We also similarly tested for differences in the ability of darts to obtain a tissue sample among the three dart types. In autumn

2010, we darted polar bears on the Alaska coast during two sampling efforts (Fig. 1): September (9 d); and October (9 d). We used PD darts to sample 30 polar bears (Fig. 3a) and PC darts to sample 18 polar bears (Fig. 3b). Two PD darts only collected hair. Three (10%) of the bears that we sampled using PD darts were darted twice because the first dart broke on impact with the bear, and one (3%) of the bears we sampled using PD darts was darted twice because the first dart failed to collect a sample. Except for missed shots, we successfully recovered all fired darts. Ceritinib mouse Excluding the two darts that only collected hair that could not be genotyped, tissue samples (n = 46) were 100% effective in genotyping and sex determination of individuals. Genetic analysis revealed that none of the bears were sampled more than once in the same sampling effort whether darted MK-2206 price with a PD or PC dart (neither type had a marking mechanism). Darting times averaged 6.8 min per bear (95% CI: 5.9–7.6 min, n = 48). In spring 2011, we darted polar bears on the sea-ice (20 d, Fig. 1). We used PC marking darts to sample and mark

41 bears (Fig. 1). These darts generally collected a small piece of skin and adipose tissue, as well as hair (Fig. 3b). Except for missed shots, we successfully recovered all fired darts. We re-darted three bears (7%) because the first dart failed to collect a sample. These samples were 100% effective in identifying sex and individual genetic identity. Genetic results indicated that we sampled one bear on two occasions. Darting times averaged 6.5 min per bear (95% CI: 5.4–7.6 min, n = 41). In autumn 2011, we darted polar bears on the Alaska coast during two sampling efforts (Fig. 1): August (6 d) and September (6 d). We used PX marking darts to sample and mark 35 bears (11 in the water and 24 on land, Fig. 3c) and PC marking darts to sample and mark

35 bears (all on land). Nine of the PX and five of the PC darts only collected a hair sample. Nine (26%) of the bears we sampled using PX darts were darted twice because the first dart failed to collect a sample. We were unable to recover three PX darts from the water because rough seas made it difficult to recover and/or selleck screening library spot the dart. Excluding darts that only collected hair, samples (n = 56) were 98% effective in genotyping individuals and identifying sex. Three of the 14 samples that only collected hair were sufficient enough to genotype 12 microsatellite loci. Genetic results indicated that two bears were sampled on two occasions and one bear was sampled on three occasions during the August sampling period, while one bear was sampled on two occasions during the September sampling period. Darting times averaged 4.2 min per bear (95% CI: 3.6–4.8 min, n = 70). We successfully quantified fatty acid profiles from all darts that collected adipose tissue (n = 45, Table 2).

This may be due to viral infections which influence both the immune system and liver function. Cholesterol levels (total cholesterol, HDL and LDL fraction) should be measured in patients who are at risk of developing CVD. If levels are elevated, treatment is indicated. As in the BMN 673 supplier general population,

being overweight is not an uncommon condition in PWH and one that is increasingly common with age. In 2001, 35% of adult Dutch PWH were overweight and 8% suffered from obesity (BMI >30 kg m−2) [17]. A high BMI is associated with a significant limitation in range of motion and with a greater chance of developing a target joint [18]. Obese PWH score lower in daily life activities compared to non-obese PWH [19]. In combination with the preexisting severe haemophiliac arthropathy, which affects activity, the BMI may increase further. High BMI is a risk factor for the development of diabetes mellitus (DM), atherosclerosis and CVD, and may further damage arthropathic joints. Therefore, regular physical activity should be advised which may be given as an individualized training programme. The prevalence of DM in PWH does not seem to be higher than in the general population, although studies are conflicting. XL184 mw Walsh et al. reported a prevalence of 24% in a cohort of PWH compared to 6.1% in control males [[20].]. However,

there have been no other studies published to confirm these findings. Glucose levels should be checked regularly, especially in obese patients. If indicated, subcutaneous injections

with insulin can be applied without bleeding complications. Although mortality from CVD is lower in PWH than in the general public, the numbers are increasing [21]. From morbidity studies it is known that CVD in PWH is not uncommon, especially not in patients with mild haemophilia, 6% of whom developed selleck products a myocardial infarction (MI) [22]. In this study, no MIs were observed in patients with severe haemophilia [22]. Research has shown that haemophilia does not protect against atherosclerosis, therefore, it is more likely that the final occlusive thrombus plays a major role in this observation [23]. Although evidence is still lacking, basically PWH should be treated in the same way as people without haemophilia. An anticoagulation therapy can be given in an individual tailored schedule and combined with coagulation therapy. Aspirin (80 mg) is well tolerated by patients with moderate and mild haemophilia with FVIII or FIX levels >5%. In PWH with clotting factor levels <1%, the risk of spontaneous bleeding is increased and in this group prophylaxis is indicated targeting trough levels of 1–5%. When aspirin is combined with clopidrogel, or when coumarin derivates are used, the risk of bleeding in PWH is substantially increased.

