European Journal of Clinical Investigation (Eur J Clin Investig )

Publisher: European Society for Clinical Investigation, Blackwell Publishing

Description

The Journal of the European Society for Clinical Investigation. The European Journal of Clinical Investigation publishes papers in the field of clinical investigation, provided they contribute to the advancement of knowledge in this field. The term 'clinical investigation' is interpreted widely and includes studies relevant to humans in health or disease, including such studies that may have taken place with animals.

  • Impact factor
    3.37
  • 5-year impact
    3.05
  • Cited half-life
    8.00
  • Immediacy index
    0.70
  • Eigenfactor
    0.01
  • Article influence
    0.90
  • Website
    European Journal of Clinical Investigation website
  • Other titles
    European journal of clinical investigation (Online)
  • ISSN
    1365-2362
  • OCLC
    46653881
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Blackwell Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
    • no listing of affected journals available as yet
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • Publisher's version/PDF cannot be used
    • On author's server, institutional server or subject-based server
    • Server must be non-commercial
    • Publisher copyright and source must be acknowledged with set statement ("The definitive version is available at www.blackwell-synergy.com")
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'Blackwell Publishing' is an imprint of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The adaptor protein p66Shc links membrane receptors to intracellular signalling pathways and has the potential to respond to energy status changes and regulate mitogenic signalling. Initially reported to mediate growth signals in normal and cancer cells, p66Shc has also been recognized as a pro-apoptotic protein involved in the cellular response to oxidative stress. Moreover, it is a key element in processes such as cancer cell proliferation, tumor progression, metastasis and metabolic reprogramming. Recent findings on the role of p66Shc in the above-mentioned processes have been obtained through the use of various tumor cell types, including prostate, breast, ovarian, lung, colon, skin and thyroid cancer cells. Interestingly, the impact of p66Shc on the proliferation rate was mainly observed in prostate tumors, while its impact on metastasis was mainly found in breast cancers. In this review, we summarize the current knowledge about the possible roles of p66Shc in different cancers.
    European Journal of Clinical Investigation 01/2015; 45(s1).
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    ABSTRACT: Background Cancer cells are widely recognized for being able to adapt their metabolism towards converting available nutrients into biomass to increase proliferation rates.Materials and methodsWe will review a series of nuclear magnetic resonance (NMR)-based stable isotope tracer methodologies for probing cancer metabolism.ResultsThe monitoring of such adaptations is of the utmost importance to unravel cancer metabolism and tumour growth. Several major metabolic targets have been recognized as promising foci and have been addressed by multiple studies in recent years. In this work are presented strategies to quantify glycolysis, pentose phosphate pathway, Krebs cycle turnover and de novo lipogenesis by NMR isotopomer analysis.Conclusions Being able to adequately define the interplay between metabolic pathways allows the monitoring of their prevalence in tissues and such information is critical for an accurate knowledge of the metabolic distinctive nature of tumours towards devising more efficient antitumorigenic strategies. Discussed methodologies are currently available in the literature, but to date, no single review has compiled all their possible uses, particularly in an interdependent perspective.
    European Journal of Clinical Investigation 01/2015; 45(s1).
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    ABSTRACT: Background Epigenetic control of gene expression is mediated by cytosine methylation/demethylation and histone modifications including methylation, acetylation and glycosylation. The epigenetic programme is corrupted in cancer cells to maintain a pattern of gene expression that leads to their de-differentiated, rapidly proliferating phenotype. Enzymes responsible for modifying histones and cytosine are sensitive to the cellular metabolite pool and can be activated by an increase in their substrates or inhibited by an increase in their products or competitors for substrate binding.Methods This review is based on publications identified on PubMed using a literature search of cytosine methylation, histone methylation, acetylation and glycosylation.ResultsIn cancer, changes in glycolytic enzymes lead to increased production of serine, increasing the pool of S-adenosylmethionine (the major methyl donor for methylation reactions) and UDP-N-acetylglucosamine (a substrate for O-linked glycosylation of histones and cytosine methyltransferases). Mutations in tricarboxylic acid cycle enzymes lead to accumulation of fumarate, succinate and hydroxyglutarate, all of which inhibit demethylation of cytosine and histones. In contrast, proline catabolism produces α-ketoglutarate and reactive oxygen, both of which promote the activity of enzymes that remove methyl groups from cytosine and histones, and the key enzyme in proline catabolism acts as a tumour suppressor.Conclusions Our emerging understanding of how the epigenetic profiles are metabolically reprogrammed in cancer cells will lead to novel diagnostic and therapeutic targets for treatment of patients.
