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Biomedical subjects

H Kalter

Publications and source records attributed to H Kalter.

13 recordsLinked to original sources
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↗
PubMed1979

Sex, side, and severity in spontaneous malformations of fetal A/JKt mice, and their associations with each other and with fetal weight.

Cleft lip and palate (CLP) and open eyelid (OL) occur spontaneously in rather high frequencies in A/JKt mice, but vary greatly in their degree, laterality, and sex distribution. CLP occurs significantly more often in females, and OL even more often in males, than in the opposite sex. The female preponderence for CLP was largely if not entirely due to the increased rate of occurrence of left and incomplete forms of the defect, and to the excess in females heavier than the female median weight; whereas the male preponderance for OL could not be explained by any clear or major disparities of these sorts. CLP and OL occurred together more often than expected in individuals, but not in litters. There was no relation between the rate of defects in successive litters of the same female; nor was a relation detected between extent and severity of defect.

Abnormalities, Multiple↗
PubMed1979

The history of the A family of inbred mice and the biology of its congenital malformations.

The A family of inbred mice which originated in 1921, came during its early development to have incorporated into its genome the tendency to several congenital malformations, among them cleft lip and palate. These sporadic abnormalities are of interest because they closely resemble their human counterparts in morphology and development, and because they share with them a multifactorial basis. The origins and development of the A family are traced, and the abnormalities are described and the forces affecting them detailed.

Animals↗
PubMed1978

Elimination of fetal mice with sporadic malformations by spontaneous resorption in pregnancies of older females.

The frequency of offspring with sporadic spontaneous malformations in A/JKt mice was significantly smaller in litters from older mothers than in litters from younger mothers. Simultaneously the fetal resorption rate was significantly larger in the older group apparently accounted for most, if not all, of the reduced malformation rate in their surviving offspring. It therefore seems that the aged uterus and the abnormal fetus are involved in the process by which such offspring are eliminated.

Age Factors↗
PubMed1976

Some sources of nongenetic variability in steroid-induced cleft palate in mice.

C57BL/6JKt female mice mated to A/JKt males were each injected im with 50 mg/kg triamcinolone 13 days post-VP, and the roles of a number of nongenetic factors underlying variability in the frequency of cleft palate (CP) induced in the fetuses were analyzed. Litter size and number of young per uterine horn, overall, were not significantly related to the CP rate. But nearly one-quarter of litters (almost all larger-sized ones) contained CP rates deviating from-mostly less than-expected on a random basis. Analysis of litters with deviant CP distribution, as well as of all suitable litters, indicated that only maternal treatment-day weight was significantly associated, inversely, with CP frequency-in spite of the treatment dosage having been weight-based. There was no clear relation between the CP and resorption rates; but litters with deviant CP distribution had a significantly greater resorption rate than the others. Fetal weight was inversely related to CP rate even in litters of uniform size. Fetuses occupying uterine positions immediately caudal to those with CP had a significantly higher CP rate than those next to normals, and conceptuses caudal to resorptuses a significantly higher resorption rate than those next to surviving fetuses; but the reverse was not true: CP and resorption rates were not greater in those next to resorptuses and surviving fetuses, respectively.

Animals↗
PubMed1976

Oncogenic response of rats with x-ray-induced microcephaly to transplacental ethylnitrosourea.

The relation of congenital malformations to tumor development was examined. Pregnant Sprague-Dawley rats were given 200 rads of X-rays on the 15th or 16th day of gestation and injections of 10 mg ethylnitrosourea (ENU)/kg 1-4 days later, or they were irradiated or injected only. Surviving weanlings that had been irradiated had micrencephaly and other malformations. Offspring exposed to ENU only had no external deformities. By 15 months of age 16.7% of the offspring exposed to X-rays and ENU prenatally had developed neurogenic tumors, whereas 62.2% of those exposed to ENU alone had developed tumors. Those only irradiated had no tumors. Both of the former groups developed oligodendrogliomas, mixed gliomas, ependymomas, and schwannomas, but the first manifestations of tumors occurred later in the group receiving the combined treatment. This delay persisted furing the subsequent period of the study.

Animals↗
PubMed1975

Prenatal epidemiology of spontaneous cleft lip and palate, open eyelid, and embryonic death in A/J mice.

Nongenetic bases of variability in the frequencies of spontaneous cleft lip and palate (CLP), open eyelid (OL), and fetal resorption were searched for in A/J mouse litters of prenatal ages 17-21 days post-VP and parities 1-7. The malformation rates did not decrease with advancing fetal age, and hence prenatal elimination does not account for the lower rates seen in newborns. Multivariate analysis indicated that the frequencies of CLP and resorption were inversely related to maternal age and directly related to litter size, and that the frequency of OL was related, directly, only to litter size; but that none were associated with maternal weight, parity, and several other variables. Regarding uterine location, the frequency of CLP was higher at the ovarian and cervical sites, OL higher at the cervical site, and resorption lower at the ovarian site, than elesewhere. CLP was significantly commoner in females, and OL commoner in males; also, since the percentage of males increased with parity, the frequency of CLP in males relative to that in females decreased with parity, and that of OL increased. Malformed offspring weighed less than normal ones; and the sex with the lower frequency of CLP or OL had the greater weight reduction. The results are discussed in relation to the frequency of malformations in human fetuses and newborns.

Animals↗
PubMed1975

Some relations between teratogenesis and mutagenesis.

The nonactinic environmental agents that have been found to induce mutations in laboratory mammals are almost without exception of a single chemical class, alkylating chemicals, whereas this class is only one of the numerous sorts of environmental agents that induce congenital structural malformations. Many other types of chemical teratogens as well as nonchemical teratogens exist. This conspicuous difference between the known means of producing these phenomena reflects the fact that the mechanism by which malformations and mutations arise are for the most part distinctly different from each other. Therefore, environmentally induced malformations and mutations cannot be equated with each other and used as mutual indicators in monitoring potential harmful effects of the environment.

Abnormalities, Drug-Induced↗