2). A 6.3 Mb region of homozygosity on chromosome 16 (25,073063-31,378235) that was shared by the proband and her affected cousin but not with the unaffected cousin harbored an excellent candidate gene,

HSD3B7. We PCR-amplified and sequenced Enzalutamide cell line the coding region of HSD3B7 in the proband using flanking oligonucleotides to amplify each of the nine exons of the gene.3 The proband and her affected first cousin (III.5) were both homozygous for a 2-basepair deletion in exon 1 of HSD3B7 (c.45_46del AG, p.T15Tfsx27) that was not present in the unaffected cousin. Exon 1 of HSD3B7 was then sequenced in the other family members. Both parents of the affected first cousin (III.5) were heterozygous CH5424802 order for the mutation. The proband’s parents were not available for sampling but four of their siblings were heterozygous for the mutation (II.2, II.4, II.7, and II.14) (Fig. 1). We confirmed the diagnosis of 3β-HSD deficiency by using negative ion FAB-MS21 to analyze the bile acids in the serum of family member III.5. The results definitively established a defect in bile acid synthesis consistent with a deficiency in the activity

of 3β-HSD (formally called 3β-hydroxy-Δ5-C27 steroid dehydrogenase/isomerase). The negative ion mass spectrum of the serum (Fig. 3) was remarkable in revealing the presence of ions consistent with an array of atypical bile acids not normally detected in serum by FAB-MS. The triplets of ions at m/z 453, 469, and 485 (sulfate conjugates) and m/z 510, 526, and 542 (glyco-sulfate conjugates) are characteristic of monohydroxy, dihydroxy, and trihydroxy bile acids, respectively, with a structural feature of a 3β-hydroxy-Δ5 structure (i.e., unsaturated C24 bile acids), respectively, and these are signature metabolites for this genetic defect Low-density-lipoprotein receptor kinase in bile acid synthesis.2, 21 There was a complete absence of the glycine and taurine conjugates of the primary bile acids of cholic (m/z 498 and 514) and chenodeoxycholic acids (m/z 448 and 464), typically observed

in patients with cholestasis when bile acid synthesis is intact. Family member III.5 was referred to a hepatologist to commence treatment with bile acids. Here we report the identification of a family with 3β-HSD deficiency in which affected individuals show striking phenotypic variability. The proband had chronic liver disease from childhood, but survived without medical care into her early 20s and then died at age 24. Her paternal first cousin (III.1) died at age 6 years of liver disease. The sister of III.1 (III.5) had an apparently self-limited liver disorder in childhood that was severe enough to require multiple hospitalizations and yet she has been asymptomatic for the last 22 years. We confirmed that she was homozygous for a null allele of HSD3B7, yet her liver function tests were normal at age 32 years. The lack of 3β-HSD activity was biochemically confirmed by FAB-MS analysis of the serum.

94 min) or perforation rate (4.2% vs. 5.1%). Sixteen SM1-EGC patients (22.2%) underwent surgical resection after ESD as an additional treatment, and lymph node metastasis was found in only 1 case. Additional surgical resection was performed for 57 patients (72.2%) of SM2-EGC patients, and lymph node metastasis selleckchem was observed in 8 of these patients. Of 33 patients who did not undergo additional

curative surgical resection, 2 patients with SM2-EGC had recurrence of lymph node metastases and underwent surgery, but no patient with SM1-EGC had lymph node metastases or local recurrence. Conclusion: ESD for SM1-EGC based on expanded criteria may be feasible, but additional long-term follow-up data are needed. Key Word(s): 1. ESD; 2. submucosal invasion; 3. early gastric cancer Presenting Author: TETSURO INOKUMA Additional Authors: YOSHIKI GPCR Compound Library high throughput SUGINOSHITA, HIROSHI THEI, SATOKO INOUE, NAOTO SHIMENO, MASAYA WADA, MASASHI FUKUSHIMA, YOHEI TANIGUCHI, HIROKI KITAMOTO, TATSUNORI MINAMIDE, KAZUYA HOSOTANI, KAZUHIRO MATSUMOTO, TAKAHIKO ITOH Corresponding Author: TETSURO INOKUMA Affiliations: Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital, Kobe

