We observed areas of restricted diffusion within the spinal cord which probably corresponded to the ischemic changes. This would concur selleck screening library with the currently accepted pathogenetic theory concerning RM. “
“While high-resolution cone-beam

computational tomographic (CBCT) angiography has gained use in intracranial vascular imaging, digital subtraction angiography (DSA) and 3-dimensional-rotational angiography (3D-RA) remain the preferred acquisition modalities for intracranial aneurysm imaging. This case report highlights the utility of the greater spatial resolution afforded by CBCT for cerebral aneurysm imaging. A 54-year-old man presenting with subarachnoid hemorrhage was confirmed to harbor a ruptured anterior communicating artery aneurysm by conventional angiography. Due to varying contrast opacification captured by different acquisition methods, dramatic aneurysm shape Ganetespib ic50 difference was observed between 2- and 3-dimensional-angiographic and CBCT models. The greater resolution of CBCT revealed in an unequivocal fashion the exact site of rupture on the aneurysm dome, visualized as a discrete irregular and elongated bleb that was not seen on either 3D-RA or DSA. High-resolution CBCT visualized the shape of the target aneurysm in greater detail than the more conventional 2D-DSA and 3D-RA, enabling

more precise computational fluid dynamics (CFD) simulations. Given that aneurysms most likely change shape either prior to rupture or upon rupture, future studies evaluating fluid dynamics using computer reconstructions should be cognizant of the differences in resolution provided by various imaging modalities. “
“Previous studies have demonstrated that cerebral dural sinus stenosis (DSS) may be a potential patho-physiological cause of idiopathic intracranial MCE公司 hypertension (IIH). Endovascular therapy for DSS is emerging as a potential alternative to treat IIH. Here, we present the results of our case series. We prospectively collected angiographic and manometric data on patients that underwent angioplasty/stenting for IIH. All patients

had failed maximal medical therapy (MMT) and had confirmed sinus stenosis. Demographic, clinical and radiological presentation, and outcomes were collected retrospectively. A total of 18 patients underwent 25 procedures. Demographics revealed a mean age of 30 (range 15-59), 83% (15/18) were female, 72% (13/18) were white, and mean body mass index of 36 (range 23-59.2). All patients presented with classic IIH. Symptom improvement or resolution was reported in 94% (17/18) of patients. All patients had resolution and/or stabilization/improvement of their papilledema. Headaches related to increased pressure improved in 56% (10/18). Re-stenosis and retreatment occurred in 33% (6/18). No procedural related complications were reported. Dural sinus angioplasty and stenting is relatively safe, feasible, and clinically efficacious for patients with symptomatic sinus stenosis who have failed standard therapy.

[74] TN is reported in up to 3.8% of patients with multiple sclerosis.[75] For this reason, imaging (MRI) forms an essential part of the work-up for TN. Management will depend on whether there is an identifiable cause, but is primarily medical, and aims to achieve symptom relief. Medical management involves the use of anticonvulsants such

as carbamazepine or oxcarbazepine.[74, 76] Second line agents include lamotrigine and baclofen. Because of the increasing number of anticonvulsants now available, many patients are referred unnecessarily late for surgical interventions this website that can offer the best quality-of-life outcomes.[77] Surgical procedures such as microvascular decompression may be performed if there is imaging

evidence of a lesion affecting the trigeminal nerve root, and the disease is causing a significant impact on quality of life.[78, 79] Other less invasive surgical procedures such as radiofrequency thermocoagulation, glycerol rhizotomy, balloon compression, or gamma knife surgery Sirolimus purchase tend to provide shorter periods of pain relief and have a higher risk of sensory loss. They are used in patients who are medically unfit for major surgery such as microvascular decompression. It remains difficult for patients and clinicians to make decisions about treatment due to a lack of high-quality evidence. Some data suggest that many patients prefer a surgical option rather than ongoing medical management.[80] Glossopharyngeal neuralgia has a similar MCE presentation to TN, although the location of the pain is different. Patients may experience paroxysmal attacks of pain felt deeply in the throat, ear, or posterior aspect of the tongue. The triggers for pain attacks include chewing, talking, drinking, and swallowing. The condition is usually managed medically with anticonvulsant drugs. Refractory

