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  • Wiley  (30)
  • Pharmacy  (30)
  • 1
    In: British Journal of Clinical Pharmacology, Wiley, Vol. 73, No. 3 ( 2012-03), p. 422-427
    Type of Medium: Online Resource
    ISSN: 0306-5251
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 1498142-7
    SSG: 15,3
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  • 2
    In: The Journal of Clinical Pharmacology, Wiley, Vol. 59, No. 3 ( 2019-03), p. 326-334
    Abstract: Mammalian targets of rapamycin inhibitors (mTORIs), including sirolimus and everolimus, are used for minimizing calcineurin inhibitors after liver transplantation. However, head‐to‐head randomized comparisons of these 2 mTORIs are lacking. We assessed the differences in renoprotection and possible mechanisms between sirolimus and everolimus in liver transplant recipients. For this prospective cohort study, we recruited liver transplant recipients whose regimens were switched from tacrolimus to sirolimus or everolimus at a Taiwan medical center. Serial changes in estimated glomerular filtration rate (eGFR), urinary N‐acetyl‐β‐D‐glucosaminidase, neutrophil gelatinase–associated lipocalin, 8‐hydroxy‐2′‐deoxyguanosine, and transforming growth factor‐β1 during 1 year after mTORI conversion were compared within and between groups. In the 61 patients analyzed, no significant change in eGFR occurred within 12 months after conversion in both mTORI groups. Among patients with baseline eGFR 〈 60 mL/min/1.73 m 2 , eGFR improved at 6 months and 1 year after conversion (+12.3 and +12.0 mL/min/1.73 m 2 , both P 〈 .05). Urinary N‐acetyl‐β‐D‐glucosaminidase decreased in both sirolimus and everolimus groups at 6 months (–68.7 ± 137.6 and –62.0 ± 92.4 U/g creatinine, both P 〈 .05), and the reduction of urinary neutrophil gelatinase–associated lipocalin was significant in the sirolimus group (–4345.1 ± 7763.5 ng/g creatinine; P 〈 .05). Neither transforming growth factor‐β1 nor 8‐hydroxy‐2´‐deoxyguanosine changed significantly. In conclusion, the renoprotective effect of mTORI conversion was significant in liver transplant recipients with renal insufficiency, which was similar for sirolimus and everolimus, in the first year and may be associated with ameliorated tubular injury. Available evidence remains insufficient to determine which mTORI conversion therapy is more effective in renoprotection in the long run.
    Type of Medium: Online Resource
    ISSN: 0091-2700 , 1552-4604
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2010253-7
    SSG: 15,3
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  • 3
    In: Phytotherapy Research, Wiley, Vol. 36, No. 9 ( 2022-09), p. 3662-3671
    Abstract: Inflammatory bowel disease (IBD) is a non‐specific chronic intestinal inflammatory disease, often presenting with abdominal pain, diarrhea, bloody stool, anorexia, and body loss. It is difficult to cure completely and a promising treatment is urgently needed. Natural compounds can offer promising chemical agents for treatment of diseases. Polydatin is a natural ingredient extracted from the dried rhizome of Polygonum cuspidatum , which has anti‐inflammatory, anti‐tumor, and dementia protection activities. The purpose of this study was to evaluate the therapeutic effect of polydatin on IBD and explore its possible mechanism. We found that polydatin could effectively suppress the differentiation of Th17 cells in vitro, but had no effect on the differentiation of Treg cells. Polydatin significantly alleviated colitis induced by dextran sulfate sodium (DSS) and 2, 4, 6‐trinitrobenzenesulfonic acid (TNBS) in mice, and dramatically decreased the proportion of Th17 cells in spleen and mesenteric lymph nodes. Mechanism investigations revealed that polydatin specifically inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation by directly binding to STAT3, leading to Th17 cell reduction and thereby alleviating colitis. These findings provide novel insights into the anti‐colitis effect of polydatin, which may be a promising drug candidate for the treatment of IBD.
