It is noteworthy that many deregulated genes were common to 20 μM

It is noteworthy that many deregulated genes were common to 20 μM amiodarone after 24-hour BAY 80-6946 molecular weight and 14-day treatments and to 100 μM tetracycline after 24-hour treatment. Two genes involved in fatty acid transport were up-regulated, SLC27A4 by both drugs and FABP1 by tetracycline after repeat treatments. Only one gene involved in mitochondrial biogenesis, PPARGC1A, was overexpressed by both amiodarone and tetracycline. By contrast, several genes involved in de novo lipogenesis were modulated by the two

drugs. Transcripts of SREBP1, THRSP, ACLY, FASN, and SCD1 were significantly augmented after 24-hour and/or 14-day treatments by amiodarone. SREBP1 and PPARG were also up-regulated, whereas THRSP was down-regulated by 100 μM tetracycline after 24-hour treatment. MLN0128 in vivo However, THRSP was overexpressed after 14-day exposure to 10 μM tetracycline. Expression of genes involved in cholesterol metabolism was also altered; thus, transcript levels of LSS were increased after 24-hour amiodarone and 14-day tetracycline treatments. In addition, SOAT1 and LPIN1 were induced by 20 μM amiodarone after both short- and long-term treatments.

Moreover, genes involved in the formation of lipid droplets, particularly PLIN4 and ADFP, were overexpressed by high concentrations of both drugs, regardless of the duration of treatment. In addition, LPL as well as GDPD3 and ASML3A, two genes involved in phospholipids degradation, were up-regulated after long-term exposure to amiodarone. Finally, the two test CYP genes were also Miconazole modulated: transcripts of CYP2E1 were decreased by both drugs, whereas those of CYP3A4 were induced only by amiodarone. No changes were noticed in ALB or ALDB transcripts regardless of the drug treatment. Comparison with oleic acid–overloaded HepaRG cells revealed that, as observed with the two drugs, genes involved in the formation of lipid droplets (ADFP and PLIN4) were up-regulated by 500 μM oleic acid at the two time points. However,

genes involved in de novo lipogenesis were markedly (FASN, THRSP) or slightly (SCD1) down-regulated, whereas CPT1A involved in FAO was increased. In addition, CYP3A4 transcripts were reduced after 24 hours and CYP2E1 levels were increased after 14 days of oleic acid overload. ALDB transcripts were also decreased after repeat oleic acid exposure. Importantly, the expression of several genes was also analyzed at the protein level by way of western blotting (Fig. 6). For all of them (PPARG, ADFP, CYP2E1, and CYP3A4), changes in protein content followed messenger RNA (mRNA) modifications after treatment with either drug or oleic acid. Liver steatosis is characterized by excessive accumulation of neutral lipids, mainly TG, into intracytoplasmic macrovesicles and microvesicles that are induced by various factors, including several drugs.

But, recent studies revealed that more stringent normal AST and A

But, recent studies revealed that more stringent normal AST and ALT levels are needed. We investigated the normal range of serum AST and ALT levels of all ages in Korea. Methods: We used the data from the fifth Korea National Health and Nutrition Examination Survey (KNHANES V, 2010–2012). The exclusion criteria were history of chronic liver disease including hepatitis B infection, hepatitis C infection, heavy alcohol drinking (>50 g/day for male and >30 g/day for female), liver cirrhosis, hepatocellular carcinoma, Selumetinib purchase and obesity (body mass index >25 kg/m2).

Results: A total number of 13246 (male 5495, female 7751) participants aged 10 years or older were analyzed. The overall upper limit of normal AST and ALT levels (95th percentile) were 32 IU/ml (29 IU/ml for females and 36 IU/ml for males) and 35 IU/ml (28 IU/ml for females and 41 IU/ml for males). According to the age, the average of AST and ALT levels were increased. The average of AST levels were peaked in the 7th decade and the ALT levels were in GS-1101 price the 6th decade, and since then were decreased. Conclusion: The upper limit of normal AST and ALT levels were different according to the sex