cases may require surgery in the form of microvascular decompression.[81] Anesthesia dolorosa is a condition arising from damage to the trigeminal nerve, usually during surgery for TN. The condition develops 3-6 months following the traumatic incident. It is characterized by “painful numbness.” Patients will report continuous facial pain in an area of numbness, often described as “burning,” “pressure,” or “stinging.” This is a typical patient description: “The right side of my face, from my chin to above my right eye, is numb and I frequently experience a ‘crawling’ sensation on the right side of my face and scalp. Also, my face has quite a bit of pressure and feels as though it is being pulled or tugged, as if in a visor. The pain is persistent, severe, and associated with a high level of psychological distress and comorbidity. It is often resistant to treatment. The area involved may include all 3 divisions of the trigeminal nerve. Examination findings may include objective sensory deficits, allodynia, and hyperalgesia or hypoalgesia.

S1a-c). In agreement with results obtained in KCAV1−/− mice,4 Balb/CCAV1−/− mice showed impaired liver regeneration. We analyzed the survival ratio of Balb/CCAV1−/− and Balb/CCAV1+/+ and the liver/body regeneration selleck index as indicators of the progression of the liver regeneration. The total postoperation survival rate

48 hours after partial hepatectomy in Balb/CCAV1−/− mice was significantly lower than in Balb/CCAV1+/+ mice (60% in Balb/CCAV1−/− versus 100% in Balb/CCAV1+/+ mice) (Fig. 1A,B). In addition, approximately 80% of the CAV1−/− mice showed significantly delayed liver regeneration, as indicated by the liver/body regeneration index (Fig. 1E). At 24 hours after partial hepatectomy the total liver/body regeneration index (1.85 ± 0.16 versus 2.57 ± 0.11, P = 0.0059, n = 6 Balb/CCAV1−/− and n = 5 Balb/CCAV1+/+ mice, respectively) and the liver/body regeneration index from the deceased (1.51 ± 0.01 versus 2.57 ± 0.11, P = 0.00044, n = 3 Balb/CCAV1−/− and n = 5 Balb/CCAV1+/+ mice, respectively) and from the surviving (2.20 ± 0.03 versus 2.57 ± 0.11, P = 0.05, n = 3 Balb/CCAV1−/− and n = 5 Balb/CCAV1+/+ mice, respectively) Balb/CCAV1−/− mice were significantly lower than in Balb/CCAV1+/+ mice (Fig. 1C,D). Furthermore, analysis of the Balb/CCAV1−/− mice that reached 48 hours of liver regeneration suggested that despite lacking CAV1, some Balb/CCAV1−/− mice might show a compensative mechanism

that allows progression of liver regeneration. However, the large variability observed in the values Selleckchem Vemurafenib of the liver/body index obtained from the Balb/CCAV1−/− mice at 48 hours of liver regeneration when compared with Balb/CCAV1+/+ mice suggested that, although still progressing, lack of CAV1 perturbs liver regeneration

and survival of Balb/CCAV1−/− mice. Taken together, the results clearly demonstrated that loss of CAV1 also impairs liver regeneration in Balb/CCAV1−/− mice. We next analyzed JAXCAV1−/− mice, the only commercial CAV1−/− mouse line available, that were used by Mayoral et al.5, 8, 13 As shown previously,5 mice demonstrated normal liver regeneration after partial hepatectomy, had similar postoperation survival rates, and after 72 hours of regeneration the liver/body regeneration index was slightly but statistically medchemexpress significantly higher than in the JAXCAV1+/+ mice (3.34 ± 0.175 versus 2.69 ± 0.116, respectively, P = 0.0038) (Fig. 2A,E), suggesting faster regeneration in JAXCAV1−/− mice. Liver regeneration depends on the supply of both glucose and fatty acids to the remnant hepatocytes during the first hours of regeneration. As observed in KCAV1−/− and Balb/CCAV1−/− mice, hepatic oxidative lipid metabolism is disrupted during fasting in JAXCAV1−/− mice (Fernandez-Rojo et al., unpubl. results). In addition, it has been shown that high glucose levels can compensate for inefficient utilization of fatty acids.