2E,F). These results implied that resistin diminished ATP levels through increasing the uncoupling effect and impairing the functions of TCA and ETC. Decrease in mitochondria content was correlated to changes in fat metabolism. Subsequently, mouse epididymal fat and liver were collected and analyzed. Histomorphological results indicated that there was no difference in weight and cell size of epididymal fat between the control and the resistin-administered groups (Fig. 3A); however, there were more, and larger, vacuoles in the hepatic cytoplasm

of the resistin-administered group (Fig. 3B). Furthermore, TAG levels were significantly higher in the resistin-administered group, compared to the control group (Fig. 3B). To understand the role of resistin in hepatic fat accumulation, HepG2 cells were cultured with FAs (as described above) and with or without 25 ng/mL of resistin 17-AAG price for 24 or 48

hours. Cells were then harvested to measure TAG and glycerol contents. Results SCH 900776 demonstrated that resistin increased TAG levels and decreased glycerol levels (Fig. 3C,D). The result also showed that resistin inhibited the activity of acyl-CoA (coenzyme A) dehydrogenase (CAD), which catalyzes the first reaction of FA β-oxidation (Fig. 3E). However, after 24 hours of treatment, resistin did not change the phosphorylation level of Akt (Ser473) (Fig. 3F). To clarify the signal transduction of resistin, the second messengers, cyclic adenosine monophosphate (cAMP) and cGMP, were measured. Resistin stimulated intracellular cAMP, but had no effect on cGMP (Fig. 4A). The cAMP-dependent protein kinase (PKA) inhibitor (H89) (50 nM) was added and was expected to block the effect of resistin, but the results indicated that inhibition did not occur (Supporting Fig. 1A). A higher concentration this website of H89 (5 μM) blocked the effect of resistin (Fig.

4B); however, at this concentration, it also inhibited protein kinase C (PKC) and cGMP-dependent protein kinase (PKG).20, 21 To distinguish the protein kinases involved in resistin action, the inhibitors, phloretin (a PKC inhibitor) and KT5823 (a PKG inhibitor), were both found to inhibit decreases observed in the mitochondria (Fig. 4C). Subsequently, to explore the upstream signal transduction of PKC, U73122 (a PLC inhibitor) was used, but could not block the effect of resistin (Supporting Fig. 1B). cGMP is a classic agonist for PKG, and cellular cGMP production is dependent on two kinds of guanylyl cyclases (GCs). The first is located on the plasma membrane and termed particulate guanylyl cyclase (pGC), whereas the second is located in the cytoplasm and termed soluble guanylyl cyclase (sGC).22 Neither BPIPP (a pGC inhibitor) nor NS2028 (an sGC inhibitor) could maintain mitochondrial content (Supporting Fig. 1C,D).

Functions of miRNAs have been characterized in the embryologic, physiologic and oncogenic process, but the role

of miRNAs in mediating tumor metastasis was addressed only recently and still absented in gastric cancer. Methods: With the human gastric cancer cell line subpopulations of elevated peritoneal metastatic activity and by means of microRNAs expression profile analysis, functional verification and clinical validation, we want to investigate the mechanism of gastric cancer PDGFR inhibitor peritoneal metastasis. Results: Three microRNAs marks and mediates gastric cancer metastasis to the peritonea, and most of them target metastasis related genes and are of previously unknown relevance to organ-specific metastatic behavior. MiR-181b promotes gastric cancer peritoneal metastasis