(AST/ALT, 29/28 IU/ml for females and 36/41 IU/ml for males) and age. The two factors are the points to be specially considered in making the new normal range of serum AST and ALT levels. Key Word(s): 1. alanine aminotransferase; 2. aspartate aminotransferase; 3. normal Presenting Author: CHOL KYOON CHO Additional Authors: CHOONG YOUNG KIM, EUN KYU PARK, HEE JOON KIM, HYUN JONG KIM, YANG SEOK KOH, JIN SHICK SEOUNG Corresponding Author: CHOL KYOON CHO Affiliations: Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Saint Carollo Clomifene Hospital Objective: microRNAs (miRNAs) are endogenous non-coding 21–23 nucleotide RNAs that are

involved in post-transcriptional regulation and they control various cellular processes, one of which is tumorigenesis. miRNAs were reported to be implicated in the pathogenesis of hepatocellular carcinoma(HCC) and the aim of this study is to evaluate the role of miRNAs in the development of HCC. Methods: To find yet-to-be-identified miRNAs associated with HCC tumorigenesis, we carried out miRNA microarray analysis with miRNAs extracted from normal and HCC liver tissues resected from the same patients. Of the miRNAs showing significantly different expression levels between normal and HCC liver tissues, we focused on miR-128. The difference in expression levels of miR-128 was verified by real-time PCR.

The operation also led to a marked decrease in type IV collagen 7

The operation also led to a marked decrease in type IV collagen 7s domain and des-y-carboxy prothrombin. In addition, B-RTO significantly decreased homeostasis model assessment (HOMA) of IR without a statistical decline of HOMA of p-cell function, suggesting a pronounced recovery from IR. The 75g oral glucose tolerance test (75-OGTT) revealed that occlusion of PSS reduced both fasting immunoreactive insulin (IRI) levels and the area under the curve for IRI, suggesting amelioration

of hyperinsulinemia in the fasting state Temsirolimus concentration and attenuation of the excessive insulin response to a glucose load. However, no significant change in preprandial or postprandial plasma glucose levels was observed. Furthermore, according to the criteria of the American Diabetes Association, B-RTO improved a 75-OGTT profile in 58.3% of patients who had impaired glucose tolerance or diabetes mellitus before the procedure. Preoperative factors statistically associated with an improvement in H〇MA-IR by B-RTO were sex=male, age<70 years, body

mass index<25, etiology=HCV, C-P class=A, and feeding vein of GV=Ieft gastric vein. Conclusions: Shunt occlusion attenuates IRrelated hyperinsulinemia through increased portal venous flow, promoted liver function, and conseguent augmented hepatic insulin clearance in cirrhotic patients with PH. Excessive insulin response and sustained hyperglycemia after meals are reportedly risk factors for both hepatic fibrosis and hepatocarcinogenesis, and thus B-RTO may be beneficial

for therapeutic management of patients with LC. Disclosures: The following people have nothing to disclose: this website Tsuyoshi Ishikawa, Takashi Matsuda, Takuya Iwamoto, Shuji Terai, Isao Sakaida [Background and Aim] Spleen stiffness (SS) can be easily measured using virtual touch guantification (VTQ), and it is expected to be important in identifying cirrhotic patients with esophageal varices (EVs). Portosystemic shunts (PSSs), which were developed to treat portal hypertension, can influence SS. However, the significance of SS for the prediction of EVs considering PSSs has not been well documented. next The aim of the present study was to determine the predictive value of SS for the presence and severity of EVs. [Patients and Methods] Between June 2008 and May 2013, 981 patients underwent liver stiffness measurement, and data on SS, EVs, and PSSs were available for 143 patients with chronic liver disease (hepatitis C virus, 86; hepatitis B virus, 19; alcoholic liver disease, 14; autoimmune hepatitis, 9; nonalcoholic steatohepatitis, 6; unknown, 9). VTQ was performed using a Siemens Acuson S2000. EVs evaluated using upper endoscopy were classified into the following 3 grades: F1, small, straight, disappearing on insufflation; F2, moderately sized, tortuous, occupying less than one-third of the lumen; and F3, large, coiled, occupying more than one-third of the lumen.