City Medical 3-mercaptopyruvate sulfurtransferase Center General Hospital, Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital,Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital, Kobe City Medical Center General Hospital Objective: [Background] Metastatic gastrointestinal

tract tumors can be seen in end-stage malignant disease, is clinically diagnosed during his lifetime was rare. Review the experience cases of metastatic gastric tumors, we report, including the endoscopic findings and therapeutic adaptation. Methods: We have experienced 17 cases (with28 lesions) of metastatic gastric tumor. 8 cases of female and 9 cases of male, 67 -year-old average age. Primary tumor were detected 7 cases of lung cancer, two cases of pancreatic cancer and bile duct cancer, one each in esophageal cancer, breast cancer, colonic cancer. Nine cases of digestive tract bleeding, abdominal pain, clinical symptoms that triggered the discovery was 8 cases is asymptomatic. At the first visit is the seven cases, the discovery period was 4–60 months after the primary tumor found in six cases other. Results: Gross morphology was submucosal tumor -like polypoid lesions with a central ulcer formation in 17 lesions, primary gastric cancer similar lesions in 6, and 2 lesions peptic ulcer similar. From the form, rather than transfer the serosal side invasion of intraperitoneal seeding, hematogenous metastases was suggested.

[[39]] For important considerations related to performing surgical

procedures in persons with hemophilia, please see “Surgery and Invasive Procedures”. Specific issues in relation to orthopedic surgery include: Orthopedic surgeons should have had specific training Ixazomib manufacturer in surgical management of persons with hemophilia. [[3]] Performing multiple site elective surgery in a simultaneous or staggered fashion to use clotting factor concentrates judiciously should be considered. (Level 3) [[50]50] Local coagulation enhancers may be used. Fibrin glue is useful to control oozing when operating in extensive surgical fields. (Level 3) [[36, 51, 52]36,51,52] Postoperative care in patients with hemophilia requires closer monitoring of pain and often higher doses of analgesics in the immediate postoperative period. (Level 5) [[36]] Good communication with the postoperative rehabilitation Roscovitine concentration team is essential [[39]]. Knowledge of the details of the surgery performed and intra-operative joint status will facilitate planning of an appropriate rehabilitation program. Postoperative rehabilitation should be carried out by a physiotherapist experienced in hemophilia management. Rehabilitation may have to progress more slowly in persons with hemophilia. Adequate pain control is essential to allow appropriate exercise and mobilization. These

principles also apply to fixation of fractures and excision of pseudotumors. Inhibitors” in hemophilia refer to IgG antibodies that neutralize clotting factors. In the current era in which clotting factor concentrates have been subjected to appropriate viral inactivation, inhibitors to FVIII Thymidine kinase or FIX are considered the most severe treatment-related complication in hemophilia. The presence of a new inhibitor should be suspected in any patient who fails to respond clinically to clotting factors, particularly if he has been previously responsive. In this situation, the expected recovery and half-life of the transfused clotting factor are severely diminished. Inhibitors are more frequently encountered

in persons with severe hemophilia compared with those with moderate or mild hemophilia. The cumulative incidence (i.e., lifetime risk) of inhibitor development in severe hemophilia A is in the range of 20–30% and approximately 5–10% in moderate or mild disease. [[53, 54]] In severe hemophilia A, the median age of inhibitor development is 3 years or less in developed countries. In moderate/mild hemophilia A, it is is closer to 30 years of age, and is often seen in conjunction with intensive FVIII exposure with surgery. [[55, 56]] In severe hemophilia, inhibitors do not change the site, frequency, or severity of bleeding. In moderate or mild hemophilia, the inhibitor may neutralize endogenously synthesized FVIII, thereby effectively converting the patient’s phenotype to severe.

[[39]] For important considerations related to performing surgical

procedures in persons with hemophilia, please see “Surgery and Invasive Procedures”. Specific issues in relation to orthopedic surgery include: Orthopedic surgeons should have had specific training RAD001 mouse in surgical management of persons with hemophilia. [[3]] Performing multiple site elective surgery in a simultaneous or staggered fashion to use clotting factor concentrates judiciously should be considered. (Level 3) [[50]50] Local coagulation enhancers may be used. Fibrin glue is useful to control oozing when operating in extensive surgical fields. (Level 3) [[36, 51, 52]36,51,52] Postoperative care in patients with hemophilia requires closer monitoring of pain and often higher doses of analgesics in the immediate postoperative period. (Level 5) [[36]] Good communication with the postoperative rehabilitation CHIR-99021 team is essential [[39]]. Knowledge of the details of the surgery performed and intra-operative joint status will facilitate planning of an appropriate rehabilitation program. Postoperative rehabilitation should be carried out by a physiotherapist experienced in hemophilia management. Rehabilitation may have to progress more slowly in persons with hemophilia. Adequate pain control is essential to allow appropriate exercise and mobilization. These