    European Journal of Clinical Investigation 01/2015; 45(s1).
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    ABSTRACT: Background Bisphenol A (BPA) is one of the most widely produced chemicals worldwide and is often used in the production of food and beverage containers. As a result of BPA contact with food, drink and toiletries, its ingestion and absorption by humans has been growing. The industrialization and modern lifestyles brought a constant exposure to several health-disturbing compounds and ushered a new era of chronic diseases. The endocrine disruptor potential of BPA is well known, but the research around its epigenotoxic effects raised further concerns whether chronic exposure to BPA can contribute to chronic human illness, including cancer in hormone-sensitive organs.Materials and methodsFocusing on computerized databases, we reviewed original and review articles which elucidate and link some of the information already available about BPA and related epigenetic alterations.ResultsA number of studies indicate that short-term administration of low or high-doses of BPA may be associated with an increased risk of epigenetic modifications, increasing the risk for carcinogenesis. However, it is clear that more studies considering real daily exposures are essential to define a real tolerable daily intake and to tighten\xA0up\xA0manufactory regulations.Conclusion In this review, we highlight some evidences suggesting a relationship between BPA exposure, genotoxic activity and epigenetic modifications, which may prime for carcinogenesis.
    European Journal of Clinical Investigation 01/2015; 45(s1).
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    ABSTRACT: Background In rodents, it has previously been shown that Necrostatin-1 (Nec-1) inhibits RIP1, a central regulator of programmed necrosis, thereby decreasing cell death and reducing infarct size after ischemia/reperfusion (I/R) injury. To address unanswered questions on feasibility and efficacy of Nec-1 in a large animal model, we assessed the effects of Nec-1 in a porcine I/R model, relevant to human disease.Materials and Methods In Dalland landrace pigs (69±3kg), I/R injury was induced by a 75-min surgical ligation of the left circumflex coronary artery (LCx). Ten minutes prior to reperfusion, pigs were randomly allocated to different Nec-1 doses (1.0mg/kg or 3.3mg/kg) or vehicle treatment (CTRL). Functional endpoints and immunohistological analyses were performed 24 hours after reperfusion.ResultsNec-1 3.3mg/kg significantly reduced infarct size (n=6; 24.4±15.6%) compared to Nec-1 1.0 mg/kg (n=5; 54.8±16.9%) or CTRLs (n=6; 62.1±26.6%; P=0.016). In line, LVEF was significantly higher in Nec-1 3.3mg/kg, compared to Nec-1 1.0mg/kg or CTRL treated animals (50.0±12.0% vs 32.5±12.9% vs 31.9±6.6% respectively, P=0.015). Hemodynamically, a preserved contractility was observed (end systolic volume at 100 mmHg (ESV100)) at 24-hours follow up (87.6±17.3 ml vs. 74.5±41.1 ml vs. 56.8±11.8 ml, respectively; P=0.032), reflecting improved cardiac function.Conclusions In the pig model of I/R injury, intravenous administration of Nec-1 prior to reperfusion was an effective and above all practical therapeutic strategy that significantly reduced infarct size and preserved left ventricular function. These data highlight the potential of cardioprotection as a promising adjuvant therapy in the setting of early reperfusion following I/R injury.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 12/2014;
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    ABSTRACT: Background Post-operative atrial fibrillation (POAF) is a common complication after cardiac surgery and predicts increased morbidity and mortality. Identification of patients at high risk of POAF with the help of circulating biomarkers may enable early preventive treatment but data are limited, especially in contemporary surgical patients.Methods Plasma concentrations of N-terminal pro B-type natriuretic peptide (NT-proBNP) and high sensitivity cardiac troponin T (hs-cTnT) were measured at enrollment, on the morning of cardiac surgery, at end-surgery, and 2 days post-surgery in 562 patients undergoing cardiac surgery, randomized to perioperative supplementation with oral fish oil or placebo in the Omega-3 Fatty Acids for Prevention of Post-Operative Atrial Fibrillation trial (OPERA). The primary endpoint was incident POAF lasting ≥ 30seconds, centrally