Genetic control of tetracycline resistance in bacteria]

Modern data on prevalence, structural and functional organization of the tetracycline resistance determinants in bacteria are reviewed. The three mechanisms of the antibiotic resistance are the tetracycline efflux, the ribosomal protection and the antibiotic modification. The problems of evolution of tetracycline resistance genes are discussed.     

Genetic determinants of tetracycline resistance of plasmids from the bacterial species Pseudomonas

The colony hybridization and tetracycline accumulation techniques made possible to demonstrate the majority of the 29 bacteria of Pseudomonas genera to harbour the plasmids carrying tet determinants belonging to classes A-C, while one strain contained a plasmid carrying tet determinant of class B. For the first time the determinants of classes D and E were found on R plasmids in Pseudomonas aeruginosa. The determinant of G class was identified on two plasmids identical to pBS221 plasmid described previously.     

The quantitative analysis of polymorphism on human chromosomes 1, 9, 16, and Y

Summary Comparative analysis of the polymorphism of C segments on chromosomes 1, 9, 16, and Y was conducted in 50 normal boys and 50 normal girls. Quantitative methods revealed that the mean lengths of C segments, their variability, and their distribution on the chromosomes mentioned are quite identical in the two groups. Methodological problems related to the study of chromosome polymorphism are discussed.     

Cerebroprotective effects of the CO-releasing molecule CORM-A1 against seizure-induced neonatal vascular injury

Endogenous CO, a product of heme oxygenase activity, has vasodilator and cytoprotective effects in the cerebral circulation of newborn pigs. CO-releasing molecule (CORM)-A1 (sodium boranocarbonate) is a novel, water-soluble, CO-releasing compound. We addressed the hypotheses that CORM-A1 1) can deliver CO to the brain and exert effects of CO on the cerebral microvasculature and 2) is cerebroprotective. Acute and delayed effects of topically and systemically administered CORM-A1 on cerebrovascular and systemic circulatory parameters were determined in anesthetized newborn pigs with implanted closed cranial windows. Topical application of CORM-A1 (10(-7)-10(-5) M) to the brain produced concentration-dependent CO release and pial arteriolar dilation. Systemically administered CORM-A1 (2 mg/kg ip or iv) caused pial arteriolar dilation and increased cortical cerebrospinal fluid CO concentration. Systemic CORM-A1 did not have acute or delayed effects on blood pressure, heart rate, or blood gases. Potential cerebroprotective vascular effects of CORM-A1 (2 mg/kg ip, 30 min before seizures) were tested 2 days after bicuculline-induced epileptic seizures (late postictal period). In control piglets, seizures reduced postictal cerebrovascular responsiveness to selective physiologically relevant vasodilators (bradykinin, hemin, and isoproterenol) indicative of cerebrovascular injury. In contrast, in CORM-A1-pretreated animals, no loss of postictal cerebrovascular reactivity was observed. We conclude that systemically administered CORM-A1 delivers CO to the brain, elicits the vasodilator and cytoprotective effects of CO in the cerebral circulation, and protects the neonatal brain from cerebrovascular injury caused by epileptic seizures.     

Urokinase stimulates whereas tissue plasminogen activator attenuates blood vessel stenosis]

Periadventitial application of the urokinase-plasminogen activator (uPA) in pluronic gel to an injured artery stimulated the neointima and neoadventitia formation as well as cell migration and proliferation in vivo. In contrast, the tissue-type plasminogen activator (tPA) reduced the number of neointimal smooth muscle cells and neointimal area and attenuated the lumen stenosis after a balloon catheter injury of the rat carotid artery. This ability to stimulate the neointima and neoadbentitia formation was found to be quite specific for the uPA. The findings suggest that this uPA property provides a specific functional target for attenuating growth of the damage.     

Participation of apolipoprotein E in the transport of cholesterol esters

It is established in the in vitro experiments that subfraction of HDL3 is able of accepting cholesterol from the atherosclerosis-afflicted aorta intima. Apoprotein E has no effect on the acceptance of cholesterol from the intima by HDL3 particles. The role of the protein under its joint incubation with the aorta intima and HDL3 is reduced to the uptake of cholesterol esters from HDL3-particles enriched by cholesterol. It is assumed that apoprotein E under certain metabolic conditions can transfer esterified cholesterol from HDL-particles on other lipoproteins as well as into tissues impoverished in the cholesterol content.     

First report on bacteria of the family <Emphasis Type="Italic">Spirochaetaceae</Emphasis> from digestive tract of endemic gastropods from Lake Baikal

Detection of bacteria of the family Spirochaetaceae in the crystalline style of 11 species of endemic gastropods from Lake Baikal is reported. Investigation by transmission and scanning electron microscopy showed that these spirochetes belonged to the genus Cristispira.     

HDL2b lipoproteins as an acceptor of cholesterol from erythrocyte membrane and the role of lecithin-cholesterol-acyltransferase during this process

The role of lecithin-cholesterol-acyltransferase (LCAT) in net cholesterol transport from erythrocyte membranes to one of high density lipoprotein subclasses--HDL2b--was studied in vitro. It was shown that an addition of partially purified LCAT to the incubation medium containing human HDL2b and human erythrocytes triggers free cholesterol transport from erythrocyte membranes to HDL2b. In this case, the rise in HDL cholesterol occurs mainly due to the formation of cholesteryl esters produced by LCAT. The significance of cholesterol ecceptor properties of HDL2b in vivo is discussed.