Indeed, using functional neuroimaging

Killgore, PD0332991 chemical structure Oki, and Yurgelun-Todd (2001) showed that sex-specific changes in amygdala and dorsolateral prefrontal cortex reactivity to affective facial expressions emerged during puberty. Our findings in the adults partly replicate previous results in a group of 68 psychology undergraduate students, in which sex differences were found in the advantage of women for the emotions sadness, surprise, anger, and disgust (Montagne et al., 2005). However, apart from the study sample, there are methodological differences between the current set-up and the previous study, in that in Montagne et al. (2005), the emotional expressions were presented in side-view perspective as well. Also, in addition to assessing accuracy for labelling (similar to the present study), sensitivity for the emotions was assessed by asking the participants to move through the animated sequence and indicate the point at which they start to recognize the expression. These methodological differences may explain the discrepancy between study findings in relation to sex differences in emotion perception (Kret & De Gelder, 2012), as some paradigms are more sensitive to small between-group MAPK inhibitor differences than others. Indeed, Hoffmann, Kessler,

Eppel, Rukavina, and Traue (2010) demonstrated that facial expressions presented at lower intensities resulted in sex differences Branched chain aminotransferase in favour of females, but this effect disappeared when full-blown emotional expressions were shown. However, we would like to emphasize that in our study (and in general), sex differences in recognition of emotional expressions are small and great overlap is present in the performance of men and women. IQ was only positively correlated with the ability to recognize disgust in the children. Possibly, the verbal label of disgust may be relatively difficult compared with the other emotions, and better

understood by children with higher levels of intelligence. Brechet, Baldy, and Picard (2009), for instance, demonstrated that the ability to understand the emotion disgust was relatively poor in children overall (i.e., only 40% correct responses even in a group of 11-year olds). Indeed, and in line with our results, intelligence was found to predict the performance on disgust in the study by Horning et al., 2012 as well. In adults, years of education (which is highly correlated with intellectual ability) correlated strongly with the recognition of fear, happiness, sadness, and the ERT Total Score. As years of education is a predictor of performance on many cognitive tests (Lezak et al., 2012), we adjusted our normative data accordingly (in addition to age). Looking at the differences in performance across the six emotions, differences were found that are in accordance with other findings (e.g., Young et al., 2002; Montagne, Kessels, et al., 2007; Ruffman et al., 2008).

044∼0.000). The AUCs (area under receiver operating characteristic curve) were 0.657∼1.000 (7 indicators >0.8); sensitivities, specificities and accuracies for PHC diagnosis were 61.8∼100.0% (4 indicators >80%), 61.1∼100.0% (6 indicators >80%) and 64.3∼100.0% (6 indicators >80%), respectively. These results indicate the method we developed is a valuable approach for aptamer application in diagnosis. Conclusion: A simple method was developed for aptamer application in diagnosis of primary hepatic carcinoma based on polyacrylamide gel electrophoresis and gray analysis. Key Word(s): 1. Aptamer; 2. Diagnosis;

3. PAGE; 4. Heptoma; Presenting Author: MEI-DI HU CHIR-99021 order Additional Authors: TING WANG, KUN-HE ZHANG, WEN-XUE CHEN, GUO-FENG XU, CHAO-ZHU HE,

XUAN ZHU, NONG-HUA LV Corresponding Author: KUN-HE ZHANG Affiliations: the First Affiliated Hospital of Nanchang University; Jiangxi Institute of Gastroenterology & Hepatology Objective: Aptamers are oligonucleotide sequences capable of binding to their targets with high specificity and affinity. We previously generated a group of aptamers against the serum of patients with primary hepatic carcinoma (PHC), and some of them were valuable in the diagnosis of PHC. Here we present the preliminary results of the capture and analysis of target proteins of the aptamers in the serum of patients with PHC for discovering new serum biomarkers of PHC. Methods: The biotinylated aptamers were incubated with pooled PHC serum and pooled normal serum to allow the binding AZD2014 mw of aptamers to their target proteins, followed by adding streptavidin-coated magnetic beads. The beads were magnetically separated and the bound proteins were eluted

