domingo, 1 de julio de 2012

Another reason why dads and hopeful dads should quit smoking now

Another Reason Why Dads and Hopeful Dads Should Quit Smoking Now

ScienceDaily (June 23, 2012) — As you decide what to get dad for Father's Day, you might want to consider what he gave you when you were conceived. If he smoked, your genes are likely damaged, and your odds for cancers and other diseases throughout your life could be increased. A new research report appearing online in the FASEB Journal, scientists show for the first time in humans that men who smoke before conception can damage the genetic information of their offspring. These inherited changes in DNA could possibly render an offspring in the womb susceptible to later disease such as cancer.

This provides evidence showing why men should be urged to stop smoking before trying to conceive in the same way women have been urged to quit. Interestingly, a fertile sperm cell takes about three months to fully develop; therefore men would ultimately need to quit smoking long before conception to avoid causing genetic problems.
"That smoking of fathers at the time around conception can lead to genetic changes in their children indicates that the deleterious effects of smoking can be transmitted through the father to the offspring," said Diana Anderson, Ph.D., a researcher involved in the work from the School of Life Sciences at the University of Bradford, in the United Kingdom. "These transmitted genetic changes may raise the risk of developing cancer in childhood, particularly leukemia and other genetic diseases. We hope that this knowledge will urge men to cease smoking before trying to conceive."
To make this discovery, Anderson and colleagues used DNA biomarkers to measure genetic changes in the paternal blood and semen around conception, as well as maternal and umbilical cord blood at delivery in families from two different European regions in central England and a Greek island. Information regarding the lifestyle, environmental and occupational exposures of these families was taken from validated questionnaires. The combined analysis of exposures and DNA biomarkers was used to evaluate the role of exposures before conception and during pregnancy in the causation of genetic changes in the offspring. These results have strong implications for the prevention of disease.
"This report shows that smoking is a germ cell mutagen. If dad uses cigarettes, his kids will be affected even before they are born," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "As Father's Day approaches, family members may want to give dads and prospective dads the help they need to quit smoking for good."

Story Source:

The above story is reprinted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

J. Laubenthal, O. Zlobinskaya, K. Poterlowicz, A. Baumgartner, M. R. Gdula, E. Fthenou, M. Keramarou, S. J. Hepworth, J. C. S. Kleinjans, F.-J. van Schooten, G. Brunborg, R. W. Godschalk, T. E. Schmid, D. Anderson. Cigarette smoke-induced transgenerational alterations in genome stability in cord blood of human F1 offspring. The FASEB Journal, 2012; DOI: 10.1096/fj.11-201194

RFA-HG-12-015: Population Architecture Using Genomics and Epidemiology (PAGE), Phase II Coordinating Center (U01)

Funding

Population Architecture Using Genomics and Epidemiology (PAGE), Phase II – Coordinating Center (U01)

RFA-HG-12-015: Population Architecture Using Genomics and Epidemiology (PAGE), Phase II Coordinating Center (U01)

Population Architecture Using Genomics and Epidemiology (PAGE), Phase II Study Investigators (U01)

Population Architecture Using Genomics and Epidemiology (PAGE), Phase II Study Investigators (U01)

RFA-HG-12-010: Population Architecture Using Genomics and Epidemiology (PAGE), Phase II Study Investigators (U01)

Differential Association of Gene Content Polymorphi... [PLoS One. 2012] - PubMed - NCBI

PLoS One. 2012;7(6):e38617. Epub 2012 Jun 8.

Differential Association of Gene Content Polymorphisms of Killer Cell Immunoglobulin-Like Receptors with Placental Malaria in HIV- and HIV+ Mothers.

Omosun YO, Blackstock AJ, Gatei W, Hightower A, van Eijk AM, Ayisi J, Otieno J, Lal RB, Steketee R, Nahlen B, Ter Kuile FO, Slutsker L, Shi YP.

Source

Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America.