through suppression of ADAM metallopeptidase domain 11. MiR-223 regulates gastric cancer peritoneal metastasis through suppression of erythrocyte membrane protein band 4.1-like 3 and activated leukocyte cell adhesion molecule. MiR-136 inhibits gastric cancer peritoneal metastasis through suppression of homeobox C10. Conclusion: This study shows that the microRNAs that mediate gastric cancer specific metastasis to peritoneum. We proved the above results in vitro and in vivo. Our results indicate that microRNAs may serve as a novel therapeutic target for treating gastric cancer peritoneal metastasis. Key Word(s): 1. gastric cancer; 2. peritoneal; 3. metastasis; 4. miRNA; Presenting Author: JIANQIN KANG Additional Selleckchem DMXAA Authors: GUOHONG ZHAO, TAO LIN, SHANHONG TANG, GUANGHUI XU, SIJUN HU, QIAN BI, LIN XUE, CHANGCUN GUO, LI SUN, SHUANG HAN, YONGZHAN NIE, BIAOLUO WANG, SHUHUI LIANG, JIE DING, KAICHUN WU Corresponding Author: SHUHUI LIANG, JIE DING Affiliations: Fourth Military Medical University,

Xijing Hospital of Digestive Disease Objective: Multidrug resistance (MDR) remains a significant challenge click here to the clinical treatment of gastric cancer (GC). In our previous study, using a phage display approach combined with MTT assays, we screened a specific peptide GMBP1 (Gastric cancer MDR cell-specific binding peptide), ETAPLSTMLSPY, which could bind to the surface of GC MDR cells specifically and internalized into MDR cells compared with control cells SGC7901 and GES. However, the role of GMBP1 in GC MDR is not fully understood. The aim of this study was to investigate the role of GMBP1 in GC MDR, screen the receptor of GMBP1 and further explore the potential mechanisms of GMBP1 in the reversal of GC MDR. Methods: Immunocytochemistry staining assay was performed to observe the subcellular localization and the binding ability of GMBP1 to MDR cells. MTT, in vitro and in vivo drug sensitivity, flow cytometry and hoechst staining assays were used to detect the role of GMBP1 in GC MDR. Western blot, proteomics methods and siRNA experiments were used to screen and identify the receptors of GMBP1 in MDR cells.

Background.— Verapamil and lithium are the most widely used drugs in the prevention of CH attacks. Lithium is considered a second-line treatment in part because of its potentially severe adverse drug reactions (ADRs). Evidence for the efficacy of lithium in CH prevention is greater in chronic than in episodic patients. In addition, because of its narrow therapeutic window and ADRs (which can be significantly reduced

with proper periodical monitoring of blood levels), lithium is recommended only in chronic CH, when other drugs are ineffective or potentially harmful. Methods.— Our primary aim learn more was to determine whether lithium reduced the number of attacks per day (attack frequency). We compared attack frequency in 3 periods: run-in, the first, and the second week of lithium treatment. Responders were defined as patients showing at least a 50% reduction in attack frequency. Results.— Lithium response was evaluated in 26 patients. Treatment led to a significant reduction in attack frequency within 2 weeks Selleck Fer-1 in a percentage of 77% of responders and 23% of nonresponders. Responders and nonresponders did not differ in terms of demographic and clinical characteristics. Only 15% of patients experienced mild ADRs. Conclusion.— Our study provides additional evidence on the effectiveness of lithium in the prevention of episodic CH. It also shows the tolerability of lithium,

given the short duration of treatment and low dosage. “
“To identify possible clinical differences between male, premenopausal, and postmenopausal female patients with burning mouth symptoms. Burning mouth symptoms are known to occur predominantly in postmenopausal women. In some rare cases, however, such symptoms may also appear in men and younger premenopausal women. There is no information on the characteristics of male and premenopausal female patients with burning mouth symptoms. A total of 22 male patients (no age limit) and 19 relatively younger premenopausal female patients (age: ≤45 years)

with a burning sensation in the mouth without any visible selleckchem signs of oral mucosal diseases were included in the experimental groups. Sixty burning mouth patients (postmenopausal females, age: ≥50 years) without oral mucosal diseases were included as a typical older postmenopausal group for comparison. All individuals in the 3 groups were subjected to clinical evaluations including an interview, a comprehensive questionnaire, a simplified psychological evaluation (Symptom Checklist-90-Revision [SCL-90-R]), blood tests, and a measurement of salivary flow rate. The male group reported taste problems less commonly (40.9%, P = .009) and less severely (median visual analog scale [VAS] = 0.00, P = .004) than the postmenopausal group (73.3%, median VAS = 4.50). The younger premenopausal group complained of paresthesia more commonly (68.4%, P = .006) and more severely (median VAS = 0.50, P = .

