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Biomedical subjects

H Kalter

Publications and source records attributed to H Kalter.

At least 19 recordsLinked to original sources
PubMed1993

Case reports of malformations associated with maternal diabetes: history and critique.

Several malformations and malformation complexes have been alleged to be associated with maternal type 1 diabetes mellitus: in particular, sacral dysplasia, caudal regression/sirenomelia, femoral dysplasia, and holoprosencephaly. For some of the malformations the claim rests on case material, and for others on theoretical considerations. The history and evolution of these ideas are presented.

Bone Diseases, Developmental↗
PubMed1991

Five-decade international trends in the relation of perinatal mortality and congenital malformations: stillbirth and neonatal death compared.

The relation between long-term temporal trends in stillbirth and neonatal death rates and the congenital malformation frequencies in such deaths were analysed, using data from hospital-based European, USA, and Canadian reports published from 1950. In the last 50 years the overall perinatal mortality rate has fairly steadily improved, decreasing by 65-80%. This was accomplished by the control of some serious problems of early life. However, lingering disorders form an ever larger proportion of the causes of perinatal mortality. Among the prominent of these are congenital malformations, accounting for nearly 30% of perinatal deaths at present. However, this figure conceals important differences between stillbirths and early neonatal deaths. For example, although stillbirth and early neonatal mortality rates have decreased to similar extents during these years, congenital malformations, which were almost equally frequent causes of death in both of them at the beginning of this period, are now about twice as common in early neonatal (one week) deaths as in stillbirths. Other differences between them are in birthweight-related malformation frequencies and in characteristic arrays of malformations. The significance of these patterns and of some geographical variations, and the likelihood of continuing improvement in the stillbirth and early neonatal mortality rates are discussed.

Americas↗
PubMed1990

Analysis of the syndrome of congenital malformations induced in genetically defined mice by acute riboflavin deficiency.

The role of genetics in the expression of a complex syndrome of teratologically induced congenital malformations was examined by the use of three inbred strains and 15 related crosses of mice. The syndrome, which included various limb, brain, orofacial, gastrointestinal, and miscellaneous malformations, was induced by an intense riboflavin deficiency produced by feeding the antagonist galactoflavin during midgestation. Analyses of the data showed that, although all three strains shared the major and most other features of the syndrome, there occurred in its manifestation vast quantitative and qualitative differences among them, in which they were resembled by their related crosses such as to constitute strain-specific malformation patterns. The results can be regarded as typifying an animal counterpart of human situations, the three strains representing in toto the mouse family, each strain individually exhibiting the variety that occurs between siblings in expressing a single syndrome.

Acute Disease↗
PubMed1987

Diabetes and spontaneous abortion: a historical review.

The recent claims that there is an increased frequency of spontaneous abortion in diabetic pregnancies prompted a reexamination of this question. More than 50 articles published in 1950 to 1986 containing relevant information provided the data for this purpose. In 8041 American and European, otherwise uninterrupted diabetic pregnancies ascertained through hospital records, mostly not specified as to the time at first examination and the interval covered, there occurred 10.0% +/- 0.3% spontaneous abortions. The frequency was significantly greater (12.7% +/- 0.7%), however, in the 1890 pregnancies observed during specifically stated extended periods. The records are marred by the lack of control pregnancies and the great absence of information regarding the variables and confounding factors that influence the spontaneous abortion rate. Nevertheless, since the results are very similar to those found in general clinical material it is most probable that there is no excess of spontaneous abortion in diabetic pregnancy. The recent claims of such an increase may have been based on the pregnant women in these studies being seen earlier and being closely examined for longer periods than has usually been the case and to the enrollment in the studies of women with unrepresentatively great risk of reproductive mishap.

Abortion, Spontaneous↗
PubMed1985

Experimental teratological studies with the mouse CNS mutations cranioschisis and delayed splotch.

Teratological experiments were made with a recessive mouse gene (cranioschisis) causing exencephaly and a semidominant gene (delayed splotch) causing spina bifida. In studies with the cranioschisis gene administration of warfarin and thyroxine resulted in frequencies of exencephaly significantly below that expected of a recessive trait, perhaps indicating selective elimination of abnormal conceptuses. Studies with the delayed splotch gene tested the hypothesis that offspring with a hereditary defect of neural-tube closure have other, unexpressed CNS defects, which may be elicited by teratological impulses. This proposition was decisively upheld by administering 5-bromo-2'-deoxyuridine, cadmium sulfate and retinoic acid, as these treatments all caused significantly greater frequencies of induced exencephaly in offspring with spina bifida than in their genetically normal littermates.

Animals↗
PubMed1982

Congenital malformations of the central nervous system and transplacental carcinogenesis: modification of ethylnitrosourea-induced brain tumors in rats by pretreatment with methylazoxymethanol.

X-irradiation of rat fetuses prior to exposing them transplacentally to the neurotropic carcinogen ethylnitrosourea (ENU) greatly reduces the frequency of offspring that develop neurogenic tumors. Since the tumor inhibition may have been related to the teratogenic effects of the irradiation of the fetal brain, it was of interest to learn whether another means of causing such brain damage would also interfere with the development of ENU-induced neurogenic tumors. For this purpose methylazoxymethanol (MAM), known to produce microencephaly, was used. Pregnant Sprague-Dawley rats were injected i.p. with 20 or 30 mg MAM/kg on the 15th day of gestation and 10 mg ENU/kg on the 16th or 20th day of gestation, or with either chemical alone. The offspring were observed during their life-span for the appearance of neurogenic tumors. MAM produced the expected microencephaly, but when administered alone caused no neurogenic tumors. ENU had no effect on brain size; and when administered alone produced high rates of offspring with neurogenic tumors (68 and 72% after treatment on the earlier and later day of gestation, respectively). The combined treatments resulted in significantly reduced frequencies of brain tumors, but did not modify the frequencies of non-brain tumors. The treatments caused relatively little or no excess pre- and postnatal mortality and for the most part had little effect on postnatal growth. Mean time of appearance of neurogenic tumors and mean number of neurogenic tumors per affected animal were unchanged by the dual treatments. There were no sex differences in tumor frequency, latency, or multiplicity. As noted, MAM reduced cerebral hemisphere size, but did not affect spinal cord size. The site of tumor inhibition by MAM thus appears to be correlated with the site of teratogenic damage. Nevertheless, various considerations led us to conclude that reduced number of target cells does not entirely explain the modifications in the frequency of tumors caused by MAM.

Animals↗