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Maternal Hyperthermia (maternal + hyperthermia)

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Life Sciences100%

Selected Abstracts

Etiology, pathogenesis and prevention of neural tube defects

CONGENITAL ANOMALIES, Issue 2 2006
Rengasamy Padmanabhan
ABSTRACT Spina bifida, anencephaly, and encephalocele are commonly grouped together and termed neural tube defects (NTD). Failure of closure of the neural tube during development results in anencephaly or spina bifida aperta but encephaloceles are possibly post-closure defects. NTD are associated with a number of other central nervous system (CNS) and non-neural malformations. Racial, geographic and seasonal variations seem to affect their incidence. Etiology of NTD is unknown. Most of the non-syndromic NTD are of multifactorial origin. Recent in vitro and in vivo studies have highlighted the molecular mechanisms of neurulation in vertebrates but the morphologic development of human neural tube is poorly understood. A multisite closure theory, extrapolated directly from mouse experiments highlighted the clinical relevance of closure mechanisms to human NTD. Animal models, such as circle tail, curly tail, loop tail, shrm and numerous knockouts provide some insight into the mechanisms of NTD. Also available in the literature are a plethora of chemically induced preclosure and a few post-closure models of NTD, which highlight the fact that CNS malformations are of hetergeneitic nature. No Mendelian pattern of inheritance has been reported. Association with single gene defects, enhanced recurrence risk among siblings, and a higher frequency in twins than in singletons indicate the presence of a strong genetic contribution to the etiology of NTD. Non-availability of families with a significant number of NTD cases makes research into genetic causation of NTD difficult. Case reports and epidemiologic studies have implicated a number of chemicals, widely differing therapeutic drugs, environmental contaminants, pollutants, infectious agents, and solvents. Maternal hyperthermia, use of valproate by epileptic women during pregnancy, deficiency and excess of certain nutrients and chronic maternal diseases (e.g. diabetes mellitus) are reported to cause a manifold increase in the incidence of NTD. A host of suspected teratogens are also available in the literature. The UK and Hungarian studies showed that periconceptional supplementation of women with folate (FA) reduces significantly both the first occurrence and recurrence of NTD in the offspring. This led to mandatory periconceptional FA supplementation in a number of countries. Encouraged by the results of clinical studies, numerous laboratory investigations focused on the genes involved in the FA, vitamin B12 and homocysteine metabolism during neural tube development. As of today no clinical or experimental study has provided unequivocal evidence for a definitive role for any of these genes in the causation of NTD suggesting that a multitude of genes, growth factors and receptors interact in controlling neural tube development by yet unknown mechanisms. Future studies must address issues of gene-gene, gene-nutrient and gene,environment interactions in the pathogenesis of NTD. [source]

Effects of maternal hyperthermia on myogenesis-related factors in developing upper limb,

BIRTH DEFECTS RESEARCH, Issue 3 2009
Jin Lee
Abstract BACKGROUND: Maternal hyperthermia is one causative factor in various congenital anomalies in experimental animals and humans. In the present study, we assessed the effects of high temperature on limb myogenesis in mice. METHODS: Pregnant mice, C57BL/6 strain, were exposed to hyperthermia (43°C, 5 minutes) on embryonic day (ED) 8. Fetuses on ED 11, 13, 15, and 17 and neonates on postnatal day (PD) 1 were collected. To characterize the effects of hyperthermia on myogenesis-related factors Pax3, MyoD, myogenin, and myosin heavy chain (MyHC) during skeletal muscle development, we performed RT-PCR, western blotting, immunohistochemistry, and transmission electron microscopy. RESULTS: Pax3 gene expression was still detected on ED 13 in hyperthermia-exposed fetuses. The expression of MyoD protein was down-regulated in fetuses exposed to hyperthermia. In contrast, myogenin and MyHC protein expression were up-regulated on PD 1 and ED 17, respectively, in the group exposed to hyperthermia. Immunohistochemical analysis confirmed the findings from western blot analysis. Compared with control neonates, a TEM study revealed immature muscle fibers in PD 1 hyperthermia neonates. Thus, our studies showed that maternal hyperthermia induced delayed expression of Pax3 and inhibited expression of MyoD proteins, which are known to play important roles in migration of myogenic progenitor cells, and in myoblast proliferation. In addition, maternal hyperthermia also delayed the expression of myogenin protein for the formation of myotubes, and MyHC protein, which is one of the final muscle differentiation factors. CONCLUSION: Our data suggest that maternal hyperthermia delays limb myogenesis in part by disregulating the expression of key myogenesis-related factors. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source]

The effect of fever, febrile illnesses, and heat exposures on the risk of neural tube defects in a Texas-Mexico border population