principles also apply to fixation of fractures and excision of pseudotumors. Inhibitors” in hemophilia refer to IgG antibodies that neutralize clotting factors. In the current era in which clotting factor concentrates have been subjected to appropriate viral inactivation, inhibitors to FVIII Amino acid or FIX are considered the most severe treatment-related complication in hemophilia. The presence of a new inhibitor should be suspected in any patient who fails to respond clinically to clotting factors, particularly if he has been previously responsive. In this situation, the expected recovery and half-life of the transfused clotting factor are severely diminished. Inhibitors are more frequently encountered

in persons with severe hemophilia compared with those with moderate or mild hemophilia. The cumulative incidence (i.e., lifetime risk) of inhibitor development in severe hemophilia A is in the range of 20–30% and approximately 5–10% in moderate or mild disease. [[53, 54]] In severe hemophilia A, the median age of inhibitor development is 3 years or less in developed countries. In moderate/mild hemophilia A, it is is closer to 30 years of age, and is often seen in conjunction with intensive FVIII exposure with surgery. [[55, 56]] In severe hemophilia, inhibitors do not change the site, frequency, or severity of bleeding. In moderate or mild hemophilia, the inhibitor may neutralize endogenously synthesized FVIII, thereby effectively converting the patient’s phenotype to severe.

Increases in the proportion of FA > .8 (P < .0001), distribution of FA (P < .0001), and distributions of longitudinal (P < .0001) and radial diffusivity (P < .0001) were observed. Histogram analysis showed increased peak frequency of FA (Fig 1C). Decreases in the distribution of MD (P < .0001) also occurred. Fiber tracking using fiber assignment by continuous tracking[9] was performed with termination criteria

set to FA < .15 and angle >60°. Tractography CCR antagonist showed displacement and compression of the corticospinal tract by the enlarged Virchow–Robin spaces (Fig 1D). Fiber density index was calculated as the number of fiber paths passing through the ROI divided by the area of the ROI in pixels. Fiber density index was 14.6 (1157/8973) as compared to 8.8 (fibers/voxels = 746/6029) for the normal contralateral tract. We report a case with enlarged Virchow–Robin spaces adjacent to the corticospinal tract, which showed increased FA, decreased MD, and thinning and compression at tractography. Increased FA suggests augmented diffusion anisotropy and structural coherence, whereas decreased MD suggests diminished diffusion magnitude. These tensor abnormalities, however, did not

correlate with any clinical signs or symptoms. Zhu and colleagues[10] found Virchow–Robin spaces were ubiquitous in 1,818 elderly patients, Ceritinib of whom 32% had enlarged Virchow–Robin spaces. In a patient with enlarged Virchow–Robin spaces, Ugawa Avelestat (AZD9668) and colleagues[11] reported normal clinical findings and sensorimotor conduction. In 2 patients with enlarged Virchow–Robin spaces just below the Rolandic cortex, Mathias et al[12] described decreased white matter tract vectors on the side of the enlarged spaces. Given normal neuropsychological

evaluations, they postulated that these represented technical limitations of tractography. We instead hypothesize that the DTI changes are due to alterations in the extravascular extracellular space (EES). Increased FA may occur from increased myelination, increased axonal diameter, increased axonal density, and/or increased directionality.[13] The case patient had increased FA that was confirmed by increased peak frequency and increased skewness at histogram analysis, and by increased longitudinal and radial diffusivity. Mass effect by enlarged Virchow–Robin spaces decreases unrestricted water in the EES that has low anisotropy. This suggests compression or increased density of normal axons, as corroborated by the increased fiber density index. DTI in acute ischemia has correlated transient increases in FA with changes in the EES.[14] In vitro nerve research has also shown that decreased EES causes decreased MD.[15] Calculation of the EES fraction VE is possible using T1 perfusion imaging but beyond the scope of this study. The main limitation is the complicated oncological history. The case patient had two primary cancers and multiple brain metastases, but none near the corticospinal tracts or motor gyri.

