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The report contains data concerning occupational and social rehabilitation of 46 patients operated on for aneurysma of the anterior communicative artery. It was established that the occupational prognosis depends upon the severity of the hemmorhage, character of surgical operation. Of significance are the conditions of work, time after the surgical operation. The authors mark that in 2/3 of the operated on patients the working capacity is being restored. A spontaneous restoration of diaturbed functions is slow and is not always sufficient. With this purpose it is expedient to repeat courses of a general tonic and special rehabilitative therapy. A favourable factor in the readaptation of patients is their early engagement in working activities. The authors give their recommendations for medical labour expert testimony for this category of patients.  相似文献   
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The influence of hepatocyte enlargement on intrahepatic hemodynamics was assessed in the isolated perfused rat liver preparation (IPRL) using two experimental models: hypotonic liver cell swelling and phenobarbitone-induced hepatocyte hypertrophy. The analysis of pressure-flow data obtained from the portal vascular bed over a flow range of 0 to 70 mL/min in the presence of a maximally-effective concentration of the vasodilator agent papaverine hydrochloride (6 x 10(-4) mol/L) enabled the calculation of P0, an estimate of the pressure required to passively distend the intrahepatic vasculature, and Gmax, the maximal portal vascular conductance. By comparison with an isotonic perfusion medium (Krebs-Henseleit buffer [KH] containing 2.5% bovine serum albumin [BSA]), perfusion with a hypotonic medium induced a significant increase in mean hepatocyte cross-sectional area (H(A)) (590 +/- 21 vs. 324 +/- 23 microm(-2), p < .05), a fall in Gmax (0.39 +/- 0.08 vs. 2.02 +/- 0.18 mL/min/g/mm hg, P < .001), and an increase in P0 (2.96 +/- 0.38 vs. 1.58 +/- 0.07 mm hg, P < .001). Phenobarbitone administered in drinking water (0.5 g/L) over a period of 60 days also induced a significant degree of hepatocyte enlargement (HA, 510 +/- 29 microm2, P < .05). On day 7, portal pressure measured in vivo in this group was significantly elevated compared with untreated controls (10.5 +/- 0.3 vs. 8.4 +/- 0.2 mm hg, P < .001), while in the IPRL Gmax was reduced (0.48 +/- 0.01 mL/min/g/mm hg, P < .001), and P0 was increased (2.23 +/- 0.17 mm hg, P < .05). However, with continued phenobarbitone treatment portal pressure, Gmax and P0 returned toward control values. The results confirm that hepatocyte enlargement is associated with a significant disturbance of intrahepatic hemodynamics but also that some adaptation occurs if hepatocyte enlargement is sustained over a prolonged period of time.  相似文献   
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We suggest that toroidal structures in the state of psi-condensation of DNA may be caused by anisotropy on a meso-scale of several thousand A, the conformation of a DNA-molecule being determined by its elasticity and neutralization of phosphate charge. We model a molecule of B-DNA on an anisotropic elastic rod subject to a torque, and make the numerical simulation of the model that reveals that under appropriate conditions, which may be effected in experimental setting by changing the concentration of polymeric solutions, there are toroidal structures having the size of a few persistence lengths, in agreement with the experimental data. On changing the elastic modulii or characteristics of the counterion layer, we see the toroidal structures turn into the spherical ones. To understand the function of anisotropy it would be interesting to investigate the Z-DNA as regards psi-condensation.  相似文献   
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Interleukin-1 beta (IL-1 beta) significantly inhibits insulin secretion from glucose stimulated islet cells. The mechanism for this inhibition has been hypothesized to be due to stimulation of the inducible form of nitric oxide synthase and a resulting increase in nitric oxide (NO) concentration. Ways to block the effect of IL-1 beta have focused on blocking the binding of IL-1 beta to the IL-1 receptor and the use of antioxidants to neutralize increases in NO. This report focuses on a 33 residue peptide synthesized based on the C-terminal region of the IL-1 beta molecule, a reported binding site of the IL-1 beta molecule, and the redoxcycling antioxidant pyrroloquinoline quinone (PQQ). The 33 residue peptide did not function as an antagonist, but as a weak agonist. High concentrations of PQQ itself inhibited glucose-dependent insulin release while low concentrations did not. PQQ had no effect on the actions of IL-1 beta. Three isosteric and isomeric analogues of PQQ were also investigated. One of the PQQ isomers had an inhibitory effect on insulin secretion at low concentrations where PQQ had no effect. These results reflect the sensitivity of islets to oxidative stress.  相似文献   
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