BIRTH DEFECTS RESEARCH, Issue 10 2004
Lucina Suarez
Abstract BACKGROUND Hyperthermia produces neural tube defects (NTDs) in a variety of animal species. Elevated maternal body temperatures may also place the developing human embryo at risk. We examined the relation between maternal hyperthermia and the development of NTDs in a high-risk Mexican-American population. METHODS Case-women were Mexican-American women with NTD-affected pregnancies who resided and delivered in any of the 14 Texas counties bordering Mexico, during 1995,2000. Control-women were randomly selected from study area residents delivering normal live births, frequency-matched to cases by hospital and year. Information on maternal fevers, febrile illnesses, exposures to heat generated from external sources, and hyperthermia-inducing activities was gathered through in-person interviews, conducted about six weeks postpartum. RESULTS The risk effect (OR) associated with maternal fever in the first trimester, compared to no fever, was 2.9 (95% CI, 1.5,5.7). Women taking fever-reducing medications showed a lower risk effect (OR, 2.4; 95% CI, 1.0,5.6) than those who did not (OR, 3.8; 95% CI, 1.4,10.9). First-trimester maternal exposures to heat devices such as hot tubs, saunas, or electric blankets were associated with an OR of 3.6 (95% CI, 1.1,15.9). Small insignificant effects were observed for activities such as cooking in a hot kitchen (OR, 1.6; 95% CI, 1.0,2.6) and working or exercising in the sun (OR, 1.4; 95% CI, 0.9,2.2). CONCLUSIONS Maternal hyperthermia increases the risk for NTD-affected offspring. Women intending to become pregnant should avoid intense heat exposures, carefully monitor and manage their febrile illnesses, and routinely consume folic acid supplements. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source]

Effects of maternal hyperthermia on myogenesis-related factors in developing upper limb,

BIRTH DEFECTS RESEARCH, Issue 3 2009
Jin Lee
Abstract BACKGROUND: Maternal hyperthermia is one causative factor in various congenital anomalies in experimental animals and humans. In the present study, we assessed the effects of high temperature on limb myogenesis in mice. METHODS: Pregnant mice, C57BL/6 strain, were exposed to hyperthermia (43°C, 5 minutes) on embryonic day (ED) 8. Fetuses on ED 11, 13, 15, and 17 and neonates on postnatal day (PD) 1 were collected. To characterize the effects of hyperthermia on myogenesis-related factors Pax3, MyoD, myogenin, and myosin heavy chain (MyHC) during skeletal muscle development, we performed RT-PCR, western blotting, immunohistochemistry, and transmission electron microscopy. RESULTS: Pax3 gene expression was still detected on ED 13 in hyperthermia-exposed fetuses. The expression of MyoD protein was down-regulated in fetuses exposed to hyperthermia. In contrast, myogenin and MyHC protein expression were up-regulated on PD 1 and ED 17, respectively, in the group exposed to hyperthermia. Immunohistochemical analysis confirmed the findings from western blot analysis. Compared with control neonates, a TEM study revealed immature muscle fibers in PD 1 hyperthermia neonates. Thus, our studies showed that maternal hyperthermia induced delayed expression of Pax3 and inhibited expression of MyoD proteins, which are known to play important roles in migration of myogenic progenitor cells, and in myoblast proliferation. In addition, maternal hyperthermia also delayed the expression of myogenin protein for the formation of myotubes, and MyHC protein, which is one of the final muscle differentiation factors. CONCLUSION: Our data suggest that maternal hyperthermia delays limb myogenesis in part by disregulating the expression of key myogenesis-related factors. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source]

The effect of fever, febrile illnesses, and heat exposures on the risk of neural tube defects in a Texas-Mexico border population

BIRTH DEFECTS RESEARCH, Issue 10 2004
Lucina Suarez
Abstract BACKGROUND Hyperthermia produces neural tube defects (NTDs) in a variety of animal species. Elevated maternal body temperatures may also place the developing human embryo at risk. We examined the relation between maternal hyperthermia and the development of NTDs in a high-risk Mexican-American population. METHODS Case-women were Mexican-American women with NTD-affected pregnancies who resided and delivered in any of the 14 Texas counties bordering Mexico, during 1995,2000. Control-women were randomly selected from study area residents delivering normal live births, frequency-matched to cases by hospital and year. Information on maternal fevers, febrile illnesses, exposures to heat generated from external sources, and hyperthermia-inducing activities was gathered through in-person interviews, conducted about six weeks postpartum. RESULTS The risk effect (OR) associated with maternal fever in the first trimester, compared to no fever, was 2.9 (95% CI, 1.5,5.7). Women taking fever-reducing medications showed a lower risk effect (OR, 2.4; 95% CI, 1.0,5.6) than those who did not (OR, 3.8; 95% CI, 1.4,10.9). First-trimester maternal exposures to heat devices such as hot tubs, saunas, or electric blankets were associated with an OR of 3.6 (95% CI, 1.1,15.9). Small insignificant effects were observed for activities such as cooking in a hot kitchen (OR, 1.6; 95% CI, 1.0,2.6) and working or exercising in the sun (OR, 1.4; 95% CI, 0.9,2.2). CONCLUSIONS Maternal hyperthermia increases the risk for NTD-affected offspring. Women intending to become pregnant should avoid intense heat exposures, carefully monitor and manage their febrile illnesses, and routinely consume folic acid supplements. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source]