4% clinical response) and 77% for CD patients (74% remission, 3 2

4% clinical response) and 77% for CD patients (74% remission, 3.2% clinical response). Sakata et al.33 has conducted a small prospective randomized trial to compare the clinical efficiency for active selleck screening library UC between LCAP and GMA;

however, they could not detect any significant difference between them. Therapeutic mechanism of GMA for UC.  The therapeutic mechanism of GMA for UC can be judged from the following background. In patients with active IBD, peripheral blood granulocyte and monocytes/macrophage levels are elevated, and cells show activation behavior and increased survival time.34–39 As these leukocytes are a major source of inflammatory cytokines,40,41 the level of neutrophil infiltration into the mucosal tissue in patients with active IBD has been directly related to the severity of intestinal inflammation and clinical relapse.42,43 Adacolumn has been developed to “tame the exuberant immune system” in patients in whom an overactive immune system, namely elevated peripheral blood neutrophils, is associated with disease progression.34 However, interestingly, the observed clinical efficacy cannot be fully explained by the KU 57788 effects of the procedure on peripheral blood leukocytes per se. We have proven that peripheral Treg (CD25HighCD4+ T-cells) expression,

which has been suppressed in active UC compared with healthy controls, was significantly increased after a single GMA session.44 The increase in CD25High+CD4+ regulatory T-cells after GMA should contribute to improved

immune function of the patient. Moreover, we have proven that the number of CD4+/FoxP3+ mucosal Treg in GMA responders decreased significantly after the fifth GMA session compared with the baseline level.45 It seems possible, therefore, that GMA might impact the circulating as well as the mucosal levels of Tregs. Likewise, several other investigators have reported favorable immunological observations associated with GMA.23,46,47 Reactivation of cytomegalovirus (CMV) infection has often exacerbated UC refractory to immunosuppressive therapies. Yoshino et al. reported the clinical effect of GMA therapy for UC patients with concomitant mucosal CMV infection, and they have proposed that GMA might be a safe and effective treatment for UC patients positive for CMV because Dapagliflozin the procedure does not induce CMV reactivation.48 Optimization of processing conditions.  Clinical effectiveness of LCAP and GMA should be regulated by blood volume for the procedure (Pv), procedure time, and procedure frequency (Qf). Pv can be calculated as: Pv = Blood flow speed (Qb) × Procedure time (Qt). Basically, slower Qb should reinforce the leukocyte removal performance of the column. Cellsorba, the LCAP column, is unsuitable for proceeding under 20 mL/min of slow Qb conditions since the platelet removal characteristics of the column could cause formation of thromboses in the Cellsorba column.

It has been reported to facilitate the exchange of phospholipids,

It has been reported to facilitate the exchange of phospholipids, unesterified cholesterol, diacylglycerides, vitamin E

(tocopherols), and lipopolysaccharides (LPS) between plasma lipoproteins, with functional consequences in vascular biology, brain physiology, reproductive biology, inflammation, and innate immunity.1 In plasma, PLTP is mainly transported by high-density lipoproteins (HDLs), and previous studies of PLTP focused on HDL. Earlier studies in mouse models provided direct support for an HDL-orientated function of PLTP, that is, with higher2 or lower3-5 levels of HDL cholesterol in transgenic mice overexpressing human PLTP and lower HDL cholesterol levels in PLTP-deficient mice.6 In fact, there is growing evidence that PLTP plays a pivotal role in HDL-mediated reverse cholesterol Bortezomib in vivo transport because of its ability (1) to generate nascent, preβ-HDL (i.e., the primary acceptors of cell-derived cholesterol), which dissociates from the surface of very-low-density lipoproteins (VLDLs) during lipolysis,7 (2) to form both preβ-HDL and large HDL2-like particles through intra-HDL remodeling,8-10 and (3) to facilitate cholesterol and phospholipid efflux from peripheral cells through an ABCA1-dependent pathway in the initiating step of reverse cholesterol

transport11-13 (see Fig. this website 1). Recent genome-wide association studies brought evidence of the association of higher PLTP transcript levels in the liver with higher HDL cholesterol concentrations.14 However, beyond PLTP gene-expression levels, the consequences of plasma PLTP activity might be highly dependent on the metabolic context and on the plasma lipoprotein profile. VDA chemical For instance, plasma PLTP activity was found

to be inversely associated with HDL-cholesterol levels, but positively associated with apolipoprotein B (apoB) levels in a cohort of Chinese patients who underwent diagnostic coronary angiography.15 HDL; high-density lipprotein; LPS, lipopolysaccharides; PLTP, phospholipid transfer protein; VLDL, very-low-density lipoprotein. In wild-type mice, most of the plasma cholesterol is transported in the HDL fraction, with smaller amounts of cholesterol in VLDL and barely detectable amounts of cholesterol in the low-density lipoprotein (LDL) fraction. It is a major limitation of the mouse model, because plasma lipoprotein profiles in humans and rabbits normally display prominent non-HDL, apoB-containing lipoproteins. Interestingly, mice genetically engineered to have a human-like plasma lipoprotein profile (in particular, with human apoB synthesis in the liver and similar plasma apoB levels to those in humans) and expressing a PLTP-deficiency trait revealed a new, unexpected role of PLTP: the ability to increase both the liver production rate and plasma levels of apoB-containing lipoproteins.