and analyzed by mass spectrometry. The spectrum of captured proteins from Non-specific serine/threonine protein kinase PHC serum was compared with that from normal serum to identify the specific targets of PHC. Results: We captured 61 proteins that expressed in PHC serum but not in normal serum, in which 7 proteins related to the human tumors according to previous reports. They might be potential serum biomarkers of PHC. The capture and analysis of aptamer targets is a new strategy to discover novel tumor biomarkers. It has been reported that aptamer-based identification of serum biomarkers of lung cancer was highly valuable in the diagnosis of lung cancer. Because the aptamers could be selected “blindly”, the strategy is powerful in the study of tumor diagnosis. Conclusion: With aptamer-based strategy, potential serum biomarkers of PHC were captured from the PHC serum. Key Word(s): 1. Aptamer; 2. Hepatoma; 3. Serum; 4. Biomarker; Presenting Author: TING WANG Additional Authors: GUO-FENG XU, KUN-HE ZHANG, WEN-XUE CHEN, MEI-DI HU, XUAN ZHU, NONG-HUA LV Corresponding Author: KUN-HE ZHANG Affiliations: the First Affiliated Hospital of Nanchang University; Jiangxi Institute of Gastroenterology & Hepatology Objective: Aptamers are artificial nucleic acid ligands capable of binding to targets with high specificity and affinity.

The fact that almost a third of the patients in either group received further TACE sessions after they went off protocol further outlines the danger of inadequate retreatment criteria for protocol compliance and consequently the success of multicenter

TACE studies. The ART score developed here is able to identify patients with good prognosis despite the presence of Child-Pugh stage B 7-9 points (Fig. 4B,C) or ascites (Fig. 4D) and would therefore provide a robust and objective evidence based tool to guide retreatment with TACE in future clinical trials. Finally, regarding the association of higher ART score values with SAEs and unplanned admissions (Table 4) and poorer OS (Figs. 3, 4), the application of this score may spare patient suffering RO4929097 order and consequential costs by avoiding treatment-related side effects. The retrospective nature and the heterogeneous TACE types (TAE, cTACE, DEB-TACE) in the training cohort may be potential limitations of this study. However, we confirmed the results in all three TACE types in the training cohort (Fig. 3C-E) and in a completely independent external (Table 1, Figs. 3F, 4) patient Selleck Silmitasertib cohort in

which most patients received conventional TACE. Additionally, the outcome of our patient population within the different Child-Pugh stages (Table 2) matches the published survival data reported in prospective clinical trials BCKDHA and meta-analysis3 and, thus,

further confirms the validity of our data. Another limitation may be the ART score assessment at heterogeneous timepoints between the first and second TACE (13-90 days), since the ART score is composed of laboratory changes that may be potentially reversible over time. However, time-related sensitivity analysis (Supporting Table 1-2) revealed no significant hint that the time of the ART score assessment influenced the results of this study. Finally, the ART score was developed by using the radiologic EASL-response criteria. Although the prognostic performance of EASL criteria in the setting of TACE seems to be equal to the performance of mRECIST criteria,25 the latter may be more adequate to dissect the prognosis of patients with partial response from that of subjects with stable disease.26 This could rely on a different definition of partial response in the two models: greater than 50% tumor reduction for EASL and greater than 30% for mRECIST criteria. Given that radiologic response is a parameter of the ART score, there is a need for prospective studies validating the ART score which include mRECIST criteria to the study design. In summary, we developed a novel and externally validated, noninvasive, objective, widely applicable prognostic (ART) score for patients with HCC allocated to retreatment with TACE. Patients with 2.

6A). The recovery of expression of RORα in the liver by tail-vein injection of Ad-RORα

led to restoration of pAMPK levels (Fig. 6B). In addition, mRNA expression of SREBP-1c, FAS, ACC, and SCD1, was significantly lower in the Ad-RORα–infected liver (Fig. 6C). In agreement with these molecular findings, hepatic triglyceride levels were reduced in the Ad-RORα–injected mice (Fig. 6D). Histological examination showed clearly that the hepatocytes of HFD-fed mice were distended by accumulation of lipid droplets. This change was attenuated in the Ad-RORα–injected mice (Fig. 6E). Together, these results indicate that RORα reduces lipid accumulation in vivo by regulating genes that are important in hepatic lipogenesis (Fig. 6F). We synthesized 50 thiourea derivatives PKC412 in vitro based on the structure of CGP52608, an RORα-activating