Background.— Verapamil and lithium are the most widely used drugs in the prevention of CH attacks. Lithium is considered a second-line treatment in part because of its potentially severe adverse drug reactions (ADRs). Evidence for the efficacy of lithium in CH prevention is greater in chronic than in episodic patients. In addition, because of its narrow therapeutic window and ADRs (which can be significantly reduced

with proper periodical monitoring of blood levels), lithium is recommended only in chronic CH, when other drugs are ineffective or potentially harmful. Methods.— Our primary aim Opaganib purchase was to determine whether lithium reduced the number of attacks per day (attack frequency). We compared attack frequency in 3 periods: run-in, the first, and the second week of lithium treatment. Responders were defined as patients showing at least a 50% reduction in attack frequency. Results.— Lithium response was evaluated in 26 patients. Treatment led to a significant reduction in attack frequency within 2 weeks Fluorouracil concentration in a percentage of 77% of responders and 23% of nonresponders. Responders and nonresponders did not differ in terms of demographic and clinical characteristics. Only 15% of patients experienced mild ADRs. Conclusion.— Our study provides additional evidence on the effectiveness of lithium in the prevention of episodic CH. It also shows the tolerability of lithium,

given the short duration of treatment and low dosage. “
“To identify possible clinical differences between male, premenopausal, and postmenopausal female patients with burning mouth symptoms. Burning mouth symptoms are known to occur predominantly in postmenopausal women. In some rare cases, however, such symptoms may also appear in men and younger premenopausal women. There is no information on the characteristics of male and premenopausal female patients with burning mouth symptoms. A total of 22 male patients (no age limit) and 19 relatively younger premenopausal female patients (age: ≤45 years)

with a burning sensation in the mouth without any visible this website signs of oral mucosal diseases were included in the experimental groups. Sixty burning mouth patients (postmenopausal females, age: ≥50 years) without oral mucosal diseases were included as a typical older postmenopausal group for comparison. All individuals in the 3 groups were subjected to clinical evaluations including an interview, a comprehensive questionnaire, a simplified psychological evaluation (Symptom Checklist-90-Revision [SCL-90-R]), blood tests, and a measurement of salivary flow rate. The male group reported taste problems less commonly (40.9%, P = .009) and less severely (median visual analog scale [VAS] = 0.00, P = .004) than the postmenopausal group (73.3%, median VAS = 4.50). The younger premenopausal group complained of paresthesia more commonly (68.4%, P = .006) and more severely (median VAS = 0.50, P = .

On the basis of the latter SRT1720 solubility dmso observation, Watanabe hypothesized that CD4+ T cells are maintained outside the intestine as memory stem cells. Since spleen and lymph nodes were dispensable for the development of chronic colitis (JI 2007), he demonstrated that, CD4+ cells preferentially reside in bone marrow (BM) of colitic mice (Gastroenterology 2007, JI 2009).[3] Importantly, these

resident BM CD4+ memory T cells are closely associated with IL-7-producing stromal cells (Gastroenterology 2007). He also demonstrated using intrarectal administration of CD4+ T cells that CD4+ T cells constantly recirculate from LP to BM (Gastroenterology 2011).[4] All of these findings indicate that the IL-7/IL-7R signal is an important target for therapy of IBD, which is a novel strategy to deplete

pathogenic memory T cells. In addition, Dr Watanabe also clarified the role of co-stimulatory molecules such as CD86 (Gastroenterology 1999), B7-H1 (JI 2003), and ICOS (Gastroenterology 2003), cytokines such as IL-18 (Gastroenterology 2000), γδ T cells (PNAS 1999, Immunity 2000), B cells (Gastroenterology 2001, JI 2004) and regulatory T cells (JI 2003, JI 2004, JI 2007, JI 2009) for the pathogenesis of IBD. Dr Watanabe next turned his attention to colitis-associated carcinogenesis, because he recognized that colon colitic cancer incidence in Asia is likely to increase in line with the increase of ulcerative colitis. First, Dr Watanabe has identified the specific gene expression (Cancer Res. 1999) and gene mutations (Cancer Res. 2003) only in colitis-associated colon cancer, click here suggesting the Selumetinib mechanism of colitis-associated carcinogenesis is different from sporadic colon carcinogenesis. In further functional studies of carcinogenesis relevant to sporadic colorectal cancer, Dr Watanabe showed that aberrant Wnt signal directly suppressed the differentiation state of cancer to degrade the Atoh1 protein, which is the master gene for

the differentiation of intestinal epithelial cells (Gastroenterology 2007).[5] More importantly, Dr Watanabe discovered that Atoh1 protein is co-expressed with beta-catenin and that inflammatory cytokines modulate Atoh1 protein stabilization in crosstalk between cytokine signaling and Wnt signaling (J Biol Chem. 2008). Finally, Dr Watanabe has obtained evidence that co-localization with Atoh1 and beta-catenin induces not only the mucinous phenotype but also the ‘cancer stemness’ and chemo-resistance in colitis-associated carcinogenesis. These studies prove that Atoh1 is involved in the malignant potential of carcinogenesis, a finding that has therapeutic implications for colitis-associated cancer. In his recent research, Dr Watanabe has examined fundamental functions of intestinal stem cells, and how this impacts on regeneration of the intestinal mucosa.

