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Carboxyl ester lipase (Cel), is a lipolytic enzyme secreted by the pancreas, which hydrolyzes various species of lipids in the gut. Cel is also secreted by mammary gland during lactation and exists in breast milk. It facilitates dietary fat digestion and absorption, thus contributing to normal infant development. This study aimed to examine whether the Cel in zebrafish embryos has a similar role of maternal lipid utilization as in human infants, and how Cel contributes to the utilization of yolk lipids in zebrafish. The cel1 and cel2 genes were expressed ubiquitously in the blastodisc and yolk syncytial layer before 24 hpf, and in the exocrine pancreas after 72 hpf. The cel1 and cel2 morphants exhibited developmental retardation and yolk sac retention. The total cholesterol, cholesterol ester, free cholesterol, and triglyceride were reduced in the morphants' body while accumulated in the yolk (except triglyceride). The FFA content of whole embryos was much lower in morphants than in standard controls. Moreover, the delayed development in cel (cel1/cel2) double morphants was partially rescued by FFA and cholesterol supplementation. Delayed and weakened cholesterol ester transport to the brain and eyes was observed in cel morphants. Correspondingly, shrunken midbrain tectum, microphthalmia, pigmentation-delayed eyes as well as down-regulated Shh target genes were observed in the CNS of double morphants. Interestingly, cholesterol injections reversed these CNS alterations. Our findings suggested that cel genes participate in the lipid releasing from yolk sac to developing body, thereby contributing to the normal growth rate and CNS development in zebrafish., Competing Interests: Declaration of competing interest Authors have declared no conflict of interest., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Autosomal-recessive omodysplasia (OMOD1) is a genetic condition characterized by short stature, shortened limbs, and facial dysmorphism. OMOD1 is caused by loss-of-function mutations of glypican 6 ( GPC6 ). In this study, we show that GPC6 -null embryos display most of the abnormalities found in OMOD1 patients and that Hedgehog (Hh) signaling is significantly reduced in the long bones of these embryos. The Hh-stimulatory activity of GPC6 was also observed in cultured cells, where this GPC increased the binding of Hh to Patched 1 (Ptc1). Consistent with this, GPC6 interacts with Hh through its core protein and with Ptc1 through its glycosaminoglycan chains. Hh signaling is triggered at the primary cilium. In the absence of Hh, we observed that GPC6 is localized outside of the cilium but moves into the cilium upon the addition of Hh. We conclude that GPC6 stimulates Hh signaling by binding to Hh and Ptc1 at the cilium and increasing the interaction of the receptor and ligand., (© 2017 Capurro et al.)

