14 However, most Hes1 null animals die by E18.5 from severe neural

tube defects and have gallbladder agenesis and hypoplasia of extrahepatic bile ducts never connecting with the IHBD system, possibly interfering MLN8237 cell line with proper ductal plate remodeling.27, 28 Moreover, those Hes1 null animals reaching birth all die within the first 24 hours and therefore are of limited informative value to study the impact of Hes1 on IHBD tubulogenesis as this process extends several days beyond birth. In addition to our observations in RbpjF/FAlbCre and Hes1F/FAlbCre animals we found that N2IC-induced morphogenetic effects in R26N2ICAlbCre animals could be reverted by the additional genetic deletion of Rbpj, but not Hes1. Although Hes1 has been clearly demonstrated to be expressed in developing bile ducts,6, 14 it is increasingly accepted that Hes1 may not be a perfect readout for Notch activity because Hes1 expression is also regulated independently of Notch.29 In support of this evidence, embryonic deletion of

Jagged1 in the portal mesenchyme resulted in severe IHBD morphogenesis defects without altered expression of Hes1.13 Furthermore, Hes1 may even function as a Notch suppressor30; in this context, we observed enhanced expression of Hey1 and Hes5 after genetic deletion of Hes1 in N2IC-expressing livers of R26N2ICHes1F/FAlbCre animals (Supporting Fig. 8), which might also argue for redundancy of these Notch targets as proposed in brain development.31 Kinase Inhibitor Library solubility dmso Inactivation of the Notch target gene Sox9 results in IHBD maturation defects32 and, therefore, Sox9 is a likely candidate to contribute to N2IC-expressing tubulogenesis in our model. However, because IHBD malformations are much more pronounced selleck chemicals llc after genetic deletion of Jagged1, RBP-Jκ or Notch2 than after deletion of Sox9,6, 7, 10, 13, 32 additional Notch targets yet to be identified are likely involved to drive Notch-induced biliary tubulogenesis.

Taken together, our results underline the vital role of canonical Notch signaling but clearly argue against a pivotal role of Hes1 as the key Notch target in IHBD formation. It should be also kept in mind that besides Notch other signaling pathways such as the TGFβ or Wnt/β-Catenin pathway act in concert to induce biliary lineage defining proteins such as Sox9, HNF1β, CK19, or osteopontin.12 The observation that Sox9 expression is induced in periportal and interlobular hepatocytes of P10 RbpjF/FAlbCre livers that later acquire an intermediate phenotype (Fig. 4) underscores that induction of biliary proteins can take place in the absence of canonical Notch signaling. Remarkably, adult hepatocytes fully retained their susceptibility to N2IC-induced biliary reprogramming.

Mice

were anesthetized (30 mg/kg of pentobarbital IP) and placed in a supine position, with the liver located at the center of the coil. Eight mice from each group (i.e., Mdr2-KO, Mdr2:CCR5 DKO, and Mdr2:CCR1 DKO) were scanned at 9, 13, and 16 months, and liver hepatomegaly and tumor formation were evaluated from multislice coronal and axial T1- and T2-weighted fast-spin echo images covering the entire liver, both coronally and axially (repetition time/echo time = 147/10 ms; flip angle = 30 degrees; field of view = 5 cm; 256 × 256 pixels; 11-13 slices with slice thickness = 1 mm). Mouse peripheral blood mononuclear cells (PBMCs) were analyzed for the ability to migrate toward RANTES in vitro. For this aim, 100 µL of chemotaxis buffer (RPMI 1640, 1% fetal calf serum [FCS]; Biological Industries, find more Kibbutz Beth Haemek, Israel) containing 2 × 105 PBMCs from either WT, CCR5-, or CCR1-deficient mice were placed into the upper chamber of a Costar 24-well Selleck Cisplatin transwell (Costar, Cambridge, MA), and 600 µL of chemotaxis buffer with or without RANTES (PeproTech EC, London, UK) were added to the bottom chamber (at indicated concentration). Cells were collected from the chambers after 4 hours of migration at 37°C, stained with antimouse Mac-1 (eBioscience, San Diego, CA), and counted by flow cytometry. Liver samples were homogenized in homogenization buffer (50 mmol/L of