Increases in the proportion of FA > .8 (P < .0001), distribution of FA (P < .0001), and distributions of longitudinal (P < .0001) and radial diffusivity (P < .0001) were observed. Histogram analysis showed increased peak frequency of FA (Fig 1C). Decreases in the distribution of MD (P < .0001) also occurred. Fiber tracking using fiber assignment by continuous tracking[9] was performed with termination criteria

set to FA < .15 and angle >60°. Tractography Palbociclib price showed displacement and compression of the corticospinal tract by the enlarged Virchow–Robin spaces (Fig 1D). Fiber density index was calculated as the number of fiber paths passing through the ROI divided by the area of the ROI in pixels. Fiber density index was 14.6 (1157/8973) as compared to 8.8 (fibers/voxels = 746/6029) for the normal contralateral tract. We report a case with enlarged Virchow–Robin spaces adjacent to the corticospinal tract, which showed increased FA, decreased MD, and thinning and compression at tractography. Increased FA suggests augmented diffusion anisotropy and structural coherence, whereas decreased MD suggests diminished diffusion magnitude. These tensor abnormalities, however, did not

correlate with any clinical signs or symptoms. Zhu and colleagues[10] found Virchow–Robin spaces were ubiquitous in 1,818 elderly patients, HSP inhibitor of whom 32% had enlarged Virchow–Robin spaces. In a patient with enlarged Virchow–Robin spaces, Ugawa Montelukast Sodium and colleagues[11] reported normal clinical findings and sensorimotor conduction. In 2 patients with enlarged Virchow–Robin spaces just below the Rolandic cortex, Mathias et al[12] described decreased white matter tract vectors on the side of the enlarged spaces. Given normal neuropsychological

evaluations, they postulated that these represented technical limitations of tractography. We instead hypothesize that the DTI changes are due to alterations in the extravascular extracellular space (EES). Increased FA may occur from increased myelination, increased axonal diameter, increased axonal density, and/or increased directionality.[13] The case patient had increased FA that was confirmed by increased peak frequency and increased skewness at histogram analysis, and by increased longitudinal and radial diffusivity. Mass effect by enlarged Virchow–Robin spaces decreases unrestricted water in the EES that has low anisotropy. This suggests compression or increased density of normal axons, as corroborated by the increased fiber density index. DTI in acute ischemia has correlated transient increases in FA with changes in the EES.[14] In vitro nerve research has also shown that decreased EES causes decreased MD.[15] Calculation of the EES fraction VE is possible using T1 perfusion imaging but beyond the scope of this study. The main limitation is the complicated oncological history. The case patient had two primary cancers and multiple brain metastases, but none near the corticospinal tracts or motor gyri.

In this respect, although this study did not show changes in IR or lipid profiles of DAPT chemical structure rats exposed to CS, it is possible that longer exposures to CS may adversely affect these metabolic factors.23-26 Interestingly, the observation of increased hepatic injury induced by CS in the absence of worsening IR, together with the knowledge that CS also worsens IR23, 24 and IR in turn worsens NAFLD,21, 22 suggests that the deleterious effect of CS in human NAFLD and in CLD in general may engage several pathways. The 4-week study design may also have resulted

in an inability to demonstrate increased hepatic fibrosis. A second study limitation also is related to the assessment selleck chemicals of hepatic fibrosis. Although CS up-regulated the expression of genes involved in fibrogenesis in obese rats, this was not associated with evident development of increased liver fibrosis. However, the absence of a leptin receptor in the Zucker rat model may have influenced these results. Evidence for this possibility is that, although a methionine-choline–deficient diet induces steatohepatitis and increased oxidative stress in Zucker rats, the occurrence of increased neovascularization, hepatic expression of vascular endothelial growth factor, and liver

fibrosis development are restricted in this model.34 Therefore, although conclusions cannot be made regarding