compound (Fig. 7A). 18 The most active, JC1-38, JC1-40, and JC1-42, induced expression of known endogenous RORα target genes such as SPARC and AGRP (Fig. 7B and Supporting Fig. 5). 23 A docking study using the X-ray crystallographic Lapatinib structure of the RORα complex with CS showed that JC1-42 fitted well into the binding pocket (Fig. 7C). These compounds induced phosphorylation of AMPK/ACC, decreased the expression as well as transcriptional activity of LXRα, and attenuated the FFA mixture–induced lipid accumulation in HepG2 cells (Fig. 7D–F). Finally, we performed in vivo experiments to evaluate the inhibitory effects of JC1-40 and JC1-42 on hepatic lipid accumulation using a safflower oil–enriched HFD model. 27 As expected, oral administration of JCI-40 or JCI-42 led to strong activation of AMPK and repression of LXRα expression in the liver of HFD-fed mice (Fig. 8A). Consistently, hepatic triglyceride levels were significantly lowered in the mice given compound (30

mg/kg) mice (Fig. 8B). Furthermore, body weight was significantly reduced by the compounds, although food intake was not much different among experimental buy Docetaxel groups (Fig. 8C). Oil-red O staining of liver tissues showed clearly that hepatic steatosis in the HFD-fed mice were attenuated by administration of JC1 compounds (Fig. 8D). In the present study, we demonstrated that RORα induced activation of AMPK and inhibition of the lipogenic function of LXRα, which conferred beneficial effects against hepatic steatosis. AMPK is activated by a variety of physiological and pathological stresses that increase the intracellular AMP/ATP ratio, either by increasing ATP consumption or by decreasing ATP production. 6 We showed clearly that RORα expression was associated with a reduction in cellular ATP levels and activation of LKB1 (Fig. 1). Interestingly, we observed that overexpression of constitutively active (CA)-AMPK or treatment with aminoimidazole carboxamide ribonucleotide (AICAR), an activator of AMPK, induced phosphorylation of RORα, which was abolished in the presence of compound C, an inhibitor of AMPK (Supporting Fig. 6A,B).

Further research including innate immune responses against structural components of microbes (bacteria and fungi) may open new possibilities for exploring an important issue of “gut and liver” settled by Nolan from his world leading endotoxin reserach.26 “
“All AASLD Practice Guidelines are updated annually. If you are viewing a Practice Guideline

that is more than 12 months old, please visit www.aasld.org for an update in the material. Ascites is the most common of the three major complications of cirrhosis, the other complications being hepatic encephalopathy and variceal hemorrhage.1 Cirrhosis is the most common cause of ascites in the United States.2 Development of ascites may be the first evidence of the presence of cirrhosis. Obesity makes the physical examination less helpful in detecting ascites.3 Imaging Selleckchem ABC294640 may provide the first evidence of the presence of ascites. Patients with ascites are frequently admitted to hospitals. Effective care of these patients can reduce the frequency of these readmissions. This version of the American Association for the Study of Liver Diseases Practice Guideline is the fourth iteration of this guideline

and represents a thorough update of the 2009 version. ALB, albumin; CI, confidence interval; HRS, hepatorenal syndrome; MAP, mean arterial pressure; NASH, nonalcoholic steatohepatitis; RR, relative risk; SBP, spontaneous bacterial peritonitis; TID, three times daily. In this revision, XAV-939 supplier the treatment options are now divided into first-line, second-line, third-line, and experimental options. There is a new section on drugs to be avoided or used with caution. Blood pressure in patients with

cirrhosis and ascites is supported by elevated levels of vasoconstrictors; these vasoconstrictors are compensating for the vasodilatory effect of nitric oxide.4 Arterial pressure independently predicts survival in patients with cirrhosis; those with a mean arterial pressure (MAP) >82 mmHg have a 1-year survival of 70%, compared to 40% for those ≤82 mmHg.5 Drugs that inhibit the effects of these vasoconstrictors would be expected to lower blood pressure; they have been documented to do so.6 Lowering Ixazomib purchase blood pressure might worsen survival. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers should be avoided or used with caution in patients with cirrhosis and ascites. The European Association for the Study of the Liver practice guideline on ascites recommends that “…they should generally not be used in patients with ascites.”7 This revised guideline reinforces this admonition. Cirrhosis cures hypertension.” In the current era, many patients, especially those with obesity and a component of nonalcoholic steatohepatitis (NASH), have hypertension before they decompensate. Normalization of systemic blood pressure is perhaps the only perquisite of cirrhosis.

