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41.
高脂血症患者C—反应蛋白含量的变化及氟伐他汀对它的影响 总被引:4,自引:1,他引:3
Dong-Sheng Chi Feng-Xia Jin Shu-Guang Yang Yu-Wen Su Bin Ge Jie Zhang Yan Zhang Yi-Li Liu 《第一军医大学学报》2002,22(12):1109-1111
OBJECTIVE: To observe the changes of C-reactive protein (CRP) level and its relationship with blood lipids, and the effects of fluvastatin on CRP and the lipids in patients with hyperlipidemia. METHODS: Serum levels of cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C) and lipoprotein(a)[Lp(a)] were measured by enzyme assay, and plasma CRP level by immunonephelometry before and after fluvastatin treatment (20 mg/d for 4 weeks) in patients with hyperlipidemia. RESULTS: CRP levels were above normal in 90.3% hyperlipidemia cases in spite of the various accompanying diseases. Fluvastatin treatment significantly reduced TC (-7.49%), TG (-14.32%), LDL (-13.88%), VLDL (-18.48%) and TC/HDL(-13.50%) levels (P<0.01), and also brought down Lp(a) concentration (-13.81%). CRP levels was very effectively reduced after the treatment (-15.92%, P<0.001). No association between basal CRP levels and basal lipids and Lp(a) concentrations was observed. Positive correlation of CRP, however, was observed after fluvastatin treatment with TC/HDL (r=0.62, P=0.041) and Lp(a) (r=0.320, P=0.011), while inverse relations were noted between CRP and HDL (r=-0.288, P=0.023). CONCLUSION: CRP levels increases markedly in patients with hyperlipidemia, a fact that is independent of the accompanying diseases. In addition to modulating blood lipid levels, fluvastatin also reduces CRP level, the latter possibly serving as an independent predictive factor for atherosclerotic cardiovascular diseases and also as an indicator for estimating the effectiveness of the treatment. 相似文献
42.
进一步研究了抗三尖杉酯碱的HL-60细胞(HR20)抗细胞凋亡的机制及该抗性和抗药性的关系。结果表明,环孢菌素A(CsA)20,10μg·ml ̄(-1)诱导HL-60细胞发生凋亡,而阻断HR20细胞于G_1期,就不能诱导细胞发生凋亡。低浓度的CsA明显增加柔红霉素在HR20细胞内的积聚,其逆转抗药性作用与阻断细胞周期运行无关。CsA10μg·ml ̄(-1)处理HR20细胞,可引起50kDa的蛋白质高度磷酸化。结果提示:环孢菌素A阻断抗三尖杉酯碱的HL-60细胞于G_1期,而诱导敏感的HL-60细胞发生凋亡,其阻断作用与抗药性无关 相似文献
43.
D. Schiffer A. Chiò M. T. Giordana A. Mauro A. Migheli M. C. Vigliani 《Acta neuropathologica》1989,77(4):369-378
Summary Neo-vascularization and endothelial hyperplasia have been shown to be very active in malignant gliomas. In this contribution the vascularization of the cortex infiltrated by malignant gliomas is morphometrically studied and the endothelial proliferations are immunohistochemically investigated and reconstructed by a three-dimensional computer-assisted procedure. Vessel density increases after tumor infiltration in some cases only. The diameter of vessels increases and so does the number of nuclei/vessel after the complete invasion of the cortex when vascular glomeruli develop. In completely infiltrated cortex with development of glomeruli and circumscribed necroses, vessel density is very low. No neoformation of vessels takes place before the complete infiltration of the cortex by the tumor. The hyperplastic formations, usually arranged parallel to the deep or outer cortical layers, take origin from the radially penetrating vessels from the meninges and their lateral branching. The hyperplasia deforms the vascular network, making it often inadequate to supply tumor cells. Immunohistochemically, the cells composing the hyperplastic structures are variably positive for factor VIII/RAg and, at a lesser extent, for -smooth muscle actin. The poorness of the vascular network in many instances of completely infiltrated cortex is responsible for the development of circumscribed necroses.Supported by Grant 87.01446.44 CNR, Rome and by A. I. R. C., Milan. Presented in part at the 63rd Annual Meeting of the American Association of Neuropathologists, Seattle, Washington, June 11–14, 1987 相似文献
44.