Tris-HCl [pH 7.6], 0.25% Triton X-100, 0.15 M of NaCl, 10 mM of CaCl2, and complete mini–ethylenediaminetetraacetic acid–free protease inhibitor cocktail [Roche Diagnostics, Mannheim, Germany]). Tissue lysates (containing 30 μg of protein) were separated on a 10% sodium dodecyl sulfate polyacrylamide gel. Blottings were incubated overnight at 4°C in a blocking buffer containing 5% skim milk and then incubated with either anti-SMA (smooth muscle actin) (Dako, Carpintera, CA) or beta-actin (Sigma-Aldrich) mouse monoclonal antibody (Ab) (diluted 1:2,000) for 2 hours at

room temperature and, subsequently, with peroxidase-conjugated goat antimouse immunoglobulin G (Dako) for 1 hour at room temperature. Total RNA was extracted from livers of 1- and 3-month-old mice (WT, Mdr2-KO, Mdr2:CCR5 DKO, and Mdr2: CCR1 DKO) using check details TRIzol reagent (Invitrogen Life Technologies, Carlsbad, CA), according to the protocol recommended by the manufacture. Complementary DNA (cDNA) was obtained by reverse transcription (RT) of 1 mg of total RNA in a final reaction volume of 25 μL containing 1× Moloney murine leukemia virus (M-MLV) RT buffer, 2.5 μmol/L of random hexamers, 0.5 mmol/L of each deoxynucleoside triphosphate, 3 mmol/L of MgCl2, 0.4 U/μL of RNase inhibitor, and 100 U/μL of M-MLV RT (Promega, Madison, WI). Quantitative real-time PCR assays, containing the primers and probe mix for transforming growth factor beta (TGF-β) and RANTES, were purchased from Applied Biosystems (Foster City, CA) and utilized according to the manufacturer’s instructions.

Perhaps, in the absence

of these objective evaluations, it is time we gave weight to traditions and clinical experiences that, in some cases, span thousands of years and millions of clinical experiences in the hands of countless non-Western practitioners.”[1] He expands on this by considering a case of a patient in his practice who is on a wide group of treatments, some prescribed, some almost unheard of and unregulated. He tracks down some of them, like a detective, in descriptions of classical Chinese Fulvestrant healing. Then he tries to give the reader his wisdom, guidance, and recommendations for the future. One of his endorsements is, when possible, to become familiar with some of the alternative systems used in treating headaches. In addition to classical Chinese, he mentions homeopathy and Ayurveda. He states, “Having LY2835219 clinical trial a referral base that includes some of these practitioners is very helpful. Integrating these approaches into one’s own practice can be even more helpful, but requires considerable commitment in time and refocusing of the practice We don’t need to embrace every alternative medical system to serve our patients, but there exists a wide variety of modalities which, whether we incorporate them into our practices or

not, need to be on our radar, and with which we need more than a passing familiarity. Moreover, we need to provide this website some guidance to our patients in these areas if we are truly to be their advocate in healthcare. For this reason, I asked Dr. Trupti Gokani, who melds Western medicine and Ayurveda in her practice, to

provide a description of the Ayurvedic system for this issue, and how she uses Ayurveda in her headache treatments.[2] This is an eye-opening review, and it immediately calls to mind Dr. Cowan’s admonition that “Because these are medical systems rather than discrete interventions, studies are much harder to come by and in general, each has its own internal logic. It is much more difficult to evaluate a system which is based on centuries of trial and error or an oral tradition.” I found Dr. Gokani’s summary riveting, and it will help me in talking with my patients who use this approach. The biggest problem in alternative care is squaring these treatments with the Western tradition and the requirement for rigorous evidence-based studies. In the third article in this month’s Headache Currents, Dr. Rebecca Wells and colleagues tease apart the requirements for adequate study in mind/body interventions in headache.[3] This article is particularly useful in that the authors tightly organize the questions that remain in evidence-based mind/body interventions, the troubles in answering the questions, and how they might be addressed.

