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41.
S Yoshii T Fuzii T Saitoh R Yamamoto N Ishida Y Hosoi M Tahara 《Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology》1992,83(3):374-382
Thirty-five patients with benign prostatic hyperplasia (age range: 45-88 years; average: 67.5 years) underwent local thermotherapy with prostathermer. Clinical therapeutic effect was evaluated in 30 of the 35 patients: 2 patients interrupting from therapy and 3 receiving pretherapeutic indwelling catheters were not included. A total of 6 treatments (2 per week) were performed, each lasting for 60 minutes. As for subjective improvement, improvement of nocturia was noted in 70.0% of all patients and sense of residual urine in 70.7%. Post-therapeutic nocturnal and daytime decreases in urination frequency were statistically significant (p less than 0.01). Objective improvement in residual urine volume occurred in 19 of the 30 cases, and elevation in uroflowmetric maximal flow rate following therapy was statistically significant (p less than 0.05). Among complications ascribable to catheter insertion were urethral bleeding (3 cases), epididymitis (1 case) and pyuria (1 case). Therapeutic result based primarily on subjective symptoms and partly on objective findings was fairly good in 17 cases (about 57%), and slightly good in 25 cases (about 83%). In conclusion, this therapy seems to be useful in the treatment of benign prostatic hyperplasia. 相似文献
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43.
Koichiroh Nandate Kenji Muranaka Koichi Shinohara Kazuyoshi Ishida Hiroko Ishida Katsuhiro Seo Hiroshi Takeshita 《Journal of anesthesia》1997,11(2):117-120
We retrospectively reviewed the records of 250 consecutive patients undergoing coronary artery bypass graft surgery (CABG)
from January 1994 through January 1996 to determine the incidence of persistent postoperative neurological dysfunction after
CABG and to compare normothermic and moderate hypothermic cardiopulmonary bypass (CPB). Normothermic CPB was used in 128 patients
(36°–37°C) and hypothermic CPB (27°–28°C) in 122 patients. Postoperative neurological dysfunction included focal motor deficits,
delayed recovery of consciousness (>24h) after surgery, and seizures within 1 week postoperatively. Persistent neurological
dysfunction was diagnosed if complete resolution had not occurred within 10 days of surgery. The incidence of persistent postoperative
neurological dysfunction was 4.1% in the hypothermic CPB group and 2.3% in the normothermic CPB group. There were no statistically
significant differences between the two groups (P=NS). These results suggest that normothermic CPB did not increase the incidence of persistent postoperative neurological
dysfunction compared to hypothermic CPB. 相似文献
44.
Elise Chiffoleau Gaëlle Bériou Patrick Dutartre Claire Usal Jean-Paul Soulillou Maria Cristina Cuturi 《American journal of transplantation》2002,2(8):745-757
A 20-day treatment with LF15-0195, a deoxyspergualine analog, induced long-term heart allograft survival in the rat without signs of chronic rejection. LF15-0195-treated recipients did not develop an anti-donor alloantibody response. Analysis of graft-infiltrating cells, IL10, TNFalpha, IFNgamma mRNA and iNOS protein expression in allografts, 5 days after transplantation, showed that they were markedly decreased in allografts from LF15-0195-treated recipients compared with allografts from untreated recipients. Surprisingly, spleen T cells from LF15-0195 recipients, 5days after grafting, were able to proliferate strongly in vitro, when stimulated with donor cells, but had reduced mRNA expression for IFNy compared with spleen T cells from untreated graft recipients. Furthermore, when T cells from naive animals were stimulated in vitro, using anti-CD3 and anti-CD28, LF15-0195 also increased T-cell proliferation in a dose-dependent fashion: however, these cells expressed less of the Th1 -related cytokines, IFNgamma and IL2, compared with untreated cells, suggesting that LF15-0195 could act on T-cell differentiation. In conclusion, we show here that a short-term treatment with LF15-0195 induced long-term allograft tolerance, decreasing the in situ anti-donor response, and we illustrate evidence for the development of regulatory mechanisms. 相似文献
45.
Ryoji Kajiwara Takahiro Matsuno Osamu Ishida Toru Sunagawa Osami Suzuki Mitsuo Ochi 《Nordisk plastikkirurgisk forening [and] Nordisk klubb for handkirurgi》2004,38(6):373-375
We report a case of an anterior interosseous nerve palsy after closed reduction and percutaneous pinning of open fractures of the radius and ulna in an adult. Operative findings showed that the anterior interosseous nerve was trapped between the distal and proximal part of the fractured radius. Treatment by neurorrhaphy gave a satisfactory result. 相似文献
46.
