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Biomedical subjects

V K Mohl

Publications and source records attributed to V K Mohl.

12 recordsLinked to original sources
PubMed1998

Hyperparathyroidism.

Hyperparathyroidism is a common cause of hypercalcemia. The hypercalcemia usually is discovered during a routine serum chemistry profile. Often, there has been no previous suspicion of this disorder. In most patients initially believed to be asymptomatic, previously unrecognized symptoms resolve with surgical correction of the disorder. The symptoms of hyperparathyroidism are vague and often similar to symptoms of depression, irritable bowel syndrome, fibromyalgia or stress reaction. Complications of primary hyperparathyroidism include peptic ulcers, nephrolithiasis, pancreatitis and dehydration. Surgical management is usually indicated. When medical management is used, routine monitoring for clinical deterioration is recommended. Preoperative localization of adenomas with technetium Tc 99m sestamibi scan is possible but may be unnecessary. An experienced surgeon should perform the parathyroidectomy.

Diagnosis, Differential↗
PubMed1997

Intrathecal analgesia for labor.

Intrathecal analgesia is a highly effective technique for pain relief in the first stage of labor. It is a technically simple procedure that can be easily learned by family physicians currently performing diagnostic lumbar puncture. Its effectiveness, simplicity, and low incidence of serious complications make it especially applicable to the practices of physicians delivering babies in areas where continuous epidural anesthesia is not available. This article describes the procedure of intrathecal analgesia, and discusses advantages, complications, side effects, and applications.

Analgesia, Epidural↗
PubMed1991

In vitro analysis of the murine heat shock response: implications for reproductive toxicology.

Lymphocytes isolated from two inbred mouse strains that differed in their genetically determined sensitivity to heat-induced exencephaly were used to compare the in vitro kinetics of heat shock protein synthesis in the two strains following hyperthermic exposure. Differences in protein synthesis were determined by densitometric analysis of autoradiograms of SDS-PAGE gels. The findings were consistent with those observed in vivo in that there was an immediate and prolonged synthesis of heat-shock proteins by lymphocytes from the heat sensitive SWV/SD strain, compared to the response observed in lymphocytes from the heat-resistant DBA/2J strain. These results indicate that an in vitro lymphocyte assay of the heat-shock response may be a useful tool for screening suspected teratogenic agents.

Animals↗
PubMed1990

Embryonic and maternal heat shock responses to a teratogenic hyperthermic insult.

Exposing embryos to elevated temperatures both in vivo and in vitro has been shown to result in the production of offspring with severe congenital abnormalities. While a direct effect of heat cannot be excluded, recent interest has been focused on the possible role that the induction of the heat shock response may have in the etiology of the observed congenital defects. In the present study, mouse embryos from inbred strains known to differ in terms of their sensitivity to heat-induced exencephaly were treated in vivo and their heat shock response determined using SDS-PAGE electrophoretic techniques. Further, the embryonic responses were compared with a maternal cell type. We observed excellent agreement between the two test systems following exposure to a teratogenic hyperthermic insult. Both the embryonic and maternal cells underwent a reduction in total protein synthesis and an enhanced synthesis of four heat shock proteins migrating with the molecular weights of 68, 70, 97, and 110 kDa. The results failed to indicate any strong correlation between the heat shock response and enhanced genetic sensitivity to hyperthermia-induced neural tube defects.

Animals↗
PubMed1990

Genetic differences in the duration of the lymphocyte heat shock response in mice.

Lymphocytes from adult mice bearing a known difference in genetic susceptibility to teratogen-induced exencephaly (SWV/SD, and DBA/2J) were evaluated for changes in protein synthesis following an in vivo heat treatment. Particular attention was paid to changes indicative of the heat shock response, a highly conserved response to environmental insult consisting of induction of a few, highly conserved proteins with simultaneous decreases in normal protein synthesis. The duration of heat shock protein induction in lymphocytes was found to be increased by 1 hr in the teratogen-sensitive SWV/SD strain as compared to the resistant DBA/2J strain. Densitometric analysis revealed a significant decrease in the relative synthesis of at least two non-heat shock proteins (36 kD and 45 kD) in the SWV/SD lymphocytes as compared to DBA/2J cells. The increased sensitivity of protein synthesis to hyperthermia in the SWV/SD lymphocytes were lost in the F1 progeny of reciprocal crosses between SWV/SD and DBA/2J mouse strains. Sensitivity to hyperthermia-induced exencephaly is recessive to resistance in these crosses. The relationship between altered protein synthesis and teratogen susceptibility is discussed.

Animals↗
PubMed1988

Common hierarchies of susceptibility to the induction of neural tube defects in mouse embryos by valproic acid and its 4-propyl-4-pentenoic acid metabolite.

The teratogenic effects of valproic acid and its 4-propyl-4-pentenoic acid (4-en) metabolite were investigated in three inbred mouse strains that were known to possess differing sensitivity to heat-induced neural tube defects. In the heat-resistant DBA/2J strain, administration of either valproic acid or the metabolite during the critical period of neural tube development failed to produce any abnormal offspring. Similar treatment in the moderately heat-sensitive LM/Bc strain resulted in up to 19.8% exencephalic fetuses. The highly heat-sensitive SWV strain was also very susceptible to the induction of neural tube defects by either valproic acid or its 4-en metabolite. When administered on gestational day 8 plus 12 hours, the parent compound produced 35% exencephalic fetuses, while the metabolite had a response frequency of 32.4%. Thus, the hierarchy of susceptibility for the induction of neural tube defects in these inbred mouse strains was exactly the same whether the teratogen was a physical agent such as hyperthermia or a chemical compound such as valproic acid. If such diverse agents as these should interact to produce malformations, then it is possible that a wide variety of other agents might interact in a similar manner to produce neural tube defects.

Animals↗
PubMed1986

Failure of epoxide formation to influence carbamazepine-induced teratogenesis in a mouse model.

The teratogenic potential of the anticonvulsant drug carbamazepine was determined following chronic oral administration in two inbred mouse strains (SWR/J and LM/Bc). The drug was administered in the animal's diet in concentrations equivalent to 0, 1,000, 1,500, or 2,000 mg/kg body weight, with treatment starting 2 wks prior to mating and continuing throughout gestation. Fetal examination failed to reveal a significant pattern of malformation in either strain at any treatment level. Levels of plasma carbamazepine and its metabolite, carbamazepine-10,11-epoxide, were determined by high pressure liquid chromatography. There was no correlation with either of these compounds and the incidence of fetal abnormality. The inherent teratogenicity of carbamazepine is significantly lower than that of other anticonvulsant drugs that have been similarly tested in an animal model.

Animals↗