Obesity has emerged as one of the most serious public health concerns in the 21st century. Obese children tend to become obese adults. The dramatic rise in pediatric obesity closely parallels the rapid increase in the prevalence of adult obesity. As overweight children become adults they face the multitude of health problems associated with obesity at younger ages. The morbidity and mortality associated with obesity continue to increase. Obesity is one of the leading causes of preventable death. Complications of obesity include cardiovascular risks, hypertension, dyslipidemia, endothelial dysfunction, type 2 diabetes mellitus and impaired glucose tolerance, acanthosis nigricans, hepatic steatosis, premature puberty, hypogonadism and polycystic ovary syndrome, obstructive sleep disorder, orthopedic complications, cholelithiasis and pseudotumor cerebri. Genetic and molecular and environmental factors play an important role in the assessment and management of obesity.

The normal umbilical cord coil index is one coil/5 cm, i.e., 0.2 +/- 0.1 coils completed per cm. We report the frequency and clinical correlations of abnormally coiled cords among 1329 cases referred to our placental pathology services. Twenty-one percent of cords were overcoiled and 13% were undercoiled. Abnormal cord coiling was seen at all gestational ages. Principal clinical correlations found in overcoiled cords were fetal demise (37%), fetal intolerance to labor (14%), intrauterine growth retardation (10%), and chorioamnionitis (10%). For undercoiled cords, the frequencies of these adverse outcomes were 29%, 21%, 15%, and 29%, respectively. Abnormal cord coiling was associated with thrombosis of chorionic plate vessels, umbilical venous thrombosis, and cord stenosis. Thus, abnormal cord coiling is a chronic state, established in early gestation, that may have chronic (growth retardation) and acute (fetal intolerance to labor and fetal demise) effects on fetal well-being. The cause of abnormal cord coiling is not known. Its effects on neurological status of survivors are also unknown. Antenatal detection of abnormal cord coil index by ultrasound could lead to elective delivery of fetuses at risk, thereby reducing the fetal death rate by about one-half. We recommend that the cord coil index become part of the routine placental pathology examination.

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Ever more frequent and closer involvement by clinical geneticists and counselors in the prenatal assessment of development mandates a better understanding of all stages of human ontogeny, but especially those of earliest development during which most of the lethal and all of the gross, multiple and complex defects of morphogenesis arise. Because of the phenomenon of universality, i.e., identical molecular inductive mechanisms involved in the process of embryonic patternformation in all vertebrates, experimental animals indeed are a most valuable approach to an understanding of the causal and formal aspects of development and are beginning to forge essential, strong bonds between molecular biologists and clinicians in a mutually supportive discipline of developmental biology. However, to grieving parents of a stillborn fetus with, say, Pentalogy of Cantrell, sirenomelia or otocephaly, mouse data o¡er little comfort or reassurance about recurrence; thus, it is imperative to make ever more e¡ective a science of human teratology (sensu lato) with participating reproductive geneticists, obstetricians, neonatologists, ultrasonographers, pediatric=fetal pathologists, cytogeneticists and pediatric geneticists to generate the diagnostic, pathogenetic and causal data necessary to counsel and to comfort the parents. Few molecular data exist on causes of blastogenetic defects in humans; however, the phenomenon of parsimony, whereby the same ''morphogenetic'' molecule, say, sonic hedgehog (SHH), is ''deployed'' simultaneously or sequentially during the morphogenesis (and even the histogenesis) of several=many embryonic primordia, makes it likely that a genetic=epigenetic disturbance of such an inductive system will have multiple e¡ects on blastogenetic, organogenetic and perhaps also histogenetic events in the embryo. If causally de¢ned, such a pattern of anomalies constitutes pleiotropy, and the embryo=fetus can be said to have a syndrome. If cause is unknown, the presumption of pleiotropy is less certain, and the fetus=infant may be said to have an ''association'' with low empiric recurrence risk.

Cross-linking of Fas (CD95, APO-1) and Fas ligand (FasL; CD95L) induces apoptosis of Fas-bearing cells. Recent evidence suggests that FasL. expression plays an important role in maintenance of immune privilege in murine testis and eye and in tumour escape from immune rejection in colon cancer, melanoma and hepatocellular carcinoma. Bcl-2 is a membrane protein that suppresses apoptosis in response to a variety of stimuli. In this paper we describe abundant expression of FasL protein and mRNA transcripts within the immune privileged environment of the placenta by immunohistochemistry and reverse transcription in-situ polymerase chain reaction methods. The syncytiotrophoblast layer, the main site of feto-maternal interface, and extravillous trophoblasts, demonstrated consistent immunoreactivity for FasL in term placentae. Co-occurrence of Fas and Bcl-2 were detected with a similar pattern of distribution with FasL. The TUNEL method revealed evidence of apoptosis in the placental tissues. We speculate that abundant presence of FasL in the trophoblast contributes to immune privilege in this unique environment, perhaps by fostering apoptosis of activated Fas-expressing lymphocytes of maternal origin. An apoptotic process mediated by FasL may also play a role in placental invasion during implantation and underscores similarities between the trophoblast and neoplastic cells.

Intestinal malrotation has an incidence of 1 per 6000 live births. The most serious consequence of malrotation is volvulus. Midgut volvulus is a rare condition in which the small bowel and proximal colon twist around the superior mesenteric artery, leading to a high-grade proximal bowel obstruction and vascular compromise of the intestine, thereby leading to infarction of the involved intestine. Midgut volvulus rarely occurs antenatally and is usually not lethal in utero. There are only 7 cases of intrauterine fetal demise caused by midgut volvulus reported in the literature. We report a case of intrauterine fetal demise at 38 weeks of gestation, due to cardiovascular failure and shock from midgut volvulus. Non-specific abnormalities, including ascites and dilated bowel, had been seen on the antenatal ultrasound from the 15th week of gestation. In addition to the volvulus, the fetus had intestinal atresia and arthrogryposis.

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