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Male Births (male + birth)
Selected AbstractsAdverse health effects of children's exposure to pesticides: What do we really know and what can be done about itACTA PAEDIATRICA, Issue 2006JOANNA JUREWICZ Abstract Children may be exposed to pesticides in several ways, such as by transplacental transfer during foetal life, by intake of contaminated breast milk and other nutrients, or by contact with contaminated subjects and areas in the environment such as pets treated with insecticides, house dust, carpets and chemically treated lawns and gardens. Exposure early in life, and particularly during periods of rapid development, such as during foetal life and infancy, may have severe effects on child health and development by elevating the risk of congenital malformations, cancer, malabsorption, immunological dysfunction, endocrine disease, and neurobehavioural deficiencies. As pesticides can also interfere with parental reproductive health, exposure of parents may have consequences for the offspring leading to reduced chance of male birth and increased risk of childhood cancer. Conclusions: Current knowledge about tolerable levels and consequences of toxic exposure to pesticides during human development is rather scarce. Owing to the high risk of exposure to pesticides, particularly in less developed countries, further elucidation by well-controlled epidemiological studies in this field it is urgently needed. The Policy Interpretation Network on Children's Health and Environment (PINCHE), which is financed by the EU DG research has suggested actions against pesticide exposure. They have been presented and discussed in this paper. Several suggestions of PINCHE concerning action needed regarding pesticides were presented in the paper. [source] Breakpoint of a balanced translocation (X:14) (q27.1;q32.3) in a girl with severe hemophilia B maps proximal to the factor IX geneJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 3 2004J. Di Paola Summary., Hemophilia B is an X-linked bleeding disorder caused by the deficiency of coagulation factor (F)IX, with an estimated prevalence of 1 in 30 000 male births. It is almost exclusively seen in males with rare exceptions. We report a girl who was diagnosed with severe (<1%) FIX deficiency at 4 months of age. Cytogenetic studies in the patient showed a balanced translocation between one of the X-chromosomes and chromosome 14, with breakpoints at bands Xq27.1 and 14q32.3. Both parents were found to have normal chromosomes. Late replication studies by incorporation of 5-bromodeoxyuridine showed non-random inactivation of the normal X-chromosome, a phenomenon frequently seen in balanced X/autosome translocations. To map the breakpoint, fluorescent in-situ hybridization was performed. A PAC DNA probe, RP6-88D7 (which contains the FIX gene) hybridized only on the normal chromosome X as well as onto the derivative 14. Using a PAC DNA probe, RP11-963P9 that is located proximal to the FIX gene, we obtained signals on the normal and derivative X and also on the derivative 14. We conclude that the breakpoint is located within the DNA sequence of this clone mapping proximal to the FIX gene. Since the FIX gene seems to be intact in the derivative 14, the breakpoint may affect an upstream regulatory sequence that subjects the gene to position effect variegation (PEV). [source] The Sex Ratio Transition in AsiaPOPULATION AND DEVELOPMENT REVIEW, Issue 3 2009Christophe Z. Guilmoto This article adopts a comparative perspective to review the recent increase in the sex ratio at birth (SRB) across Asia. It first describes and compares the most recent birth statistics in Asia in order to identify commonalities in the gradual rise of SRBs observed from Armenia to South Korea. This comparison provides the basis for identifying specific transition patterns in the changes in SRBs. Their recent rise is then interpreted in a social and historical framework borrowed from fertility decline and based on three preconditions: access to sex-selection technology, preference for male births, and pressure from low fertility. On a broader plane, the process of growing imbalances in the sex composition of the population gives rise to a tragedy of the commons. This article indicates the factors that appear most likely to trigger a turnaround in this transitional demographic situation and to facilitate a return to biologically normal sex ratios in the future. [source] Secular trends of hypospadias prevalence and factors associated with it in southeast China during 1993,2005BIRTH DEFECTS RESEARCH, Issue 6 2010Lei Jin Abstract BACKGROUND The aim of this study is to describe the prevalence of hypospadias and its time trends during 1993,2005 in southeast China, and to explore the potential risk factors. METHODS The study population included all male live and still births (at least 20 weeks of gestation) in 11 cities and counties in Jiangsu and Zhejiang Provinces in Southeast China born during January 1, 1993, through December 31, 2005. RESULTS Overall prevalence of hypospadias was 5.8 per 10,000 male births and presented an increasing trend during 1993,2005 (with , of 3.94, p = 0.047). Prevalence of coronal hypospadias and those with unknown sites increased from 1.7 and 0.3 per 10,000 male births in 1993 to 3.6 and 1.4 per 10,000 male births in 2005, respectively (with , of 7.29 and 9.05, p = 0.007 and p = 0.002, respectively), but prevalence of perineal hypospadias decreased (with , of 7.13, p = 0.008). Maternal fever during first trimester, birth of twins or more children, and year of birth were independent risk factors for hypospadias, with odds ratios of 4.14 (95% CI, 1.32,12.83), 3.37 (95% CI, 1.73,6.58), and 1.04 (95% CI, 1.00,1.08), respectively, after adjusting for confounding factors with multivariable logistic regression analysis. CONCLUSIONS Prevalence of hypospadias increased during 1993,2005 in the two provinces in southeast China. Maternal fever in the first trimester and birth of twins or more children are associated with the risk for hypospadias. Birth Defects Research (Part A), 2010. © 2010 Wiley-Liss, Inc. [source] Molecular epidemiology of hypospadias: Review of genetic and environmental risk factorsBIRTH DEFECTS RESEARCH, Issue 10 2003Jeanne M. Manson Hypospadias is one of the most common congenital anomalies in the United States, occurring in approximately 1 in 125 live male births. It is characterized by altered development of the urethra, foreskin, and ventral surface of the penis. In this review, the embryology, epidemiology, risk factors, genetic predisposition, and likely candidate genes for hypospadias are described. Recent reports have identified increases in the birth prevalence of mild and severe forms of hypospadias in the United States from the 1960s to the present. Studies in consanguineous families and small case series have identified allelic variants in genes controlling androgen action and metabolism that cause hypospadias, but the relevance of these findings to the general population is unknown. Concern has also focused on whether exposure to endocrine disrupting chemicals (EDC) with antiandrogenic activity is the cause of this increase. Hypospadias is believed to have a multifactorial etiology in which allelic variants in genes controlling androgen action and metabolism predispose individuals to develop this condition. When genetic susceptibility is combined with exposure to antiandrogenic agents, a threshold is surpassed, resulting in the manifestation of this birth defect. A clear role for exposure to antiandrogenic environmental chemicals has yet to be established in the etiology of hypospadias, although results from laboratory animal models indicate that a number of environmental chemicals could be implicated. Molecular epidemiology studies that simultaneously examine the roles of allelic variants in genes controlling androgen action and metabolism, and environmental exposures are needed to elucidate the risk factors for these anomalies and the causes of the increased rate of hypospadias. Birth Defects Research (Part A), 2003. © 2003 Wiley-Liss, Inc. [source] | ||||||||||