    Type of Medium: Online Resource
    ISSN: 0951-418X , 1099-1573
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1493490-5
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  • 4
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 123, No. 3 ( 2018-09), p. 308-313
    Abstract: Genetic risk factors could cause cutaneous adverse drug reactions ( cADR s) in patients after treatment with clarithromycin. This study explored the association of HLA class I genes with clarithromycin‐ cADR s in Han Chinese patients. A total of 12 clarithromycin‐ cADR patients and 34 clarithromycin‐tolerant controls were recruited for the high‐resolution genotyping of HLA class I genes ( HLA ‐A , HLA ‐B and HLA ‐C ). The population controls consisted of 283 Han Chinese retrieved from the MHC database for validated comparison. A molecular docking analysis of HLA ‐A*02:07 protein and clarithromycin was conducted using glide module with Schrödinger Suite. Among all tested HLA alleles, the carrier frequencies of HLA ‐A*02:07 (58% versus 5.9%, OR = 22.40, 95% CI = 3.58–139.98, p = 8.20 × 10E‐5, pc = 1.1 × 10E‐3) and HLA ‐B*46:01 (50% versus 5.9%, OR = 16.00, 95% CI = 2.59–98.99, p = 0.002, pc = 0.03) were significantly higher in clarithromycin‐ cADR s than in clarithromycin‐tolerant controls. However, when compared to population controls, only HLA ‐A*02:07 , and not HLA ‐B*46:01 , reached statistical significance (58% versus 15.5%, OR = 7.61, 95% CI = 2.31–25.04, p = 1.2 × 10E‐4, pc = 1.7 × 10E‐3). Furthermore, molecular docking data revealed that clarithromycin could bind to and interact with HLA ‐A*02:07 in two possible binding situations. These data suggest that HLA ‐A*02:07 might be a genetic risk factor for developing clarithromycin‐ cADR s in Han Chinese and serve as a useful biomarker for personalized medicine to prevent clarithromycin‐ cADR s.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2151592-X
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  • 5
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 125, No. 6 ( 2019-12), p. 508-517
    Abstract: Methimazole (MMI) has been used in the therapy of Grave's disease (GD) since 1954, and drug‐induced liver injury (DILI) is one of the most deleterious side effects. Genetic polymorphisms of drug‐metabolizing enzymes and drug transporters have been associated with drug‐induced hepatotoxicity in many cases. The aim of this study was to investigate genetic susceptibility of the drug‐metabolizing enzymes and drug transporters to the MMI‐DILI. A total of 44 GD patients with MMI‐DILI and 118 GD patients without MMI‐DILI development were included in the study. Thirty‐three single nucleotide polymorphisms (SNPs) in twenty candidate genes were genotyped. We found that rs12422149 of SLCO2B1 , rs2032582_AT of ABCB1 , rs2306283 of SLCO1B1 and rs4148323 of UGT1A1 exhibited a significant association with MMI‐DILI; however, no significant difference existed after Bonferroni correction. Haplotype analysis showed that the frequency of SLCO1B1*1a (388A521T) was significantly higher in MMI‐DILI cases than that in the control group (OR = 2.21, 95% CI = 1.11‐4.39, P  = 0.023), while the frequency of SLCO1B1*1b (388G521T) was significantly higher in the control group (OR = 0.52, 95% CI = 0.29‐0.93, P  = 0.028). These results suggested that genetic polymorphisms of SLCO1B1 were associated with susceptibility to MMI‐DILI. The genetic polymorphism of SLCO1B1 may be important predisposing factors for MMI‐induced hepatotoxicity.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2151592-X
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  • 6
    In: Clinical Pharmacology & Therapeutics, Wiley, Vol. 110, No. 4 ( 2021-10), p. 1119-1126
    Abstract: Our previous study showed that parenteral anticoagulation therapy (PACT) in the context of aggressive antiplatelet therapy failed to improve clinical outcomes in patients undergoing percutaneous coronary intervention for non–ST‐segment elevation acute coronary syndrome (NSTE‐ACS). However, the role of PACT in patients managed medically remains unknown. This observational cohort study enrolled patients with NSTE‐ACS receiving medical therapy from November 2014 to June 2017 in the Improving Care for Cardiovascular Disease in China‐Acute Coronary Syndrome project. Eligible patients were included in the PACT group and non‐PACT group. The primary outcomes were in‐hospital all‐cause mortality and major bleeding. The secondary outcome included minor bleeding. Among 23,726 patients, 8,845 eligible patients who received medical therapy were enrolled. After adjusting the potential confounders, PACT was not associated with a lower risk of in‐hospital all‐cause mortality (adjusted odds ratio (OR), 1.25; 95% confidence interval (CI), 0.92–1.71; P  = 0.151). Additionally, PACT did not increase the incidence of major bleeding or minor bleeding (major bleeding: adjusted OR, 1.04; 95% CI, 0.80–1.35; P  = 0.763; minor bleeding: adjusted OR, 1.27; 95% CI, 0.91–1.75; P  = 0.156). The propensity score analysis confirmed the primary analyses. In patients with NSTE‐ACS receiving antiplatelet therapy, PACT was not associated with a lower risk of in‐hospital all‐cause mortality or a higher bleeding risk in patients with NSTE‐ACS receiving non‐invasive therapies and concurrent antiplatelet strategies. Randomized clinical trials are warranted to reevaluate the safety and efficacy of PACT in all patients with NSTE‐ACS who receive noninvasive therapies and current antithrombotic strategies.
