5A,B). These results indicate not only that a GAS6 deficiency sensitizes mice to I/R-induced liver damage but also that the elevation of serum GAS6 levels is a protective strategy against liver I/R injury. Our findings have disclosed a novel role for GAS6 in hepatocellular defense against hypoxia and I/R and have expanded our knowledge of the biological

facets of this atypical member of the vitamin K–dependent family, which has negligible anticoagulant function but is recognized to be involved in cancer, inflammation, and the regulation of liver regeneration and fibrosis.1, 2, 5, 6 Specifically, we have shown that GAS6 is dispensable for the activation of JNK and NF-κB during hepatic I/R but is required for efficient AKT phosphorylation in hepatocytes; this agrees with previous findings reported for other cell types.3 In addition to increased susceptibility to

hepatic I/R injury, GAS6-null mice exhibit enhanced BGB324 research buy expression of IL-1β and TNF, and this suggests that GAS6 may mediate the suppression of liver inflammation during I/R. These findings are in line with previously reported data on human Idasanutlin research buy and murine monocytes/macrophages20, 21, 32 and Sertoli cells30 via the regulation of TAM receptor signaling.1 Together, our findings indicate that the susceptibility to hepatic I/R injury in the absence of GAS6 reflects the combination of the inability to turn on survival pathways dependent on AKT activation and the overstimulation of inflammatory cytokines. Interestingly, this hepatoprotective role displayed by GAS6 against I/R contrasts

with findings in mouse hearts subjected to warm ischemia, in which GAS6 promoted graft destruction by enhancing interactions between endothelial cells, platelets, and leukocytes33; this exemplifies the importance of organ-dependent mechanisms in GAS6 signaling. The outcome of GAS6-null mice after hepatic I/R is reversible upon the addition of GAS6, and this suggests the maintenance of TAM receptors in the null mice and the functional interaction of GAS6 with TAM receptors. Among TAM receptors, most of the protective effects of GAS6 described in different cell types are due to the binding of GAS6 to Axl.34-37 In 上海皓元 contrast to these findings, Axl seems to play a minor role in hepatic I/R because increased Axl phosphorylation was not detected after I/R exposure. Instead, Mer becomes phosphorylated in WT mice after I/R, and this response is blunted in GAS6-KO mice. Moreover, recent data on differentiated monocytes and macrophages have shown that GAS6 inhibits TNF and IL-1β stimulation in response to LPS via Mer activation.21 Moreover, the binding of GAS6 to Mer but not to Axl or Tyro3 results in the activation of AKT via glycogen synthase kinase 3β phosphorylation, which in turn prevents NF-κB activation. Together, these data and the present study expand our knowledge of the biological impact of the GAS6-Mer interaction, which elicits a combined anti-inflammatory and survival pathway to protect against hepatic I/R.

5A,B). These results indicate not only that a GAS6 deficiency sensitizes mice to I/R-induced liver damage but also that the elevation of serum GAS6 levels is a protective strategy against liver I/R injury. Our findings have disclosed a novel role for GAS6 in hepatocellular defense against hypoxia and I/R and have expanded our knowledge of the biological

facets of this atypical member of the vitamin K–dependent family, which has negligible anticoagulant function but is recognized to be involved in cancer, inflammation, and the regulation of liver regeneration and fibrosis.1, 2, 5, 6 Specifically, we have shown that GAS6 is dispensable for the activation of JNK and NF-κB during hepatic I/R but is required for efficient AKT phosphorylation in hepatocytes; this agrees with previous findings reported for other cell types.3 In addition to increased susceptibility to

hepatic I/R injury, GAS6-null mice exhibit enhanced selleck chemicals expression of IL-1β and TNF, and this suggests that GAS6 may mediate the suppression of liver inflammation during I/R. These findings are in line with previously reported data on human Selleck C59 wnt and murine monocytes/macrophages20, 21, 32 and Sertoli cells30 via the regulation of TAM receptor signaling.1 Together, our findings indicate that the susceptibility to hepatic I/R injury in the absence of GAS6 reflects the combination of the inability to turn on survival pathways dependent on AKT activation and the overstimulation of inflammatory cytokines. Interestingly, this hepatoprotective role displayed by GAS6 against I/R contrasts

