study evaluated independent effects of maternal and paternal age on risk of autism spectrum disorder. A case-cohort design was implemented using data from 10 US study sites participating in the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network. The 1994 birth cohort included 253,347 study-site births with complete parental age information. Cases included 1,251 children aged 8 years with complete parental age information from the same birth cohort and identified as having an autism spectrum disorder based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision criteria. After adjustment for the other parent's age, birth order, maternal education, and other covariates, both maternal and paternal age were independently associated with autism (adjusted odds ratio for maternal age ≥35 vs. 25–29 years = 1.3, 95% confidence interval: 1.1, 1.6; adjusted odds ratio for paternal age ≥40 years vs. 25–29 years = 1.4, 95% confidence interval: 1.1, 1.8). Firstborn offspring of 2 older parents were 3 times more likely to develop autism than were third- or later-born offspring of mothers aged 20–34 years and fathers aged <40 years (odds ratio = 3.1, 95% confidence interval: 2.0, 4.7). The increase in autism risk with both maternal and paternal age has potential implications for public health planning and investigations of autism etiology.
Epidemiology and Infection - Current Issue
Volume 136 Issue 12
Mon, 01 Dec 2008 00:00:00 -0000
Epidemiology and Infection, Volume 136 Issue 12 Increased frequency in 2007 - now 8 issues per year! Epidemiology and Infection publishes original reports and reviews on all aspects of infection in humans and animals. Particular emphasis is given to the epidemiology, prevention and control of infectious diseases. The field covered is broad and includes the zoonoses, tropical infections, food hygiene, vaccine studies, statistics and the clinical, social and public-health aspects of infectious disease. Papers covering microbiology and immunology which have an epidemiological relevance are part of this broad field. Papers come from medical and veterinary scientists worldwide. It has become the key periodical in which to find the latest reports on recently discovered infections and new technology. For those concerned with policy and planning for the control of infections, the papers on mathematical modelling of epidemics caused by historical, current and emergent infections, will be of particular value. To celebrate 100 years of the journal, a series of important papers has been selected and each, together with a modern commentary on the paper by an expert, will be published on-line. This journal has now moved over to electronic submission, using the Scholar One system. Click here to go to the submission website. Guidance on how to upload your manuscript is available on the site by clicking "User Tutorials". Online manuscript submission (now) available, please go to http://mc.manuscriptcentral.com/cup/hyg
The transmission and control of XDR TB in South Africa: an operations research and mathematical modelling approach
Review ArticlesS. BASU, A. P. GALVANI, Epidemiology and Infection, Volume 136 Issue 12 , pp 1585-1598Abstract
Latest Issue of International Journal of Medical Microbiology
Editorial - ETOX turned twenty
Sebo P.
Pathogenomics of mobile genetic elements of toxigenic bacteria
Hacker J.Hochhut B.Middendorf B.Schneider G.Buchrieser C.Gottschalk G.Dobrindt U.
Subscribe to Microbiology RSS feed 
NQO1 Polymorphisms and De Novo Childhood Leukemia: A HuGE Review and Meta-Analysis
Guha, N., Chang, J. S., Chokkalingam, A. P., Wiemels, J. L., Smith, M. T., Buffler, P. A. Fri, 21 Nov 2008 00:00:00 -0000
Polymorphisms in NQO1, a gene coding for the phase II enzyme involved in the detoxification of quinone carcinogens, have been associated with childhood leukemia in some studies, although the observed direction and magnitude of effects have been inconsistent. Therefore, the authors systematically reviewed all published reports describing the effect of NQO1 in de novo childhood leukemia and conducted a meta-analysis of 7 case-control studies that examined the association between NQO1*2 and childhood leukemia. Although a family-based study previously demonstrated overtransmission of this allele among childhood acute lymphoblastic leukemia cases, the meta-analysis showed that the presence of a NQO1*2 variant allele, which reduces the activity of the enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1), had no significant effect on childhood leukemia. However, there was an increased risk associated with having at least 1 copy of the NQO1*2 allele in a subset of cases with MLL translocations (summary odds ratio = 1.39, 95% confidence interval: 0.98, 1.97). Heterogeneity between studies may be due to differences in population exposures to NQO1 substrates and small sample sizes, as well as potential population stratification in non-family-based studies. Therefore, further research is warranted on the role of NQO1 polymorphisms in the etiology of childhood leukemia, especially among MLL-positive leukemias.
