[Completion technology of pelvic surgery accompanying with cystectomy in elderly and senile patients].

Results of treatment of 204 elderly and senile patients who underwent cystprostatectomy or anterior pelvic exenteration are analyzed. A comparative analysis of two groups of patients whose operation ended with the traditional drainage through the anterior abdominal wall (n = 100), and bilateral perineal drainage (n = 104) is presented. Bilateral perineal drainage after operations on the pelvic organs, accompanied by cystectomy and extended lymphadenectomy in conjunction with the restoration of the peritoneum lateral pelvic walls, improves postoperative recovery of intestinal peristalsis, promotes an earlier reduction in the intensity of pain and morbidity in the early postoperative period. Perineal installation of drains is a simple in design and safe procedure. We recommend bilateral perineal drainage after operations on the pelvic organs, accompanied by cystectomy and extended lymphadenectomy.

[Pelvic exenteration in surgery for colorectal cancer].

A total of 1436 patients with colorectal cancer underwent resective surgery: 244 (15.6%) received combined interventions, 94 (41.9%) pelvic exenteration (PE), 38 (40.4%) complete PE, 9 (9.6%) of which were infralevator and 29 (30.8%) supralevator. In 56 (59.6%) patients posterior PE was performed, supralevator was performed in 17 (18.1%) cases and infralevator in 39 (41.5%) cases. In 47 (69.1%) of 68 supralevator PE recipients colonic anastomosis was formed. In 21 (38.9%) patients a terminal colostoma was formed, in 29 (76.3%) of 38 patients incontinent urinary diversion was formed. Continent urinary diversion was performed in 9 (23.7%) patients. Twenty six (27.6%) patients had 43 post-operative complications which were lethal in 7 (26.9%) cases.

Programmed cell death in plants: protective effect of tetraphenylphosphonium and tetramethylrhodamine cations used as transmembrane quinone carriers.

Tetraphenylphosphonium (TPP(+)) and tetramethylrhodamine ethyl ester (TMRE(+)) cations used as transmembrane carriers of ubiquinone (MitoQ) and plastoquinone (SkQ, SkQR) in mitochondria prevented at nanomolar concentrations the chitosan- or H(2)O(2)-induced destruction of the nucleus in epidermal cells of epidermis isolated from pea leaves. The protective effect of the cations was potentiated by palmitate. Penetrating anions of tetraphenylboron (TB(-)) and phenyl dicarbaundecaborane also displayed protective effects at micromolar concentrations; the effect of TB(-) was potentiated by NH(4)Cl. It is proposed that the protective effect of the penetrating cations and anions against chitosan is due to suppression of the generation of reactive oxygen species in mitochondria as a result of the protonophoric effect of the cations plus fatty acids and the anions plus NH(4)(+). Phenol was suitable as the electron donor for H2O2 reduction catalyzed by horseradish peroxidase, preventing the destruction of cell nuclei. The penetrating cations and anions, SkQ1, and SkQR1 did not maintain the peroxidase or peroxidase/oxidase reactions measured by their suitability as electron donors for H(2)O(2) reduction or by the oxidation of exogenous NADH.

Programmed cell death in plants: protective effect of mitochondrial-targeted quinones.

Ubiquinone or plastoquinone covalently linked to synthetic decyltriphenylphosphonium (DTPP(+)) or rhodamine cations prevent programmed cell death (PCD) in pea leaf epidermis induced by chitosan or CN(-). PCD was monitored by recording the destruction of cell nuclei. CN(-) induced the destruction of nuclei in both epidermal cells (EC) and guard cells (GC), whereas chitosan destroyed nuclei in EC not in GC. The half-maximum concentrations for the protective effects of the quinone derivatives were within the pico- and nanomolar range. The protective effect of the quinones was removed by a protonophoric uncoupler and reduced by tetraphenylphosphonium cations. CN(-)-Induced PCD was accelerated by the tested quinone derivatives at concentrations above 10(-8)-10(-7) M. Unlike plastoquinone linked to the rhodamine cation (SkQR1), DTPP(+) derivatives of quinones suppressed menadione-induced H(2)O(2) generation in the cells. The CN(-)-induced destruction of GC nuclei was prevented by DTPP(+) derivatives in the dark not in the light. SkQR1 inhibited this process both in the dark and in the light, and its effect in the light was similar to that of rhodamine 6G. The data on the protective effect of cationic quinone derivatives indicate that mitochondria are involved in PCD in plants.

[Ways to improve the quality of life of elderly and senile patients after the operation by Brikker].

The present study is devoted to improving quality of life of patients in elderly and senile age after operation of Bricker by finding the optimal method of forming ureterointestinal anastomosis. From 2007 to 2009 103 patients of elderly and senile age with diseases requiring removal of the bladder were treated in the Lenigrad Regional Oncology Centre. All the patients were made cystectomy. Patients were divided into two groups: In 1st group, the ureterointestinal anastomosis was formed a classical way "end to side" described Bricker, in the 2nd group ureterointestinal anastomosis was performed by the method of Wallace - "common area". Pathological conditions developed in patients in late postoperative period were as follows: hydronephrosis in early and later stages, obstructive pyelonephritis, frequent attacks of chronic pyelonephritis, chronic renal failure, urinary fistula. Formation of ureterointestinal anastomosis by Wallace during surgery reduces the amount of later postoperative complications. Quality of life was better after the formation of ureterointestinal anastomosis by Wallace.