Additional Supporting Information may be found in the online version of this article. “
“Fulminant hepatitis (FH) is a disease characterized by massive destruction of hepatocytes with severe impairment of liver function.

The pathogenesis of FH is not fully understood, but hyperactivity of T cells and macrophages with excessive production of cytokines are important hallmarks https://www.selleckchem.com/products/PLX-4720.html of the condition. In this study, we investigated the role of interleukin (IL)−25 in FH. IL-25 expression was evaluated in patients with FH and in livers of mice with FH induced by D-galactosamine (D-Gal) and lipopolysaccharide (LPS). Mice were treated with IL-25 before D-Gal/LPS-induced FH and before or after concanavalin A (ConA)-induced FH. Mononuclear cells were isolated from livers of mice treated with or without IL-25 and analyzed for GR1+CD11b+ cells. CFSE-labeled T cells were cocultured with GR1+CD11b+ cells and their proliferation was evaluated

by flow cytometry. Mice were also treated with a depleting anti-GR1 antibody before IL-25 and D-Gal/LPS administration. IL-25 was constitutively expressed in mouse and human liver and down-regulated during FH. IL-25 prevented D-Gal/LPS-induced FH and this effect was associated with increased infiltration of the liver with cells coexpressing GR1 and CD11b. In vitro studies showed that GR1+CD11b+ cells isolated from mice given IL-25 inhibited T-cell proliferation. Consistently, in vivo depletion of GR1+ cells abrogated the protective effect of IL-25 in experimental D-Gal/LPS-induced FH. IL-25 was both preventive and therapeutic in ConA-induced FH. see more Conclusions: IL-25 expression is markedly reduced during human and experimental FH. IL-25 promotes liver accumulation of GR1+CD11b+cells with immunoregulatory properties. (Hepatology 2013;58:1436–1450) Fulminant hepatitis (FH) (also termed fulminant liver failure or acute liver

failure [ALF]), in patients without previous liver disease, is caused by massive destruction of hepatocytes with resultant severe impairment of liver function, followed by hepatic encephalopathy, and, in many cases, progressive multiorgan failure.[1] Viruses, drugs, and toxins are the major causes of FH.[1] Although many pharmacological approaches have been proposed to recover liver function, transplantation Sorafenib is the only definitive treatment for FH.[2] However, transplantation-related problems, such as lack of donors, surgery-associated complications, risk of rejection, and side effects of immunosuppressive drugs suggest the necessity of novel effective treatments.[1, 2] The pathogenesis of FH is not fully understood, but circumstantial evidence suggests that an exaggerated, poorly controlled immune response plays a major role in the pathological process.[3] FH is characterized by infiltration of immune cells into the liver and the production of inflammatory cytokines and reactive oxygen species, which promote apoptosis and necrosis of hepatocytes.

Defect or deficiency in FVIII causes haemophilia A, a severe hereditary bleeding disorder. Epigenetics inhibitor Intravenous administration of plasma-derived FVIII or recombinant FVIII

concentrates restores normal coagulation in haemophilia A patients and is used as an effective therapy. In this work, we studied the biophysical properties of clinically potent recombinant FVIII forms: human FVIII full-length (FVIII-FL), human FVIII B-domain deleted (FVIII-BDD) and porcine FVIII-BDD bound to negatively charged phospholipid vesicles at near-physiological conditions. We used cryo-electron microscopy (Cryo-EM) as a direct method to evaluate the homogeneity and micro-organization of the protein-vesicle suspensions, which are important for FVIII therapeutic properties. Applying concurrent Cryo-EM, circular dichroism and dynamic light scattering studies to the three recombinant FVIII selleck chemicals llc forms when bound to phospholipid vesicles revealed novel properties for their functional, membrane-bound state. The three FVIII constructs have similar activity, secondary structure distribution and bind specifically to negatively charged phospholipid membranes. Human and porcine FVIII-BDD induce strong aggregation of the vesicles, but the human FVIII-FL form does not. The proposed methodology is effective in characterizing and identifying