Disruption of steroid hormone signaling has been implicated independently in the developmental abnormalities resulting from maternal phthalate plasticizer exposure and developmental zinc deficiency. This study investigated if secondary zinc deficiency may result from dietary exposure to a low level of di-2-ethylhexyl phthalate (DEHP) through gestation and if this could be associated with altered steroid metabolism. The interaction between marginal zinc nutrition and DEHP exposure to affect pregnancy outcome, zinc status, and steroid metabolism was also assessed. For this purpose, rats were fed a diet containing an adequate (25 mg/kg) or marginal (10 mg/kg) level of zinc without or with DEHP (300 mg/kg) from gestation day (GD) 0 until GD 19. Steroid profiles were measured in dam liver, plasma, adrenal glands, and in fetal liver by UPLC/MS-MS. In dams fed the adequate zinc diet, DEHP exposure decreased maternal weight gain and led to hepatic acute-phase response and zinc accumulation. The latter could compromise zinc availability to the fetus. DEHP and marginal zinc deficiency caused several adverse effects on the maternal and fetal steroid profiles. Interactions between DEHP exposure and marginal zinc deficient nutrition affected 17OH pregnenolone and corticosterone, while pregnenolone levels were specifically affected by DEHP exposure. Maternal marginal zinc deficiency specifically affected maternal progesterone and aldosterone, and presented evidence of increased androgen aromatization activity in maternal and fetal tissues. Results stress the potential major impact of mild DEHP exposure on maternal/fetal steroid metabolism that can be potentiated by nutritional and chronic disease states leading to zinc deficiency., (© The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Background: Malnutrition places a direct and indirect burden on individuals, especially children and communities. Malnutrition or growth failure can occur because of various reasons. This study aimed to determine the prevalence of thinness, underweight, stunting, and their related factors in students aged 6-12 years in Semnan province, central Iran., Participants and Methods: Using multistage sampling, a total of 2195 primary students in Semnan province, between November 2012 and March 2013, were selected randomly and the prevalences of wasting, underweight, and stunting among the students were estimated. Students' weights were measured using a Burer digital scale (Germany), with an accuracy of 100 g. Students' heights were measured using a nonstretchable tape measure. The BMI was calculated. Using the CDC 2000 standards, values less than the fifth percentile of BMI, weight-for-age, and height-for-age were defined as thinness, underweight, and stunting, respectively., Results: In the total sample, 12.5, 9.2, and 9.0% of the students, respectively, were affected by thinness, underweight, and stunting. Lack of access to a computer increased the odds ratio (OR) of thinness by 1.38 times [OR=1.38, 95% confidence interval (CI): 1.06-1.78, P=0.015). Other variables (including age) did not show a significant association with the prevalence of thinness. Similarly, of all the variables studied, only access to a computer showed a significant association with the prevalence of underweight (OR=1.37, 95% CI: 1.02-1.84, P=0.036). The prevalence of stunting was associated significantly with a history of parasitic infection (OR=2.32, 95% CI: 1.53-3.51, P<0.001) and living in rural areas (OR=1.57, 95% CI: 1.15-2.16, P=0.005)., Conclusion: The prevalence of malnutrition among students is high. Hence, families and stakeholders must pay special attention to various measures including healthcare services to improve the condition. Education, health, and support programs must be strengthened and continued.

Objective: To conduct genetic testing and prenatal diagnosis for a pregnant women with growth retardation, severe mental retardation, and a history of adverse pregnancies., Methods: G-banded chromosome analysis, fluorescence in situ hybridization (FISH), and whole genome DNA microarray were used to analyze the patient and her fetus., Results: The women was found to be a chimera containing two cell lines with 47 and 46 chromosomes, respectively. Both have involved deletion of 18q21.2q23. FISH analysis suggested that the cell line containing 47 chromosomes has harbored a chromosome marker derived from chromosome 15. The marker has contained chromosome 15p involving the SNRPN locus and part of 15q, which gave rise to a karyotype of 47,XX,del18q21.3,+ish mar D15Z1+ SNRPN+[82]/46,XX,del18q21.3[18]. Whole genome DNA microarray confirmed that a 3.044 Mb fragment from 15q11.2q12 was duplicated, which involved NIPA1, SNRPN and other 17 OMIM genes. Duplication of this region has been characterized by low mental retardation, autism, developmental delay. Meanwhile, there was a 17.992 Mb deletion at 18q21.33q23, which contained 39 OMIM genes including TNFRSF11A and PHLPP1. This fragment was characterized by mental retardation, developmental delay, short stature, and cleft palate. Whole genome microarray analysis confirmed that there was a 17.9 Mb deletion at 18q21.33q23, which has been implemented with mental retardation, general growth retardation, short stature, and cleft palate. After genetic counseling, the family decided to terminate the pregnancy at 21st week., Conclusion: Combined chromosome karyotyping, FISH, and whole genome DNA microarray can determine the origin of marker chromosomes and facilitate delineation of its correlation with the clinical phenotype.