adjudicated and confirmed electrocardiographically.ResultsHigher levels of NT-proBNP and hs-cTnT before surgery were associated with older age, renal or cardiac dysfunction and EuroSCORE. NT-proBNP peaked on post-operative day 2 (2172 [1238-3758] ng/L, median [Q1-Q3]), while hs-cTnT peaked at the end of surgery (373 [188-660] ng/L). Fish oil supplementation did not alter the time course of the cardiac biomarkers (p>0.05). Concentrations of NT-proBNP or hs-cTnT, on the morning of surgery, or changes in their level between morning of surgery and post-surgery, were not significantly associated with POAF after adjustment for clinical and surgical characteristics.Conclusion Among patients undergoing cardiac surgery, NT-proBNP and hs-cTnT are related to clinical and surgical characteristics, have different perioperative time courses but are not independently associated with risk of POAF.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 12/2014;
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    ABSTRACT: Background The increased cardiovascular risk present in chronic kidney disease (CKD) is related to the development of endothelial dysfunction, whose mechanisms are still unclear. Accumulation of toxins and proinflammatory cytokines may constitute danger associated molecular patterns (DAMP) to which endothelial cells are continuously exposed. Potential involvement of mechanisms recognizing DAMP, such as TLR and inflammasomes, has been explored.Material & Methods Endothelial cells in culture were exposed to sera samples collected from patients with CKD: i) stages 4-5 not on dialysis (PreD), ii) on maintenance hemodialysis (HD), and iii) peritoneal dialysis (PD). Changes in TLR4 and ICAM-1 expression, reactive oxygen species (ROS) production, and TLR4 signaling were explored. Assembly of NALP3 inflammasome components was also investigated.ResultsTLR4 was expressed at the cell surface and increased significantly in response to PreD, HD and PD sera, paralleling with the activation of the cell stress protein Akt and the inflammation related transcription factor NFκB, with elevated surface ICAM-1 expression and ROS production. TLR4 blockade partially decreased these effects. Exposure of cells to uremic sera induced assembly of NALP3 components, with caspase-1 activation, especially in response to HD and PD sera.ConclusionsTLR4 and NALP3 inflammasome, crucial elements of innate immunity, contribute to the development and perpetuation of endothelial dysfunction in response to the uremic toxicity. These mechanisms constitute potential therapeutic targets to improve endothelial dysfunction and to reduce the increased cardiovascular risk in CKD.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 12/2014;
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    ABSTRACT: A common challenge of scientific research is an inability to randomly assign subjects to a treatment that varies on only one variable. The inability to randomly assign variation on a single treatment variable necessarily limits the strength of causal inferences made from the data, one of the central goals of scientific analysis. Herein, we describe packet randomization experiments (PREs), an experimental design that improves the internal validity of observational studies by eliminating a class of observed and unobserved potential confounders. We introduce this design as an intermediary between purely observational studies and true randomized trials. We then discuss the inferential properties of PRE design and describe its application to different phenomena, including obesity, breastfeeding, and parabiosis. Finally, we describe a situation in which confounders uncontrolled by packet randomization can be asymptotically controlled for by conditioning on certain covariates. The application of this design will improve decisions about clinical, public health, and policy actions insofar as it offers researchers new insight into cause and effect relationships among variables.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 12/2014;