the lack of increased angiogenesis and liver fibrosis development reported in the study by Azzalini et al., the CS-induced worsening of histological injury and apoptosis support the concept that CS may cause fibrosis progression in NASH.35 Additional studies in different animal models are needed to clarify and substantiate the profibrogenic effects of CS in NAFLD suggested by gene up-regulation. Finally, this study has demonstrated that CS increases hepatic Roflumilast apoptosis in the livers of obese rats. This is of great importance given the crucial role of apoptosis in NAFLD progression. However, the exact apoptotic pathways involved were not identified. A key observation was that CS decreased caspase-3–driven apoptosis in both obese and control rats, and this suggests that CS induces a caspase-3–independent pathway in NAFLD. Further studies are warranted to elucidate the exact mechanism behind CS-induced apoptosis in NAFLD. In summary, the study by Azzalini et al.33 demonstrates that CS worsens liver injury in a rat model of obesity-related NAFLD. These results, together with other experimental data,25-29 provide compelling evidence that CS exacerbates NAFLD. Similarly, clinical studies in CLD have consistently indicated that CS aggravates liver injury in humans.8, 9, 11-17 There are very few published studies on the effects of CS in human NAFLD.

In this respect, although this study did not show changes in IR or lipid profiles of 3-deazaneplanocin A mw rats exposed to CS, it is possible that longer exposures to CS may adversely affect these metabolic factors.23-26 Interestingly, the observation of increased hepatic injury induced by CS in the absence of worsening IR, together with the knowledge that CS also worsens IR23, 24 and IR in turn worsens NAFLD,21, 22 suggests that the deleterious effect of CS in human NAFLD and in CLD in general may engage several pathways. The 4-week study design may also have resulted

in an inability to demonstrate increased hepatic fibrosis. A second study limitation also is related to the assessment selleck of hepatic fibrosis. Although CS up-regulated the expression of genes involved in fibrogenesis in obese rats, this was not associated with evident development of increased liver fibrosis. However, the absence of a leptin receptor in the Zucker rat model may have influenced these results. Evidence for this possibility is that, although a methionine-choline–deficient diet induces steatohepatitis and increased oxidative stress in Zucker rats, the occurrence of increased neovascularization, hepatic expression of vascular endothelial growth factor, and liver

fibrosis development are restricted in this model.34 Therefore, although conclusions cannot be made regarding

the lack of increased angiogenesis and liver fibrosis development reported in the study by Azzalini et al., the CS-induced worsening of histological injury and apoptosis support the concept that CS may cause fibrosis progression in NASH.35 Additional studies in different animal models are needed to clarify and substantiate the profibrogenic effects of CS in NAFLD suggested by gene up-regulation. Finally, this study has demonstrated that CS increases hepatic PAK5 apoptosis in the livers of obese rats. This is of great importance given the crucial role of apoptosis in NAFLD progression. However, the exact apoptotic pathways involved were not identified. A key observation was that CS decreased caspase-3–driven apoptosis in both obese and control rats, and this suggests that CS induces a caspase-3–independent pathway in NAFLD. Further studies are warranted to elucidate the exact mechanism behind CS-induced apoptosis in NAFLD. In summary, the study by Azzalini et al.33 demonstrates that CS worsens liver injury in a rat model of obesity-related NAFLD. These results, together with other experimental data,25-29 provide compelling evidence that CS exacerbates NAFLD. Similarly, clinical studies in CLD have consistently indicated that CS aggravates liver injury in humans.8, 9, 11-17 There are very few published studies on the effects of CS in human NAFLD.

20 Moreover, the HCV titer did not significantly increase after B cell depletion with rituximab (Fig. 6), which is inconsistent with B cells harboring significant amounts of virus. Alternative suggestions include B cell stimulation by HCV core Selleckchem Protease Inhibitor Library and E2,10, 21-23 but this also cannot explain the restricted repertoire of pathogenic B cells in HCV-related MC. Thus, we favor the hypothesis that a combination of multiple factors, including chronic antigen stimulation,23 elevated B cell growth factor expression,17 and genetic predisposition,24 trigger B cell clonal expansion. Rituximab therapy is an alternative treatment approach for MC patients who have failed antiviral therapy. All patients enrolled

in our study responded effectively to rituximab,7 as B cells were undetectable within 2 months (Fig. 6) and were recovered 6-12 months after