Although the trophic actions of serotonin (5-HT) are well established, only few developmental defects have been reported in mouse strains with constitutive hyposerotonergia. We analyzed postnatal growth and cortical development in three different mutant mouse strains with constitutive reductions in central 5-HT levels. We compared two previously published mouse strains with severe (-95%) depletions of 5-HT, the tryptophan hydroxylase (Tph) 2(-/-) mouse line and VMAT2(sert-cre) mice, with a new strain, in which VMAT2 deletion is driven by Pet1 (VMAT2(pet1-cre)) in 5-HT raphe neurons leading to partial (-75%) reduction in brain 5-HT levels. We find that normal embryonic growth and postnatal growth retardation are common features of all these mouse strains. Postnatal growth retardation varied from mild to severe according to the extent of the brain 5-HT reduction and gender. Normal growth was reinstated in VMAT2(sert-cre) mice by reconstituting central 5-HT stores. Growth abnormalities could not be linked to altered food intake or temperature control. Morphological study of the cerebral cortex over postnatal development showed a delayed maturation of the upper cortical layers in the VMAT2(sert-cre) and Tph2(-/-) mice, but not in the VMAT2(pet1-cre) mice. No changes in layer-specific gene expression or morphological alterations of barrel cortex development were found. Overall, these observations sustain the notion that central 5-HT signaling is required for the preweaning growth spurt of mouse pups. Brain development appeared to be immune to severe central 5-HT depletion for its overall growth during prenatal life, whereas reduced brain growth and delayed cortical maturation development occurred during postnatal life. Reduced developmental 5-HT signaling during postnatal development might modulate the function and fine structure of neural circuits in ways that affect adult behavior.

Objectives: To evaluate growth for children born very preterm with particular focus on those born small-for-gestational age (SGA) or with ex utero growth restraint (GR), and to identify risk factors for short stature at 5 years of age., Study Design: Population-based study of children born at less than 33 completed weeks of gestation (Étude Epidémiologique sur les Petits Ages Gestationnels (EPIPAGE)). Short stature was defined as height <-2SD on WHO growth curves. Ex utero GR was considered to have occurred in children with appropriate size for gestational age at birth and with a height and/or weight below -2SD at 2 years of corrected age. Logistic regression models were used to test associations between risk factors and short stature., Results: The authors measured height at 5 years of age for 1,597 of 2,193 children (73%), 5.6% (95% CI 4.6 to 6.9) of whom were diagnosed as having a short stature. Height was measured at 2 and 5 years of age in 1417 children. Among these, 24% of those born SGA and 36% of those with ex utero GR (p=0.002) had a short stature at 5 years. Predictors of short stature were SGA or birth length <-2SD, maternal height ≤ 160 cm, gestational age <29 weeks and systemic corticosteroids. Breastfeeding at discharge decreased the risk of short stature., Conclusions: Short stature at 5 years of age is common in children born preterm. The highest incidence was observed in the group with ex utero GR. Systemic steroids have a long-term impact on growth and should be used with caution. Breastfeeding at discharge appeared to be protective.

Objective: To explore the effects of maternal smoking during pregnancy on offspring growth using three approaches: (1) multiple adjustments for socioeconomic and parental factors, (2) maternal-paternal comparisons as a test of putative intrauterine effects and (3) comparisons between two birth cohort studies., Methods: Population-based birth cohort studies were carried out in Pelotas, Brazil, in 1993 and 2004. Cohort members were followed up at 3, 12, 24 and 48 months. Multiple linear regression analysis was used to examine the relationships between maternal and paternal prenatal smoking and offspring anthropometric indices. In the 2004 cohort, the association of smoking with trunk length, leg length and leg-to-sitting-height ratio at 48 months was also explored., Results: Maternal smoking during pregnancy was associated with reduced z scores of length/height-for-age at each follow-up in both cohorts and reduced leg length at 48 months in the 2004 cohort. Children older than 3 months born to smoking women showed a higher body mass index-for-age z score than children of non-smoking women., Conclusions: The results of this study strongly support the hypothesis that maternal smoking during pregnancy impairs linear growth and promotes overweight in childhood.

Large (>90%) for gestational age (LGA) fetuses are usually identified incidentally. Detection of the LGA fetus should first prompt the provider to rule out incorrect dates and maternal diabetes. Once this is done, consideration should be given to certain overgrowth syndromes, especially if anomalies are present. The overgrowth syndromes have significant clinical and molecular overlap, and are associated with developmental delay, tumors, and other anomalies. Although genetic causes of overgrowth are considered postnatally, they are infrequently diagnosed prenatally. Here, we review prenatal sonographic findings in fetal overgrowth syndromes, including Pallister-Killian, Beckwith-Wiedemann, Sotos, Perlman, and Simpson-Golabi-Behmel. We also discuss prenatal diagnosis options and recurrence risks.

