摘要:

AbstractWe hypothesized that susceptibility to the genetic and environmental factors that disrupt cardiac development is associated with race and sex. To evaluate this hypothesis, we asked whether the prevalence of specific cardiac malformations differs by race and sex. We attempted to include all infants born alive in the State of Louisiana from January 1, 1988, through December 31, 1989, and diagnosed by echocardiography, catheterization and/or autopsy within a year of birth as having one of ten specific cardiac malformations. The prevalence of atrioventricular canal defects (AVCD) per 1,000 live births was significantly higher for black females (.744) compared to black males (.198) and for white females (.414) compared to white males (.116). Complete transposition of the great arteries (TGA) was significantly higher for white males (.559) compared to white females (.122); in contrast, TGA was not significantly different for black males (.198) and black females (.169). Obstructive left heart syndrome (OLHS)—aortic stenosis and/or coarctation of the aorta—was significantly higher for white males (.652) compared to white females (.317); in contrast, OLHS was not significantly different for black males (.264) and black females (.169). Single ventricle (SV) was significantly higher for whites (.202) compared to blacks (.067). We did not find that race and sex were associated with differences in the prevalence of tetralogy of Fallot and hypoplastic left heart syndrome. The numbers of infants with anomalous pulmonary venous return, tricuspid atresia, double outlet right ventricle, or truncus arteriosus were too small to measure an association with race and sex. These results demonstrate that the prevalence of a subset of cardiac malformations differs by race and sex. Selective fetal survival and differential susceptibility to cardiac malformations may be associated with these findings. © 1992 Wiley‐Lis

ISSN:0040-3709    

DOI:10.1002/tera.1420460311

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractA case‐control study of birth defects was carried out in Kandang Kerbau Hospital in Singapore for a three‐year period from January 1986 until December 1988. This paper presents the descriptive profile of birth defects among livebirths seen in that hospital. Out of 44,842 livebirths, 678 babies were found to have birth defects, giving a prevalence of 15.13 per 1000 livebirths (95% CI 14.0–16.2). The musculoskeletal system was the most frequently affected system accounting for 161 cases with a prevalence of 3.59 per 1,000 livebirths (95% CI 3.06–4.19), followed by 111 cases with defects of the gastrointestinal system (2.47 per 1,000 livebirths 95% CI 2.04–2.98), 88 cases of chromosomal disorders (prevalence of 1.96 per 1,000 livebirths 95% CI 1.57–2.42), 78 cases with defects of the cardiovascular system (1.74 per 1,000 live‐births 95% CI 1.38–2.17), 73 cases with defects of the urogenital system (1.63 per 1,000 livebirths 95% CI 1.28–2.05), and 52 cases with defects of the central nervous system (1.16 per 1,000 livebirths 95% CI 0.87‐1.52). The prevalence of cleft lip, cleft palate in isolation, and cleft lip and palate combined was 1.72 per 1,000 livebirths and the occurrence of Down's syndrome was 1 in 700 livebirths. When reviewed 6 weeks postpartum, the rate of false positives at birth was 4%. In a control group of 709 “normal” cases at birth, the rate of cases not detected at birth but detected at 6 week follow‐up, false negatives was 0.84

ISSN:0040-3709    

DOI:10.1002/tera.1420460312

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractIt has been shown that multiple exposures of gravid rats to cocaine during late gestation result in significant incidences of severe malformations. Hind limb reduction defects were frequent findings in this study. Other studies have shown that comparable abnormalities can be induced in experimental animals by various procedures including vascular clamping, direct fetal exposure to epinephrine, uterine handling following laparotomy, as well as by exposure to hyperbaric oxygen. This paper reviews these and other studies, and presents a novel mechanistic hypothesis that explains their common findings. It is proposed that in each instance, conceptual hypoxia results from hypoperfusion caused by transient vasoconstriction. Following the resumption of normal perfusion, reactive oxygen species are generated by the ischemia/reperfusion mechanisms thought to underlie many pathobiologic lesions. It is proposed that the conceptus is particularly vulnerable to the toxicity of oxygen radicals because of its low antioxidant activities and the highly reduced state of its undifferentiated cells. Sensitivity to cocaine and uterine handling appears to be enhanced during late gestation and it is hypothesized that this results from changes in oxygenation and iron content that increase both the substrate and catalyst for generation of reactive oxygen species. © 1992 Wiley‐Liss, I

ISSN:0040-3709    

DOI:10.1002/tera.1420460313

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractThe administration of multiple doses of cocaine on a single day during late gestation is teratogenic in rats in which hind limb ectrodactyly is a major finding (Webster and Brown‐Woodman, '90). We have previously hypothesized that these limb malformations result from the generation of reactive oxygen species during the process of ischemia/reperfusion in vivo. In order to study the direct effects of cocaine versus the aberrant oxygenation it may induce, we have developed a system for culturing rat embryos between days 14 and 15 of gestation. Growth and development of cultured embryos are comparable to that of in vivo controls. Exposure to normoxia (95% O2) with or without cocaine failed to induce limb malformations and exposure to a single long period of hypoxia (20% O2) only reduced limb growth in the anterior‐posterior axis. By contrast, embryos receiving multiple brief exposures to hypoxia developed a significant incidence of hind limb ectrodactyly that appeared indistinguishable from that induced by cocaine in vivo. By incubating day 14 embryos in a nitroblue tetrazolium derivative, 1‐[4,5‐dimethylthiazol‐2‐yl]‐2,5‐diphenyltetrazolium bromide (MTT), it was shown that superoxide anion radical appears in the digital rays following two episodes of reperfusion. Little reaction product was seen under the other conditions. Finally, mitochondrial electron transport particles prepared from teratogenically sensitive limb buds spontaneously “leak” electrons to form superoxide anion radical whereas those from insensitive heart fail to do so. We propose that cocaine and other exposures that can transiently reduce conceptal oxygenation during late gestation are teratogenic by virtue of their capacity to induce ischemia/reperfusion. This process generates toxic oxygen radicals that can overwhelm the immature antioxidant defenses. ©

ISSN:0040-3709    

DOI:10.1002/tera.1420460314

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

摘要:

AbstractA monoclonal antibody to the 72 kDa heat shock protein and Western blot analysis blot analysis were used to determine the induction, accumulation and turnover of hsp 72 after day 10 rat embryos were exposed to elevated temperatures (40°–43°C) for various lengths of time (2.5 minutes to 18 hours). Embryos exposed to temperatures that exceed the normal culture temperature (37°C) by 4°C or more for as little as 2.5 minutes (43°C) or 15 minutes (41, 42°C) synthesized and accumulated detectable amounts of heat‐inducible hsp 72. Hsp 72 could not be detected by Western blot analysis of proteins from embryos cultured at 40°C or below. Once induced, hsp 72 can be detected in embryos for 24–48 hours after they are removed from the hyperthermic conditions and returned to normothermic conditions. Our results also indicate that hsp 72 is induced by all hyperthermic exposures that induce alterations in rat embryo growth and development; therefore, hsp 72 is a potential biomarker for heat‐induced embryotoxicity. © 1992

ISSN:0040-3709    

DOI:10.1002/tera.1420460315

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420460316

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420460301

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1992

数据来源: WILEY