I. C. Chi L. R. Wilkens C. B. Champion R. E. Machemer R. Rivera 《Advances in Contraception》1989,5(2):101-119
The possible effect of breastfeeding on intrauterine device (IUD) insertion events was investigated. Analysis included a total of 6493 women who enrolled in multicenter IUD clinical trials over a ten-year period. Findings indicate that breastfeeding exerts a protective effect on the incidence of moderate to severe insertional pain and reduces the need for cervical dilatation to facilitate insertion. The pain protection effect was most evident in breastfeeding women who were still in lactational amenorrhea. Subjects with amenorrhea, both breastfeeding and non-breastfeeding, had a significantly lower incidence of pain at IUD insertion than the corresponding menstruating subjects. This effect may be related to a higher secretion of beta-endorphin in the breastfeeding and lactational amenorrheic subjects.
Resumen Se investigaron en este estudio los posibles efectos del amamantamiento sobre la inserción de dispositivos intrauterinos (DIU). El estudio comprendió 6493 mujeres que participaron en ensayos clínicos en diversos centros durante un período de diez años. Los resultados indican que el amamantamiento ejerce un efecto protector contra la aparición de dolores moderados a fuertes en el momento de la inserción y reduce la necesidad de dilatar el cuello del útero para facilitar la inserción. Este efecto de protección contra el dolor predominó entre las mujeres que amamantaban y se hallaban aún en amenorrea de lactación. Las mujeres con amenorrea, tanto las que amamantaban como las que no lo hacían, señalaron un nivel de dolor significativamente menor en el momento de inserción del DIU que aquéllas cuyo ciclo menstrual se había reanudado. Este efecto puede estar relacionado con una mayor secreción de -endorfina en las mujeres en período de amamantamiento o de amenorrea de lactación.
Resumé Cette étude présente les effets possibles de l'allaitement au sein sur des phénomènes liés à l'insertion de dispositifs intra-utérins (DIU). La recherche portait 6493 femmes inscrites dans plusieurs centres pour participer à des essais cliniques pendant une période de dix ans. On a constaté que l'allaitement au sein a un effet protecteur contre l'apparition de douleurs modérées à fortes au moment de l'insertion et qu'il réduit la nécessité de dilater le col utérin en vue de faciliter l'insertion. Cet effet de protection contre les douleurs prédominait chez les femmes qui allaitaient et se trouvaient encore en aménorrhéc de lactation. Les douleurs au moment de l'insertion étaient significativement moins fréquentes au moment de la pose du DIU chez celles qui, allaitant ou non, étaient encore en période d'aménorrhée, que chez celles dont le cycle menstruel avait repris. Cet effet peut être lié à une sécrétion plus abondante de -endorphine chez les femmes en période d'allaitement ou d'aménorrhée de lactation.相似文献
45.
Increased expression of osteopontin gene in atypical teratoid/rhabdoid tumor of the central nervous system. 总被引:4,自引:0,他引:4
Chung-Lan Kao Shih-Hwa Chiou Yann-Jang Chen Sher Singh Han-Tso Lin Ren-Shyan Liu Chih-Wen Lo Chi-Chang Yang Chin-Wen Chi Chen-hsen Lee Tai-Tong Wong 《Modern pathology》2005,18(6):769-778
The atypical teratoid/rhabdoid tumor, primary to the central nervous system, is a highly malignant and aggressive neoplasm of infancy and childhood. Although having distinct biological features and clinical outcomes, it is frequently misdiagnosed as primitive neuroectodermal tumor/medulloblastoma. To further distinguish the underlying pathogenesis and to identify biological markers for clinical use, an atypical teratoid/rhabdoid tumor-derived cell line was established and its gene expression pattern analyzed in comparison to the human astrocyte SVG12 cell line and the human DAOY medulloblastoma cell line using a complementary DNA microarray method. The osteopontin gene was found specifically upregulated in atypical teratoid/rhabdoid tumor cells. This specificity was confirmed by immunohistochemistry in pathological sections of tissues from atypical teratoid/rhabdoid tumor patients. Even though the role of osteopontin in the cytopathogenesis of atypical teratoid/rhabdoid tumor still needs to be determined, our data support that overexpressed osteopontin is a potential diagnostic marker for atypical teratoid/rhabdoid tumor. 相似文献
46.