Background: Growth faltering in West African children has previously been associated with dietary exposure to aflatoxins, particularly upon weaning. However, in animal studies in utero exposure to low levels of aflatoxin also results in growth faltering., Objective: This study investigated the effect of in utero aflatoxin exposure on infant growth in the first year of life in The Gambia., Methods: Height and weight were measured for 138 infants at birth and at regular monthly intervals for one year. Aflatoxin-albumin (AF-alb) adduct level was measured in maternal blood during pregnancy, in cord blood and in infants at age 16 weeks., Results: The geometric mean AF-alb levels were 40.4 pg/mg (range 4.8-260.8 pg/mg), 10.1 pg/mg (range 5.0-189.6 pg/mg) and 8.7 pg/mg (range 5.0-30.2 pg/mg) in maternal, cord and infant blood, respectively. AF-alb in maternal blood was a strong predictor of both weight (P = 0.012) and height (P = 0.044) gain, with lower gain in those with higher exposure. A reduction of maternal AF-alb from 110 pg/mg to 10 pg/mg would lead to a 0.8 kg increase in weight and 2 cm increase in height within the first year of life., Conclusions: This study shows a strong effect of maternal aflatoxin exposure during pregnancy on growth in the first year of life and thus extends earlier observations of an association between aflatoxin exposure during infancy and growth faltering. The findings imply value in targeting intervention strategies at early life exposures.

Animal knockout experiments have offered the opportunity to study genes that play a role in growth and development. In the last few years, reports of patients with genetic defects in GH-IGF-I axis have greatly increased our knowledge of genetically determined causes of short stature. We will present the animal data and human reports of genetic disorders in the GH-IGF-I axis in order to describe the role of the GH-IGF-I axis in intrauterine and postnatal growth. In addition, the effects of the GH-IGF-I axis on the development and function of different organ systems such as brain, inner ear, eye, skeleton, glucose homeostasis, gonadal function, and immune system will be discussed. The number of patients with genetic defects in the GH-IGF-I axis is small, and a systematic diagnostic approach and selective genetic analysis in a patient with short stature are essential to identify more patients. Finally, the implications of a genetic defect in the GH-IGF-I axis for the patient and the therapeutic options will be discussed.

Aim: To explore the effects of maternal glucose on birthweight, infant and childhood growth in non-diabetic pregnant women using routinely collected data., Methods: Routinely collected data were extracted retrospectively from two clinical databases. These data comprised measurements of maternal random plasma glucose, infant birthweight, infant and child weight and height at 6-8 weeks, 24-36 weeks and 96-120 weeks in 6263 cases. After data cleaning, 4681 were analysed., Results: When the data were analysed in thirds, a positive association between birthweight standard deviation scores (SDS), weight SDS and height SDS with maternal random plasma glucose (RPG) was observed. Regression analysis of birthweight SDS and RPG was significant (P < 0.001). Babies were approximately 48 g heavier at birth for each 1 mmol/l increase of mother's RPG. Infants who showed 'catch-up' growth (as shown by change in weight SDS) at 2 years were born to mothers with lower glucose levels than infants who showed 'catch-down' growth (P < 0.001)., Conclusions: Random maternal glucose concentrations (taken at 28 weeks' gestation) in the normal range are positively related to birthweight. Glucose concentrations also predict greater weight and length in infancy. Despite this, babies born to mothers with higher glucose concentrations within the normal range show significant 'catch-down' growth in infancy as shown by a fall in weight SDS.