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    ABSTRACT: While the randomized clinical trial is considered to provide the highest level of evidence in clinical medicine, its superiority to other study designs in the context of prevention studies is debated. The purpose of this review was (i) to gather evidence about challenges facing both randomized controlled trials and observational designs for the conduct of population-based chronic disease prevention interventions and (ii) to consider the suitability of recently proposed hybrid designs for population-based prevention intervention studies.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background During the progression of the metabolic syndrome (MetS), cardiovascular diseases (CVD) appear clinically in many individuals and cause death. As a result, it is essential to set-up an optimal animal model to study the mechanism of MetS leading to CVD. SIRT1 and AMPK are the master regulators of lipid and carbohydrate metabolism. The objective of this study was to establish a miniature pig model of Western diet-induced MetS and investigate the role of SIRT1/AMPK during MetS development.Methods Five-month-old Lee-Sung (LS) and Lanyu (LY) minipigs were each randomly assigned to 2 groups: control diet (C) and Western diet (W), in a 6-month experimental period.ResultsWestern diet caused obesity in both minipig models. Compared with the CLS pigs, WLS pigs exhibited hypercholesterolemia. However, WLY pigs maintained a similar plasma lipid profile to the CLY pigs. Western diet caused a lower antioxidant capacity in the liver of both pig models. WLS pigs had higher triglyceride accumulation in the liver than CLS pigs, whereas WLY and CLY pigs had similar hepatic triglyceride accumulation. Compared with CLS pigs, WLS pigs had a lower hepatic SIRT1 expression, whereas WLY pigs had a higher expression of AMPK, FOXO1 and SIRT1 than CLY pigs.Conclusion Long-term feeding of the Western diet to Lee-Sung miniature pigs not only caused obesity but also induced MetS and fatty liver, whereas, Western diet induced obesity in Lanyu pigs without metabolic dysfunctions. SIRT1/AMPK and their downstream pathways might be one of the possible regulators for pathological obesity in Lee-Sung pigs.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background Although there is no direct evidence, it is generally believed that bed rest shifts the hemostatic system towards hypercoagulability; thus, immobilized patients are commonly treated with anticoagulants. We, therefore, aimed to investigate whether long-term bed rest actually leads to an elevated risk for thromboembolic events.Materials and methodsEleven healthy men were enrolled in our study (bed rest campaign in MEDES Clinique d'Investigation, Toulouse, France). Besides various standard laboratory methods, we used calibrated automated thrombography (CAT) and thrombelastometry (TEM). Activation of samples with minute amounts of relipidated tissue factor allowed sensitive detection of hyper- or hypocoagulable states.ResultsCAT and TEM values were not indicative of bed rest-induced hypercoagulability. On the contrary, several parameters were indicative of a tendency towards a hypocoagulable state. Peak and thrombin formation velocity (VELINDEX) were significantly decreased during bed rest compared to baseline. CTs were significantly increased and alpha angles were significantly decreased, indicating attenuated clot formation. Moreover, F1+2 and TAT values were significantly decreased during bed rest, indicating suppressed coagulation activation. FVII plasma levels were also significantly decreased during the first week of bed rest.Conclusions Our data indicate that the re-ambulation period is associated with a tendency towards hypercoagulability: ttPeak and StartTail were significantly shorter, Peak and VELINDEX were significantly higher compared to baseline. Moreover, plasma levels of F1+2, TAT, FVII, and FVIII were significantly higher compared to baseline. The results from our study suggest that bed rest by itself is not associated with hypercoagulable states in healthy subjects.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Recent trends in health care financing and delivery is increasingly generating situations where interests of physicians and patients may not necessarily align. As a result, each party is incentivized to act strategically according to their best interest. This situation can be best approached using game theory precepts. When both doctor and patient act according to their individual strategic interests, which are not aligned, both “players” are worse off. We argue that everyone would be better off if the current health “game” structure is changed to better align doctors’ and patients’ interests while rebuilding trust in the medical profession. Instead of competition, society should incentivize alignment of interests of doctors and patients. When the payoffs of different players are similar, the game theory conflict does not apply. Moreover, selection of rational strategies would be facilitated by improvements in the evidence base of medicine (unbiased knowledge of the probabilities of outcomes with different treatment options) and more accurate knowledge of the patient's and physician's values including those of regret, guilt, and frustration that dominate health care decision-making but are rarely explicitly acknowledged.