Effect of Ca2+ on programmed death of guard and epidermal cells of pea leaves.

The effect of Ca2+ on programmed death of guard cells (GC) and epidermal cells (EC) determined from destruction of the cell nucleus was investigated in epidermis of pea leaves. Ca2+ at concentrations of 1-100 microM increased and at a concentration of 1 mM prevented the CN(-)-induced destruction of the nucleus in GC, disrupting the permeability barrier of GC plasma membrane for propidium iodide (PI). Ca2+ at concentrations of 0.1-1 mM enhanced drastically the number of EC nuclei stained by PI in epidermis treated with chitosan, an inducer of programmed cell death. The internucleosomal DNA fragmentation caused by CN(-) was suppressed by 2 mM Ca2+ on 6 h incubation, but fragmentation was stimulated on more prolonged treatment (16 h). Presumably, the disruption of the permeability barrier of plasma membrane for PI is not a sign of necrosis in plant cells. Quinacrine and diphenylene iodonium at 50 microM concentration prevented GC death induced by CN(-) or CN(-) + 0.1 mM Ca2+ but had no influence on respiration and photosynthetic O2 evolution in pea leaf slices. The generation of reactive oxygen species determined from 2',7'-dichlorofluorescein fluorescence was promoted by Ca2+ in epidermal peels from pea leaves.

Programmed cell death in plants: protective effect of phenolic compounds against chitosan and H2O2.

Addition of chitosan or H2O2 caused destruction of nuclei of epidermal cells (EC) in the epidermis isolated from pea leaves. Phenol, a substrate of the apoplastic peroxidase-oxidase, in concentrations of 10(-10)-10(-6) M prevented the destructive effect of chitosan. Phenolic compounds 2,4-dichlorophenol, catechol, and salicylic acid, phenolic uncouplers of oxidative phosphorylation pentachlorophenol and 2,4-dinitrophenol, and a non-phenolic uncoupler carbonyl cyanide m-chlorophenylhydrazone, but not tyrosine or guaiacol, displayed similar protective effects. A further increase in concentrations of the phenolic compounds abolished their protective effects against chitosan. Malate, a substrate of the apoplastic malate dehydrogenase, replenished the pool of apoplastic NADH that is a substrate of peroxidase-oxidase, prevented the chitosan-induced destruction of the EC nuclei, and removed the deleterious effect of the increased concentration of phenol (0.1 mM). Methylene Blue, benzoquinone, and N,N,N',N'-tetramethyl-p-phenylenediamine (TMPD) capable of supporting the optimal catalytic action of peroxidase-oxidase cancelled the destructive effect of chitosan on the EC nuclei. The NADH-oxidizing combination of TMPD with ferricyanide promoted the chitosan-induced destruction of the nuclei. The data suggest that the apoplastic peroxidase-oxidase is involved in the antioxidant protection of EC against chitosan and H2O2.

Chitosan-induced programmed cell death in plants.

Chitosan, CN(-), or H(2)O(2) caused the death of epidermal cells (EC) in the epidermis of pea leaves that was detected by monitoring the destruction of cell nuclei; chitosan induced chromatin condensation and marginalization followed by the destruction of EC nuclei and subsequent internucleosomal DNA fragmentation. Chitosan did not affect stoma guard cells (GC). Anaerobic conditions prevented the chitosan-induced destruction of EC nuclei. The antioxidants nitroblue tetrazolium or mannitol suppressed the effects of chitosan, H(2)O(2), or chitosan + H(2)O(2) on EC. H(2)O(2) formation in EC and GC mitochondria that was determined from 2',7'-dichlorofluorescein fluorescence was inhibited by CN(-) and the protonophoric uncoupler carbonyl cyanide m-chlorophenylhydrazone but was stimulated by these agents in GC chloroplasts. The alternative oxidase inhibitors propyl gallate and salicylhydroxamate prevented chitosan- but not CN(-)-induced destruction of EC nuclei; the plasma membrane NADPH oxidase inhibitors diphenylene iodonium and quinacrine abolished chitosan- but not CN(-)-induced destruction of EC nuclei. The mitochondrial protein synthesis inhibitor lincomycin removed the destructive effect of chitosan or H(2)O(2) on EC nuclei. The effect of cycloheximide, an inhibitor of protein synthesis in the cytoplasm, was insignificant; however, it was enhanced if cycloheximide was added in combination with lincomycin. The autophagy inhibitor 3-methyladenine removed the chitosan effect but exerted no influence on the effect of H(2)O(2) as an inducer of EC death. The internucleosome DNA fragmentation in conjunction with the data on the 3-methyladenine effect provides evidence that chitosan induces programmed cell death that follows a combined scenario including apoptosis and autophagy. Based on the results of an inhibitor assay, chitosan-induced EC death involves reactive oxygen species generated by the NADPH oxidase of the plasma membrane.