K Mochitate K Ishida T Ohsumi T Miura 《Journal of toxicology and environmental health》1992,35(4):247-260
To investigate how alveolar macrophages adapt themselves to oxidative pollutants in the long term, rats were exposed to a strong oxidant, ozone (O3), or a weak oxidant, nitrogen dioxide (NO2), for a maximum duration of 12 wk. After exposures, alveolar macrophages were collected by pulmonary lavage. Throughout 11 wk of exposure to 0.2 ppm O3, the specific activities of glucose-6-phosphate dehydrogenase (G6PDH) and glutathione peroxidase of the peroxidative metabolic pathway and pyruvate kinase and hexokinase of the glycolytic pathway were 40-70% elevated over the controls in alveolar macrophages. The population of alveolar macrophages was consistently 60% higher than the controls. The small-sized macrophages, immature macrophages, preferentially increased. To the contrary, the thymidine incorporation per cell was always 20-30% lower than in the controls, although the total incorporation remained unchanged. No infiltration of polymorphonuclear leukocytes occurred. By 12 wk of exposures to 1.2 and 4.0 ppm NO2, the population of alveolar macrophages increased 30% over the control. Among the enzymes examined, however, only the G6PDH activity increased 10% for 4.0 ppm NO2. No increase in the enzyme activities occurred for 1.2 ppm NO2. Based on these results, alveolar macrophages adapt themselves to the long-term exposure of O3 or NO2 by recruiting immature macrophages through an apparent influx of monocytes. During the exposure to O3, the peroxidative metabolic and glycolytic pathways are enhanced persistently in alveolar macrophages, whereas both pathways were not enhanced by the exposures to NO2. 相似文献
47.
48.
A case-control study of breast cancer among Japanese women: with special reference to family history and reproductive and dietary factors 总被引:8,自引:0,他引:8
Dr. Ikuko Kato Dr. Shigeto Miura Fijio Kasumi Takuji Iwase Hideya Tashiro Yoshihiro Fujita Hiroki Koyama Tadashi Ikeda Kiyoshi Fujiwara Keiichi Saotome Kazuaki Asaishi Rikiya Abe Mitsuhiro Nihei Tsunehiro Ishida Takao Yokoe Hiroshi Yamamoto Motoi Murata 《Breast cancer research and treatment》1992,24(1):51-59
Summary To study the effects of family history and reproductive, anthropometric, and dietary factors on the risk of breast cancer among low risk populations, we conducted a hospital-based case-control study involving 908 patients with breast cancer and their matched controls, in Japan. A positive family history of breast cancer significantly increased the risk of breast cancer (odds ratio = 1.52, 95% confidence interval: 1.14–2.03). The risk further increased with increasing number of family members affected. Obesity, single marital status, fewer births, a late childbirth, and less consumption of green-yellow vegetables and dairy products were also associated with an increased risk of breast cancer. These associations were independent in multivariate analyses. There was no increase in risk associated with consumption of high fat foods. When analyzed by menopausal status, the association with family history of breast cancer, especially in the first degree of relatives, was more evident for premenopausal breast cancer. The associations with obesity and lower consumption of dairy products were more pronounced for postmenopausal breast cancer, while those with lower parity and single marital status were stronger for premenopausal breast cancer. 相似文献
49.
Norihiro Ishida Koji Hayashi Asuka Hattori Keiichiro Yogo Toru Kimura Tatsuo Takeya 《Journal of bone and mineral research》2006,21(1):48-57
We found that a chemokine receptor gene, CCR1, acts downstream of NFAT2 in RANKL-stimulated RAW264 and bone marrow cells. The upstream regulatory region of CCR1 showed RANKL-dependent and CsA-suppressible promoter activity. Downregulation of the expression and function of CCR1 suppressed cell migration. INTRODUCTION: We previously reported that the expression of NFAT2 induced by RANKL is a key process for progression to multinucleated cells in an in vitro osteoclastogenesis system. Identifying the target genes of NFAT2 would thus be informative about the differentiation process. We focused here on chemokine and chemokine receptor genes that act downstream of NFAT2 in RAW264 cells as well as osteoclast precursors prepared from bone marrow cells. MATERIALS AND METHODS: RAW264 mouse monocyte/macrophage line cells were cultured with or without cyclosporin A (CsA) in the presence of RANKL or glutathione S-transferase (GST). Osteoclast precursors were prepared from bone marrow cells. RANKL-inducible and CsA-suppressible genes were searched for by microarray analysis, and expression was confirmed by quantitative RT-PCR. Promoter activity was measured by luciferase gene reporter assay. Short interfering (si)RNA for CCR1 was introduced in RAW264 cells. Cell migration activity was examined using a Boyden chamber assay. RESULTS AND CONCLUSIONS: We identified the chemokine receptor gene CCR1 as a gene showing significant differential expression profiles in osteoclastogenesis in the presence versus the absence of CsA, an inhibitor of NFAT. This property was unique to CCR1 among the chemokine and chemokine receptor genes examined in both RAW264 and bone marrow cells. The upstream regulatory region was isolated from CCR1, and its RANKL-dependent and CsA-suppressible promoter activity was confirmed. The functional significance of CCR1 was assessed by monitoring the migration of cells in a transwell migration assay, and this activity was abolished when either CsA- or CCR1 siRNA-treated cells were used. Moreover, treatment with a Galpha inhibitor pertussis toxin (PTX) or methiolynated-regulated on activation, normal T cells expressed and secreted (Met-RANTES), an antagonist of CCR1, suppressed multinucleated cell formation in the bone marrow cell system. Together, these results suggest that the CCR1 signaling cascade is under the control of NFAT2 and seems to enhance the migration of differentiating osteoclasts. 相似文献
50.