However, a significant heterogeneity in survival among RCTs remained even after stratifying patients and study features, and heterogeneity in the survival rates persisted even in the stratum of high-quality studies, implying that this was not explained by study validity alone. Therefore, the evaluation of the methodological quality did not seem to influence the variability of the assessed outcome, because of the mean high quality of the studies (75% of these RCTs were high-quality studies). Heterogeneity of these rates among RCTs may reflect

both inclusion of patients with different stages of disease and variability in the molecular Navitoclax molecular weight characteristics and biological behavior of the tumor, which are not included in any of the currently available staging systems. In our analysis, when studies were separated according to the BCLC stage, the 1-year survival was much higher in RCTs including only BCLC B or C patients (34%) than in those also including BCLC D patients (11%). This provides further evidence that the BCLC staging system has a good discriminative capacity for prognosticating survival not only in patients with early HCC41 but also in those with intermediate/advanced HCC. However, data on direct ABT737 BCLC stage were

lacking in several trials, and caution must be exercised when interpreting results from subgroup exploratory analyses. We found by meta-regression analysis that ECOG performance status and portal vein thrombosis are robust predictors of death in untreated patients as reported by Tandon and Garcia-Tsao42 in a recent systematic review of 72 studies on prognostic indicators in HCC. These

上海皓元 two individual parameters, both included in the BCLC classification, may explain in large part why this staging system provides accurate information on prognosis in the setting of HCC. A remarkable difference in survival was found between occidental (North American and European) and oriental (Asia-Pacific) studies. The high prevalence of HBV-related liver disease found in Asia-Pacific countries may account for the different survival observed between oriental and occidental studies in which a high prevalence of HCV-related liver disease was observed. However, the potential role of HBV as a prognostic factor disappears when Asian-Pacific location of the studies and HBV-related disease were both included in a multivariate model. The survival differences between occidental and Asian studies may be explained by differences in the distribution of other risk and prognostic factors. In fact, the worse survival observed in the Asia-Pacific study36 could be explained by the higher prevalence of patients in advanced stage than in the SHARP study.

Ahmed, Ola Ahmed, Auhood Nassar, Mai

Lotfy, Abeer Bahnassy Background/Aims: Hypoxia is deprivation of an adequate oxygen supply and induces hypoxic apoptosis. Hypoxia inducible factor-1α (HIF-1α) and interleukin (IL-8) activate tumor survival in different pathways. We evaluated whether adenovirus-mediated small hairpin RNAs for HIF-1α (shHIF-1α) and IL-8 (shIL-8) induced apoptosis in hepatocellular carcinoma (HCC) and endothelial cell lines. see more Methods: The HCC cell line was infected with adenovirus expressing shRNA for HIF-1α and IL-8 and maintained under hypoxic conditions (1% O2, 24 h). The expression levels of HIF-1α and apoptotic and growth factors were examined by real-time quantitative polymerase chain reaction and Western blotting. We also investigated apoptosis by terminal deoxynucleotidyl ICG-001 in vivo transferase dUTP nick-end-labeling assay (flow assisted cytometry and immunofluorescence) and measured cytochrome c levels. Results: Inhibiting HIF-1α and IL-8 up-regulated the expression of apoptotic factors

while simultaneously down-regulating anti-apoptotic factors. Knockdown of HIF-1α and IL-8 increased cytochrome c concentration and enhanced DNA fragmentation in the HCC cell line and human umbilical vein endothelial cells (HUVECs). Moreover, the culture supernatant collected from knockdown of HIF-1α and IL-8 in the HCC cell line induced apoptosis in HUVECs under hypoxia. Conclusions: These data suggest that adenovirus-mediated knockdown of HIF-1α and IL-8 induced apoptosis

in HCC and triggered apoptosis in vascular endothelial cells. MCE公司 Disclosures: The following people have nothing to disclose: Sung Hoon Choi, Seung Up Kim, Do Young Kim, Weon Sang Ro, Sang Hoon Ahn, Seungtaek Kim, Chae Ok Yun, Kwang-Hyub Han, Jun Yong Park [Backgrounds] Transforming growth factor (TGF)-β induces epithelial-mesenchymal transition (EMT) which is a crucial step for invasion and metastasis in various types of cancer. Reduced expression of E-cadherin, a hallmark of EMT, is reported in hepatocellular carcinoma (HCC), however, involvement of microRNAs (miRNAs) in this process is poorly understood. CDH1, which encodes E-cadherin, has CpG islands in the promoter region. DNA methylation of CpG islands are regulated by DNA methyltransferases (DNMTs) which are the targets of miR-29a. We investigated the involvement and role of miR-29a in epigenetic regulation of E-cadherin expression during the process of EMT induced by TGF-β. [Methods] Human HCC cell lines, PLC/PRF/5 and HepG2 were treated with 1-10 ng/ml of TGF- β for ∼72 hours to induce EMT. Expression of E-cadherin was examined by using real-time qPCR and immunoblotting. Methylation specific PCR (MSP) was performed to determine the methylation level of CpG islands in the E-cadherin promoter that contains E-boxes. To force the expression of miR-29a, cells were electroporated with synthetic precursor miR-29a.

