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31.
Jong-Moon Lee Kun-Woo Park Woo-Keun Seo Moon Ho Park Changsu Han Inho Jo Sangmee Ahn Jo 《Movement disorders》2007,22(16):2446-2449
There have been a few studies and inconsistent results regarding the coincidence of Parkinson's disease (PD) and atherosclerotic diseases, such as cerebrovascular disease. Carotid intima-media thickness (IMT) is a known marker for subclinical atherosclerosis. The aim of this study was to investigate the carotid IMT between PD patients and controls. We studied 43 patients with PD and 86 matched controls. The carotid IMT in PD patients was significantly smaller than in controls (0.796 +/- 0.179 mm vs. 0.913 +/- 0.237 mm, P < 0.05). In multivariate analysis, the carotid IMT was inversely associated with the duration of levodopa medication and the severity of PD. These results suggest that PD patients have a lower risk of atherosclerosis. 相似文献
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The promoting effect of the Chinese medicinal herb, Wikstroemia chamaedaphne and Tung oil extracts (WC and HHPA) on carcinoma of uterine cervix induced by HSV-2 or MCA in mice was studied. The results showed that WC and HHPA extracts were not carcinogenic themselves. After carcinogen HSV-2 and MCA treatment, WC and HHPA were added separately. The inducing rates by HSV-2 increased from 7.4% to 21.1% and 26.3%, those by MCA increased from 56.5% to 82.8% and 84.4%. There was a significant difference between the combined groups and groups with HSV-2 or MCA only. The experimental results suggest that these two kinds of extracts play a promoting effect on carcinogenesis. The relation between the carcinogenesis of uterine cervix or nasopharynx and WC or HHPA extracts is discussed. 相似文献
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将动、静脉阻断法用于恒速灌流的在体山羊左肺,使其总压力降区分为动脉端、静脉端及中间段三部分。大肠杆菌内毒素主要升高肺静脉端压力降及肺毛细血管压;山莨菪碱可显著缓解内毒素所致的改变,但对正常肺血管各段压力降无明显影响。5-羟色胺主要升高肺动脉端压力降,对肺静脉端及毛细血管压无明显影响。去甲肾上腺素及组胺主要升高肺静脉端压力降及肺毛细血管压,但对肺动脉端无明显影响。去甲肾上腺素和组胺可能介导内毒素性肺动脉高压。 相似文献
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Su Jin Park Su Jin Kim Yumie Rhee Ji Hyun Byun Seong Hwan Kim Myoung Hee Kim Eun Jig Lee Sung-Kil Lim 《Journal of bone and mineral research》2007,22(6):889-896
The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation. 相似文献
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