Seven Lipoprotein Lipase Gene Polymorphisms, Lipid Fractions, and Coronary Disease: A HuGE Association Review and Meta-Analysis
Sagoo, G. S., Tatt, I., Salanti, G., Butterworth, A. S., Sarwar, N., van Maarle, M., Jukema, J. W., Wiman, B., Kastelein, J. J. P., Bennet, A. M., de Faire, U., Danesh, J., Higgins, J. P. T. Fri, 21 Nov 2008 00:00:00 -0000
Lipoprotein lipase (LPL) is a key enzyme in lipoprotein metabolism and a major candidate gene for coronary heart disease (CHD). The authors assessed associations between 7 LPL polymorphisms and lipid fractions and CHD risk in population-based cohort, case-control, and cross-sectional studies published by January 2007. Meta-analyses of 22,734 CHD cases and 50,177 controls in 89 association studies focused on the relations of the T-93G (rs1800590), D9N (rs1801177), G188E, N291S (rs268), PvuII (rs285), HindIII (rs320), and S447X (rs328) polymorphisms to high density lipoprotein cholesterol, triglycerides, myocardial infarction, or coronary stenosis. Carriers of 9N or 291S had modestly adverse lipid profiles. Carriers of the less common allele of HindIII or of 447X had modestly advantageous profiles. The combined odds ratio for CHD among carriers was 1.33 (95% confidence interval (CI): 1.14, 1.56) for 9N, 1.07 (95% CI: 0.96, 1.20) for 291S, 0.89 (95% CI: 0.81, 0.98) for the less common HindIII allele, and 0.84 (95% CI: 0.75, 0.94) for 447X. For T-93G (odds ratio (OR) = 1.22, 95% CI: 0.98, 1.52) and PvuII (OR = 0.96, 95% CI: 0.89, 1.04), there were null associations with lipid levels or CHD risk; information on G188E was limited (OR = 2.80, 95% CI: 0.88, 8.87). The study of LPL genotypes confirms the existence of close interrelations between high density lipoprotein cholesterol and triglyceride pathways. The influence of these genotypes on CHD risk warrants further investigation.
The Effect of Racial Residential Segregation on Black Infant Mortality
Hearst, M. O., Oakes, J. M., Johnson, P. J. Fri, 21 Nov 2008 00:00:00 -0000
Economic differences and proximal risk factors do not fully explain the persistent high infant mortality rates of African Americans (blacks). The authors hypothesized that racial residential segregation plays an independent role in high black infant mortality rates. Segregation restricts social and economic advantage and imposes negative environmental exposures that black women and infants experience. The study sample was obtained from the 2000–2002 US Linked Birth/Infant Death records and included 677,777 black infants residing in 64 cities with 250,000 or more residents. Outcomes were rates of all-cause infant mortality, postneonatal mortality, and external causes of death. Segregation was measured by using the isolation index (dichotomized at 0.60) from the 2000 US Census Housing Patterns. Propensity score matching methods were used. After matching on propensity scores, no independent effect of segregation on black infant mortality rates was found. Results show little statistical evidence that segregation plays an independent role in black infant mortality. However, a key finding is that it is difficult to disentangle contextual effects from the characteristics of individuals.
Invited Commentary: Residential Segregation and Health--The Complexity of Modeling Separate Social Contexts
Acevedo-Garcia, D., Osypuk, T. L. Fri, 21 Nov 2008 00:00:00 -0000
When researching racial disparities in health, residential segregation cannot be ignored. Because of segregation, contextual differences by race are so pronounced that ignoring them may lead to misestimating the effect of individual-level factors. However, given the stark racial separation of social contexts, researching how residential segregation and neighborhood inequality contribute to racial health disparities remains methodologically challenging. Estimating the contribution of neighborhood effects to health disparities would require overlap in the racial distributions of neighborhood environment, for example, in the distributions of neighborhood poverty. Because of segregation, though, the extent of such overlap is extremely restricted. Previous analyses of the 2000 US Census found, on average, only a 24% overlap between the distribution of neighborhood poverty for black children and that for white children in metropolitan areas. Propensity score methods may be 1 useful tool for addressing limited overlap or exchangeability. However, as shown by their application to the segregation and health relation, their use should be informed by a sound conceptualization of the scale of the social exposure of interest, the hypothesized pathways between the exposure and the health outcome, and possible unmeasured confounders.