Abstract

Pregnant women have abundant natural killer (NK) cells in their placenta, and NK cell function is regulated by polymorphisms of killer cell immunoglobulin-like receptors (KIRs). Previous studies report different roles of NK cells in the immune responses to placental malaria (PM) and human immunodeficiency virus (HIV-1) infections. Given these references, the aim of this study was to determine the association between KIR gene content polymorphism and PM infection in pregnant women of known HIV-1 status. Sixteen genes in the KIR family were analyzed in 688 pregnant Kenyan women. Gene content polymorphisms were assessed in relation to PM in HIV-1 negative and HIV-1 positive women, respectively. Results showed that in HIV-1 negative women, the presence of the individual genes KIR2DL1 and KIR2DL3 increased the odds of having PM, and the KIR2DL2/KIR2DL2 homozygotes were associated with protection from PM. However, the reverse relationship was observed in HIV-1 positive women, where the presence of individual KIR2DL3 was associated with protection from PM, and KIR2DL2/KIR2DL2 homozygotes increased the odds for susceptibility to PM. Further analysis of the HIV-1 positive women stratified by CD4 counts showed that this reverse association between KIR genes and PM remained only in the individuals with high CD4 cell counts but not in those with low CD4 cell counts. Collectively, these results suggest that inhibitory KIR2DL2 and KIR2DL3, which are alleles of the same locus, play a role in the inverse effects on PM and PM/HIV co-infection and the effect of KIR genes on PM in HIV positive women is dependent on high CD4 cell counts. In addition, analysis of linkage disequilibrium (LD) of the PM relevant KIR genes showed strong LD in women without PM regardless of their HIV status while LD was broken in those with PM, indicating possible selection pressure by malaria infection on the KIR genes.

PMID:: 22715396; [PubMed - in process]
PMCID:: PMC3371008

Free PMC Article

Differential Association of Gene Content Polymorphisms of Killer Cell Immunoglobulin-Like Receptors with Placental Malaria in HIV− and HIV+ Mothers

Cancer in children with nonchromosomal birth defects. [J Pediatr. 2012] - PubMed - NCBI

J Pediatr. 2012 Jun;160(6):978-83. Epub 2012 Jan 11.

Cancer in children with nonchromosomal birth defects.

Fisher PG, Reynolds P, Von Behren J, Carmichael SL, Rasmussen SA, Shaw GM.

Source

Department of Neurology, Stanford University, Palo Alto, CA; Department of Pediatrics, Stanford University, Palo Alto, CA; Department of Neurosurgery, Stanford University, Palo Alto, CA; Department of Human Biology, Stanford University, Palo Alto, CA.

Abstract

OBJECTIVE:

To examine whether the incidence of childhood cancer is elevated in children with birth defects but no chromosomal anomalies.

STUDY DESIGN:

We examined cancer risk in a population-based cohort of children with and without major birth defects born between 1988 and 2004, by linking data from the California Birth Defects Monitoring Program, the California Cancer Registry, and birth certificates. Cox proportional hazards models generated hazard ratios (HRs) and 95% CIs based on person-years at risk. We compared the risk of childhood cancer in infants born with and without specific types of birth defects, excluding infants with chromosomal anomalies.

RESULTS:

Of the 4869 children in the birth cohort with cancer, 222 had a major birth defect. Although the expected elevation in cancer risk was observed in children with chromosomal birth defects (HR, 12.44; 95% CI, 10.10-15.32), especially for the leukemias (HR, 28.99; 95% CI, 23.07-36.42), children with nonchromosomal birth defects also had an increased risk of cancer (HR, 1.58; 95% CI, 1.33-1.87), but instead for brain tumors, lymphomas, neuroblastoma, and germ cell tumors.

CONCLUSION:

Children with nonchromosomal birth defects are at increased risk for solid tumors, but not leukemias. Dysregulation of early human development likely plays an important role in the etiology of childhood cancer.
Copyright © 2012 Mosby, Inc. All rights reserved.

PMID:: 22244463; [PubMed - in process]

Nocardia amikacinitolerans sp. nov... [Int J Syst Evol Microbiol. 2012] - PubMed - NCBI

Int J Syst Evol Microbiol. 2012 Jun 15. [Epub ahead of print]

Nocardia amikacinitolerans sp. nov., an amikacin-resistant human pathogen.