This postmarketing surveillance study evaluated patient satisfaction before and after switching to the new Bio-Set reconstitution method. Napabucasin research buy Male children and adults

with haemophilia A were enrolled from nine European countries. A preference questionnaire was administered to patients after Bio-Set training and at the end of the observation period (≥20 exposure days or 3 months). Physician assessments of patient compliance and satisfaction were conducted at the end of the observation period. Patients (N = 306) received a mean ± SD of 28 ± 23 infusions of rFVIII-FS with Bio-Set. A majority of patients (82%) preferred the Bio-Set method, with domain scores for ease of use, safety from needlesticks, and speed of reconstitution being highest after training and at the end of the observation period. The Bio-Set method received higher mean scores than previous reconstitution methods for worry/safety and ease/confidence domains at both selleck kinase inhibitor time points. Physician-reported patient compliance with the Bio-Set method was similar or greater compared with the previous method for 94%

of the patients, with physicians reporting that 92% of the patients were satisfied or very satisfied with Bio-Set. Thirteen adverse events (AEs) occurred in nine patients, and five serious AEs occurred in five patients; none was related to rFVIII-FS. No de novo or recurrent inhibitor development was observed during the observation period. rFVIII-FS with Bio-Set was well tolerated and well accepted by haemophilia A patients, which may improve treatment compliance. “
“Forty per cent of haemophilia A (HA) patients have click here missense mutations in the F8 gene. Yet, all patients with identical mutations are not at the same risk of developing factor VIII (FVIII) inhibitors. In severe HA patients, human leucocyte antigen (HLA) haplotype was identified as a risk factor for onset of FVIII inhibitors. We hypothesized that missense

mutations in endogenous FVIII alter the affinity of the mutated peptides for HLA class II, thus skewing FVIII-specific T-cell tolerance and increasing the risk that the corresponding wild-type FVIII-derived peptides induce an anti-FVIII immune response during replacement therapy. Here, we investigated whether affinity for HLA class II of wild-type FVIII-derived peptides that correspond to missense mutations described in the Haemophilia A Mutation, Structure, Test and Resource database is associated with inhibitor development. We predicted the mean affinity for 10 major HLA class II alleles of wild-type FVIII-derived peptides that corresponded to 1456 reported cases of missense mutations. Linear regression analysis confirmed a significant association between the predicted mean peptide affinity and the mutation inhibitory status (P = 0.006). Significance was lost after adjustment on mutation position on FVIII domains.

Overall survival at 3 years was about 16% (Fig. 3B) ranging from 31% to 11.4% in non-PVT versus PVT, respectively. In each BCLC strata, survival tended to favor patients with Child-Pugh class A disease over patients with Child-Pugh class B disease (Table 2). Within the BCLC-C category, median survival and TTP deteriorated as the level of

PVT extended (14 months for PV1-2 versus 8 months for PV3-4; P = 0.052). Tumor control rate by Y90RE significantly affected patient outcome (Fig. 3C). In responders versus nonresponders, a significant 3-year survival difference was registered (18.4% versus 9.1%; P = 0.009). This related to the positive GSK1120212 in vivo effect of Y90RE in the more consistent sample of HCCs with PVT (25% versus 4.4% in responders versus nonresponders, respectively; P = 0.02), whereas in intermediate stage patients, survival comparison among responders versus nonresponders did not show significant differences (Fig. 3D). Predictors of tumor progression and patients’ survival are summarized in Table 3. Tumor characteristics (size >6 cm: hazard ratio [HR], 4.42 [1.95-10.00]; extension involving >25% of the liver: HR, 3.46 [1.31-9.13]) and tumor control rate (HR, 37.43 [7.73-181.35]) were significantly related to TTP at univariate analysis. In the multivariate FK228 model, tumor response by EASL criteria was the sole variable affecting TTP (P < 0.001) and the second