Maternal Body Mass Index and Lifestyle Exposures and the Risk of Bilateral Renal Agenesis or Hypoplasia: The National Birth Defects Prevention Study
Slickers, J. E., Olshan, A. F., Siega-Riz, A. M., Honein, M. A., Aylsworth, A. S., for the National Birth Defects Prevention Study Fri, 21 Nov 2008 00:00:00 -0000
Increased maternal body mass index, maternal smoking, and alcohol exposure during pregnancy have been inconsistently reported as potential risk factors for renal birth defects. The low incidence of the most severe renal anomaly, bilateral renal agenesis or hypoplasia (RA/H), has limited the ability to study this fatal defect. Using data from the National Birth Defects Prevention Study, a multicenter case-control study, the authors explored potential relations between RA/H and maternal body mass index, smoking, alcohol, and caffeine exposures. Data available for 75 infants with RA/H born between 1997 and 2003 and for randomly selected control infants without known birth defects (n = 868) were assessed by a model adjusted for folic acid use, all four exposures of interest, and study center. Bilateral RA/H was associated with a body mass index of greater than 30 kg/m2 prior to pregnancy (adjusted odds ratio (aOR) = 1.92, 95% confidence interval (CI): 1.00, 3.67), smoking during the periconceptional period (aOR = 2.09, 95% CI: 1.08, 4.03), and binge drinking during the second month of pregnancy (aOR = 3.64, 95% CI: 1.19, 11.1). These results support the need for further exploration into the potential mechanisms by which such exposures could interfere with early fetal kidney formation resulting in RA/H.
Advanced Parental Age and the Risk of Autism Spectrum Disorder
Durkin, M. S., Maenner, M. J., Newschaffer, C. J., Lee, L.-C., Cunniff, C. M., Daniels, J. L., Kirby, R. S., Leavitt, L., Miller, L., Zahorodny, W., Schieve, L. A. Fri, 21 Nov 2008 00:00:00 -0000
This study evaluated independent effects of maternal and paternal age on risk of autism spectrum disorder. A case-cohort design was implemented using data from 10 US study sites participating in the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network. The 1994 birth cohort included 253,347 study-site births with complete parental age information. Cases included 1,251 children aged 8 years with complete parental age information from the same birth cohort and identified as having an autism spectrum disorder based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision criteria. After adjustment for the other parent's age, birth order, maternal education, and other covariates, both maternal and paternal age were independently associated with autism (adjusted odds ratio for maternal age ≥35 vs. 25–29 years = 1.3, 95% confidence interval: 1.1, 1.6; adjusted odds ratio for paternal age ≥40 years vs. 25–29 years = 1.4, 95% confidence interval: 1.1, 1.8). Firstborn offspring of 2 older parents were 3 times more likely to develop autism than were third- or later-born offspring of mothers aged 20–34 years and fathers aged <40 years (odds ratio = 3.1, 95% confidence interval: 2.0, 4.7). The increase in autism risk with both maternal and paternal age has potential implications for public health planning and investigations of autism etiology.
American Journal of Epidemiology - recent issues
NQO1 Polymorphisms and De Novo Childhood Leukemia: A HuGE Review and Meta-Analysis
Guha, N., Chang, J. S., Chokkalingam, A. P., Wiemels, J. L., Smith, M. T., Buffler, P. A. Fri, 21 Nov 2008 00:00:00 -0000
Polymorphisms in NQO1, a gene coding for the phase II enzyme involved in the detoxification of quinone carcinogens, have been associated with childhood leukemia in some studies, although the observed direction and magnitude of effects have been inconsistent. Therefore, the authors systematically reviewed all published reports describing the effect of NQO1 in de novo childhood leukemia and conducted a meta-analysis of 7 case-control studies that examined the association between NQO1*2 and childhood leukemia. Although a family-based study previously demonstrated overtransmission of this allele among childhood acute lymphoblastic leukemia cases, the meta-analysis showed that the presence of a NQO1*2 variant allele, which reduces the activity of the enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1), had no significant effect on childhood leukemia. However, there was an increased risk associated with having at least 1 copy of the NQO1*2 allele in a subset of cases with MLL translocations (summary odds ratio = 1.39, 95% confidence interval: 0.98, 1.97). Heterogeneity between studies may be due to differences in population exposures to NQO1 substrates and small sample sizes, as well as potential population stratification in non-family-based studies. Therefore, further research is warranted on the role of NQO1 polymorphisms in the etiology of childhood leukemia, especially among MLL-positive leukemias.