目的:利用高脂饮食加空气干燥术建立一种稳定、重复性好、有较典型动脉粥样硬化病理改变的动物模型。方法:32只日本大耳白兔随机分为模型组(n=24)、对照组(n=8)。模型组给予高脂饲料喂养加空气干燥术,术中结扎左侧颈动脉分支血管,对照组正常饲料喂养,分别于术后第2、4、8、12周处死动物。取颈动脉组织切片HE染色,光镜下观察。结果:(1)75%兔颈总动脉存在细小血管分支,暂时结扎侧支血管后干燥效果更好。(2)对双侧颈动脉实施手术,结扎左侧分支,成模率更高。部分斑块显示出不稳定性。结论:采用改进后高脂饮食加空气干燥术可成功建立兔颈动脉粥样硬化模型,其病理特点适合于目前临床研究。 相似文献
47.
In-Suk Kim Eun Sil Park Jae Young Lim Chang-Seok Ki Hyun Sook Chi 《Journal of Korean medical science》2008,23(6):1105-1108
Although acquired mutations in the GATA1 gene have been reported for Down syndrome-related acute megakaryoblastic leukemia (DS-AMKL) in Caucasians, this is the first report of a Korean Down syndrome patient with AMKL carrying a novel mutation of the GATA1 gene. A 3-yr-old Korean girl with Down syndrome was admitted to our hospital complaining of pallor and fever. The findings of a peripheral blood smear and bone marrow study were compatible with the presence of AMKL. A chromosome study showed 48,XX,-7,+21c,+21,+r[3]/47,XX,+21c[17]. Following GATA1 gene mutation analysis, a novel mutation, c.145dupG (p.Ala49GlyfsX18), was identified in the N-terminal activation domain of the GATA1 gene. This mutation caused a premature termination at codon 67 and expression of an abnormal GATA-1 protein with a defective N-terminal activation domain, and the absence of full-length GATA-1 protein. This case demonstrates that a leukemogenic mechanism for DS-AMKL is contributed by a unique collaboration between overexpressed genes from trisomy 21 and an acquired GATA1 mutation previously seen in Caucasians and now in a Korean patient. 相似文献
48.
Fibroblast growth factor 2 induces differentiation and apoptosis of Askin tumour cells 总被引:7,自引:0,他引:7
Kim MS Kim CJ Jung HS Seo MR Juhnn YS Shin HY Ahn HS Thiele CJ Chi JG 《The Journal of pathology》2004,202(1):103-112
Peripheral primitive neuroectodermal tumour (PNET)/Ewing's sarcoma (ES) and neuroblastoma (NB) are related tumours of neural crest origin with primitive neural characteristics. Fibroblast growth factor 2 (FGF2) is a critical signalling molecule for primitive neural crest cells. The treatment of NB cells with FGF2 variably affects biological characteristics such as growth and differentiation, while in PNET/ES, FGF2 predominantly induces apoptosis. The JK-GMS Askin tumour cell line can be induced to differentiate upon treatment with nerve growth factor (NGF), indicating the integrity of the cellular machinery necessary for differentiation. The present study assesses whether FGF2 can induce differentiation in JK-GMS cells. JK-GMS cells expressed high-affinity FGF receptors (FGFRs), and treatment with FGF2 induced phosphorylation of FGFR1 together with activation of extracellular signal-regulated kinases (ERK1/ERK2) and c-Jun N-terminal kinase (JNK). Subsequent biological effects were growth inhibition, neuronal differentiation, and apoptosis, and these changes were associated with increased expression of neurofilaments, reduction of c-myc and bcl-2 expression, and activation of caspase 3. Treatment of the cells with a specific inhibitor of the MAPK/extracellular signal-regulated kinase (MEK)-1, PD98059, predominantly inhibited the effects of FGF2 on growth, differentiation, and apoptosis, while an inhibitor of JNK reduced apoptosis, indicating that the ERK1/2 and JNK pathways are critical components of FGF2-mediated effects in JK-GMS cells. Additional comparative analyses of FGF2-mediated effects in two ES cell lines (CADO-ES, RD-ES) and a PNET cell line (SK-N-MC) showed pronounced differentiation in SK-N-MC, but not in CADO-ES or RD-ES cells. This study demonstrates that FGF2 can induce neuronal differentiation of PNET including Askin tumour. These findings clearly indicate that the FGF2-mediated signalling pathway plays a critical role in controlling the major properties of PNET cells and may provide a potential therapeutic target for PNET. 相似文献
49.