34 This FK506 purchase suggests a pleiotropic role of BAF60a in cellular and organismal biology by integrating endocrine, metabolic, and circadian signals. The possible regulation of BAF60a by the intrinsic circadian clock is supported by several independent lines of evidence, including (1) a 24-hour-period oscillation of BAF60a expression in the absence of external time cues (constant darkness); (2) a phase relationship with components of the core clock machinery such as Bmal1; and (3) a disruption of rhythmic BAF60a expression in the animals with abnormal circadian clock. However, it has not escaped our attention that feeding rhythms alone can drive rhythmic

gene transcription under constant darkness even in the complete absence of a functional clock.5 In addition, only a small number of rhythmic transcripts in the liver are direct targets of clock regulators.9 In fact, our results showed

that several metabolic tissues such as skeletal muscle, heart, and kidney lack robust BAF60a rhythmicity, whereas they have nice oscillations of clock components. Acalabrutinib order Based on these findings, we conclude that BAF60a may not be a direct target of circadian oscillators. The findings of Gatfield et al.26 support our conclusion and shed some light on the mechanism through which BAF60a is regulated. In this study, miR-122 was shown to serve as the node linking clock components (such as Rev-erbα) to the circadian expression of BAF60a. It is of particular interest to identify more molecules mediating the regulation of BAF60a by circadian oscillators. Although the molecular clocks operate in virtually all cell types, genome-wide profiling experiments have established that a hallmark of circadian gene expression in mammals is tissue-specific.5, 9 Given that BAF60a is ubiquitously expressed, the specificity of BAF60a regulation should be achieved by simultaneously orchestrating BAF60a and other tissue-specific transcriptional factors, whose circadian expression is restricted to a subset of peripheral organs/tissues. One good example is the nuclear receptor PPARα, which is a clock-controlled metabolic sensor mostly

expressed in the liver, where it regulates fatty acid β-oxidation.35, 36 Importantly, BAF60a and PPARα have a functional crosstalk in the liver.24 The tissue-specific phase of MCE公司 BAF60a oscillation is another aspect of its circadian regulation in the periphery. For instance, the phase in heart and in kidney shares a similar pattern, but differs from that in liver. This may result from tissue-specific quantitative properties of the clock and the involvement of tissue-specific upstream transcriptional or posttranscriptional regulators for BAF60a. We further show that BAF60a is involved in the regulation of a specific metabolic gene network in the liver. Notably, the knockdown of BAF60a impaired the rhythmic expression of genes involved in gluconeogenesis, fatty acid β-oxidation, and mitochondrial respiration.

34 This FG4592 suggests a pleiotropic role of BAF60a in cellular and organismal biology by integrating endocrine, metabolic, and circadian signals. The possible regulation of BAF60a by the intrinsic circadian clock is supported by several independent lines of evidence, including (1) a 24-hour-period oscillation of BAF60a expression in the absence of external time cues (constant darkness); (2) a phase relationship with components of the core clock machinery such as Bmal1; and (3) a disruption of rhythmic BAF60a expression in the animals with abnormal circadian clock. However, it has not escaped our attention that feeding rhythms alone can drive rhythmic

gene transcription under constant darkness even in the complete absence of a functional clock.5 In addition, only a small number of rhythmic transcripts in the liver are direct targets of clock regulators.9 In fact, our results showed

that several metabolic tissues such as skeletal muscle, heart, and kidney lack robust BAF60a rhythmicity, whereas they have nice oscillations of clock components. EPZ-6438 datasheet Based on these findings, we conclude that BAF60a may not be a direct target of circadian oscillators. The findings of Gatfield et al.26 support our conclusion and shed some light on the mechanism through which BAF60a is regulated. In this study, miR-122 was shown to serve as the node linking clock components (such as Rev-erbα) to the circadian expression of BAF60a. It is of particular interest to identify more molecules mediating the regulation of BAF60a by circadian oscillators. Although the molecular clocks operate in virtually all cell types, genome-wide profiling experiments have established that a hallmark of circadian gene expression in mammals is tissue-specific.5, 9 Given that BAF60a is ubiquitously expressed, the specificity of BAF60a regulation should be achieved by simultaneously orchestrating BAF60a and other tissue-specific transcriptional factors, whose circadian expression is restricted to a subset of peripheral organs/tissues. One good example is the nuclear receptor PPARα, which is a clock-controlled metabolic sensor mostly