cessation of therapy. Prior to treatment, HCV-infected patients with MC displayed not only an increased frequency of immature Ku-0059436 mw transitional B cells in the blood, but also an altered ratio of T1 to T2 immature transitional B cells. Uninfected controls generally have a 1:3 ratio of T1:T2 immature transitional B cells, but this ratio decreased to 1:5-1:6 in HCV-infected patients with MC. The altered T1:T2 ratio was not linked to apoptosis as immature B cells from HCV-infected patients with MC expressed lower levels of Bcl-2 than those of HCV-infected patients without MC and uninfected controls (data not shown). Rather, Farnesyltransferase it was related to cryoglobulin levels, which decreased in parallel with the in vivo proliferation rate (as measured by Ki-67 levels) of T2 immature transitional B cells (Fig. 6). In conclusion, we propose a model in which infection with HCV induces apoptosis of naïve mature B cells resulting in an increased size of the immature B cell subset. This process is accelerated in the presence of MC. Furthermore, MC promotes the proliferation of T2 immature transitional

B cells, resulting in a decreased T1/T2 ratio. Treatments that reduce cryoglobulin levels such as rituximab restore a normal T1/T2 ratio with reduced proliferation of T2 immature transitional B cells. These data provide a mechanistic explanation for the observed maintenance of normal B cell numbers and the increase in immature transitional B cells in the blood of chronic HCV patients with MC. We thank Catherine Rehm and Laura Heytons for the collection of patient samples during rituximab therapy. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Repeat hepatic resection for recurrent hepatocellular carcinoma (HCC) is effective in improving long-term outcome in selected patients. In the present study, we attempted to identify the prognostic factors influencing overall and recurrence-free survival after the second hepatic resection.

We defined needle-specific technical success as successful puncture of a duct or area of interest. Procedural success was defined as successful placement of a prosthesis or therapeutic injection. Clinical success was defined as resolution of collection, significant improvement in laboratory parameters and/or avoidance of any subsequent unplanned intervention. Results: A total of 158 patients (mean age 67.5, male Staurosporine order 58%) underwent 158 interventional EUS procedures using the flexible 19-gauge needle. Malignant etiology was present in 79% of patients. EUS-guided biliary drainage (54%) and pancreatic pseudocyst drainage

(22%) were the most common indications. There was no significant difference with regards to needle specific technical

or clinical success between the two groups (Table 1). However procedural success is more likely to occur with echoendoscope in the straight position. The overall complication rate was similar between the 2 groups (Table 1). Conclusion: This large multicenter study suggests that the flexible 19-gauge needle was effective for use in interventional EUS procedures with an acceptable complication rate. The needle specific technical success rate was comparable when the echoendoscope was in a straight versus angulated position. Table 1: Patient and procedure-related outcome by route of access.   Transesophageal transgastric Transduodenal transjejunal transcolonic Overall p-value Number, n (%) 100 (63.3) 58 (36.7) 158   Procedure time (mins) mean (SD) 62.2 (37.14) 70.3 (29.80) 64.5 (34.5) Selleckchem PF-562271 0.11 Mean follow up (mths) 3.99 4.06 3.97 0.48 Needle specific technical success 95 (95) 54 (93.1%) 149 (94.4%) 0.62 Procedure successfully completed 90 (90) 45 (77.6%) 135 (87.3%) GBA3 0.03 Clinical success 61 (61) 38 (65.5%) 99 (62.6%) 0.81 Complications 16 (16) 12 (20.7) 28 (17.7) 0.96 Mortality 1 (1) 0 (0) 1 (0.6) V Kumbhari,1 P Saxena,1 AC Storm,1 M Solanki,1 Okolo PI III1 1Department of Medicine and Division

of Gastroenterology and Hepatology, John Hopkins Hospital and Medical Institution, Baltimore, MD, USA Background and Aims: Surgically altered GI anatomy is increasingly encountered by the endoscopist due to the rising prevalence of bariatric surgery, liver transplant, and pancreaticoduodenectomy. The prevalence of biliary pathology is increased in these patients as bile stone formation may complicate rapid weight loss in post-bariatric patients, and post-operative biliary and enteral strictures and leaks may complicate hepatobiliary surgery. Limitations of current deep enteroscopy platforms include lack of widespread availability and limited therapeutic potential due to the smaller calibre working channel. Using a standard endoscopy platform, the Through-the-Scope Balloon Catheter (TSBC) marketed as NaviAid−AB (SMART Medical Systems Ltd.