beta 2-Adrenomimetics before and after extracorporeal lithotripsy

The paper shows it possible to use the method of total internal reflection-fluorescence for study of the kinetics of protein adsorption onto the surface of intraocular lenses (IOL) made from optically transparent hydrophobic polymers and hydrogels. The nature of the materials (polymethylmethacrylate, silicone, p-HEMA, p-HEMA-collagen copolymer) used for IOL on the adsorption and desorption of human serum albumin was studied.     

Determination of likelihood of the development of pleural empyema in patients with cancer after pneumonectomy

Management of 150 patients with lung cancer after pneumonectomy has shown that the basic factors causing the onset of postoperative pleural empyema are chronic nonspecific pulmonary diseases, pronounced obstructive syndrome and right heart overload, tumor histology, local tumor size and cancer complications, duration and techniques of surgery, duration of controlled lung ventilation, as well as the onset of postoperative suppurative tracheobronchitis and surgical wound suppuration. The likelihood of empyema development may be assessed only upon analysis of the combination of risk factors with reference to their low informative value, preoperative patients' condition and intraoperative factors which have an equal impact on the onset of this complication. The efficacy of the algorithm elaborated is as follows: if the likelihood of empyema development exceeds 50%, it occurs in 96.3% of cases, if the likelihood of the complication is less than 10%, the postoperative period is uncomplicated in 87.8% of patients.     

Micro vs. macro: structural-functional organization of avian micro- and macrochromosomes

Karyotypes of lower vertebrates mainly consist of microchromosomes. In higher vertebrates, microchromosomes are present in each class of the most primitive orders. Birds have more microchromosomes in their karyotype than other vertebrates. Accumulation of microchromosomes in the avian karyotype probably occurred after separation of birds from reptilians in Triassic, but prior to radiation of ancestors of the modern orders (late Cretaceous-early Jurassic). In this review, the structural, molecular, and functional organization of avian macro- and microchromosomes and their participation in genetic processes are discussed. The average size of an avian microchromosome is about 12.4 Mb, which is ten times less than the size of an average macrochromosome. In contrast to macrochromosomes, medium and small avian chromosomes lack the highest level of chromosomal organization: their chromonemes do not have spiral coiling. Microchromosomal euchromatin largely consists of GC-rich R regions. More than half of the mapped avian genes are located on microchromosomes. Crossing-over frequency in microchromosomes is approximately threefold higher than in macrochromosomes. This may be caused by high GC content and recombination hot spots, which are present on each microchromosome. High recombination frequency in microchromosomes increases the probability of their correct meiotic segregation.     

Empty sella and headache

Empty sella is an anatomical condition caused by herniation of the subarachnoid space into the pituitary fossa through an incompetent sellar diaphragm. Headache seems to be one of the most frequently reported symptoms. We studied 13 headache patients (12 females, 1 male) presenting with primary empty sella (PES) on CT scan. The characteristics of the headache were analyzed and plasma levels of pituitary hormones or cortisol assessed. We confirmed the nonspecific nature of the headache in PES even though the majority of our patients complained of daily headache, mostly localized anteriorly. Hormone plasma levels were within normal range in all the patients assessed. However, four patients reported earlier endocrine disorders and more than half of the patients presented with obesity. In our opinion, PES should be suspected in middle-aged overweight women with daily headache even in the absence of endocrine symptomatology.     

Characterization of the antiproliferative signal mediated by the somatostatin receptor subtype sst5