Background: Cornelia de Lange syndrome (CdLS) is a multiple congenital anomaly syndrome characterised by a distinctive facial appearance, prenatal and postnatal growth deficiency, psychomotor delay, behavioural problems, and malformations of the upper extremities. Recently mutations in NIPBL, the human homologue of the Drosophila Nipped-B gene, were found to cause CdLS. Mutations have been found in 39% of reported cases., Methods: Patients were enrolled in the study and classified into one of four groups based on clinical examination: classic, mild, possible, or definitively not CdLS. Three dimensional photography was taken of 20 subjects, and compared between groups. Behaviour was assessed with specific attention to autism. We searched for mutations in NIPBL and correlated genotype with phenotype., Results: : We found mutations in 56% of cases., Conclusions: Truncating mutations were generally found to cause a more severe phenotype but this correlation was not absolute. Three dimensional facial imaging demonstrated the potential for classifying facial features. Behavioural problems were highly correlated with the level of adaptive functioning, and also included autism. No correlation of behaviour with the type of mutation was found.

In order to test the Thrifty Phenotype Hypothesis on hearing, data from two cross-sectional studies on hearing were re-evaluated. The data sets comprised 500 18-year-old conscripts, and 483 noise-exposed male employees. Sensorineural hearing loss (SNHL) was over-represented among conscripts with a short stature (odds ratio=2.2) or hearing loss in the family (odds ration=4.2), but not among noise-exposed conscripts (odds ratio=0.9-1.3). Among noise-exposed short employees, hypertension and age exhibited a negative impact on high frequency hearing thresholds, while among tall employees hypertension had no effect on hearing and the influence of age was less pronounced (p<0.01 for body height; p<0.02 for age, hypertension and the interaction between body height and hypertension; p<0.05 for the interaction between body height and age). This suggests that mechanisms linked to fetal programming and growth retardation and/or insulin-like growth factor 1 levels during fetal life, such as a delayed cell cycle during the time window when the cochlea develops, may cause SNHL in adulthood.

Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-gamma constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid-binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited hypertriglyceridemia, impaired glucose tolerance, and decreased insulin sensitivity. Mice expressing the Pref-1/hFc transgene exclusively in liver under the control of the albumin promoter also showed a decrease in adipose mass and adipocyte marker expression, suggesting an endocrine mode of action of Pref-1. These findings demonstrate the inhibition of adipogenesis by Pref-1 in vivo and the resulting impairment of adipocyte function that leads to the development of metabolic abnormalities.

Objectives: To compare long term outcomes of a randomised controlled trial of anti-smoking education in pregnancy and to examine the same outcomes according to maternal pregnancy smoking behaviour., Design: Follow up of the population included in the randomised controlled trial nine years later and of ex-smokers and non-smokers within the same hospital population., Setting: A maternity hospital in Birmingham with follow up of children in schools and mothers at home., Population: 1218 smokers recruited to the trial; also 191 ex-smokers at booking and 414 non-smokers throughout pregnancy., Methods: Children were assessed individually by psychologists in schools, and mothers interviewed at home to obtain additional information relevant to cognitive development and growth. Information on smoking during pregnancy was obtained from mothers and obstetric data from computerised case-notes, both recorded immediately following delivery., Main Outcome Measures: Height, weight, IQ and neurological soft signs at 9.4 years., Results: Differences in birthweight and length between the intervention and control groups were confirmed but no intervention-control differences were found at age 9.4 for weight, height, IQ or neurological soft signs. Differences were found for height and IQ according to mothers pregnancy smoking behaviour, but smoking did not remain an independent predictor after taking account of confounding factors. Alternative classifications of smoking behaviour, taking account of the gestation at stopping and mean cigarette consumption throughout pregnancy likewise showed no effect., Conclusions: The well established early hazards of smoking during pregnancy seem to be resolved by later childhood, with no evidence of direct long term effects on growth or cognitive functioning.