The author is grateful to Professors Sven Björkman, Peter Collins

The author is grateful to Professors Sven Björkman, Peter Collins and Kathelijn Fischer for their helpful suggestions during BGJ398 preparation of this manuscript. The author stated that he had no interests which might be perceived as posing a conflict or bias. “
“The administration of therapeutic factor VIII (FVIII) to treat or

prevent haemorrhages in haemophilia A patients results, in up to 30% of the cases, in the development of inhibitory anti-FVIII antibodies. Much debate has taken place on the relevance of the nature of the FVIII product as a risk factor for inhibitor development. Thus, the plasma-derived vs. recombinant origin, the second vs. third generation of the product, or the presence of the B domain have been controversially evoked. A few years ago, Refacto®

AF, a third-generation recombinant B domain-deleted FVIII was marketed. The aim of this study was to compare the immunogenicity of Refacto® AF to that of two recombinant full-length FVIII products: Helixate® and Advate®. For the three recombinant FVIII products, we compared the binding to the mannose-sensitive endocytic receptor CD206, the dose-dependent endocytosis by immature monocyte-derived dendritic cells (DCs), the activation by FVIII-loaded DCs of a FVIII-specific HLA-DRB1*0101-restricted Bortezomib price mouse T-cell hybridoma and the induction of inhibitory anti-FVIII IgG in FVIII-deficient Janus kinase (JAK) mice. At elevated FVIII concentrations, Refacto® AF was less endocytosed than full-length recombinant products. At lower concentrations, however, Refacto® AF was endocytosed by DCs and activated T cells as well

as Helixate® and Advate®. The levels of inhibitory anti-FVIII IgG induced by Refacto® AF in FVIII-deficient mice were lower or equal to that induced by Helixate® and Advate® respectively. The predicted immunogenicity of Refacto® AF is identical to or lower than that of the two recombinant full-length FVIII products available on the French market. “
“Summary.  Many diseases and injuries can impair joint mobility. Normal reference values are needed to determine extent of impairment to assess and monitor joint motion. There is very little published data describing normal joint range of motion (ROM) for healthy men and women across a wide span of ages. We enrolled male and female subjects aged between 2 and 69 years who were free from conditions that could potentially limit joint mobility for the study. Nine licensed physical therapists used universal goniometers to determine passive joint motion bilaterally of elbow flexion, extension, supination and pronation, shoulder flexion, hip flexion and extension, knee flexion and extension, and ankle dorsiflexion and plantarflexion. Descriptive statistics were calculated for male and female subjects in four age groups: 2–8, 9–19, 20–44 and 45–69 years.

In this study, individual plants of the F3 population derived fro

In this study, individual plants of the F3 population derived from Pongsu Seribu 2 and Mahsuri were used for pathogenesis assays and inheritance studies of blast resistance. The study was performed with two of the most virulent Malaysian M. grisea pathotypes: P7.2 and P5.0. For blast

screening, plants were scored based on the IRRI Standard Evaluation System (SES). F3 populations showed a segregation ratio of 3R:1S for pathotype P7.2, indicating that resistance to this pathotype is likely controlled by a single nuclear gene. Chi-square analysis showed that the F3 families segregated in a 15R:1S ratio for pathotype P5.0. Therefore, locus interactions or epitasis of blast resistance occur against pathotype P5.0 in the F3 population derived from Pongsu Seribu Saracatinib cell line 2 and Mahsuri. This can be explained by the presence of two independent dominant genes that when present simultaneously, provide resistance to the M. gresia pathotype P5.0. These results indicated that blast resistance in rice is due to the combined selleck screening library effects of multiple loci with major and minor effects. The genetic data generated here will be useful in the breeding of local cultivars

for resistance to field blast. The methodology reported here will facilitate the mapping of genes and quantitative trait loci (QTLs) underlying fantofarone the blast resistance trait. “
“A total