with findings in mouse hearts subjected to warm ischemia, in which GAS6 promoted graft destruction by enhancing interactions between endothelial cells, platelets, and leukocytes33; this exemplifies the importance of organ-dependent mechanisms in GAS6 signaling. The outcome of GAS6-null mice after hepatic I/R is reversible upon the addition of GAS6, and this suggests the maintenance of TAM receptors in the null mice and the functional interaction of GAS6 with TAM receptors. Among TAM receptors, most of the protective effects of GAS6 described in different cell types are due to the binding of GAS6 to Axl.34-37 In medchemexpress contrast to these findings, Axl seems to play a minor role in hepatic I/R because increased Axl phosphorylation was not detected after I/R exposure. Instead, Mer becomes phosphorylated in WT mice after I/R, and this response is blunted in GAS6-KO mice. Moreover, recent data on differentiated monocytes and macrophages have shown that GAS6 inhibits TNF and IL-1β stimulation in response to LPS via Mer activation.21 Moreover, the binding of GAS6 to Mer but not to Axl or Tyro3 results in the activation of AKT via glycogen synthase kinase 3β phosphorylation, which in turn prevents NF-κB activation. Together, these data and the present study expand our knowledge of the biological impact of the GAS6-Mer interaction, which elicits a combined anti-inflammatory and survival pathway to protect against hepatic I/R.

The incidence of retained surgical foreign materials and instruments inside

patients is estimated to be 1 in 1,000 to 1,500 intra-abdominal operations. Several studies reported that the risk increases in emergency surgeries, when unplanned procedures occur and in obese patients. A change in surgical teams, excessive loss of blood and long duration of surgery are other associated factors. In our case, the first surgery was an emergency and there was a change in the procedure when converting from a laparoscopy to a laparotomy. Usually, retained foreign abdominal bodies are made of cotton and called gossypibomas. They are detected incidentally. Aseptic fibrinous inflammatory reactions and adhesions encapsulate the CDK inhibition gossypiboma that remains asymptomatic for a long time. In our case, the foreign body was not made of cotton but contained metallic and plastic matrix. Imaging techniques revealed the radio-opaque nature of the retained foreign body. To ensure that nothing has been left in the patient, counting of swabs and instruments is recommended. However, correct reconciliation is reported in the majority of incidents of retained foreign bodies. A new system

has been developed that automates counting and checking utilizing radio frequency identification of individual sponges and packs. The tags attached to the sponges are identified continuously during a procedure rather than episodically as in the traditional click here protocol. Detection does not involve X-irradiation. The increase in cost must be balanced against the potential benefits. “
“We read with great interest the article by Petta et al.1 regarding the association of 25-OH vitamin D (25[OH]D) levels with the response to interferon-based therapy in genotype 1 (G1) chronic hepatitis C (CHC). They found that low 25[OH]D levels were associated with severe fibrosis and low responsiveness to interferon-based therapy in this

patient group. Although the authors discussed their findings comprehensively, we think that there are two additional issues that need to be clarified. First, a MCE great number of studies have indicated that low serum 25[OH]D levels are associated with metabolic syndrome and obesity.2 Ford et al.3 showed that low serum 25[OH]D levels are associated with metabolic syndrome in US adults. Additionally, insulin resistance and CHC infection are clearly linked. Moreover, insulin resistance is a parameter for the response of therapy in G1 CHC.4 However, the authors apparently did not find a similar correlation in their patient group. For that reason, we think that it would have been noteworthy if the authors had taken into consideration the potential effects of metabolic syndrome and particularly insulin resistance on their results.