p57Kip2, one of the cyclin-dependent kinase (CDK) inhibitors, has been suggested to be a tumor suppressor candidate. To elucidate its biological roles in mouse development and tumorigenesis, we created p57Kip2-deficient mice. The p57Kip2-deficient mice exhibited a cleft palate and defective bone formation resulting in severe dyspnea. Most of the p57Kip2-deficient mice died within 24 h after birth, while about 10% of them survived beyond the weaning period. All of the surviving mice showed severe growth retardation. The males showed immaturity of the testes, prostate and seminal vesicles, and the females showed vaginal atresia, immaturity of the uterus, and an increased number of atretic follicles. Although Yan et al. and Zhang et al. have already reported p57Kip2-deficient mice, they could not investigate the phenotypes of the surviving p57Kip2-deficient mice. Also, most of the symptoms of Beckwith-Wiedemann syndrome could not be reproduced in the mutant mice. Embryonic fibroblasts prepared from p57Kip2-deficient mice showed no differences in the proliferation rate and saturation density, suggesting that G1 arrest is largely independent of p57Kip2 function. Our results suggest that p57Kip2 plays a critical role in development, but do not support the hypothesis that the p57Kip2 gene is a tumor-suppressor gene or is responsible for Beckwith-Wiedemann syndrome.

Objective: To assess the growth curves of uninfected infants born to type 1 human immunodeficiency virus (HIV-1) seropositive mothers by means of standardised anthropometric indices., Methods: The z scores (National Center for Health Statistics-World Health Organization data) of weight for age, length for age, and weight for length of 92 uninfected full term infants born to HIV positive mothers were compared with those of 65 bottle fed full term infants born to healthy mothers at 0, 1, 2, 3, 4, 6, 9, 12, 18, and (in a subgroup) 24 months of age. Confounders were also recorded., Results: The study population had a lower length for age z score at birth (95% confidence intervals (CI): 0.02, -0.58) and higher weight for length z scores at 1 (95% CI: 0.21, 0.63), 2 (95% CI: 0.25, 0.66), and 3 (95% CI: 0.0, 0.48) months compared with the reference group. After a temporary recovery, the length for age z score difference increased progressively from the 4th month onwards and was significant at 18 (95% CI: -0.31, -1.05) and 24 (95% CI: -0.02, -0.91) months. The difference between the length for age z scores at birth was associated with maternal covariates, but the between group difference at 18 months was apparent even after adjustment for covariates., Conclusion: Uninfected infants born to HIV positive mothers have a rapid weight gain immediately after birth. A decrease in length progression during the second year might be a result of the social risk connected with the family environment and an unfavourable programming related to the maternal HIV status.

We examined blood pressure and heart rate (HR) in relation to glucose and arterial PO2 (PaO2) at approximately 121 days (early) and at approximately 140 days (late) gestation in 12 growth-restricted and 10 control fetal lambs. Mild growth restriction (relative to maternal weight) was produced by withdrawal of 25 ml/day of maternal blood during the second half of pregnancy (P < 0.05). Fetuses from this model are hypoglycemic during early and late gestation but hypoxemic only during late study. Mean systolic and diastolic pressures in the experimental group were approximately 8.0 mmHg lower than the corresponding values in controls at both studies (P < 0.05). Fetal HR (FHR) was 15.4 beats/min lower (P < 0.05) in 10 but was higher than control in 2 experimental fetuses that were also not growth restricted. There were significant correlations between late systolic pressure and HR and PaO2 (r = 0.54, P = 0.046 and r = 0.50, P = 0.049, respectively) and between FHR and blood pressure and birth weight/maternal weight (P < 0.05). We conclude that, in this model, fetal blood pressure and HR may serve as good indicators of hypoxemia and growth restriction.

A new mouse mutant, tail short variable (Tsv) produces a reduction deformity of the tail, growth retardation, and, in adults, a mild anemia. Genetic and embryological studies show that on all genetic backgrounds there is variable viability of Tsv/Tsv and Tsv/+ and phenotypic overlap within these and with +/+. A modifier is located to a short segment of chromosome 7, which alters the tail length of Tsv/+ mice up to 15%. The modifier, Tsv, and a coat texture mutant come from the same wild Peru mouse. The tail deformity is associated with, and may be caused by, a vascular disruption of the caudal aorta starting on day 11 of gestation. Thus Tsv appears to be different from each of the thirty known mouse mutants involving the tail. It is suggested that Tsv could be a mouse model for human conditions involving transverse terminal limb defects such as Moebius and de Lange syndromes.

