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31.
It has been checked if the "limits of the acceptable doses of ultraviolet radiation of monochromatic radiation at the workplace" (NIOSH-standard of USA) are adhered to in the vicinity of welders' work stations in a factory hall. For recording of UV-doses polysulphon films have been used. According to these investigations non-welders are exposed to doses of UV-radiation which exceed the limits recommended by about eight times. Clinical examinations of these persons showed chronic damage of the external parts of the eyes in a higher percentage than in a control group. It is pointed to the necessity of taking protective measures to shield persons working in the vicinity of welding job sites from ultraviolet radiation.  相似文献   
32.
The study was undertaken to evaluate the relationship betweennon-responsiveness to hepatitis B (HBV) vaccination in haemodialysedpatients and HBs antigen (Ag) presentation and recognition dependingon TCR/CD3 receptors expression. We have found that the causeof the blunted response to HBV vaccination is multifactorialand seems to be associated with the following: (1) A reducednumber of TCR/CD3 antigen receptor complexes on freshly isolateduraemic CD4 T cells, especially in non-responders. (2) The bluntedproliferative response of uraemic CD4 T cells isolated fromnon-responders and stimulated for 6 days by autologous monocytespresenting HBsAg was associated with the decreased density ofthe TCR/CD3 receptors. (3) Moreover, in uraemic non-respondersthe expression of adhesion and accessory molecules on monocytes(intercellular adhesion molecule-1/ ICAM-1, HLA-DR/Ia/) wassignificantly decreased following the culture with autologousmonocytes serving as HBsAg-presenting cells. CD4 molecules andlymphocyte function antigen-1ß /LFA-1ß/on helper-inducer T cells were increased before and after theculture. (4) These findings were also associated with a diminishedbinding capacity of IL-1ß and IL-6 to their receptorson helper-inducer T cells. (5) IL-2, IFN- and IL-4 productionwas decreased in uraemic non-responders, especially after 72h of the culture. (6) Inhibited proliferation of helper-inducerT cells in uraemic non-responders was only partially reversiblein the presence of exogenous IL-1ß, IL-6, IL-2 andIFN-. (7) HLA typing of uraemic non-responders was associatedwith extended haplotype: HLA A1, B8, DR3, DR7, DQ2.  相似文献   
33.
Severe degenerative features of the nervous system of a hitherto unknown kind, associated with a neuromuscular disorder with histopathological features of congenital muscular dystrophy, are reported in two female siblings. The clinical profile was characterized by generalized hypotonia followed by spastic tetraplegia, contractures, polyneuropathy, lack of cognitive development and progressive microcephaly. There was no involvement of the eyes. Neuropathological examination of the brain of one sibling, who died at the age of 30 months, revealed subtotal loss of neurons in the cerebral and cerebellar cortex and in the ventral pons, and secondary loss of myelin in the cerebral and cerebellar subcortical white matter. Sural nerve biopsy in the other sibling, who had a similar neurological affection, showed a lack of large myelinated fibers.This investigation is part of the research program Disorders of the Neuromuscular System of the University of Nijmegen  相似文献   
34.
The evaluation for the abstracts submitted for the annual meeting of the German Neurosurgical Society together with the Swiss Neurosurgical Society in Munich 1999, is presented as it has developed during the meetings of the last years. 597 abstracts were reviewed by the 30 members of the review committee according to a 5 point grading system. Cut off for acceptance was a mean grading of 2.7 points. Abstracts better than 2.4 were accepted, abstracts worse than 2.7 were rejected. Experimental studies were judged slightly better than clinical studies: the mean grading of clinical and experimental studies was 2.55 +/- 0.5 vs. 2.72 +/- 0.6 (p < 0.02). All abstracts with a mean grading of 2.4-2.7 and a standard deviation > 1.0 were discussed in a meeting of the review committee. 353 abstracts were accepted. Some of the abstracts submitted for oral presentation had to be converted to poster presentations. Among others the decision was based on the grading of the abstract.  相似文献   
35.
