[18 incompatible medicaments that impair treatment].
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Biomedical subjects
Publications and source records attributed to J R Li.
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The foramen of Huschke, which appears during the embryological development of the tympanic bone, usually closes by the age of five years. A review of 377 dried skulls revealed that the foramen of Huschke was present in adult life in 7% of the skulls examined. A patent foramen of Huschke in the adult may, in rare cases, be the cause of temporomandibular joint herniation or fistulization through the anterior wall of the bony external canal.
In vitro development of embryos collected from the same gilts mated at first and third estrus was compared. Embryos from one to eight cells were collected from gilts 36 to 48 h after detection of estrus. Embryos were cultured for 8 d in Whitten's medium in a humidified atmosphere of 5% CO2 in air at 37 degrees C and were observed daily. No differences were detected among percentages of one- to eight-cell embryos developing into morulae from gilts in first or third estrus (P greater than .05). Similar percentages of one- to two-cell embryos from gilts mated at first and third estrus developed into blastocysts (45.8 and 55.2%, respectively), expanded blastocysts (10.4 and 24.1%, respectively) and hatching blastocysts (4.2 and 3.4%, respectively; P greater than .05). Fewer three- to eight-cell embryos from gilts in first estrus than from gilts in third estrus developed into blastocysts (63.4 and 91.1%) and expanded blastocysts (14.6 and 55.6%; P less than .01). Similar percentages of embryos with abnormal morphology were observed among morulae developing from one- to eight-cell embryos collected from gilts mated at first and third estrus (14.9 and 9.9%, respectively; P greater than .05). In contrast, more morphologically abnormal embryos were observed among blastocysts developing from gilts mated at first estrus than at third estrus (31.2% and 14.0%, respectively; P less than .05). The results suggest that the reduced in vitro development of embryos collected from gilts mated at first estrus may be due to an aberration in blastocoel formation and expansion.
Two patients with blunt head injury were examined by CT scanning. It was found that there was brainstem hemorrhage with unremarkable changes in the other parts of the brain. Physical examination showed signs of upper brainstem lesion such as discoordination, bilateral Babinski signs, and internuclear ophthalmic palsy without persistent coma and decerebrate rigidity. The diagnosis of primary brainstem injury, well healed, was established. Basing on the results of these 2 cases, we believe that primary brainstem injury does exist, but it is not necessarily associated with persistent coma and decerebrate rigidity. CT scanning for diagnosing such cases is emphasized.
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The objective of this paper is to review the extent and mechanisms of lipoprotein alterations in pregnancy, present new data relating to placental lipid transport in normal humans and diabetic animals and consider possible effects on fetal growth and development in normal and diabetic pregnancy. The concentration of all lipoprotein fractions increases during pregnancy. VLDL cholesterol and triglyceride increase 2.5-fold over prepregnancy levels and LDL cholesterol increases 1.6-fold, all with peak levels at term. HDL cholesterol is maximally increased in midgestation by 1.45-fold and subsequently declines to 1.15-fold at term. The mechanisms of these lipoprotein changes have not been studied in humans but the hypertriglyceridemia in animal models is related to enhanced VLDL entry into the circulation. In addition, diminished adipose tissue lipoprotein lipase (LPL) activity in late gestation may cause a rerouting of triglyceride fatty acids to other tissues such as muscle and uterus for oxidation, rather than storage, since triglyceride transport is not reduced in pregnancy. All of these changes appear to be sex hormone mediated. In diabetic pregnancies, the available data indicate that triglyceride concentrations are increased and HDL cholesterol concentrations are decreased with reference to lipoproteins in nondiabetic pregnant women. Previously unpublished data show that a transplacental FFA gradient exists across the umbilical circulation in the direction of the fetus and is proportional to the maternal FFA concentration. No gradient is seen for triglyceride or total plasma cholesterol. However, transport of unmeasured amounts of triglyceride fatty acids may still occur via placental LPL and be exaggerated in diabetes where LPL declines in adipose tissue but not in placenta. The mechanism of transplacental cholesterol transport remains to be defined. Preliminary studies suggest that it depends on HDL as well as LDL since both can provide cholesterol for placental progesterone synthesis. In addition, fetal weight and length are associated with maternal apoproteins A-I and A-II, both major apoproteins of HDL. By lowering HDL in pregnancy, diabetes mellitus could negatively affect these relationships. In conclusion, sex hormone mediated modifications of lipoprotein physiology are described in pregnancy which may enhance triglyceride fatty acid transport to muscle for oxidation and LDL and HDL cholesterol delivery to growing maternal and fetal tissues, a process that diabetes could globally disrupt.
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