A newborn infant with the polyasplenia sequence, intrauterine growth retardation, cutaneous nevi, and minor anomalies was found to have mosaicism for ring chromosome 7. This patient's anomalies are markedly different from those of previous patients reported with this cytogenetic anomaly.

Consecutive ultrasonic measurement of fetal biparietal diameter (B.P.D.) and fetal chest area was carried out in 152 normal and 59 complicated pregnancies between 25 and 40 weeks of gestation. In normal pregnancy the mean fetal head area (B.P.D.2) varied from 45.0 cm2 at 25 weeks to 98.0 cm2 at 40 weeks. The mean chest area varied from 31.3 cm2 at 25 weeks to 94.3 cm2 at 41 weeks. A normal curve of the head-to-chest relation was constructed. In the group of complicated pregnancies, two types of fetal growth retardation could be recognized. The first type was characterized by a normal head-to-chest relationship (symmetric type), the second type was characterized by an abnormal head-to-chest relationship (asymmetric type; relatively large head area). During fetal growth acceleration head-to-chest-relationship was abnormal (relatively large chest area).

Eight patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex, ranging in age from 4 to 33 months, were evaluated for the presence of dysmorphic features recently described as human immunodeficiency virus embryopathy. Birth data and growth charts were available. Growth failure, a prominent box-like head, large wide eyes, and a well-formed philtrum were seen in the majority of patients. The significance of hypertelorism, obliquity of eyes, long palpebral fissures, blue scleras, depressed bridge of nose, and prominent upper vermilion border is discussed.

The radiological appearance of bone maturity can be used as a criterion for fetal maturity. This examination with limited irradiation to the fetus is an alternative to amniocentesis. The practice of the latter is not without risk. The authors carried out 194 examinations of the contents of the uterus to look at the epiphyses of the knee between the 34th and 40th week of amenorrhoea. The found three groups: 1) those with normal development; 2) those with delayed development and 3) those with more advanced development. They did not find significant correlation between small-for-dates growth and bony maturity. On the other hand, where there was increased growth of the fetus in cases where maternal diabetes was excluded there was demonstrated that bony maturity accelerated with the presence of Béclard's point from the 34th week onwards. With such great variation in the dates of the appearance of points of ossification the presence of epiphyseal points in the knee cannot be taken as a criterion to establish fetal maturity nor the minimum duration of the pregnancy.

Murine trisomy 19 (Ts19) can be regarded as a general model of human trisomies. It is the only autosomal trisomy in the mouse that survives the perinatal period. Therefore, it is the only animal model available for postnatal investigations of trisomy-specific mental retardation. To evaluate the extent of developmental retardation during the late-embryonic and fetal period of gestation, total body weight development was documented for 60 Ts19-fetuses and compared with that of 219 euploid in utero-mates. In addition, a postnatal study on body-weight development of 77 Ts19-neonates and 74 euploid littermates was performed starting on day 1 postpartum and continuing until spontaneous death or until day 22. Forty-seven Ts19-individuals were further tested in nine behavioural test systems in order to determine their neurophysiological developmental profile. Findings were compared with age-dependent morphologic and physiologic parameters. The data obtained in the present study show a significant retardation of organ- and body-weight development in Ts19-mice starting on day 14 of gestation. Retardation of physiological parameters is progressive and persists throughout the perinatal and postnatal periods. Furthermore, the trisomic individuals showed specific behavioural abnormalities.

Serial serum Ca values in 47 infants with intrauterine growth retardation were analyzed in relation to clinical and biochemical factors. Serum Ca concentrations in IUGR infants fell within the 95 percent confidence limits for serum Ca in infants whose birth weights were appropriate for gestational age. Serum Ca concentrations in IUGR infants were significantly correlated with birth asphyxia and bicarbonate therapy for acidosis. Serum Ca concentration at 24 hours of age was inversely correlated with serum P values. Thus the incidence of neonatal hyocalcemia in IUGR infants is not increased above the incidence expected from their respective gestational ages. Infants with IUGR who are well at birth do not appear to develop neonatal hypocalcemia, but IUGR infants who are asphyxiated at birth develop significant hypocalcemia.