Seven Lipoprotein Lipase Gene Polymorphisms, Lipid Fractions, and Coronary Disease: A HuGE Association Review and Meta-Analysis
Sagoo, G. S., Tatt, I., Salanti, G., Butterworth, A. S., Sarwar, N., van Maarle, M., Jukema, J. W., Wiman, B., Kastelein, J. J. P., Bennet, A. M., de Faire, U., Danesh, J., Higgins, J. P. T. Fri, 21 Nov 2008 00:00:00 -0000
Lipoprotein lipase (LPL) is a key enzyme in lipoprotein metabolism and a major candidate gene for coronary heart disease (CHD). The authors assessed associations between 7 LPL polymorphisms and lipid fractions and CHD risk in population-based cohort, case-control, and cross-sectional studies published by January 2007. Meta-analyses of 22,734 CHD cases and 50,177 controls in 89 association studies focused on the relations of the T-93G (rs1800590), D9N (rs1801177), G188E, N291S (rs268), PvuII (rs285), HindIII (rs320), and S447X (rs328) polymorphisms to high density lipoprotein cholesterol, triglycerides, myocardial infarction, or coronary stenosis. Carriers of 9N or 291S had modestly adverse lipid profiles. Carriers of the less common allele of HindIII or of 447X had modestly advantageous profiles. The combined odds ratio for CHD among carriers was 1.33 (95% confidence interval (CI): 1.14, 1.56) for 9N, 1.07 (95% CI: 0.96, 1.20) for 291S, 0.89 (95% CI: 0.81, 0.98) for the less common HindIII allele, and 0.84 (95% CI: 0.75, 0.94) for 447X. For T-93G (odds ratio (OR) = 1.22, 95% CI: 0.98, 1.52) and PvuII (OR = 0.96, 95% CI: 0.89, 1.04), there were null associations with lipid levels or CHD risk; information on G188E was limited (OR = 2.80, 95% CI: 0.88, 8.87). The study of LPL genotypes confirms the existence of close interrelations between high density lipoprotein cholesterol and triglyceride pathways. The influence of these genotypes on CHD risk warrants further investigation.
The Effect of Racial Residential Segregation on Black Infant Mortality
Hearst, M. O., Oakes, J. M., Johnson, P. J. Fri, 21 Nov 2008 00:00:00 -0000
Economic differences and proximal risk factors do not fully explain the persistent high infant mortality rates of African Americans (blacks). The authors hypothesized that racial residential segregation plays an independent role in high black infant mortality rates. Segregation restricts social and economic advantage and imposes negative environmental exposures that black women and infants experience. The study sample was obtained from the 2000–2002 US Linked Birth/Infant Death records and included 677,777 black infants residing in 64 cities with 250,000 or more residents. Outcomes were rates of all-cause infant mortality, postneonatal mortality, and external causes of death. Segregation was measured by using the isolation index (dichotomized at 0.60) from the 2000 US Census Housing Patterns. Propensity score matching methods were used. After matching on propensity scores, no independent effect of segregation on black infant mortality rates was found. Results show little statistical evidence that segregation plays an independent role in black infant mortality. However, a key finding is that it is difficult to disentangle contextual effects from the characteristics of individuals.
Invited Commentary: Residential Segregation and Health--The Complexity of Modeling Separate Social Contexts
Acevedo-Garcia, D., Osypuk, T. L. Fri, 21 Nov 2008 00:00:00 -0000
When researching racial disparities in health, residential segregation cannot be ignored. Because of segregation, contextual differences by race are so pronounced that ignoring them may lead to misestimating the effect of individual-level factors. However, given the stark racial separation of social contexts, researching how residential segregation and neighborhood inequality contribute to racial health disparities remains methodologically challenging. Estimating the contribution of neighborhood effects to health disparities would require overlap in the racial distributions of neighborhood environment, for example, in the distributions of neighborhood poverty. Because of segregation, though, the extent of such overlap is extremely restricted. Previous analyses of the 2000 US Census found, on average, only a 24% overlap between the distribution of neighborhood poverty for black children and that for white children in metropolitan areas. Propensity score methods may be 1 useful tool for addressing limited overlap or exchangeability. However, as shown by their application to the segregation and health relation, their use should be informed by a sound conceptualization of the scale of the social exposure of interest, the hypothesized pathways between the exposure and the health outcome, and possible unmeasured confounders.