7 times higher in cirrhosis patients than in healthy controls (0.026 versus 0.007, respectively; click here P = 0.001, χ2 test; Table 2). Silent single nucleotide polymorphisms (SNPs) and intronic SNPs showed similar allele frequencies in patients and healthy controls35 (Supporting Table 3). The overall cumulative frequency of TERT gene missense variants in patients with hepatic cirrhosis was significantly greater than in 528 healthy controls (P = 0.0009, Fisher’s exact test; Table 2). Of note, none of the patients with mutations had hepatocellular carcinoma. One had

undergone liver transplantation and two died during the study period (of head and neck cancer and one of progressive liver disease; Table 3). Germline origin of gene variants was demonstrated by analysis of DNA obtained from peripheral blood leukocytes and buccal mucosa in all patients tested, except for two patients, one with the TERC n. 37AG mutation and another with the

TERT 441E deletion, who died before the study was complete. Leukocyte telomere length in the six patients with cirrhosis and mutations who were tested was below the median based on a reference group of 175 healthy individuals varying in age from 0 to 99 years, as measured by qPCR (Fig. 1B). PI3K Inhibitor Library cost The leukocyte telomere lengths of the two patients carrying novel TERT mutations (Patients C and D) were in the shortest quartile for healthy controls. Leukocyte telomere length was also measured for 44 patients with cirrhosis without identifiable telomerase missense mutations from whom peripheral blood find more leukocytes were collected; they had significantly shorter telomeres in comparison to controls (Fig. 1C; P = 0.0004). The mean age-adjusted telomere length in patients with cirrhosis was −0.114 (95% confidence interval, −0.162, −0.06), compared to 0.001 (95%, −0.04, 0.04) in controls. Eighty-two percent of patients with cirrhosis had telomere lengths below the median for their age. To evaluate whether mutations in TERC and TERT decreased telomerase enzymatic activity (its ability to

synthesize telomeric repeats), telomerase-deficient VA13 cells were transfected with plasmids containing wildtype or mutant TERT and TERC constructs (or transfected with an empty vector). Novel TERT codon Pro530Leu and codon Thr882Ile mutations produced significant reduction in telomerase activity as compared to wildtype TERT (Fig. 1D). In our transfection experiments, TERC 37AG mutation resulted in increased telomerase enzymatic activity in comparison to wildtype TERC. However, previous studies indicated that this mutation modulates telomerase activity from 75%13 to 100%31 of wildtype function. TERT 441Glu deletion has been previously found to generate ≈40% of wildtype telomerase activity, whereas the telomerase activity produced by the TERT codon Ala1062Thr variant is ∼60% of wildtype TERT.

Anorexia nervosa (AN) affects mainly adolescent females in developed countries including the USA, Europe and Japan. The majority of patients develop AN due to abnormal eating habits resulting from a desire to be lean or fear of becoming obese after exposure to psychiatric stress. In Japan, the prevalence of AN has been increasing rapidly;[1] according to annual

reports issued by the Ministry of Health, Labour and Welfare, the incidence of eating disorders increased 10-fold in the 20 years since 1980, and the number of AN cases in particular increased fourfold during the 5 years since selleck the mid 1990s. The prevailing explanation for this increase is the change of lifestyle in Japan including the increased variety of social circumstances.

AN is associated with a number of complications including liver injury, especially elevation of the serum alanine aminotransferase (ALT) level in more than 30% of cases.[2] Furthermore, rare cases of severe liver injury resulting in acute liver failure have been reported.[3-5] However, the precise mechanism involved in the pathogenesis of liver injury associated with AN remains unclear. Moreover, few reports have documented the clinical features of AN complicated by liver injury. Some have indicated an association with low body mass index (BMI),[6, 7] although the roles of other clinical surrogate markers are unclear. The aim of the present study was to clarify the clinical features of AN complicated by liver injury and the clinical factors this website influencing hepatic complications. In clinical settings, it is important to predict the onset of severe liver injury associated with AN, which could be potentially life-threatening, and therefore it was anticipated that the information obtained from the present study would be of value to clinicians in assessing find more the risk of developing this serious complication. This retrospective observation study was conducted between January 2010 and December 2011 at the Department of Gastroenterology and Department of Neuropsychiatry, Yamagata University Hospital. During this

2-year period, a total of 37 patients were admitted under a diagnosis of AN. These patients comprised both newly referred patients and established outpatients with exacerbation. There were also first admissions and repeat admissions due to deterioration of the patients’ condition. The diagnosis of AN was made by a psychiatrist in accordance with the criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) on the basis of information obtained by interview from the patients and their families. The exclusion criteria were: (i) a history of hepatic disease, (ii) established infection with hepatitis viruses (HBV or HCV), (iii) drug abuse, (iv) excessive alcohol intake, and (v) presence of autoimmune liver disease.

