Nonfiction 1

Teratology in the twentieth century plus ten by Harold Kalter

By Harold Kalter

Serious congenital malformations are an immense contributor to the newborn loss of life cost around the world. Their nonhereditary reasons are a number of and intricate, and contain infectious and metabolic hazards, illness medicine, dietary inadequacy, medicinal items, environmental brokers and pollution, between them. the reason for many even though continues to be unknown.

The wide variety of those factors makes the defects of curiosity to these of quite a lot of scientific and investigatory backgrounds, especialy clinicians, basic scientists, and environmentalists.

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By this work Fred Hale (who, incidentally, did not have a doctorate degree) demonstrated conclusively for the first time that an absence or insufficiency of an environmental factor – a nutritional element – of great and vital human necessity, could cause serious malformations in mammalian embryos. And he clinched the proposition with breeding and nutrition experiments that ruled out the possibility of genetic factors being responsible in any way for them. Discovery Greeted Skeptically Even so, the nutritional origin of the eye defects was greeted skeptically, as shown by an exchange of views following the delivery of his paper at a meeting of the Association for Research in Ophthalmology in Atlantic City on June 11, 1935 – in which he held his own very well (Hale 1935a).

When] examination of the records disclosed the workings of a pediatric intern with an undue fondness for this diagnosis” (Stevenson et al. 1950); absent umbilical artery, in newborn children of diabetic women (Neave 1967), which a pathology study from the same hospital found rarely in autopsies of infants of diabetic births (Driscoll et al. 1960). A perhaps common and only slowly recognized cause of an increased frequency are changed diagnostic methods and criteria. For example, a jump in the frequency of ventricular septal defect, first thought to be due to surged diagnosis, was later found to have been due to the detection of small septal defects overlooked by less intense diagnostic methods (Laursen 1980, Newman 1985, Spooner et al.

Rubella studies have been made with macaque monkeys, baboons, hamsters, rats, mice, rabbits, and ferrets. The findings were varied and inconsistent. Transplacental passage of virus seldom occurred, but when it did infection often led to fetal growth retardation, abortion, and neonatal death. Some young fetal monkeys had histological changes in ear, eye, and skin, and rats had lenticular opacities and atrophic interventricular septa, but none of these outcomes was independently confirmed. In other words, the teratogenicity of the rubella virus in non-human animals is unproven (Oxford and Sutton 1968, Elizan et al.

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