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Tien-Yuan?Wu Ying?Huang Chengyue?Zhang Zheng-Yuan?Su Sarandeep?Boyanapalli Tin?Oo?Khor Hu?Wang Hongxia?Lin Murugesan?Gounder Leonid?Kagan Ioannis?P.?Androulakis Ah-Ng?Tony?KongEmail author 《Journal of pharmacokinetics and pharmacodynamics》2015,42(4):401-408
3,3′-Diindolylmethane (DIM) has been investigated as a potential anti-cancer chemopreventive agent in many preclinical and clinical studies. In this study, we sought to characterize the pharmacokinetics of DIM and to build a pharmacokinetic (PK) and pharmacodynamic (PD) model of the DIM-induced gene expression of phase II drug metabolizing enzymes (DME), which potentially links DIM’s molecular effects to its in vivo chemopreventive efficacy. DIM (10 mg/kg) was administered intravenously (i.v.) to male Sprague–Dawley rats and blood samples were collected at selected time points for 48 h. The plasma concentration of DIM was determined using a validated HPLC method. The mRNA expression of NQO1, GSTP1 and UGT1A1 in blood lymphocytes was measured using quantitative PCR. An indirect response model was employed to relate the concentration of DIM to the expression of the genes NQO1, GSTP1 and UGT1A1, which were chosen as PD markers for DIM. After i.v. administration, the plasma concentration of DIM declined quickly, and the expression of target genes increased significantly, peaking at 1–2 h and then returning to basal levels after 24 h. The parameters in the PK–PD model were estimated. The PK–PD model aptly described the time delay and magnitude of gene expression induced by DIM. Our results indicate that DIM is effective at inducing various phase II DME, which are capable of detoxify carcinogens. This PK–PD modeling approach provides a framework for evaluating the acute effects of DIM or other similar drugs in clinical trials. 相似文献
83.
Doundoulakis Ioannis Gavriilaki Maria Tsiachris Dimitris Arsenos Petros Antoniou Christos-Konstantinos Dimou Smaro Soulaidopoulos Stergios Farmakis Ioannis Akrivos Evangelos Stoiloudis Panagiotis Notas Konstantinos Kimiskidis Vasilios K. Giannakoulas George Paraskevaidis Stylianos Gatzoulis Konstantinos A. Tsioufis Konstantinos 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》2022,36(5):951-958
Cardiovascular Drugs and Therapy - Atrial high-rate episodes (AHREs) recorded with cardiac implantable electronic devices (CIEDs) have been associated with the development of clinical atrial... 相似文献
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Brandon N. Nicolay Paul S. Danielian Filippos Kottakis John D. Lapek Jr Ioannis Sanidas Wayne O. Miles Mantre Dehnad Katrin Tsch?p Jessica J. Gierut Amity L. Manning Robert Morris Kevin Haigis Nabeel Bardeesy Jacqueline A. Lees Wilhelm Haas Nicholas J. Dyson 《Genes & development》2015,29(17):1875-1889
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Urological complications,vesicoureteral reflux,and long‐term graft survival rate after pediatric kidney transplantation 下载免费PDF全文
Fabio C. M. Torricelli Andreia Watanabe Affonso C. Piovesan Ioannis M. Antonopoulos Elias David‐Neto William C. Nahas 《Pediatric transplantation》2015,19(8):844-848
To describe a single‐center experience with kidney transplantation and then study some donor and recipient features that may impact on graft survival and urological complication rates. We reviewed our database searching for pediatric patients who underwent kidney transplantation from August 1985 through November 2012. Preoperative data and postoperative complications were recorded. Graft survival rates were analyzed and compared based on the type of donor, donor's age from deceased donors, and recipients' ESRD cause. Kaplan–Meier curves with log rank and Wilcoxon tests were used to perform the comparisons. There were 305 pediatric kidney transplants. The mean recipient's age was 11.7 yr. The mean follow‐up was 11.0 yr. Arterial and venous thrombosis rates were 1.6% and 2.3%, respectively, while urinary fistula and symptomatic vesicoureteral reflux were diagnosed in 2.9% and 3.6% of cases, respectively. Deceased kidney transplantation had a lower graft survival rate than living kidney transplantation (log rank, p = 0.005). Donor's age (p = 0.420) and ESRD cause (p = 0.679) were not significantly related to graft survival rate. In long‐term follow‐up, type of donor, but not donor's age, impacts on graft survival rate. ESRD cause has no impact on graft survival rate, showing that well‐evaluated recipients may have good outcomes. 相似文献
86.