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Chronic inflammatory diseases and systemic autoimmune conditions can result in the development of inflammatory vascular disease (IVD). The inflammatory response in the vascular bed involves several partners including pro-inflammatory cells (macrophages, lymphocytes, monocytes and neutrophils), as well as vascular smooth muscle cells, extracellular matrix components, and endothelial cells [1]. The latter play an important role since vascular injury can be initiated by their increased activation, increased expression of adhesion molecules and recruitment of pro-inflammatory cells [2-4].This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: The concept of axial Spondyloarthritis (axSpA) includes patients with non-radiographic axSpA and ankylosing spondylitis (AS). Inflammatory and chronic/structural changes of the sacroiliac joints and the spine are pathognomonic in patients who are diagnosed with axSpA. In the last years, the evaluation of the natural course of axSpA has been in the focus of research, especially with respect to the relationship between inflammation or postinflammatory changes (detected by magnetic resonance imaging (MRI)) and bone formation (detected by conventional radiographs).Based on the analysis of spinal MRI data, development of new syndesmophytes is directly associated with the parallel occurrence of inflammatory and postinflammatory (fatty) changes in the edges of the vertebral bodies. In contrast, vertebral edges that show only inflammation but no transformation into fatty lesions show a decreased relative risk for development of new bone formation over time.These data are crucial in the understanding of the long-term clinical course of patients with axSpA in daily practice. According to these results, it becomes obvious that anti-inflammatory treatment, especially by using tumor-necrosis-factor alpha (TNFa)-blockers, has the best effect on the radiographic outcomes when it is started in an early disease stage, where only inflammation is driving the disease activity and where structural, postinflammatory changes have not yet occurred.An inhibitory effect on radiographic progression had not been demonstrated during the first 2 years of continuous anti-TNFa treatment, however, very recently first studies reported a decreased rate of radiographic progression when patients were continuously treated with TNFa-blockers for a time period of ≥4 years.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background Angiopoietin-1 (Ang-1) is an essential mediator of angiogenesis by establishing vascular integrity, whereas angiopoietin-2 (Ang-2) acts as its natural inhibitor.Objective We aimed to determine the levels of angiopoietins in sputum supernatants of patients with optimally treated asthma and to investigate whether smoking represents a significant covariate on the above possible processes.Methods Eighty-seven patients with asthma (42 smokers) and 28 healthy subjects (14 smokers) were studied. All subjects underwent lung function tests, bronchial hyperresponsiveness assessment and sputum induction for cell count identification and measurement of Ang-1, Ang-2, VEGF, TGF-β1, MMP-2, IL-13, ECP, and IL-8 in supernatants. Airway vascular permeability (AVP) index was also assessed.ResultsAng-1 (ng/ml) levels were significantly higher in patients with asthma compared to normal subjects. Smoking significantly increased Ang-1 levels [median, interquartile ranges 24(13-37) in smoking asthmatics vs. 10 (7-14) in non smoking asthmatics vs. 5.3(3.7-6.5) and 4.6 (3.8-5.7) in healthy smokers and non smokers respectively, p<0.001]. Similar results were observed for Ang-2 (pg/ml) [168 (132-203) vs 124 (82-152) vs 94(78-113) vs 100 (96-108) respectively, p<0.001]. Regression analysis in the whole study population showed a significant negative association for Ang-1 with AVP index, and MMP-2. Smoking was a significant covariate for both Ang-1& Ang-2 in asthmatic patients.Conclusions Ang-1 & Ang-2 levels are up regulated in patients with optimally treated asthma. Our data support a possible role for smoking in the angiogenetic process in asthma.