Reactive oxygen species in programmed death of pea guard cells.

Hydrogen peroxide potentiates CN(-)-induced apoptosis of guard cells recorded as destruction of cell nuclei in the epidermis from pea leaves. A still stronger effect was exerted by the addition of H2O2 and NADH, which are the substrates of the plant cell wall peroxidase producing O2*- coupled to the oxidation of NADH. The CN(-)-or (CN(-) + H2O2)-induced destruction of guard cell nuclei was completely removed by nitroblue tetrazolium (NBT) oxidizing O2*- and preventing there-by the subsequent generation of H2O2. The reduced NBT was deposited in the cells as formazan crystals. Cyanide-induced apoptosis was diminished by mannitol and ethanol, which are OH* traps. The dyes Rose Bengal (RB) and tetramethylrhodamine ethyl ester (TMRE) photosensitizing singlet oxygen production suppressed the CN(-)-induced destruction of the cell nuclei in the light. This suppression was removed by exogenous NADH, which reacts with 1O2 yielding O2*-. Incubation of leaf slices with RB in the light lowered the photosynthetic O2 evolution rate and induced the permeability of guard cells for propidium iodide, which cannot pass across intact membranes. Inhibition of photosynthetic O2 evolution by 3-(3',4'-dichlorophenyl)-1,1-dimethylurea or bromoxynil prevented CN(-)-induced apoptosis of guard cells in the light but not in the dark. RB in combination with exogenous NADH caused H2O2 production that was sensitive to NBT and estimated from dichlorofluorescein (DCF) fluorescence. Data on NBT reduction and DCF and TMRE fluorescence obtained using a confocal microscope and data on the NADH-dependent H2O2 production are indicative of generation of reactive oxygen species in the chloroplasts, mitochondria, and nuclear region of guard cells as well as with participation of apoplastic peroxidase. Cyanide inhibited generation of reactive oxygen species in mitochondria and induced their generation in chloroplasts. The results show that H2O2, OH*, and O2*- resources utilized for H2O2 production are involved in apoptosis of guard cells. It is likely that singlet oxygen generated by RB in the light, judging from the permeability of the plasmatic membrane for propidium iodide, makes Photosystem II of chloroplasts inoperative and induces necrosis of the guard cells.

Cyanide-induced death of cells in plant leaves.

Destruction of guard cell nuclei in epidermis isolated from leaves of pea, maize, sunflower, and haricot bean, as well as destruction of cell nuclei in leaves of the aquatic plants waterweed and eelgrass were induced by cyanide. Destruction of nuclei was strengthened by illumination, prevented by the antioxidant alpha-tocopherol and an electron acceptor N,N,N ,N -tetramethyl-p-phenylenediamine, and removed by quinacrine. Photosynthetic O2 evolution by the leaf slices of a C3 plant (pea), or a C4 plant (maize) was inhibited by CN- inactivating ribulose-1,5-bisphosphate carboxylase, and was renewed by subsequent addition of the electron acceptor p-benzoquinone.

[Carcinogen activity of the new drug thymodepressin studied in chronic tests on rats and mice]. / Izuchenie kantserogennoi aktivnosti novogo lekarstvennogo sredstva - timodepressina v chronicheskikh opytakh na krysakh i myshakh.

The new drug thymodepressin was subcutaneously injected in doses 0.0145 and 0.145 mg/kg in rats and mice over a period of 104 weeks. No statistically significant difference in the tumor frequencies between the test and control groups was observed during this period of time. It is concluded that thymodepressin is not carcinogenic.

[The use of the orthostatic test in practical medical flight expertise in civil aviation]. / Ispol'zovanie ortostaticheskoi proby v praktike vrachebno-letnoi ékspertizy v grazhdanskoi aviatsii.

Comparison of results from HDT administered with different techniques showed that 5-10 min in vertical position are enough to adequately evaluate mechanisms of circulation control. By that time hemodynamic shifts get stabilized. More precise assessment of the circulation regulation can be made when HDT is administered from initial supine rather than sitting position. Analysis of the ECG dynamics allows to elicit latent myocardial injuries. The exact quantitative characteristic of orthostatic disturbances makes it possible to give their pathophysiological estimate.

[The role of occupational and social stress in the development of non-ischemic arrhythmia in pilots]. / Rol' professional'nogo i sotsial'nogo stressa v vozniknovenii neishemicheskikh aritmii u pilotov.

In the absence of coronary heart disease and ischemic responses to exercise, many highly skilled pilots have been shown to have arrhythmias of non-ischemic origin. The occupational stress-exercise on a flight trainer reveals such arrhythmias much more frequently than bicycle ergometric exercise. Under social stress, namely during medical- and flying examination which decides if a pilot is professionally fit, 24-hour monitoring in the out- and inpatient settings detects premature+ ventricular contractions of non-ischemic origin in high-grade pilots; the contractions regularly decreasing or ceasing during a true flight. Thus, the social stress in pilots is a stronger arrhythmogenic factor than is the routine occupational stress.