Chuen -Mao Yang Hui -Liang Tsao Chi -Tso Chiu Lir -Wan Fan Sheu -Meei Yu 《Pflügers Archiv : European journal of physiology》1996,432(4):708-716
The effects of increases in cellular adenosine 3′5′-cyclic monophosphate (cAMP) on 5-hydroxytryptamine-(5-HT-) induced generation
of inositol phosphates (IPs) and increases in intracellular Ca2+ ([Ca2+]i) were investigated using canine cultured tracheal smooth muscle cells (TSMCs). Cholera toxin and forskolin induced concentration-
and time-dependent cAMP formation with half-maximal effects (−logEC50) produced at concentrations of 7.0 ± 0.5 and 4.9 ± 0.4 respectively. Pretreatment of TSMCs with either forskolin or dibutyryl
cAMP inhibited 5-HT-stimulated responses. Even after treatment for 24h, these agents still inhibited the 5-HT-induced Ca2+ mobilization. The inhibitory effects of these agents produced both depression of the maximal response and a shift to the
right of the concentration response curves of 5-HT. The water-soluble forskolin analogue L-858051 [7-deacetyl-7β-(γ-N-methylpiperazino)-butyryl forskolin] significantly inhibited the 5-HT-stimulated accumulation of IPs. In contrast, the addition
of 1,9-dideoxy forskolin, an inactive forskolin analogue, had little effect on this response. Moreover, SQ-22536 [9-(tetrahydro-2-furanyl)-9-H-purin-6-amine], an inhibitor of adenylate cyclase, and both H-89 [N-(2-aminoethyl)-5-isoquinolinesulphonamide] and HA-1004[N-(2-guanidinoethyl)-5-isoquinolinesulphonamide], inhibitors of cAMP-dependent protein kinase (PKA), attenuated the ability
of forskolin to inhibit the 5-HT-stimulated accumulation of IPs. These results suggest that activation of cAMP/PKA was involved
in these inhibitory effects of forskolin. The AlF4
−-induced accumulation of IPs was inhibited by forskolin, suggesting that G protein(s) are directly activated by AlF4
−- and uncoupled from phospholipase C by forskolin treatment. These results suggest that activation of cAMP/PKA might inhibit
the 5-HT-stimulated phosphoinositide breakdown and consequently reduce the [Ca2+]i increase or inhibit both responses independently.
Received: 14 March 1996/Accepted: 10 April 1996 相似文献
50.
Malignant rhabdoid tumor is a distinct renal tumor in children. It had been regarded as a rhabdomyosarcomatoid variant of Wilms' tumor, but it is now thought as a separate entity. We report a case of malignant rhabdoid tumor of the kidney in a 26-month-old girl who presented with a left abdominal mass. Grossly, a large mass in the lower pole of the left kidney was well encapsulated and measured 4 x 4 x 3.5cm. On cross section, it was soft and yellowish white and showed multifocal necroses. The mass was mainly located in the medial medullary portion and compressed the renal pelvis laterally. Microscopically, the tumor masses were hypercellular and anaplastic without definite blastematous elements. In larger portion, the tumor cells had abundant eosinophilic cytoplasm and hyaline globules. In addition to the classic "rhabdoid" feature, alveolar, sclerosing, and lymphomatous patterns were seen. Ultrastructurally, tumor cells with abundant cytoplasm contained tangles of intermediate filament corresponding to vimentin in immunostaining. 相似文献