expressed in the liver, where it regulates fatty acid β-oxidation.35, 36 Importantly, BAF60a and PPARα have a functional crosstalk in the liver.24 The tissue-specific phase of 上海皓元 BAF60a oscillation is another aspect of its circadian regulation in the periphery. For instance, the phase in heart and in kidney shares a similar pattern, but differs from that in liver. This may result from tissue-specific quantitative properties of the clock and the involvement of tissue-specific upstream transcriptional or posttranscriptional regulators for BAF60a. We further show that BAF60a is involved in the regulation of a specific metabolic gene network in the liver. Notably, the knockdown of BAF60a impaired the rhythmic expression of genes involved in gluconeogenesis, fatty acid β-oxidation, and mitochondrial respiration.

It provides a detailed analytical means of studying broader aspects of carnivoran feeding ecology, such as predation habits, carrying capacity, ecological hunting requirements and species interactions, which are important aspects of carnivoran management. “
“The Italian Peninsula was one of the main refugia in southern Europe during the climatic oscillations of the Pleistocene, and was considered a ‘hotspot’ of biodiversity. A number of phylogeographic analyses identified highly divergent lineages NVP-AUY922 concentration in Italy that apparently did not contribute to the post-glacial

re-colonization of Europe, supporting the existence of refugia within refugia in the southern-most part of Italy. For the bank vole Myodes glareolus, genetic analyses highlighted a low variability for this species on the Italian peninsula, suggesting that cryptic refugia of central Europe were the main source of postglacial re-colonization in Europe.

In this work, we analysed the mtDNA phylogeography of M. glareolus with a special emphasis on the Italian refugium. We extended previous analyses by including new sequences from a wider range of samples across Y-27632 nmr the Italian peninsula. Our results suggest a high mitochondrial diversity of the bank vole in Italy and support the existence of an ancient and deeply divergent population in the Calabria region. This population did not participate to the recent re-colonization of Italy while we highlight the possible occurrence of multiple and more recent colonization events between Europe and Italy. The phylogeographic pattern observed in Italy appears compatible with refugia-within-refugia scenario. “
“Live-capture is a necessary component for the scientific study and management of most mammals, but it may negatively affect their health and physiology. We compared blood parameters related to the

stress response (nominal base levels) from red squirrels Tamiasciurus hudsonicus 上海皓元 after capture of up to 4.5 h in five different live trap models (Hava-hart, Sherman, Tomahawk 102, Tomahawk 103 and ‘Special Squirrel’ trap) with true base levels (obtained in less than three minutes). In addition, we evaluated the capture rate in the five trap models. We found that (1) prolonged time in live traps altered stress hormone concentrations compared with true base levels, but maximum corticosteroid-binding capacity was unaffected; (2) squirrels captured in a trap model with reduced visibility (a roof cover – Hava-hart) had significantly lower (c.

0001). There were 1.9 times more microvesicles in esophageal adenocarcinoma than in Barrett’s esophagus (P = 0.0043). Conclusions:  The study demonstrates distinctive alterations

of the mucosa stroma extracellular matrix in the metaplasia-dysplasia-adenocarcinoma sequence. The findings suggest that the redistribution of collagen fibers and increases in numbers of matrix microvesicles may play roles in the formation of specialized intestinal metaplasia and the development of adenocarcinoma. “
“The liver has robust regenerative potential in response to damage, but hepatic steatosis weakens this potential. We found that the enhanced integrated stress response (ISR) mediated by phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF2α) impairs regeneration in hepatic steatosis and that growth arrest and DNA damage-inducible 34 (Gadd34)-dependent suppression of ISR plays a crucial role in fatty PD-1/PD-L1 inhibitor cancer liver regeneration. Although the mice fed an HFD for 2 weeks developed moderate fatty liver with no increase in eIF2α phosphorylation before 70% hepatectomy, they showed impaired liver regeneration due to reduced buy TSA HDAC proliferation and increased death of hepatocytes with increased phosphorylation of

eIF2α and ISR. An increased ISR through Gadd34 knockdown induced C/EBP homologous protein (CHOP)-dependent apoptosis and receptor-interacting protein kinase 3-dependent necrosis, resulting in increased hepatocyte death during fatty liver regeneration. Further, Gadd34 knockdown and increased phosphorylation of eIF2α decreased cyclin D1 protein and reduced hepatocyte proliferation. In contrast, enhancement of Gadd34 suppressed phosphorylation of eIF2α and reduced