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: BackgroundA highly polymorphic Cytosine-Adenosine (CA) repeat sequence microsatellite has been identified in the promoter region of IGF1 gene. Several studies investigated the relationship between IGF1-(CA)n polymorphism and IGF1 levels, with conflicting results. Aim of this study was to investigate the influence of this polymorphism on clinical and biochemical characteristics of acromegalic patients.Methods Eighty-eight acromegalic patients and 104 normal subjects were included in the study. Blood DNA was extracted and analyzed by microsatellite technique using capillary electrophoresis. Patients and controls were subdivided in 19/19 (homozygous for the (CA)19 allele), 19/X (heterozygous for the (CA)19 allele) and X/X (any other genotype).ResultsThe genotype frequency was significantly different between patients and controls, the proportion of 19/19 being lower (28.4% vs 50.0%) and 19/X and X/X higher in acromegalic patients than in controls (P = 0.004). There were no significant differences in age, gender, basal and nadir GH, IGF1-SDS, tumor size, metabolic parameters, outcome, and treatment among the three groups. The different frequency of genotypes in acromegalic patients vs controls, as well as the lack of relationship between IGF1-(CA)n polymorphism and clinical and biochemical data in acromegalic patients, was confirmed by using an additional alternative genotyping considering (CA)19 and (CA)20 homozygotes and heterozygotes vs alleles with more than 19/20 repeats or less.Conclusions Our results do not support the hypothesis that IGF-(CA)n alleles may have a significant role in determining clinical, biochemical and outcome of patients with acromegaly. The possible role of IGF1 polymorphism on susceptibility to acromegaly remains to be investigated.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background Acotiamide is a first-in-class drug that is used to treat functional dyspepsia. It is considered that acotiamide acts as an antagonist on muscarinic autoreceptors in the enteric nervous system and inhibits acetylcholinesterase activity. We examined the effect of acotiamide on gastric emptying in healthy adult humans.Materials and methodsTwelve healthy adult males were enrolled in this double-blind crossover study. Acotiamide or placebo was administered orally in the 12 subjects 30 minutes before ingestion of a nutritional liquid meal (400Kcal/400mL). Six of the 12 participants took 100mg of acotiamide or placebo, and 6 of the 12 participants took 300 mg of acotiamide or placebo in a double-blind crossover fashion. All subjects underwent measurement of gastric emptying by the 13C breath test.ResultsAfter the meal with placebo was ingested, the %dose/h curve ascended. The %dose/h curve after a meal with 100mg or 300 mg of acotiamide ascended in an identical manner compared with the results with placebo. No significant differences were observed at any studied time point, and there were no significant changes in gastric emptying parameters (gastric emptying coefficient, t 1/2 ex and t lag ex).ConclusionsA single administration of 100mg or 300mg of acotiamide did not affect gastric emptying after a liquid meal in healthy adult humans. Acotiamide has profound effects on restoring delayed gastric emptying and impaired accommodation in patients with FD but may have no effect on gastric emptying in healthy subjects. Such pharmacological actions have not been observed in previous gastroprokinetic studies.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Estrogen is an important risk factor for cholesterol cholelithiasis not only in women of childbearing age taking oral contraceptives and postmenopausal women undergoing hormone replacement therapy, but also in male patients receiving estrogen therapy for prostatic cancer. In women, hormonal changes occurring during pregnancy markedly increase the risk of developing gallstones. We investigated whether the potent cholesterol absorption inhibitor ezetimibe could prevent the formation of estrogen-induced cholesterol gallstones in mice.
    European Journal of Clinical Investigation 10/2014;