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951.
平滑肌细胞源性趋化因子所致单核细胞迁移的钙依赖性研究 总被引:4,自引:0,他引:4
本文以培养的兔主动脉平滑肌细胞条件培养基作为趋化因子的来源,用改良的Boyden小室微孔滤膜法进行单核细胞的迁移试验,并观察戊脉胺和细胞外Ca2+对其影响。用Fura-2检测单核细胞胞液游离钙浓度,并观察上述条件培养基及戊脉胺对其影响。结果表明,该条件培养基对单核细胞有明显趋化作用并被戊脉胺所抑制;它也能明显地升高单核细胞胞液游离钙浓度,并被戊脉胺所抑制。细胞外Ca2+也能影响单核细胞的迁移。以上结果提示,单核细胞迁移对细胞内、外Ca2+均有依赖性。 相似文献
952.
Melanie S. Weaver Young-Hee Lee Jimmy L. Morris Patrick K. Randall Timothy Schallert Steven W. Leslie 《Alcoholism, clinical and experimental research》1993,17(3):643-650
The present studies investigated the effects of glutathione (GSH; γ-glutamylcysteinylglycine) and its oxidized form (GSSG) on neuronal N -methyl-D-aspartate (NMDA) receptor activation in both acute and chronic preparations of ethanol exposure. It was demonstrated using fura-2-loaded dissociated brain cells from newborn rat pups that both GSH and GSSG (0–4 mM) produced concentration-dependent increases in intracellular calcium similar to those produced by NMDA and other agonists of the NMDA receptor. GSH-stimulated calcium entry was not inhibited by low intoxicating concentrations of ethanol, which contrasts with ethanol's typical inhibitory effect on NMDA-stimulated receptor activation. Behavioral studies in adult rats demonstrated that ethanol-induced sleep times were significantly decreased when 10 μl of GSSG (20 mM) were administered intracere-broventricularly approximately 5 min before an intraperitoneal injection of 20% (w/v) ethanol (3 g/kg). These findings suggest that the less potent effect of ethanol on GSH-stimulated calcium entry as well as the reduction in ethanol-induced sleep times may be related to the presence of glycine in the peptide. The glycine found in GSH may activate the glycine site and block or reduce ethanol's action on this site. It appears that although GSH may play an important role in the activation of the NMDA receptor, this action does not involve a process that is sensitive to acute ethanol exposure. In contrast, when rat pups were chronically exposed to ethanol via prenatal exposure before the fura-2 preparation, increases in NMDA- and GSH-stimulated calcium entry were significantly decreased relative to those in pair-fed and ad libitum-fed controls. Thus, chronic in utero exposure to ethanol may alter the NMDA-receptor complex, such that calcium entry mediated by NMDA or GSH activation is significantly reduced. 相似文献
953.
Bodo Klump Chih-Jen Hsieh Karlheinz Holzmann Michael Gregor Rainer Porschen 《Gastroenterology》1998,115(6):1381-1386
Background & Aims: Inactivation of the CDKN2/p16INK4A tumor-suppressor gene is one of the most frequent genetic alterations in human malignancies. In esophageal adenocarcinomas, mutations of the p16 gene or homozygous deletions of the gene locus 9p21 are rare. This study investigated whether p16 promoter hypermethylation is an alternative mechanism for p16 gene inactivation during neoplastic progression in Barrett's esophagus. Methods: A methylation-specific polymerase chain reaction protocol was applied. A total of 95 specimens from 14 patients with Barrett's esophagus were analyzed longitudinally. The p16 promoter status was compared with histomorphological findings. Results: p16 promoter hypermethylation was detected in 9 of the 10 patients who had displayed dysplasia at some time during surveillance, whereas none of the patients who had not displayed dysplasia during surveillance had p16 promoter hypermethylation. p16 promoter hypermethylation was detected in 3% (2 of 67) of the samples without dysplasia, 60% (3 of 5) of the samples with lesions indefinite for dysplasia, 55.6% (10 of 18) of the specimens with low-grade dysplasia, and 75% (3 of 4) of the specimens with high-grade dysplasia. Conclusions: These data suggest that p16 promoter hypermethylation is a common mechanism of p16 gene inactivation during neoplastic progression in Barrett's esophagus.GASTROENTEROLOGY 1998;115:1381-1386 相似文献
954.
Gerard Cortina Johannes Hofer Thomas Giner Therese Jungraithmayr 《Pediatrics international》2015,57(2):e42-e44
A 15‐year‐old girl presented with acute bilateral loss of central visual acuity due to hypertensive retinopathy level IV. She was found to have unrecognized malignant arterial hypertension associated with end‐stage renal failure. At the time of diagnosis she also had severe left ventricular hypertrophy (LVH). Hypertension was successfully treated with combined anti‐hypertensive therapy, but renal function did not recover. The patient underwent successful kidney transplant 4 months later and over a period of 20 months hypertensive retinopathy and LVH gradually resolved. This report emphasizes the importance of routine measurement of blood pressure and describes the possible consequences of unrecognized arterial hypertension in children. Early diagnosis and appropriate treatment are necessary to avoid development and progression of target organ damage and promote better long‐term cardiovascular prognosis. 相似文献
955.