of 35 isolates of Fusarium oxysporum f.sp. eustomae obtained from diseased Eustoma grandiflorum plants in northern Italy, showing typical Fusarium wilt symptoms, were analysed for their genetic variability and molecular identification. Genetic diversity of the isolates was studied by using random amplified polymorphic DNA (RAPD). This analysis clustered the isolates into three groups at a genetic similarity of 69%. Sequence analysis of RAPD fragments led to the design of a pair of specific primers that amplify a 505-bp SCAR (sequence characterized amplified region) marker (SCAR505) which was used to rapidly detect F. oxysporum f.sp. eustomae on Eustoma grandiflorum plants. In a temperature-controlled chamber, detection of the pathogen by PCR was 100% successful in root and stem samples of infected but still symptomless plants. The diagnostic procedure could be completed in 1 day and allowed rapid and reliable detection of the pathogen in asymptomatic plants in the early stages of disease development. “
“Among the Chili breeding lines from the Asian Vegetable Research Center, two were chosen for the screening of a larger selection of Cucumber mosaic virus (CMV) isolates, mainly from Asian countries. The chili line (VC246) showed a resistance against several CMV-isolates and was compared with chili line VC27a that was susceptible to CMV infection.

Poised to be the world’s second largest economy, China may develo

Poised to be the world’s second largest economy, China may develop more Westernized diseases through changes in living conditions, lifestyle, habits, diet, hygiene, and their associated effects on the intestinal microbiome

that may further drive this unprecedented increase of immune-mediated diseases. In summary, the incidence of IBD in Asia remains significantly lower than that in the West. However, we are now seeing a slow but steady increase in IBD incidence that mirrors early increases previously observed in the West. While the etiology and pathogenesis of IBD in Asian populations may be different to that observed in Caucasian populations with regard to both genetic[10-12] and environmental[13, 14] risk factors, these observations may not mitigate a potential looming IBD epidemic in Asia. Now that Zeng et al. have established a study ACP-196 clinical trial population in Guangdong province that can be used to accurately determine IBD incidence, it is essential that these investigators continue to perform incidence studies at intervals to track changes in IBD incidence over time. Such a sentinel site in mainland China will be vital in estimating the effect of IBD incidence changes across much of Asia. “
“The paired box 5 (PAX5) is a member of PAX transcription factors family involved

in the regulation of embryonic development. However, the role of PAX5 in carcinogenesis is largely unclear. We identified that PAX5 is involved in human cancer by methylation-sensitive representational difference analysis. We examined the biological RG 7204 functions and related molecular mechanisms of PAX5 in hepatocellular carcinoma (HCC). Promoter methylation of PAX5

was evaluated by methylation-specific polymerase chain reaction (PCR) and bisulfite genomic sequencing (BGS). The functions of ectopic PAX5 expression were determined by viability assay, colony formation, and cell cycle analyses, along with in vivo tumorigenicity assays. The PAX5 target signal pathway was identified by promoter luciferase assay, chromosome immunoprecipitation (ChIP), and pathway PCR array. PAX5 is expressed in normal human liver tissue, but silenced or down-regulated Sulfite dehydrogenase in 83% (10/12) of HCC cell lines. The mean expression level of PAX5 was significantly lower in primary HCCs as compared to their adjacent normal tissues (P < 0.0001). The promoter methylation contributes to the inactivation of PAX5. Restoring PAX5 expression in silenced HCC cell lines suppressed cell proliferation, induced apoptosis in vitro, and inhibited tumor growth in nude mice (P < 0.0001). The pathway luciferase reporter assay indicated that PAX5 activated p53 and p21 signaling. ChIP analysis demonstrated that PAX5 directly bound to the p53 promoter.