Barth RF  Soloway AH  Goodman JH  Gahbauer RA  Gupta N  Blue TE  Yang W  Tjarks W 《Neurosurgery》1999,44(3):433-50; discussion 450-1
Boron neutron capture therapy (BNCT) is based on the nuclear reaction that occurs when boron-10, a stable isotope, is irradiated with low-energy thermal neutrons to yield alpha particles and recoiling lithium-7 nuclei. For BNCT to be successful, a large number of 10B atoms must be localized on or preferably within neoplastic cells, and a sufficient number of thermal neutrons must be absorbed by the 10B atoms to sustain a lethal 10B (n, alpha) lithium-7 reaction. There is a growing interest in using BNCT in combination with surgery to treat patients with high-grade gliomas and possibly metastatic brain tumors. The present review covers the biological and radiobiological considerations on which BNCT is based, boron-containing low- and high-molecular weight delivery agents, neutron sources, clinical studies, and future areas of research. Two boron compounds currently are being used clinically, sodium borocaptate and boronophenylalanine, and a number of new delivery agents are under investigation, including boronated porphyrins, nucleosides, amino acids, polyamines, monoclonal and bispecific antibodies, liposomes, and epidermal growth factor. These are discussed, as is optimization of their delivery. Nuclear reactors currently are the only source of neutrons for BNCT, and the fission reaction within the core produces a mixture of lower energy thermal and epithermal neutrons, fast or high-energy neutrons, and gamma-rays. Although thermal neutron beams have been used clinically in Japan to treat patients with brain tumors and cutaneous melanomas, epithermal neutron beams now are being used in the United States and Europe because of their superior tissue-penetrating properties. Currently, there are clinical trials in progress in the United States, Europe, and Japan using a combination of debulking surgery and then BNCT to treat patients with glioblastomas. The American and European studies are Phase I trials using boronophenylalanine and sodium borocaptate, respectively, as capture agents, and the Japanese trial is a Phase II study. Boron compound and neutron dose escalation studies are planned, and these could lead to Phase II and possibly to randomized Phase III clinical trials that should provide data regarding therapeutic efficacy.  相似文献   
36.
1 Adenosine 5'-triphosphate (ATP) is an enteric neurotransmitter which acts at purine receptors on intestinal nerve and muscle. This study set out to shed light on the receptor mechanisms by which exogenous and endogenous ATP influences intestinal peristalsis. 2 Peristalsis in isolated segments of the guinea-pig small intestine was triggered by a perfusion-induced rise of the intraluminal pressure. Motor changes were quantified by alterations of the peristaltic pressure threshold (PPT) at which propulsive muscle contractions were elicited. 3 ATP (>/= 3 microM) increased PPT and abolished peristalsis at concentrations of 100-300 microM. Adenosine 5'-O-2-thiodiphosphate (ADPbetaS, 3-100 microM) was more potent, whereas alpha,beta-methylene ATP (alpha,beta-meATP, 3-100 microM) was less potent, than ATP in depressing peristalsis. 4 8-Phenyltheophylline (10 microM) attenuated the anti-peristaltic effect of 10 and 30 microM ATP but not that of higher ATP concentrations. Apamin (0.5 microM) counteracted the ability of ATP, ADPbetaS and alpha,beta-meATP to enhance PPT. Suramin (300 microM) and pyridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 150 microM) antagonized the inhibitory effect of alpha,beta-meATP on peristalsis but did not alter the effect of ATP and ADPbetaS. 5 PPADS (50-150 microM) reduced PPT by as much as 50%. This stimulant effect on peristalsis was prevented by suramin (300 microM) but left unaltered by apamin (0.5 microM) and NG-nitro-L-arginine methyl ester (300 microM). 6 These data show that exogenous and endogenous ATP inhibits intestinal peristalsis via different apamin-sensitive purinoceptor mechanisms. Exogenous ATP depresses peristalsis mostly via suramin- and PPADS-insensitive P2 receptors, whereas endogenous purines act via P2 receptors sensitive to both suramin and PPADS.  相似文献   
37.
The effect of a previous exposure to hyperbaric oxygen (HBO) on the synthesis capacity of prostaglandin (PG) and thromboxane (TX) was investigated in the brain of male rats. Three groups of rats were used:
  1. Neurotoxic HBO (n = 11): The rats were exposed to sixfold the atmospheric pressure (101.3 kPa), i.e., 6 absolute atmospheres (ATA), of pure O2 up to the first convulsion (6 ATA O2);
  2. Mild hyperoxia (n = 10): The rats were exposed to compressed air at the same absolute pressure and for a similar time than that of the neurotoxic HBO group (here PO2 is 1.26 ATA);