Microsatellite instability in gallbladder carcinoma: two independent genetic pathways of gallbladder carcinogenesis 总被引:10,自引:0,他引:10
Yoshida T Sugai T Habano W Nakamura S Uesugi N Funato O Saito K 《Journal of gastroenterology》2000,35(10):768-774
Although the genetic basis for gallbladder carcinogenesis has not been clarified, considerable evidence has shown that genetic
alterations play an important role in the development and progression of human cancers. In this study, we analyzed 30 gallbladder
carcinomas to investigate the role of genetic alterations in their tumorigenesis, and to study correlations with their clinicopathological
features. Tissue samples were obtained from 30 patients with gallbladder carcinoma (11 men and 19 women; mean age, 62 years;
age range, 38–80 years). Genomic DNAs were extracted from fresh tumor tissue. We examined loss of heterozygosity (LOH) in
the p53, APC, DCC, RB, and NM23-H1 gene regions by polymerase chain reaction (PCR)-LOH assay using an automated fluorescent DNA sequencer employing four microsatellite
markers (p53, APC, DCC, NM23-H1). Five additional microsatellite markers were used for the determination of microsatellite
instability (MSI). LOH was found at p53 in 9 of 15 informative cases (60%), at DCC in 10 of 22 (45%), at APC in 5 of 15 (33%), at RB in 1 of 8 (13%), and at NM23-H1 in 1 of 15 (7%). MSI was observed in 5 of 30 cases (17%) in at least one chromosomal loci of these nine microsatellite markers.
None of the patients with MSI-positive tumors showed lymph node metastasis, and there was an inverse correlation between MSI
and the presence of LOH in gallbladder carcinoma. These results suggest that there are two independent genetic pathways in
gallbladder carcinogenesis; that is, an MSI pathway and an LOH pathway.
Received: December 24, 1999 / Accepted: May 26, 2000 相似文献
956.
957.
Diarrhoea and weight loss are frequently reported adverse events in rheumatoid arthritis (RA) patients receiving the disease-modifying antirheumatic drug (DMARD) leflunomide. According to the available literature these side effects occur mostly during the first 6 months of treatment, are rather mild and rarely lead to treatment withdrawal. In this report, we describe the clinical, endoscopic and histologic findings in two RA patients with severe diarrhoea and important weight loss more than 12 months after starting treatment with leflunomide. In both cases the symptoms were caused by colitis, but one had ulcerative and the other microscopic colitis. Despite treatment with budesonide the complaints only improved after withdrawal of leflunomide, making a causal relationship between this drug and the pathogenesis of colitis probable. The heterogeneous histopathological findings in these two patients, however, do not allow us to draw any definitive conclusions about the mechanism by which leflunomide causes diarrhoea and weight loss in RA patients. We conclude that persistent diarrhoea or weight loss in patients taking leflunomide can be more serious than what is previously reported in the literature. In such cases leflunomide treatment should be stopped and an endoscopic examination of the colon is recommended. Given the long half-life of this drug a washout procedure with cholestyramine should be considered whenever the problem is severe or persistent. 相似文献
958.
Velimir Matkovic MD PhD Nancy Badenhop-Stevens RD MSc Eun-Jeong Ha PhD Zeljka Crncevic-Orlic MD PhD Albert Clairmont MD 《Clinical reviews in bone and mineral metabolism》2002,1(3-4):233-248
Bone accretion during childhood is proportional to the rate of growth. During this time, interval height velocity is relatively
slow for both boys and girls. As a direct consequence of this, calcium retention in the body of an average child is lower
than the calcium retention in an adolescent. Bone size, bone mass, and bone mineral areal density of the regional skeletal
sites increase on average by about 4%/yr from childhood to late adolescence and young adulthood, when most of the bone mass
is accumulated. Calcium needs are greater during adolescence (pubertal growth spurt) than in childhood or adulthood. According
to calcium balance studies, the threshold in take for adolescents is about 1500 mg/d. Inadequate calcium intake during growth
may increase the risk of childhood fractures and predispose certain individuals to a lower peak bone mass. 相似文献
959.
960.
Reem Z. Sharaiha Kaveh Hajifathalian Rekha Kumar Katherine Saunders Amit Mehta Bryan Ang Daniel Skaf Shawn Shah Andrea Herr Leon Igel Qais Dawod Enad Dawod Kartik Sampath David Carr-Locke Robert Brown David Cohen Andrew J. Dannenberg Srihari Mahadev Louis J. Aronne 《Clinical gastroenterology and hepatology》2021,19(5):1051-1057.e2