Maternal Body Mass Index and Lifestyle Exposures and the Risk of Bilateral Renal Agenesis or Hypoplasia: The National Birth Defects Prevention Study
Slickers, J. E., Olshan, A. F., Siega-Riz, A. M., Honein, M. A., Aylsworth, A. S., for the National Birth Defects Prevention Study Fri, 21 Nov 2008 00:00:00 -0000
Increased maternal body mass index, maternal smoking, and alcohol exposure during pregnancy have been inconsistently reported as potential risk factors for renal birth defects. The low incidence of the most severe renal anomaly, bilateral renal agenesis or hypoplasia (RA/H), has limited the ability to study this fatal defect. Using data from the National Birth Defects Prevention Study, a multicenter case-control study, the authors explored potential relations between RA/H and maternal body mass index, smoking, alcohol, and caffeine exposures. Data available for 75 infants with RA/H born between 1997 and 2003 and for randomly selected control infants without known birth defects (n = 868) were assessed by a model adjusted for folic acid use, all four exposures of interest, and study center. Bilateral RA/H was associated with a body mass index of greater than 30 kg/m2 prior to pregnancy (adjusted odds ratio (aOR) = 1.92, 95% confidence interval (CI): 1.00, 3.67), smoking during the periconceptional period (aOR = 2.09, 95% CI: 1.08, 4.03), and binge drinking during the second month of pregnancy (aOR = 3.64, 95% CI: 1.19, 11.1). These results support the need for further exploration into the potential mechanisms by which such exposures could interfere with early fetal kidney formation resulting in RA/H.
Advanced Parental Age and the Risk of Autism Spectrum Disorder
Durkin, M. S., Maenner, M. J., Newschaffer, C. J., Lee, L.-C., Cunniff, C. M., Daniels, J. L., Kirby, R. S., Leavitt, L., Miller, L., Zahorodny, W., Schieve, L. A. Fri, 21 Nov 2008 00:00:00 -0000
This study evaluated independent effects of maternal and paternal age on risk of autism spectrum disorder. A case-cohort design was implemented using data from 10 US study sites participating in the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network. The 1994 birth cohort included 253,347 study-site births with complete parental age information. Cases included 1,251 children aged 8 years with complete parental age information from the same birth cohort and identified as having an autism spectrum disorder based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision criteria. After adjustment for the other parent's age, birth order, maternal education, and other covariates, both maternal and paternal age were independently associated with autism (adjusted odds ratio for maternal age ≥35 vs. 25–29 years = 1.3, 95% confidence interval: 1.1, 1.6; adjusted odds ratio for paternal age ≥40 years vs. 25–29 years = 1.4, 95% confidence interval: 1.1, 1.8). Firstborn offspring of 2 older parents were 3 times more likely to develop autism than were third- or later-born offspring of mothers aged 20–34 years and fathers aged <40 years (odds ratio = 3.1, 95% confidence interval: 2.0, 4.7). The increase in autism risk with both maternal and paternal age has potential implications for public health planning and investigations of autism etiology.
Epidemiology and Infection - Current Issue
Volume 136 Issue 12
Mon, 01 Dec 2008 00:00:00 -0000
Epidemiology and Infection, Volume 136 Issue 12 Increased frequency in 2007 - now 8 issues per year! Epidemiology and Infection publishes original reports and reviews on all aspects of infection in humans and animals. Particular emphasis is given to the epidemiology, prevention and control of infectious diseases. The field covered is broad and includes the zoonoses, tropical infections, food hygiene, vaccine studies, statistics and the clinical, social and public-health aspects of infectious disease. Papers covering microbiology and immunology which have an epidemiological relevance are part of this broad field. Papers come from medical and veterinary scientists worldwide. It has become the key periodical in which to find the latest reports on recently discovered infections and new technology. For those concerned with policy and planning for the control of infections, the papers on mathematical modelling of epidemics caused by historical, current and emergent infections, will be of particular value. To celebrate 100 years of the journal, a series of important papers has been selected and each, together with a modern commentary on the paper by an expert, will be published on-line. This journal has now moved over to electronic submission, using the Scholar One system. Click here to go to the submission website. Guidance on how to upload your manuscript is available on the site by clicking "User Tutorials". Online manuscript submission (now) available, please go to http://mc.manuscriptcentral.com/cup/hyg
The transmission and control of XDR TB in South Africa: an operations research and mathematical modelling approach
Review ArticlesS. BASU, A. P. GALVANI, Epidemiology and Infection, Volume 136 Issue 12 , pp 1585-1598Abstract
Latest Issue of International Journal of Medical Microbiology
Editorial - ETOX turned twenty
Sebo P.