Six- to 8-week-old female C57Bl/6 wild-type mice were fed a diet deficient in methionine and choline for 5 weeks. Control animals received a diet supplemented with methionine (3 g/kg) and choline bitartrate (2 g/kg) (Dyets Inc., Bethlehem, PA). Poly(I:C) (InvivoGen, San Diego, CA), a synthetic dsRNA (5 mg/kg), or cytidine–phosphate–guanosine-rich DNA (CpG)-ODN (InvivoGen, San Diego, CA; 5 mg/kg) or LPS (Sigma-Aldrich Co., St. Louis, MO; 0.5 mg/kg) were injected intraperitoneally for 2 or 6 hours. The

study was approved by the Institutional Animal Use and Care Committee at the University of Massachusetts. Serum alanine aminotransferase (ALT) levels were determined Cisplatin price using a kinetic method (D-TEK, Bensalem, PA), and liver triglyceride levels were assessed using

an L-Type Triglyceride H kit (Wako Chemicals USA Inc., Richmond, VA). Serum cytokine levels were determined by way of BD Cytometric Bead Array (BD Biosciences, Sparks, MD). Liver thiobarbituric acid reactive substances (TBARS) were assayed using whole liver homogenates and an Oxi-TEK TBARS assay kit (ZeptoMetrix Corp., Buffalo, NY). Serum high-mobility group box protein-1 (HMGB1) protein levels were measured by enzyme-linked immunosorbent assay (IBL Transatlantic, Toronto, Ontario, Canada). Sections of formalin-fixed livers were stained with hematoxylin and eosin. All slides were analyzed by way of microscopy. RNA was purified using an RNeasy kit (Qiagen Sciences, Germantown, MD) and on-column DNA digestion. CHIR-99021 purchase Complementary DNA was transcribed with the Reverse Transcription System (Promega Corp., Madison, WI). Real-time quantitative polymerase chain reaction was performed using the iCycler (Bio-Rad Laboratories Inc., Hercules, CA) as described12; primer sequences

are shown in Table 1. Isolation of mitochondrial and cytosolic fraction from fresh liver tissue was based on the principle of differential centrifugation using a Mitochondrial Extraction kit (Imgenex Co., San Diego, CA). Whole liver lysates or mitochondrial medchemexpress fractions were extracted and Western blotting was performed as described.12 The following antibodies were employed: MAVS (Santa Cruz Biotechnology Inc., sc-6881), cytochrome c (Imgenex, IMG101-A), caspase 1 p10 (Santa Cruz Biotechnology Inc., sc-514), cleaved caspase 8 (Imgenex, IMG5703), RIP3 (Abcam, ab72106), β-actin (Abcam, ab6276), β-tubulin (Abcam, ab6046), and Tim23 (BD Biosciences, 611222). A Native PAGE Novex Bis-Tris Gel System (Invitrogen Life Science, Carlsbad, CA) was used. Liver samples were lysed using 5% Digitonin as a mild detergent and separated on Native PAGE Novex 3-12% Bis-Tris gels. Proteins were transferred to a polyvinylidene difluoride (PVDF) membrane, fixed with 8% acetic acid, diluted in distilled water and identified with specific primary antibodies followed by horseradish peroxidase–labeled secondary antibodies and chemiluminescence assay.

Six- to 8-week-old female C57Bl/6 wild-type mice were fed a diet deficient in methionine and choline for 5 weeks. Control animals received a diet supplemented with methionine (3 g/kg) and choline bitartrate (2 g/kg) (Dyets Inc., Bethlehem, PA). Poly(I:C) (InvivoGen, San Diego, CA), a synthetic dsRNA (5 mg/kg), or cytidine–phosphate–guanosine-rich DNA (CpG)-ODN (InvivoGen, San Diego, CA; 5 mg/kg) or LPS (Sigma-Aldrich Co., St. Louis, MO; 0.5 mg/kg) were injected intraperitoneally for 2 or 6 hours. The

study was approved by the Institutional Animal Use and Care Committee at the University of Massachusetts. Serum alanine aminotransferase (ALT) levels were determined PLK inhibitor using a kinetic method (D-TEK, Bensalem, PA), and liver triglyceride levels were assessed using