Conclusion: For the previously published criteria, biochemical

responses at the sixth month can be used in place of those evaluated after 1 year of UDCA therapy. Our findings justify a more rapid identification of patients who need new therapeutic approaches. (HEPATOLOGY 2013) Primary biliary cirrhosis (PBC) is an autoimmune liver disease characterized by the presence of highly specific antimitochondrial antibodies and progressive destruction of intrahepatic bile ducts, resulting in chronic cholestasis, portal inflammation, and fibrosis, which can ultimately lead to cirrhosis and hepatic failure.1, 2 Ursodeoxycholic acid (UDCA) is currently the only approved medical treatment selleckchem for PBC. Despite improved prognosis selleck chemical in many patients treated with UDCA, the transplant-free survival rate remains significantly lower in patients with a suboptimal biochemical response.3-8 Thus, there is a continued need for new therapeutic options for treating PBC. The biochemical response to UDCA, especially

changes in the serum activities of alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), may serve as a strong predictor of long-term outcome

in patients with PBC6-10 and thus could have a role in clinical practice and therapeutic trials by identifying patients with a poor prognosis. Previously published criteria for predicting outcome of treatment were mainly based on biochemical response selleck compound after 1 or 2 years of UDCA therapy.6-9 However, it is helpful to identify as soon as possible patients who will get optimal benefit from alternative therapy. It has been recommended that therapeutic trials should target patients with incomplete biochemical response after 3 to 6 months of UDCA treatment.11 However, a biochemical response as early as 3 to 6 months was evaluated in only a few large independent cohorts of patients, including two studies using the Mayo criteria and Ehime criteria.12, 13 Today, more and more patients are diagnosed at an early stage of PBC. Given the slow disease progression and limited availability of study participants, traditional hard endpoints, such as the occurrence of death or liver transplantation, are considered unfeasible in clinical trials.11 Accordingly, more extended endpoints in homogeneous cohorts of patients are required to define clinically relevant criteria of biochemical response in patients with PBC.

Hydrazine is a major hydrolytic metabolite of INH (Fig. 2) and is currently believed to be one of the key players contributing to INH hepatotoxicity. Hydrazine

is not only a strong reducing agent but has also been implicated in interfering with energy metabolism. For example, hydrazine depletes ATP in hepatocytes (preceding cell Selleck Fulvestrant injury) and causes the formation of megamitochondria in rat liver.[37-39] In cultured rat hepatocytes, hydrazine causes acute toxicity in a concentration-dependent manner, characterized by glutathione depletion, increase in glutathione disulfide, loss of catalase activity, and lactate dehydrogenase release.[40] Also, hydrazine depletes the levels of pyridine nucleotides in cultured rat hepatocytes.[41] The in vitro

concentrations used to elicit these effects (low millimolar range) are clearly high and greater than the plasma concentrations measured in patients; however, the repeated and/or cumulative effects of even low levels of hydrazine in the liver are not known. More recently, nuclear magnetic resonance (NMR) spectroscopic Selleckchem Saracatinib and metabolomics studies have shed more light on the mechanisms underlying hydrazine toxicity. For example, in a rat study, proton NMR spectroscopy revealed that hydrazine caused a dose-dependent increase in plasma and urinary lactate concentrations,[42] suggesting interference with mitochondrial function. selleck screening library Metabolomics studies in rats have revealed that hydrazine (120 mg/kg) caused increases in plasma citrulline levels (suggesting mitochondrial urea cycle impairment) and decreases in urine succinate concentrations.[43]

Similarly, in mice, hydrazine (100 mg/kg p.o.) produced hepatotoxicity and mitochondrial dysfunction, as inferred from the depletion of tricarboxylic acid (TCA) cycle intermediates and increases in lactate levels.[44] One way to study the causal role of hydrazine in INH-induced hepatic injury is to experimentally block its formation from the parent INH and to compare the outcome with that in the absence of the chemical inhibitor. In rabbits, studies with the acyl amidase inhibitor bis-p-nitrophenyl phosphate (BNPP), an irreversible inhibitor with an IC50 of 2 μM, clearly protected from the mild hepatotoxicity induced by INH as assessed by the decreased activity of liver enzymes in the plasma, indicating that hydrazine indeed may be key in the development of acute INH hepatotoxicity.[45] There is evidence for a contribution of the adaptive and/or innate immune system to INH-associated hepatotoxicity, and excellent reviews have recently discussed this topic.[6, 46] One of the basic mechanisms leading to the formation of a hapten, which subsequently could elicit an immune response, is the covalent modification of a protein by a reactive drug intermediate.