differences in therapeutic recombinant FVIII membrane-bound forms near physiological conditions, because protein-containing aggregates are considered to be a factor in increasing the immunogenicity of protein therapeutics. This will provide better characterization and development of safer and more effective FVIII products with implications for haemophilia A treatment. “
“Summary.  Inhibitors of factor VIII (FVIII) have been studied for more than 50 years, but diagnostic 17-DMAG (Alvespimycin) HCl and therapeutic challenges remain. To describe the features that distinguish alloantibodies from autoantibodies, list predisposing factors, and review methods for tolerance induction and autoantibody suppression. Review of key articles published during the past half-century that have advanced knowledge in this field. Alloantibodies generally bind to the A2

or C2 domains of FVIII and disrupt the formation of the FVIII–FIX complex. They exhibit type 1 reaction kinetics, are saturable by FVIII, and display anamnesis. In contrast, autoantibodies usually bind to the C2 domain of FVIII, interfering with phospholipid and von Willebrand factor binding. They have type-2 kinetics and are poorly neutralized by FVIII. Repeated exposures to FVIII induce tolerance in 70–80% of haemophiliacs with inhibitors, whereas drugs that deplete B-lymphocytes restore self-tolerance to FVIII in a similar percentage of non-haemophiliacs. Future work should focus on improving assays that detect and quantify inhibitors, examining the pathophysiology of inhibitor formation using contemporary immunologic tools, and investigating new treatment modalities.

14 Indeed, the use of these tools can make pathologists, even those not specializing in HCC, more confident in the fine diagnostics of this challenging field. This is particularly true for small HCC, which is the most curable form and is particularly difficult to recognize with imaging.

Forner et al.3 reported that concordant noninvasive imaging techniques were successful in 1- to 2-cm HCC detection in patients with cirrhosis in only 33% of cases. We previously reported that a panel of three markers was able to detect 2- to 5-cm G1 HCCs in 49% of cases (with 72.9% accuracy) when at least two of the three markers were positive.6 We conducted the present study with a homogeneous series of small HCCs (≤2 cm) and, for comparison, nonsmall HCCs sampled by a fine-needle approach (20-21 gauge) with the aim of determining whether the addition of a novel EX 527 ic50 marker (CHC) to the previously validated panel could maintain or even increase the panel’s diagnostic accuracy in the detection of small HCC. Notably, the series was preliminary divided into HCC cases (including small G1 HCCs) and non-HCC cases (LGDNs and HGDNs) according to the diagnosis of malignancy or dysplasia made by expert pathologists; the “uncertain

for HCC” category, which could be optimally evaluated only in a prospective study, was omitted. We intentionally buy Staurosporine challenged the new panel with a retrospective series collected with fine needles (20-21 gauge) because this mini-invasive approach may minimize the risks of bleeding and seeding and thus be more acceptable

in clinical practice. CHC was chosen because it is an endothelial marker, works well as an internal standard for nonparenchymal liver cells, and, as already suggested in a surgical series, is overexpressed in the cytoplasm of malignant hepatocytes.15 In contrast, most nonmalignant hepatocytes were reported by Seimiya et al.15 to be negative for staining or to until have weak to moderate staining intensity. We had the same experience in our preliminary study of CHC immunoreactivity in HCC and non-HCC tissues, and we concluded that only CHC overexpression, which is optimally evaluated by a comparison to adjacent nontumoral tissue (which is mostly negative), can be taken as supportive proof of malignancy. In the same article, Seimiya et al. endorsed the use of this marker in combination with GPC3 to improve its efficacy. However, CHC has not been validated in routine core biopsy samples of HCC; this is the real diagnostic challenge for pathologists. With the new panel, absolute specificity (100%) for HCC detection was obtained only when staining with at least two markers (regardless of which ones) was seen (66/86, 76.7%).

Key Word(s): 1. upper gastrointestinal hemorrhage; 2. nursing

care; 3. treatment Presenting Author: ZHIE WU Additional Authors: JIN TAO, YANPING LIANG Corresponding Author: ZHI E WU Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University; Third Affiliated Hospital, Sun Yat-Sen University Objective: To AZD9668 in vitro evaluate the efficacy of hood-assisted endoscopic esophageal injection sclero-therapy in patients with esophageal varices. Methods: Three hundred and sixty two adult patients with esophageal varices treated by EIS in our hospital from January 2011 to January 2014 were randomly divided into two groups: 180 patients (group A) were treated by hood-assisted endoscopy and 182 by direct injection (group B). The time required of the endoscopic treatment, the success rate and postoperative incidence of adverse reactions were compared between the two groups. Results: The time required of endoscopic treatment (6.61 min ± 1.52 min in group A vs 9.35 min ± 1.48 min in Group B, p < 0.05)

