Lead in the mother-newborn system as an indicator of chemical load hazard in unfavorable environmental areas

The paper deals with the studies of the levels of lead in the biological media in women in labour and their neonatal infants who live in poor environmental areas. A comparison was made of the levels of lead in the biological media of the women in labour and neonates from the experimental and control groups. There was a relationship between the levels of lead in the biological media of the newborn and the mother. A total of 7 different biosubstrates from the women in labour and neonatal babies were examined. The studies were made by atomic absorption spectrophotometry on a Perkin Elmer 3110 device.     

Rapid progression of passaged mouse hepatocarcinoma associated with the loss of cell polarity

Two transplantable differentiated mouse hepatocarcinomas were obtained in B6 D2 F1 mice from primary tumors induced by initiation (NDEA)-promotion (phenobarbital) protocol. Both HC were slowly growing with time from passage to passage of 5-7 months (s-HC). A fast-growing variant with time between passages of 2-3 weeks appeared in one mouse on the third passage (f-HC). The three HC strains constantly retained their phenotype. The s-HCs were characterized by prominent cell polarity according to organization of the cytoskeleton and distribution of domain-specific membrane-associated markers. Cell polarity was completely destroyed in the fast-growing variant. Cell adhesion in the latter tumor was very low. An in vitro growing strain of f-HC was easily obtained enabling experimental study of regulation of progression in HCs.     

The rehabilitation of patients with diabetes mellitus and ischemic heart disease

The results of bicycle ergometry testing were studied in 20 patients with diabetes mellitus of type II without clinical signs of circulatory insufficiency, 21 patients with postinfarction cardiosclerosis with undisturbed carbohydrate tolerance, and in 18 healthy persons. The blood level of glucose in patients with diabetes mellitus was investigated on an empty stomach and 30, 60 and 120 min. after physical exercising. Similar changes of bicycle ergometry results were found in diabetic and CHD patients. In compensation of diabetes in response to graded physical exercise glycemic changes were absent, in decompensation glycemia increased in 30 and 60 min. and returned to the basal level 120 min. after testing. Since the results of bicycle exercises in diabetic (compensated) and CHD patients were the same, the principles of their physical rehabilitation must be identical. In patients with decompensated diabetes mellitus a hyperglycemic reaction to graded physical exercise serves the basis for reduction of motor activity in patients with decompensated diabetes mellitus.     

Application of vacuum drainage of purulent wound in the treatment of phlegmon of maxillofacial region with predominance of putrefactive-necrotic lesions

There was established high efficacy of method of the low dosed vacuum draining of wound with predominance of putrefactive-necrotic affection was established in patients with phlegmon of maxillofacial region.     

Role of ERK1/2 and p38 mitogen-activated protein kinases in the regulation of thrombospondin-1 by TGF-beta1 in rat proximal tubular cells and mouse fibroblasts

Thrombospondin-1 (TSP-1) inhibits angiogenesis and activates latent TGF-beta1, both of which are strongly associated with progression of renal disease. Recently, it was reported that Smad2 but not Smad3 regulates TSP-1 expression in response to TGF-beta1 in rat tubular epithelial cells as well as in mouse fibroblasts. This study investigated the role of ERK1/2 and p38 mitogen-activated protein kinases (MAPK). TGF-beta1 activated both ERK1/2 and p38 in the rat proximal tubular cell line NRK52E. Blocking ERK1/2 and p38 inhibited TGF-beta1-induced TSP-1 mRNA and protein expression. Next, the cross-talk between Smad2 and ERK1/2 or p38 was examined. Whereas blocking of ERK1/2 or p38 failed to inhibit TGF-beta1-induced Smad2 activation, inhibition of Smad2 by Smad7 overexpression inhibited the phosphorylation of ERK1/2 but not p38 in response to TGF-beta1. Similar results were observed using mouse fibroblasts from Smad2 knockout embryos, in that TGF-beta1 was able to activate p38 but not ERK1/2 in this cell line. In conclusion, TSP-1 expression is regulated by both ERK1/2 and p38 MAPK in rat proximal tubular cells and mouse fibroblasts in response to TGF-beta1. The ERK1/2 activation is dependent on Smad2 activation, whereas the p38 activation occurs independent of Smad2. Because TSP-1 is a major antiangiogenic molecule and an activator of TGF-beta1, this provides an important insight to the mechanism by which TGF-beta1 may mediate interstitial fibrosis and progressive renal disease.