We investigated cell proliferation modulated by cholecystokinin (CCK) and somatostatin analogue RC-160 in CHO cells bearing endogenous CCKA receptors and stably transfected by human subtype sst5 somatostatin receptor. CCK stimulated cell proliferation of CHO cells. This effect was suppressed by inhibitor of the soluble guanylate cyclase, LY 83583, the inhibitor of the cGMP dependent kinases, KT 5823, and the inhibitor of mitogen-activated protein (MAP) kinase kinase, PD 98059. CCK treatment induced an increase of intracellular cGMP concentrations, but concomitant addition of LY 83583 virtually suppressed this increase. CCK also activated both phosphorylation and activity of p42-MAP kinase; these effects were inhibited by KT 5823. All the effects of CCK depended on a pertussis toxin-dependent G protein. Somatostatin analogue RC-160 inhibited CCK-induced stimulation of cell proliferation but it did not potentiate the suppressive effect of the inhibitors LY 83583 and KT 5823. RC-160 inhibited both CCK-induced intracellular cGMP formation as well as activation of p42-MAP kinase phosphorylation and activity. This inhibitory effect was observed at doses of RC-160 similar to those necessary to occupy the sst5 recombinant receptor and to inhibit CCK-induced cell proliferation. We conclude that, in CHO cells, the proliferation and the MAP kinase signaling cascade depend on a cGMP-dependent pathway. These effects are positively regulated by CCK and negatively influenced by RC-160, interacting through CCKA and sst5 receptors, respectively. These studies provide a characterization of the antiproliferative signal mediated by sst5 receptor.     

Genetic disorders in house mice after the accident at Chernobyl power plant

Genetic effects were studied in house mice caught from 1986 to 1994 in regions polluted by radionuclides as a result of the Chernobyl disaster. The dose rates of gamma-radiation on the soil surface ranged from 0.02 to 200 mR/h. The frequency of reciprocal translocations in mouse spermatocytes was relatively low, but increased with the dose rate. Embryo mortality was increased only in the progeny of male mice caught in 1987 in the area with maximum contamination. The frequency of mice heterozygous for recessive lethal mutations decreased with the time after the accident.     

The effect of alpha-1-acidic glycoprotein on neutrophil chemiluminescence and lipid peroxidation in experimental thermal trauma

Induced chemoluminescence of neutrophils was distinctly inhibited both in intact mice and the animals with thermal injury after administration of acid alpha 1-glycoprotein. At the same time, the glycoprotein decreased the rate of thermal burn-induced activation of lipid peroxidation in rat blood, skin and liver tissue. Antioxidative and therapeutic effects of acid alpha 1-glycoprotein in burns appear to be related to regulation of neutrophil activity.     

Heparin promotes proteolytic inactivation by thrombin of a reactive site mutant (L444R) of recombinant heparin cofactor II

A heparin cofactor II (HCII) mutant with an Arg substituted for Leu444 at the P1 position (L444R-rHCII) was previously found to have altered proteinase specificity (Derechin, V. M., Blinder, M. A., and Tollefsen, D. M. (1990) J. Biol. Chem. 265, 5623-5628). The present study characterizes the effect of glycosaminoglycans on the substrate versus inhibitor activity of L444R-rHCII. Heparin increased the stoichiometry of inhibition of L444R-rHCII with alpha-thrombin (compared with minus glycosaminoglycan) but decreased it with R93A,R97A,R101A-thrombin, a mutant thrombin that does not bind glycosaminoglycans. Dermatan sulfate decreased the stoichiometry of inhibition of L444R-rHCII with both proteinases. SDS-polyacrylamide gel electrophoresis showed no proteolysis of L444R-rHCII when incubated with R93A,R97A,R101A-thrombin in the absence or the presence of glycosaminoglycan or with alpha-thrombin and dermatan sulfate. In contrast, greater than 75% of the L444R-rHCII was converted to a lower molecular weight form when incubated with alpha-thrombin/heparin. A time course of alpha-thrombin inhibition by L444R-rHCII/heparin showed a rapid but transient inhibition with approximately 80% of the alpha-thrombin activity being regained after 6 h of incubation. In contrast, all other combinations of inhibitor, proteinase, and glycosaminoglycan resulted in complete and sustained inhibition of the proteinase. Heparin fragments of 8-20 polysaccharides in length rapidly accelerated L444R-rHCII inhibition of both alpha-thrombin and R93A,R97A,R101A-thrombin. After extended incubations, R93A,R97A,R101A-thrombin was completely inhibited by L444R-rHCII with all the heparin fragments, but approximately 30-50% of alpha-thrombin activity remained with fragments long enough to bridge HCII-thrombin. These results collectively indicate that ternary complex formation, mediated by heparin, increases L444R-rHCII inactivation by alpha-thrombin.