Ezeoke I, Klenk HP, Pötter G, Schumann P, Moser BD, Lasker BA, Nicholson A, Brown JM.

Source

Centers for Disease Control and Prevention;

Abstract

Five isolates from clinical human sources were evaluated. Analysis of the near full length 16S rRNA gene showed 99.9-100 % similarity among the strains. The results of a comparative phylogenetic analysis of the 16S rRNA gene sequences indicated that the isolates belonged to the genus Nocardia. Phenotypic and molecular analyses were performed on the clinical isolates. Traditional phenotypic analyses included morphologic, biochemical/physiological, chemotaxonomic and antimicrobial susceptibility profiling. Molecular studies included 1441-bp 16S rRNA and 1246-bp gyrB gene sequence analyses, as well as DNA-DNA hybridizations. Biochemical analysis failed to differentiate the putative novel species from its phylogenetic neighbors; however, molecular studies were able to distinguish the patient strains and confirm them as a single species. Based on 16S rRNA gene sequence analysis, similarity between the isolates and their closest relatives (Nocardia araoensis, Nocardia arthritidis, Nocardia beijingensis and Nocardia niwae) were less than or equal to 99.3 %. Partial gyrB gene sequence analysis showed 98-99.7 % relatedness among the isolates. Nocardia lijiangensis and Nocardia xishanensis were the isolates' closest related species based on gyrB gene sequence analysis and showed 95.7 and 95.3 % similarity, respectively. Resistance to amikacin and molecular analyses, including DNA-DNA hybridization, distinguished the five patient strains from their phylogenetic neighbors, and the results of this polyphasic study indicated a novel species of Nocardia for which we propose the name Nocardia amikacinitolerans sp. nov., with strain W9988T (=DSM 45539 T = CCUG 59655T) as the type strain.

PMID:: 22707533; [PubMed - as supplied by publisher]

Genetic Characterization of Cryptospo... [Zoonoses Public Health. 2012] - PubMed - NCBI

Zoonoses Public Health. 2012 Jun 20. doi: 10.1111/j.1863-2378.2012.01507.x. [Epub ahead of print]

Genetic Characterization of Cryptosporidium spp. in Diarrhoeic Children from Four Provinces in South Africa.

Abu Samra N, Thompson PN, Jori F, Frean J, Poonsamy B, du Plessis D, Mogoye B, Xiao L.

Source

Epidemiology Section, Department of Production Animal Studies, University of Pretoria, Pretoria, South Africa CIRAD, UR AGIRs, Department of Zoology and Entomology, Mammal Research Institute, University of Pretoria, Pretoria, South Africa National Institute for Communicable Diseases, South African Rotavirus Surveillance Programme, University of the Witwatersrand, Johannesburg, South Africa Division of Foodborne, Waterborne and Environmental Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA.

Abstract

The diversity of Cryptosporidium at species, subtype family and subtype level in diarrhoeic children was investigated in four provinces in South Africa. A total of 442 stool samples from children <5 years of age were collected under a large rotavirus surveillance programme and analysed by Ziehl-Neelsen acid-fast staining. Fifty-four (12.2%) were positive for Cryptosporidium, of which 25 were genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) and DNA sequence analyses of the 18S rRNA gene. The majority of genotyped specimens were identified as C. hominis (76%), and a high genetic diversity was found with five different C. hominis subtype families (Ia, Ib, Id, Ie and If). Cryptosporidium parvum was found in 20% of the isolates, and three subtype families were identified (IIc, IIe and IIb), with subtype family IIc being the most common. One specimen was identified as C. meleagridis of the subtype family IIId. These results are in accordance with findings from other developing countries and report for the first time the presence in South Africa of C. meleagridis, various subtypes of C. parvum and the subtype family Ie of C. hominis. The results suggest that C. hominis and anthroponotic C. parvum subtypes are the major cause of cryptosporidiosis in South Africa. Further molecular studies are needed to better understand the epidemiology and public health importance of Cryptosporidium in humans in South Africa.
© 2012 Blackwell Verlag GmbH.