Streaking camera in the high intensity regime.

The laser-induced decay of an atomic system in an intense infrared and perturbative extreme ultraviolet (XUV) pulse is considered within Keldysh and streaking ionization channels. The streak camera method is discussed for two cases corresponding to different ranges of photoelectron momentum: i) the streaking channel significantly dominates the Keldysh channel and ii) the Keldysh channel of ionization is dominant, while two channels may interfere. The retrieval of XUV pulse parameters for these two cases is discussed and supported by numerical calculations.

[Microbial degradation of glyphosate herbicides (review)].

This review analyzes the issues associated with biodegradation of glyphosate (N-(phosphonomethyl)glycine), one of the most widespread herbicides. Glyphosate can accumulate in natural environments and can be toxic not only for plants but also for animals and bacteria. Microbial transformation and mineralization ofglyphosate, as the only means of its rapid degradation, are discussed in detail. The different pathways of glyphosate catabolism employed by the known destructing bacteria representing different taxonomic groups are described. The potential existence of alternative glyphosate degradation pathways, apart from those mediated by C-P lyase and glyphosate oxidoreductase, is considered. Since the problem of purifying glyphosate-contaminated soils and water bodies is a topical issue, the possibilities of applying glyphosate-degrading bacteria for their bioremediation are discussed.

New approaches to identification and activity estimation of glyphosate degradation enzymes.

We propose a new set of approaches, which allow identifying the primary enzymes of glyphosate (N-phosphonomethyl-glycine) attack, measuring their activities, and quantitative analysis of glyphosate degradation in vivo and in vitro. Using the developed approach we show that glyphosate degradation can follow different pathways depending on physiological characteristics of metabolizing strains: in Ochrobactrum anthropi GPK3 the initial cleavage reaction is catalyzed by glyphosate-oxidoreductase with the formation of aminomethylphosphonic acid and glyoxylate, whereas Achromobacter sp. MPS12 utilize C-P lyase, forming sarcosine. The proposed methodology has several advantages as compared to others described in the literature.

[Pathogenesis of gallbladder cholesterolemia]. / Patogenez kholesteroza zhelchnogo puzyria.

Disturbances in cholesterol metabolism may be essential in pathogenesis of gallbladder cholesterosis (GBC). HDL cholesterol in the blood is subnormal. Physicochemical changes in the superficial layer of HDL induce impairment of free cholesterol esterification. Blood lipids and their apoprotein component are important for bile cholesterol level. In gallbladder contractile dysfunction but unaffected absorption there is enhanced passive and active cholesterol transport from the supersaturated bile to the cytoplasm of the epithelial cells from the bladder mucosa. Mechanism of intensive absorption of the lipids by macrophages operates primarily via modification of their apoprotein component. Modification of apoprotein occurs both in blood and gallbladder. Modified apoprotein is recognized by the macrophage and is absorbed by it together with transported lipids. In accumulation of great quantities of lipids in the macrophage it becomes big, slow, stays in the mucous or submucous layer of the wall and finally transforms into the foam cell. Moreover, deterioration of HDL cholesterol acception in GBC leads to slow discharge of cholesterol from the bladder wall.

[Immunomorphologic detection of apoprotein B antigenic determinants in the gallbladder wall in cholesterosis and cholelithiasis]. / Immunomorfologicheskoe vyiavlenie otdel'nykh antigennykh determinant apoproteina B v stenke zhelzhnogo puzyria pri kholesteroze i zhelchnokamennoi bolezni.

The presence and location of apoprotein B (Apo B) antigenic determinants in cholesterosis and cholelithiasis in gall bladder wall were detected for elaboration of modified Apo B role in pathogenesis of these diseases. Macroscopically changed parts of gall bladder (GB) wall of patients with gall bladder cholesterosis (GBC), and also macroscopically unchanged parts of GB wall of patients with cholelithiasis (CL) after cholecystectomy were studied. Macroscopically unchanged parts of GB wall obtained during autopsy of persons without symptoms of GB pathology were used as a control. Apo B location was studied with monoclonal (MAB 5F8 to Apo B) and polyclonal (PAB) antibodies; Apo B modified by malonic dialdehyde and oxidized by Cu2+ (4C11), Apo A with MAB1C5. Antibodies to CD 68 (specific marker of macrophages) was positive control, antibodies to trichinella--negative control. The most intensive accumulation of modified Apo B was revealed in foam cells region with accumulate lipids and form polyps that testifies to connection of apoproteins with lipids and foam cells and suggests their role in pathogenesis of GBC. More intensive staining of GB epithelial cells, particularly on GB peripheral parts by antibodies to apoproteins compared with surrounding tissues shows that bile is the source of detected modified apoproteins. Increase of absorption and accumulation of apoproteins in GB wall were also revealed in CL but these processes are less intensive than in GBS.

[High-density lipoproteins in cholesterosis of the gall bladder]. / Lipoproteidy vysokoi plotnosti pri kholesteroze zhelchnogo puzyria.

The composition of serum high-density lipoproteins (HDL) was studied in 64 patients with polypous cholesterosis (PC). The spectrum of serum lipids in patients with PC was characterized by the lower concentrations of HDL cholesterol (42.0 +/- 2.5 mg/dl; p < 0.05) and higher concentrations of low-density lipoproteins (LDL) cholesterol (169.9 +/- 6.9 mg/dl; p < 0.01) than those in the controls. The decreased HDL cholesterol, or hypoalphacholesterolemia was associated with quantitative changes in HDL phospholipids (PL) (66.48 +/- 3.4; p < 0.01) and with changes in the composition of individual PL by lowering the proportion of lecithin (47.13 +/- 2.19 mg/dl; p < 0.01). It may be suggested that the lower amount of HDL cholesterol is caused by the decreased HDL acception of free cholesterol from the peripheral cell membranes due to the impaired complexation of PL with free cholesterol and associated the altered PL composition of the superficial monolayer of a lipoprotein particle. At the same time the physicochemical changes in Hdl superficial layer are a cause of abnormal free cholesterol esterification and the impaired plunge of esterified cholesterol into the nucleus of a HDL particle, which facilitates the conversion of HDL to LDL and may explain elevated LDL levels in cholesterosis. The findings suggest that serum lipids are involved in the development of cholesterosis.

[Morphological evidence of the possible role of cytochrome P-450 in the development of an autoimmune process in the liver]. / Morfologicheskie svidetel'stva vozmozhnoi roli tsitokhroma P-450 v razvitii autoimmunnogo protsessa v pecheni.

Morphological alterations in rat's liver during lipid peroxidation induction by paraqat were studied. Infiltration of liver by lymphocytes, macrophages and plasma cells was studied. On ultrastructure level profound extension of rough reticulum cistern and destruction of mitochondrial cristae were revealed by immunohistochemical methods. Cytochrom P-450 was localized on the fibrin fibers.