CHOP expression and hepatocyte apoptosis without affecting hepatocyte proliferation, clearly improving fatty liver regeneration. In more severe fatty liver of leptin receptor-deficient db/db mice, forced expression of hepatic Gadd34 also promoted hepatic regeneration after hepatectomy. Conclusion: Gadd34-mediated regulation of ISR acts as a physiological defense mechanism against impaired liver regeneration due to steatosis and is thus a possible therapeutic target for impaired regeneration in hepatic steatosis. This article is protected by copyright. All rights reserved. “
“PNPLA3 (adiponutrin), a novel patatin-like phospholipase domain-containing enzyme, is expressed MCE at high level in fat, but also in other tissues including liver. Polymorphisms in PNPLA3 have been linked to obesity and insulin sensitivity. Notably, a nonsynonymous variant rs738409(G) allele of the PNPLA3 gene was found to be strongly associated with both nonalcoholic and alcoholic fatty liver disease. We have generated Pnpla3−/− mice by gene targeting. Loss of Pnpla3 has no effect on body weight or composition, adipose mass, or development, whether the mice were fed regular chow or high-fat diet or bred into the genetic obese Lepob/ob background.

Our results suggest that candidates with low MELD scores have a significantly lower risk of dying after LDLT. To select appropriate selleck inhibitor candidates for LDLT, donor risk must be balanced by a reasonable chance of success in the recipient. To justify the risk incurred by the donor, timing of LT should be done to achieve the lowest post-LT mortality. Clinical features of 364 adult LDLT recipients Disclosures: The following people have nothing to disclose: Murat Dayangac, Murat Akyildiz, Necdet Guler, Levent Oklu, Yildiray Yuzer, Yaman Tokat Purpose: To determine the effectiveness

of percutaneous and endoscopic therapeutic interventions for biliary strictures and leaks following liver transplantation in children. Material and Methods: Retrospective analysis of 38 consecutive pediatric patients (18 girls, mean age at transplant 5.9 years)

treated at our institution from 1997 to 2010 for biliary leak and/or biliary stricture following liver transplantation (29 deceased donor liver transplants, 9 living related liver transplants) was performed. Six patients had a choledochocholedochostomy while the rest had a Roux-en-Y hepaticojejunostomy biliary anastomosis. Patients with a hepaticojejunostomy anastomosis were managed by a percutaneous approach (percutaneous tran-shepatic biliary drain placement followed by balloon dilation of the stricture), whereas endoscopic approach was feasible in 8 of the patients with choledochocholedochostomy. 32 patients had a stricture at the biliary anastomosis, while 6 patients had an anastomotic leak. Minimally invasive approach GDC-0980 was considered clinically successful if it resulted in patency of the narrowed biliary segment (<30% residual stenosis) and/or correction of the biliary

leak. Results: After an average of 9.1 years of follow-up, non-surgical management was clinically successful for 4 patients (67%) with a biliary leak and for 25 patients (78%) with a stricture. Surgical revision of the anastomosis was eventually required in 3 patients with a leak, and long-term clinical success was achieved in 3 patients (50%). For patients that had developed a biliary stricture, surgical revision was ultimately required MCE公司 in 14 patients, with 7 patients proceeding straight to surgery and 7 patients requiring surgical revision after recurrent stricture developed a median of 2.2 months of initial drain removal. Long-term clinical success was achieved in 18 patients (56%) with a biliary stricture. Patients that had long-term failure (n=14) were compared to patients with long-term success (n=18) and were found to have lower median age at transplantation (p=0.09), lower median age at stricture diagnosis (p=0.03), and had a choledochojejunostomy biliary anastomosis (p=0.05). Conclusions: Percutaneous and endoscopic management of biliary strictures and leaks after liver transplantation in children is associated with a durable result in approximately 50% of patients.