[MATRIX METALLOPROTEINASE 9 AND TISSUE INHIBITOR OF MATRIX METALLOPROTEINASES TYPE 1 SERUM CONCENTRATIONS AND GENETIC POLYMORPHISM IN SENILE AORTIC STENOSIS].

The study of the serum levels of matrix metalloproteinase 9 (MMP9) and tissue inhibitor of matrix metalloproteinases type 1 (TIMP1) was conducted involving 108 patients aged over 65, with calcinosis and/or calcific aortic valve (AV) stenosis. The purpose of the study was to identify the molecular and genetic markers responsible for the development of senile aortic stenosis. Besides, there was also typing of polymorphic loci of MMP9 gene A8202G (rs1169732) and TIMP1 gene C536T(rs11551797) performed. The comparison group included 46 patients whose examination revealed no evidence of AV calcinosis present in them. Association of senile aortic stenosis with a significant increase in the serum TIMP1 levels (257,5 (151,5-325,9) pg/ml vs 129,7 (86,2-229) pg/ml, p < 0.05) has been detected, while the TIMP1 concentration going beyond 258,1 pg/ml in the elderly people over 65 years can be considered as a high-precision marker of the pathology under discussion. The MMP9 (A8208G) as well as TIMP1 (C5367) genetic polymorphisms are not associated with calcific aortic stenosis.

Aesthetic vaginal labioplasty.

Labia minora that protrude past the labia majora are aesthetically and functionally unsatisfactory to some women. Historically, female circumcision has been practiced in Islamic/Arabic countries for many centuries and is still commonly practiced in these countries. Three case reports present middle-aged women who were dissatisfied with the size and protuberance of the labia minora, and an aesthetic labioplasty was performed in these three women. The technical aspects of this procedure are outlined, and a representative case with 3-month follow-up is presented pictorially.

Effects of uridine and inosine on glucose metabolism in skeletal muscle and activated lipolysis in adipose tissue.

In a first series of experiments, the effects of uridine and inosine on glucose metabolism in rat diaphragm muscle incubated in Krebs-bicarbonate buffer were studied. Uridine in concentrations of 10(-4) to 10(-6) M stimulated the uptake of glucose and increased the content of glycogen, but had no effect on the production of lactate. When diaphragm muscles were incubated in the buffer without glucose, uridine (10(-4)-10(-6) M) had no effects on the content of glycogen and on the production of lactate. On the other hand, inosine in concentrations of 10(-4) to 10(-6) M stimulated the uptake of glucose and the production of lactate, but had no effect on the content of glycogen in the muscle. In a second series of experiments, uridine (10(-4)-10(-5) M) and inosine (10(-4)-10(-7) M) inhibited the relase of glycerol from isolated rat epididymal adipose tissue in Krebs-bicarbonate buffer. Uridine and inosine in concentrations of 10(-4) M inhibited the epinephrine (10(-5) M)-, the norepinephrine (10(-5) M)- and the theophylline (10(-3) M)-stimulated lipolysis. Dibutyryl 3',5'-adenosine monophosphate-stimulated lipolysis was further activated in the presence of 10(-4) M uridine or inosine. Dose-response curves studies suggested that inosine, but not uridine, has a common receptor site with epinephrine in adipose tissue. These results demonstrated that both nucleosides stimulated the glucose uptake, but only uridine increased the synthesis of glycogen in the muscle. Both nucleosides also inhibited lipolysis in adipose tissue. The mechanism of antilipolytic action of these nucleosides is unknown, but one of the receptor sites for inosine might be adenylate cyclase.

Myocardial metabolism and performance in hypoxia: effect of epinephrine.

Effects of epinephrine (10(-5) M) on mechanical performance, glycolysis, glycogenolysis, lipolysis, and metabolism of adenine nucleotides were studied in isolated hypoxic rabbit hearts. The exposure of hearts to hypoxia decreased their mechanical performance and heart rate, but increased their utilization of glucose by 50% and the release of lactate by 139%. Myocardial stores of glycogen and ATP declined by 53 and 84%, respectively, but their breakdown products such as lactate, pyruvate, AMP, and inosine accumulated in these hearts. Myocardial content of free fatty acids decreased, and the amount of glycerol increased in hypoxic hearts. Epinephrine stimulated mechanical performance and heart rate of hypoxic hearts, but decreased myocardial glycogen and ATP even more by 62 and 33%, respectively. Though glucose utilization remained unchanged, the release of lactate increased by 66% from hypoxic hearts treated with epinephrine. However, epinephrine failed to stimulate myocardial lipolysis in hypoxic hearts. These metabolic changes due to epinephrine would lead to accelerated depletion of energetic reserves in hypoxic heart and its earlier deterioration.