Pathogenomics of mobile genetic elements of toxigenic bacteria
Hacker J.Hochhut B.Middendorf B.Schneider G.Buchrieser C.Gottschalk G.Dobrindt U.
Sites:
American Type Culture Collection (ATCC): ATCC is a global bioresource center that stores and distributes biological materials such as cell lines, bacteria, animal and plant viruses and antisera, fungi, protozoa, algae, clones and other molecular genomic materials. We also manage databases and offer repository management and other labora...Antimicrobial Resistance Surveillance (BSAC Working Party): Information about antimicrobial resistance surveillance programmes run by BSAC (British Society for Antimicrobial Chemotherapy) and links to related sites.
Association for Professionals in Infection Control and Epidemiology, Inc.: Association for Professionals in Infection Control and Epidemiology is an association of healthcare professionals working to reduce, control and prevent infections associated with or acquired in a healthcare setting.
Bacterial Toxins: Friends or Foes?: Overview of the biochemistry and mechanism of action of bacterial toxins from the Center for Disease Control (CDC).
Candida albicans Pseudomonas Helicobacter epidemiology: Molecular epidemiology, virulence factors, virulence genes of pathogenic microorganisms.
CDC Division of Healthcare Quality Promotion: Issues in Healthcare Settings: Articles and statistics related to infectious diseases and hospitals and hospital personnel.
Clinical Microbiology Software: Interpretation and Report of Antimicrobial Susceptibility Test.: This is based on "rule-base expert system" and freeware. End-user can modify and add rules. This is assistant software to interpret and report antimicrobial( antibiotics ) susceptibility tests for clinical microbiology department,
Common Cold: A comprehensive source of information on the common cold that facilitates informed decisions about cold prevention and treatment.
Department of Medical Microbiology of the University of Zurich: Homepage of the Department of Medical Microbiology, University Zurich
Family Practice Notebook: Infectious Disease: Covers Bacteria, Emerging, Examination, Faver, Fever, Fungus, Helminth, Immune, Immunization, Parasite, Prion, Procedure, Sexually Transmitted Disease, Travel, Vector and Virus. Related chapters from other specialties include Dermatology, Ophthalmology, Gastroenterology, HIV, Laboratory, Neurolo...
General Practice Notebook - Infectious disease: Coverage of this medical speciality.
Genomics and Bacterial Pathogenesis: This review summarises the current methodologies used in genome analysis
Global Infectious Diseases and Epidemiology Network: GIDEON - Provides information, including disease, therapy and vaccine lists, support and demo of GIDEON. Medical software for the fields of infectious diseases and microbiology targeted at doctors and lab specialists.
Infection Control: Recent litterature abstracts on infection control updated every three months
Infectious disease information: Information about infectious disease in overview form, provided by Aventis.
Know Your Enemy: Determining the Genetic Blueprint of Disease-Causing Microorganisms, NIAID Fact Sheet: A fact sheet from the National Institute of Allergy and Infectious Diseases (NIAID) explaining, in simple terms, the objectives behind the finished and ongoing sequencing projects of pathogen genomes.
Medical Microbiology Synopsis: Site provides an overview of medical microbiology for students of medicine. Typical and atypical microbial flora are listed per specimen source and characterized in flowchart diagrams that can be easily memorized.
Microbiology at Mount Sinai Hospital, Toronto, Canada: We are a comprehensive, primary-source, Canadian microbiology and infectious diseases site. This site contains data from population and laboratory based surveillance programs, frequently requested papers and protocols, our current in use Lab Manual, as well as a forum for frequently asked q...
Physiopathological role of microbial metallogeny: Page personnelle de Stephane PLOUVIER
Reservoirs of Antibiotic Resistance Network: ROAR - Alliance for the Prudent Use of Antibiotics: A network, interactive database and information source organized around antibiotic resistance.
Reviews in Medical Microbiology: Journal of the Pathological Society of Great Britain and Ireland. Covering developments and techniques in medical microbiology, virology, mycology, parasitology, clinical microbiology, and hospital infection.
The United Kingdom National Culture collection: Fireworks Splice HTML
Using DNA Microarrays to Study Host-Microbe Interactions: This article provides a detailed introduction to DNA microarray technology and their application to the identification of host-pathogen interactions and virulence factors.
This directory is based on the Open Directory and may have been modified