Liver function tests can serve as the basis for accurate decision

Liver function tests can serve as the basis for accurate decision-making regarding the need for liver transplantation in the setting of acute failure or in patients with chronic liver disease. The liver metabolic breath test relies on measuring exhaled 13C tagged methacetin, which is metabolized only by the liver. Measuring this liver-specific substrate by means of molecular correlation spectroscopy is a rapid, non-invasive method

for assessing liver function at the point-of-care. The 13C methacetin breath test (MBT) is a powerful tool to aid clinical hepatologists in bedside decision-making. Our recent findings regarding the ability of point-of-care 13C MBT to assess the hepatic functional reserve in Opaganib molecular weight patients with acute and chronic liver disease are reviewed along with suggested treatment algorithms for common liver disorders. “
“Beta-catenin plays important roles in liver physiology and hepatocarcinogenesis. While studying the role of β-catenin in diet-induced steatohepatitis, we recently found that liver-specific β-catenin knockout (KO) mice exhibit intrahepatic cholestasis. This study was undertaken to further characterize the role of β-catenin in biliary physiology. KO mice and wild-type (WT) littermates were fed standard chow or a diet supplemented with 0.5% cholic acid for 2 weeks. Chow-fed KO

mice had higher serum and hepatic total bile acid levels and lower bile flow rate than WT mice. Expression ABT-263 molecular weight levels of bile acid biosynthetic genes were lower and levels of major bile acid exporters were similar, which therefore could not explain the KO phenotype. Despite loss of the tight junction protein claudin-2, KO mice had preserved functional integrity of tight junctions. KO mice had bile canalicular morphologic abnormalities as evidenced by staining for F-actin and zona occludens 1. Electron microscopy revealed dilated and tortuous bile canaliculi in KO livers along with decreased canalicular and sinusoidal

microvilli. KO mice on a cholic acid diet had higher hepatic and serum bile acid levels, bile ductular reaction, increased Phospholipase D1 pericellular fibrosis, and dilated, misshapen bile canaliculi. Compensatory changes in expression levels of several bile acid transporters and regulatory genes were found in KO livers. Conclusion: Liver-specific loss of β-catenin leads to defective bile canalicular morphology, bile secretory defect, and intrahepatic cholestasis. Thus, our results establish a critical role for β-catenin in biliary physiology. (HEPATOLOGY 2010) Beta-catenin, the primary effector of the canonical Wnt signaling pathway, plays critical roles in hepatocarcinogenesis and liver development.1-6 However, its role in adult liver physiology is not well understood. Cytoplasmic levels and localization of β-catenin are tightly regulated (reviewed in MacDonald et al.7). In the absence of Wnt signaling, β-catenin is bound in the cytoplasm by a multiprotein complex.

Since the majority of university researchers are not subject to t

Since the majority of university researchers are not subject to the rules of conduct of a professional body, their name will only routinely enter the public domain if a paper is formally retracted, and even then the reasons Epigenetics Compound Library supplier for the retraction are not always evident. The danger of this practice is that it can allow serial offenders to move from university to university largely unimpeded. Professor Anthony Segal at University College London (UCL) made this point recently when one of his postdoctoral researchers had been subject to allegations of research misconduct at two other leading universities before

coming to UCL;[29] his work with Professor Segal was eventually found to be wanting, and a high-profile paper was formally retracted from Nature. Ways must be found to allow institutions to exchange information of this nature without fear of litigation. A similar situation has occurred in the case of Professor Melendez, where investigation of allegations of research misconduct have been conducted at three universities: two in the UK, University of Liverpool and the University of Glasgow, and at the National University of Singapore. So far, these investigations have resulted in 12 retractions from leading journals, but it is reported that the universities

felt unable to communicate freely about the investigations even though there must have been some overlap LY2835219 as Melendez had worked in all three institutions.[22] Professor Segal has suggested that there should be a register for laboratory scientists and that maintenance of registration would be an indication of a researcher’s integrity.[29] The concept of the “research passport” has already been entertained and might go some way to affirm the importance for a researcher to have a clean record with, say, a relevant professional body or learned society. For medical and dental researchers in the UK, for example, a finding of serious research misconduct could put their registration in jeopardy and could limit C59 cell line the right to work in the UK as a practitioner.

Might it be reasonable to put similar stipulations on other researchers who currently escape this sanction by not being subject to the regulations of a professional regulator? Finally, I would suggest that we need more research to understand better the motivations of those that commit misconduct and why they feel able to go against the high-level principles that are now accepted to be intrinsic to the integrity of research across the disciplines. How important is the notion that research misconduct is worth the risk because the chances of getting caught appear to be slight? In a fascinating article in The New York Times Magazine (April 28, 2013) by Yudhijit Battacharjee, the story behind the 55 retractions by the Dutch social psychologist, Professor Diederik Stapel, is revealed in a face-to-face interview.