  3. Normoxia at atmospheric pressure (PO2 is 0.21 ATA) for control.
There was no convulsion in groups 2 and 3. Decompression of the high pressure groups lasted 15 min. After decapitation, samples of the frontal cortex and the striatum were taken, weighed, washed, and then incubated in Krebs-Ringer bicarbonate for 1 h. The release of eicosanoids in the medium was determined by enzyme immunoassay. Mild hyperoxia only significantly reduced in the striatum the release of 6-keto-PGF1α (1.3±2.4 vs 10.9±6.6 pg/mg wet tissue,p< 0.001; mean±SD) and PGE2 (3.2±2.7 vs 7.8±6.5 pg/mg wet tissue,p< 0.05), whereas TXB2 did not change. Neurotoxic hyperoxia reduced significantly in both cortex and striatum the release of 6-keto-PGF1α (8.7±5.1 vs 29.3±13.0,p< 0.001 and 3.2±4.3 vs 10.9±6.6,p< 0.01 respectively) and PGE2 (8.3± 5.8 vs 15.2± 6.4,p < 0.05 and 3.1± 2.9 vs 7.8±6.5,p< 0.05 respectively) without affecting TXB2 release. These inactivations could be related to reactive oxygen species (ROS) induced by HBO. Taking into account the known sensitivities to ROS of the enzymes of the eicosanoid cascade, the effects of HBO on PGs could be related to a hyperoxic deactivation of PGI synthase in striatum, beginning with nonneurotoxic hyperoxia with a possible associated deactivation of PGE synthase activity in both cortex and striatum in hyperbaric neurotoxic hyperoxia. The decrease in 6-keto-PGF1α reflecting the decrease in prostacyclin could lead to vasoconstriction (which in turn decreased local oxygen partial pressure) and also to platelet aggregation, since TXB2 was not affected in the process. As this inactivation began well before the neurotoxicity threshold of HBO, the following changes in eicosanoids may therefore take some non-specific part in the HBO-induced brain damage.  相似文献   
38.
Performance of 11 commercially available 4- and 5-F aortic flush catheters was evaluated with respect to the extent of upstream injection, catheter motion, and downstream homogeneity of a 10-, 15-, and 20-mL/sec bolus of 76% meglumine sodium diatrizoate at room temperature. Tests were made in a pulsatile aortic flow model containing circulating fluid isoviscous to blood. The injection process was recorded on videotape. Homogeneity of the contrast material bolus was determined spectrophotometrically from samples collected from the center and each of the four quadrants of the vessel lumen. Upstream contrast material injection between 1.5 and 7 cm in length emerged from all catheters; it was lowest with one of the "tennis racket" designs from one and a new spiral end-loop design (Halo) from another manufacturer. All catheters, except the most rigid and largest-caliber catheter (5.8 F) showed considerable shaft motion at the higher injection rates. Downstream contrast material mixing homogeneity was always best at the highest injection rate but altogether was better for the Halo catheter than for any other catheter tested. It is concluded that all tested 4- and 5-F aortic flush catheters show some undesirable features, but certain design modifications improve performance and comparative testing is helpful to distinguish such features.  相似文献   
39.
BACKGROUND AND PURPOSE: Small emboli arising from a friable plaque during carotid endarterectomy (CEA) constitute an important risk of perioperative ischemic complications. To evaluate the incidence and significance of silent cerebral ischemic lesions of embolic origin after CEA, we prospectively examined a series of surgical patients with high-grade carotid stenosis by using diffusion-weighted MRI (DWI). We also tried to correlate postoperative ischemic lesions with the occurrence of sonographic cerebral embolic signals, the presence of plaque ulcerations, and the use of intraoperative shunting. METHODS: Of a consecutive series of 53 patients undergoing elective CEA for high-grade carotid stenosis, 48 patients with unchanged postoperative neurological status were prospectively studied with DWI of the brain the day before and the day after the operation. The magnetic resonance images were analyzed by 2 neuroradiologists blinded to the clinical result of the operation. Any new hyperintense signal was interpreted as a postoperative ischemic lesion. RESULTS: Forty-six (95.8%) of 48 patients had unchanged postoperative brain DWI. In 2 patients (4.2%), a new single asymptomatic hyperintense signal was observed on the side of the operation. Both lesions were small and presumably of embolic origin. They were not related to sonographic embolic signals, plaque ulcerations, or intraoperative shunting. CONCLUSIONS: These results suggest that the incidence of silent ischemic brain lesions of embolic origin after CEA is low and does not correlate with the occurrence of intraoperative sonographic microemboli. They confirm that CEA is a safe procedure that carries a low risk of postoperative cerebral events.  相似文献   
40.
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