was shortened in the hood-assisted group. The success rate was 100% in group A and VX-809 supplier 93.8% in group B. The postoperative incidence of complications was significantly reduced in the hood-assisted group (26.7% vs 35.1%, p < 0.05). Conclusion: Our results indicate that the hood-assisted EIS method can make endoscopic view show clearly, easy to locate, and help to shorten operation time, reduce complications and increase the success rate of operation. Key Word(s): 1. esophageal varices; 2. esophageal injection sclera-therapy; 3. hood-assisted Presenting Author:

RYOICHI YAMAKAWA Additional Authors: MASAYA IWATA, SATORU NYZUKI, MANABU HARADA, KUNIHIRO KAWAUCHI Corresponding Author: RYOICHI YAMAKAWA Affiliations: Kaetsu Hospital, Kaetsu Hospital, Kaetsu Hospital, Kaetsu Hospital Objective: Colonic diverticular bleeding is one of the most common causes of lower intestinal bleeding. Although most bleeding episodes are mild and stop spontaneously, massive bleeding requiring therapeutic intervention occurs in a significant number of patients. Therapeutic barium enema was first reported in 1970. The effectiveness and the less invasiveness of this therapy has been reported. However it has not been performed widely. The aim of this study was to evaluate the effectiveness and adverse STK38 events of barium enema for the treatment of colonic diverticular bleeding. Methods: We examined 90 consecutive patients admitted between January 2000 and March 2014 with colonic diverticular bleeding. The diagnosis was made when all three of the following criteria were fulfilled, 1) There was fresh lower intestinal bleeding, 2) Diverticulum were detected by colonoscopy or barium enema, 3) It was possible to exclude other diseases which caused lower intestinal bleeding. Results: 90 patients (49 males, 41 females, median age 75.0 years, range 29–97) were included. 59 patients (65.6%) were considered to bleed from the left colon and 31 (34.4%) from the right.

18 Actually, none of the patients who eventually had a liver biopsy were found to have cirrhosis. However, we cannot fully exclude that a proportion of the patients had a certain degree of intrahepatic portal venous obstruction preceding the development of acute extrahepatic PVT. Previous retrospective studies have identified local factors in 25% of acute PVT patients. The results in this prospective study were similar (21%), meaning that the reason why thrombosis develops in this particular vein remains unanswered in most patients. However, this study suggests that intrahepatic vascular disease is an underestimated risk factor for acute

PVT.19 Obliterative portal venopathy or nodular regenerative hyperplasia was documented in only 3% of Selleck VX-770 patients. However, intrahepatic vascular YAP-TEAD Inhibitor 1 ic50 disease accounted for 25% of those who underwent liver biopsy, because there were some anomalies in liver tests or imaging. Using comprehensive investigations with updated tools, a general risk factor for venous thrombosis was identified in 52% of patients. There was a predominance of MPD (21% of

patients), G20210A prothrombin gene mutation (14%), and antiphospholipid syndrome (9%). Thirty-six percent of patients had a local factor with a general risk factor, and 25% had no identified factor. These results support the recommendation that all acute

PVT patients—with or without local factors—should be investigated for prothrombotic disorders and considered for early anticoagulation without waiting for test results. A randomized controlled trial of anticoagulation for acute PVT is not realistic due to the rarity and heterogeneity of this disorder. This study has clarified the overall outcome of early anticoagulation therapy using homogeneous inclusion criteria and endpoints. Treatment recommendations were closely followed so that only seven patients could not receive early Demeclocycline anticoagulation therapy. Eighty-nine percent of the anticoagulated patients received heparin-based therapy, and 83% had anticoagulation initiated within 5 days of diagnosis. The main outcomes were an absence of thrombus extension, and a high rate of recanalization. Furthermore, the incidence of intestinal infarction was only 3% in patients with superior mesenteric vein obstruction. This is similar to results in a medical series of 33 patients treated with early anticoagulation,11 but much lower than in unselected or surgical patients (20%–50%) who did not all receive anticoagulation.4 Analyses of suboptimal power failed to disclose any differences according to the type of anticoagulation agents or the delay in initiating anticoagulation.