3A2). Similar results were also observed in Huh-7 cells (data not shown). Thus, Snai1 is critical for FoxC1-induced reduction of E-cadherin expression. To determine whether FoxC1 regulates Snai1 and E-cadherin transcription, Snai1 and E-cadherin promoter luciferase constructs ([−1511/+140]Snai1 and pGL3-E-cadherin) were cotransfected with pCMV-FoxC1. The luciferase reporter assay showed that FoxC1 transactivated Snai1 promoter activity, but inhibited E-cadherin transcription. Furthermore, the short interfering RNA (siRNA)-mediated knockdown of Snai1 in FoxC1-overexpressing SMMC7721 cells partially relieved the click here suppression of E-cadherin promoter-driven luciferase activity (Fig. 3B1).

To define the roles of the cis-regulatory elements www.selleckchem.com/products/PD-0325901.html of the Snai1 promoter in response to FoxC1 regulation, reporter constructs containing serial 5′ deletions of the Snai1 promoter ([−1511/+140]Snai1, [−922/+140]Snai1, [−694/+140]Snai1, and [−354/+140]Snai1) were cotransfected with pCMV-FoxC1. The luciferase reporter assay showed that a deletion from

nt −1511 to nt −694 had no effect on FoxC1-induced Snai1 promoter activity. However, further deletion from nt −694 to nt −354 significantly decreased FoxC1-induced Snai1 promoter activity (Fig. 3B2), indicating that the sequence between nt −694 and −354 was critical for the activation of the Snai1 promoter by FoxC1. The third putative FoxC1-binding site was in this region. A luciferase reporter assay showed that mutation of the third FoxC1-binding site significantly reduced FoxC1-induced transactivation

of the Snai1 promoter (Fig. 3B2). A chromatin immunoprecipitation (ChIP) assay confirmed the direct binding of FoxC1 to the third FoxC1-binding site in the Snai1 promoter in HCC cells (Fig. 3C). To determine whether FoxC1 binds to the Snai1 promoter under physiological conditions, three healthy liver tissues (healthy control) and three HCC tissues were collected. A ChIP assay showed that the FoxC1-binding activity to the Snai1 promoter was much higher in HCC tissues than in healthy controls (Supporting Figure 7). These results suggested that FoxC1 transactivated Snai1 expression, thereby leading to the inhibition of E-cadherin transcription in HCC cells. To study the possible role of Snai1 in FoxC1-mediated invasion and metastasis, SMMC7721-FoxC1 find more cells were infected with LV-shSnai1 lentivirus to knock down Snai1 expression. Snai1 knockdown significantly reduced FoxC1-enhanced cell migration and invasion (Fig. 3D). To determine the effect of Snai1 on FoxC1-mediated metastasis, two cells lines were transplanted into livers of nude mice. Ten weeks after orthotopic implantation, BLI showed the presence of lung metastasis in mice implanted with SMMC7721-FoxC1 plus LV-shcontrol cells, but no lung metastasis occurred in mice implanted with SMMC7721-FoxC1 plus LV-shSnai1 cells (Fig. 3E1). Histological analysis (Fig.

(2) The SES-CD correlated with CDEIS significantly (r = 0.970, P < 0.0001). Weaker correlation detected between learn more the Bjorkesten scoring (r = 0.743) and the SES-CD or CDEIS (r = 0.738). (3) Weaker correlation discovered between CDEIS and Crohn’s Disease Activity Index (CDAI) (r = 0.378, P = 0.001 < 0.05). Moreover, significant correlation were found between Bjorkesten scoring and HCT (r = −0.302) or age (r = −0.296, both P < 0.05). Conclusion: (1) CDEIS score over 6 may prompt severe mucosal injury which also had a higher level of biological markers and perianal disease. (2) CDEIS, SES-CD and Bjorkesten scoring systems demonstrated close