Koutroubakis IE Petinaki E Dimoulios P Vardas E Roussomoustakaki M Maniatis AN Kouroumalis EA 《International journal of colorectal disease》2003,18(3):254-259
BACKGROUND AND AIMS: Initiation of a fibrotic process has been suggested as part of the intestinal response to chronic inflammation in inflammatory bowel disease. YKL-40 has been proposed as a new serum marker of fibrosis. We studied compared the serum levels of YKL-40 in patients with ulcerative colitis or Crohn's disease with inflammatory and healthy controls. PATIENTS AND METHODS: YKL-40 serum levels were measured in 179 patients with inflammatory bowel disease (94 ulcerative colitis, 85 Crohn's disease), in 23 with intestinal inflammation of other causes, and 70 matched healthy controls using a commercially available enzyme-linked immunosorbent assay. YKL-40 levels were assessed in terms of disease activity, type and localization. RESULTS: Mean serum YKL-40 levels were 102.6+/-82.7 ng/ml in ulcerative colitis patients and 112.2+/-83.7 ng/ml in Crohn's disease patients, significantly higher than in healthy controls (64.1+/-21.4 ng/ml) but not significantly different from inflammatory controls (77.8+/-23.1 ng/ml). Disease activity and C-reactive protein levels were significantly correlated with YKL-40 levels in both ulcerative colitis and Crohn's disease. Crohn's disease patients with ileum localization had significantly higher YKL-40 levels than those with ileocolonic or colonic disease. Patients with stenotic disease had mean YKL-40 levels not significantly different than those with nonstenotic disease. CONCLUSION: Serum levels of YKL-40 are increased in patients with inflammatory bowel disease, and this is associated with the inflammatory process rather than with the degree of fibrosis. 相似文献
87.
Effects of CCR5-Delta32 and CCR2-64I alleles on HIV-1 disease progression: the protection varies with duration of infection 总被引:5,自引:0,他引:5
Mulherin SA O'Brien TR Ioannidis JP Goedert JJ Buchbinder SP Coutinho RA Jamieson BD Meyer L Michael NL Pantaleo G Rizzardi GP Schuitemaker H Sheppard HW Theodorou ID Vlahov D Rosenberg PS;International Meta-Analysis of HIV Host Genetics 《AIDS (London, England)》2003,17(3):377-387
OBJECTIVE: To examine temporal variation in the effects of CCR5-Delta32 and CCR2-64I chemokine receptor gene polymorphisms on HIV-1 disease progression. DESIGN: Pooled analysis of individual patient data from 10 cohorts of HIV-1 seroconverters from the United States, Europe, and Australia. METHODS: We studied HIV-1 seroconverters of European (n = 1635) or African (n = 215) ancestry who had been genotyped for CCR5-Delta32 and CCR2-64I. We used Cox proportional hazards models with time-varying coefficients to determine whether the genetic protection against AIDS (1987 case definition) and death varied with time since seroconversion. RESULTS: Protection against AIDS conferred by CCR5-Delta32 held constant at a 31% (RH 0.69, 95% CI 0.54, 0.88) reduction in risk over the course of HIV-1 infection, whereas protection against death held constant at a 39% reduction in risk (RH 0.61, 95% CI 0.45, 0.88). When the period from AIDS to death was isolated, the survival benefit of CCR5-Delta32 diminished 2 years after AIDS. Protection against AIDS conferred by CCR2-64I was greatest early in the disease course. Compared with individuals without CCR5-Delta32 or CCR2-64I, individuals with one or two copies of CCR2-64I had a 58% lower risk of AIDS during the first 4 years after seroconversion (RH 0.42, 95% CI 0.23, 0.76), a 19% lower risk during the subsequent 4 years (RH 0.81, 95% CI 0.59, 1.12), and no significant protection thereafter. CONCLUSION: The protection against AIDS provided by CCR5-Delta32 is continuous during the course of infection. In contrast, the protection provided by CCR2-64I is greatest early in the course of infection. 相似文献
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