    Type of Medium: Online Resource
    ISSN: 0009-9236 , 1532-6535
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2040184-X
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  • 7
    In: Medicinal Research Reviews, Wiley, Vol. 42, No. 6 ( 2022-11), p. 2025-2066
    Abstract: Carbohydrate‐based drug discovery has gained more and more attention during the last few decades. Resin glycoside is a kind of novel and complex glycolipids mainly distributed in plants of the family Convolvulaceae. Over the last decade, a number of natural resin glycosides and derivatives have been isolated and identified, and exhibited a broad spectrum of biological activities, such as cytotoxic, multidrug‐resistant reversal on both microbial pathogens and mammalian cancer cells, antivirus, anticonvulsant, antidepressant, sedative, vasorelaxant, laxative, and α‐glucosidase inhibitory effects, indicating their potential as lead compounds for drug discovery. A systematic review of the literature studies was carried out to summarize the chemistry and biological activity of resin glycosides from Convolvulaceae species, based on various data sources such as PubMed, Web of Science, Scopus, and Google scholar. The keyword “Convolvulaceae” was paired with “resin glycoside,” “glycosidic acid,” “glycolipid,” or “oligosaccharide,” and the references published between 2009 and June 2021 were covered. In this article, we comprehensively reviewed the structures of 288 natural resin glycoside and derivatives newly reported in the last decade. Moreover, we summarized the biological activities and mechanisms of action of the resin glycosides with pharmaceutical potential. Taken together, great progress has been made on the chemistry and biological activity of resin glycosides from Convolvulaceae species, however, more exploratory research is still needed, especially on the mechanism of action of the biological activities.
    Type of Medium: Online Resource
    ISSN: 0198-6325 , 1098-1128
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2001841-1
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  • 8
    Online Resource
    Online Resource
    Wiley ; 2009
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 36, No. 12 ( 2009-12), p. 1177-1182
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 36, No. 12 ( 2009-12), p. 1177-1182
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2020033-X
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  • 9
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 35, No. 8 ( 2008-08), p. 904-908
    Abstract: Clopidogrel is one of the most important antithrombotic drugs but has different efficacies in different populations. The aim of the present study was to evaluate the contribution of CYP2C19 genetic polymorphisms to the inhibition of ADP‐induced platelet aggregation by clopidogrel in healthy Chinese volunteers. Eighteen healthy male volunteers (six CYP2C19*1/CYP2C19*1 , six CYP2C19*1/CYP2C19*2 and *3 and six CYP2C19*2/CYP2C19*2 and *3 ) were enrolled in the study. Each subject took 300 mg clopidogrel on the first day and then 75 mg once daily for 2 consecutive days. Blood samples were taken to measure ADP‐induced platelet aggregation at baseline and 4, 24 and 72 h after administration of the first dose of clopidogrel. There were significant decrease in 2 and 5 mmol/L ADP‐induced platelet aggregation at 4, 24 and 72 h after clopidogrel among the three CYP2C19 genotypes compared with baseline ( P  〈  0.001). The change in 5 mmol/L ADP‐induced platelet aggregation in subjects with the CYP2C19*1/CYP2C19*1 genotype was greater than that in subjects with the CYP2C19*2/CYP2C19*2 and *3 genotype at 4 h (49.0 ± 15.5 vs 29.7 ± 17.4%, respectively; P  = 0.029), 24 h (48.7 ± 20.5 vs 25.0 ± 17.6%, respectively; P  = 0.035) and 72 h (45.5 ± 15.2 vs 26.5 ± 15.8%, respectively; P  = 0.030) after clopidogrel administration. In conclusion, CYP2C19*2 and CYP2C19*3 genetic polymorphisms reduced clopidogrel inhibition of ADP‐induced platelet aggregation, with the degree of inhition dependent on the genetic polymorphism present.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 2020033-X
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  • 10
    In: British Journal of Pharmacology, Wiley, Vol. 175, No. 5 ( 2018-03), p. 810-829
    Abstract: The aim of this study was to investigate the ameliorative effects of corilagin on intrahepatic cholestasis induced by regulating liver farnesoid X receptor (FXR)‐associated pathways in vitro and in vivo . Experimental Approach Cellular and animal models were treated with different concentrations of corilagin. In the cellular experiments, FXR expression was up‐regulated by either lentiviral transduction or GW4064 treatment and down‐regulated by either siRNA technology or treatment with guggulsterones. Real‐time PCR and Western blotting were employed to detect the mRNA and protein levels of FXR, SHP1, SHP2, UGT2B4, BSEP, CYP7A1, CYP7B1, NTCP, MRP2 and SULT2A1. Immunohistochemistry was used to examine the expression of BSEP in liver tissues. Rat liver function and pathological changes in hepatic tissue were assessed using biochemical tests and haematoxylin and eosin staining. Results Corilagin increased the mRNA and protein levels of FXR, SHP1, SHP2, UGT2B4, BSEP, MRP2 and SULT2A1, and decreased those of CYP7A1, CYP7B1 and NTCP. After either up‐ or down‐regulating FXR using different methods, corilagin could still increase the mRNA and protein levels of FXR, SHP1, SHP2, UGT2B4, BSEP, MRP2 and SULT2A1 and decrease the protein levels of CYP7A1, CYP7B1 and NTCP, especially when administered at a high concentration. Corilagin also exerted a notable effect on the pathological manifestations of intrahepatic cholestasis, BSEP staining in liver tissues and liver function. Conclusions and Implications Corilagin exerts a protective effect in hepatocytes and can prevent the deleterious activities of intrahepatic cholestasis by stimulating FXR‐associated pathways.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
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