correlation. For scoring of endoscopic activity in clinical routine, Bjorkesten scoring or SES-CD might replace the CDEIS. Key Word(s): 1. Crohn’s disease; 2. CDEIS; 3. SES-CD; 4. Bjorkesten scoring; Presenting Author: LV SUCONG Additional Authors: CHEN BAILI, XIAO YINGLIAN, U0126 CHAO KANG, HE YAO, ZENG ZHIRONG, GAO XIANG, HU PINJIN, CHEN MINHU Corresponding Author: CHEN MINHU Affiliations: The First Affiliated Hospital of Sun Yat-Sen University Objective: To compare

the efficacy of step-up and top-down infliximab therapy on patients with Crohn’s disease. Methods: A prospective study was performed by the First Affiliated Hospital of Sun Yat-sen University. Confirmed CD patients were enrolled into step-up and top-down group. Baseline data, clinical efficacy rate, mucosal healing rates at week 10 and 30, fistula closure rates at week 10 and 30, follow-up therapy and adverse events were collected for this study. Results: (1) 77 CD patients were enrolled, with 32 in step-up group

and 45 in top-down group. No significant difference at baseline characters of each group except male gender (P = 0.012 < 0.05). (2) There were significant difference in clinical efficacy rates (P = 0.002) selleck kinase inhibitor and mucosal healing rates at week 30 (P = 0.007), while no significant difference were detected of mucosal healing rates at week 10. Fistula closure rates at week 10 and 30 of step-up group were 9.37% and 12.5% respectively. Fistula closure rates at week 10 and 30 of top-down group were 13.3% and 17.7% respectively. Difference of fistula closure rates of each group at both week10 and 30 were not significant. (3) 17 patients in step-up group adopted AZA as follow-up treatment, while 28 patients in top-down group adopted AZA as follow-up treatment. (4) The prevalence of adverse events in step-up and top-down group were 3.1%(1/32) and 11.1%(5/45) respectively. Conclusion: (1) Top-down infliximab therapy could achieve higher clinical efficacy rate and mucosal healing rate at week 30, thus, might be a better choice for doctors. (2) Early adoption of infliximab and immunosuppressants might improve prognosis of CD patients according to its higher fistula closure rate and lower surgery rate. (3) Infliximab therpy combine with anti-tuberculosis drugs and anti-HBV drugs might reduce the prevalence of adverse events. Key Word(s): 1.

However, the final choice of the type and duration of anticoagulation TSA HDAC cell line treatment

was left to the judgment of the referring specialist according to the risk of bleeding based on past and recent history; the possible need for urgent invasive therapy for local factors; and a history of intolerance to heparin. Therefore, patients were included in the descriptive analyses but excluded from the therapeutic and prognostic analyses if they received only antiplatelet agents, were not given anticoagulation, or were given anticoagulation beyond 30 days after the retrospectively defined date of diagnosis (as defined below). Date of diagnosis corresponded to the date of the imaging study where diagnostic criteria were

met after centralized review. As a result, this website in some patients, the date of diagnosis could precede or follow by a few days the date when the clinical diagnosis was actually made. Radiological images were collected and reviewed by expert radiologists during a centralized national review. The following segments were examined: portal vein, right and left portal vein branches, and terminal segment of the superior mesenteric and splenic veins. Patency was defined as visualization of a completely normal selleck chemicals llc venous segment; obstruction as the presence of solid material in the vascular lumen or obliteration of the normal lumen; and recanalization as the normal appearance of a previously obstructed segment. Cavernoma was defined as the presence of clear porto-portal collaterals.

A diagnosis of mesenteric infarction was based on evidence in a pathology specimen. Patients were followed from the date of diagnosis until death, study closure (May 1, 2006), or the date of the last visit. Clinical, laboratory and radiological data were collected at diagnosis, at predefined intervals (1, 3, 6, 12, 18, 24 months), and during significant clinical events. Blood samples were obtained for centralized etiological workup. Risk factors for thrombosis were investigated as described.13, 14 All collected data were confirmed by national and international experts before freezing for analyses. Endpoints included: (1) patency of the portal vein trunk and at least one of its main right or left branches as a result of recanalization or lack of extension; (2) patency of the superior mesenteric and splenic veins; and (3) bleeding, intestinal infarction, or death.