(P = 0.048) after Child-Pugh class independently affecting survival outcomes. In Table 4, the observed grade 3-4 clinical and laboratory toxicities at 3 and 6 months are reported. Among post-Y90RE relevant clinical toxicities, the most common included anorexia (15.4%) and clinically detectable ascites (9.6%), whereas at laboratory sampling, altered bilirubin affected 27% of the series, paralleled by alkaline phosphatase elevation in 19.2% selleck chemicals and lymphocyte count reduction in 15.4%. No significant differences in toxicity

were registered within each category when PVT patients were compared with non-PVT patients. There were no gastroduodenal ulcers or pulmonary toxicities. Within 6 months of therapy, 36.5% of the patients suffered from at least one episode of liver decompensation, with no difference among PVT versus non-PVT patients: seven out of 19 patients eventually recovered with no need of hospitalization, whereas in 12 patients (27.3% of the entire series), liver decompensation led to death. Forty-four patients died during the median 3 years of follow-up. The causes of death were tumor progression in 28 cases (63.6%), liver failure in 12 cases (27.3%) and non liver–non tumor-events in 4 cases (9.1%). Thirty- and ninety-day mortality were 0% and 3.8% (n=2) respectively: both deaths were not treatment-related as occurred at 3 months in tumor progressing PVT patients.

The expression of Sonic Hedgehog (SHH), a ligand of the HH pathway, was analyzed by immunohistochemistry in 84 NAFLD patients with different stages of fibrosis. In these patients, SHH expression increases concomitantly to fibrosis stage, ballooning, signaling pathway portal inflammation, and fibrosis. Interestingly, at the univariate analysis age, body mass index, waist circumference, homeostasis model assessment-insulin resistance, essential hypertension, and fibrosis stage strongly correlated with hepatic expression of

SHH. In HH signaling, the interaction of SHH with the cell surface receptor Patched depresses Smoothened (SMO) activity, leading to nuclear localization of glioblastoma family transcription factors (GLI1, 2, and 3) that regulate the expression of cell-specific target genes.2 Interestingly, Guy and colleagues1 observed a significant correlation between nuclear accumulation of GLI2, liver fibrosis, and other risk factors for NAFLD. Accordingly, we found that GLI2 was overexpressed in liver extracts from rats treated with high fat/high fructose (HF/HFr) diet as compared with standard diet (Fig. 1A). We previously selleck chemicals llc demonstrated that rats fed a HF/HFr diet histologically resemble human NAFLD, developing a rare fibrosis with increased collagen VI.3 Here we show that this dietetic regimen also increases hyaluronic

acid (HA) circulating levels (Fig. 1B). HA, as well as osteopontin, is an important ligand for CD44, a marker of cancer stem cells, whose expression is inhibited by SMO antagonists.4 We hypothesize that an interaction network may exist between HA and HH signaling. This hypothesis is strongly supported by data from Patched1 mutant see more mice (Ptch1+/−), in which the HH pathway is constitutively

activated and displays high levels of circulating HA with respect to Ptch1+/+ mice (Fig. 1c). These results may explain why these mice are susceptible to developing fibrosis in diet-induced NAFLD.5 In conclusion, the relationships between the HH pathway and CD44 ligands, such as HA, may be critical for the comprehension of mechanisms that lead to fibrosis and hepatocellular carcinoma from NAFLD. Simonetta Pazzaglia M.D.*, Loredana Cifaldi M.D.†, Anna Saran M.D.*, Valerio Nobili M.D.‡, Doriana Fruci M.D.†, Anna Alisi Ph.D.‡, * Laboratory of Radiation Biology and Biomedicine, Agenzia Nazionale per le Nuove Tecnologie, l’Energia e lo Sviluppo Economico Sostenibile (ENEA) CR-Casaccia, Rome, Italy, † Oncohaematology Department, ‡ Liver Research Unit, Bambino Gesù Children’s Hospital, IRCCS, Rome, Italy. “
“In the March 2013 issue of Hepatology, in the article titled “Inhibition of hedgehog signaling attenuates carcinogenesis in vitro and increases tumor necrosis of cholangiocellular carcinomas” (volume 57, pages 1035-1045; doi: 10.1002/hep.26147), by Mona El Khatib, Anna Kalnytska, Vindhya Palagani, Uta Kossatz, Michael P. Manns, Nisar P. Malek, Ludwig Wilkens, and Ruben R. Plentz, the photomicrographs a and b of Fig. 2D are identical.