an L-Type Triglyceride H kit (Wako Chemicals USA Inc., Richmond, VA). Serum cytokine levels were determined by way of BD Cytometric Bead Array (BD Biosciences, Sparks, MD). Liver thiobarbituric acid reactive substances (TBARS) were assayed using whole liver homogenates and an Oxi-TEK TBARS assay kit (ZeptoMetrix Corp., Buffalo, NY). Serum high-mobility group box protein-1 (HMGB1) protein levels were measured by enzyme-linked immunosorbent assay (IBL Transatlantic, Toronto, Ontario, Canada). Sections of formalin-fixed livers were stained with hematoxylin and eosin. All slides were analyzed by way of microscopy. RNA was purified using an RNeasy kit (Qiagen Sciences, Germantown, MD) and on-column DNA digestion. Navitoclax clinical trial Complementary DNA was transcribed with the Reverse Transcription System (Promega Corp., Madison, WI). Real-time quantitative polymerase chain reaction was performed using the iCycler (Bio-Rad Laboratories Inc., Hercules, CA) as described12; primer sequences

are shown in Table 1. Isolation of mitochondrial and cytosolic fraction from fresh liver tissue was based on the principle of differential centrifugation using a Mitochondrial Extraction kit (Imgenex Co., San Diego, CA). Whole liver lysates or mitochondrial MCE fractions were extracted and Western blotting was performed as described.12 The following antibodies were employed: MAVS (Santa Cruz Biotechnology Inc., sc-6881), cytochrome c (Imgenex, IMG101-A), caspase 1 p10 (Santa Cruz Biotechnology Inc., sc-514), cleaved caspase 8 (Imgenex, IMG5703), RIP3 (Abcam, ab72106), β-actin (Abcam, ab6276), β-tubulin (Abcam, ab6046), and Tim23 (BD Biosciences, 611222). A Native PAGE Novex Bis-Tris Gel System (Invitrogen Life Science, Carlsbad, CA) was used. Liver samples were lysed using 5% Digitonin as a mild detergent and separated on Native PAGE Novex 3-12% Bis-Tris gels. Proteins were transferred to a polyvinylidene difluoride (PVDF) membrane, fixed with 8% acetic acid, diluted in distilled water and identified with specific primary antibodies followed by horseradish peroxidase–labeled secondary antibodies and chemiluminescence assay.

Serum from HCC patients contained higher concentration TGF-β1 than those from cirrhosis and healthy control. Flow cytometry indicated that blocking TGF-β1 stimulated HCC cells proliferation and knockdown it leaded to G1 arrest. Colony formation assay displayed that silencing TGF-β1 affect proliferation of cancer cells. And animal experiments showed that interference TGF-β1 decreased the metastatic nodules in lungs.

Conclusion: Cancer secreted-TGF-β1 is necessary for proliferation of HCC cells. Knockdown Epigenetics inhibitor TGF-β1 could inhibit tumor growth and decrease metastases. The findings suggest that TGF-β1 could be a potential therapeutic target for HCC treatment. Key Word(s): 1. HCC; 2. TGF-β1; 3. metastasis; Presenting Author: HIROKI UCHIDA Additional Authors: YUKIO IWASHITA, KIMINORI WATANABE, TAKAHIDE KAWASAKI, YUICHIRO KAWANO, YOKO KOMORI, KAZUHIRO YADA, MASAYUKI OHTA, SEIGO KITANO Corresponding Author: HIROKI UCHIDA Affiliations: Oita university Objective: Surgical resection for hepatocellular carcinoma (HCC) is regarded as a curable treatment. A tumor adhering to the major hepatic vessels sometimes causes a need to perform hepatectomy without surgical margin. The aim of this study was to evaluate the short-term

outcomes see more of hepatectomy with null surgical margin for HCC. Methods: rom January 2010 to December 2012, 70 patients who underwent curative hepatectomy for HCC in Oita University were analyzed. They were divided into two group with null margin group and negative margin group. These two groups were compared in terms of clinicopathological characteristics, perioperative features, and short-term outcomes. MCE Results: Nineteen patients (27.1%) had been performed hepatectomy with null margin diagnosed pathologically. Mean intraoperative

blood loss was greater and operation time was longer in the null margin group as compared to those in the negative margin group. There were no significant differences in overall survival, disease free survival and other clinicopathological features between the two groups. In the null margin group, 12 patients had recurrence (59.1%) and the recurrence site was liver in all the patients. Four of the 12 patients (33%) had recurrence at the resected stump of the liver and the mean period of recurrence was 10.8 months. Conclusion: Hepatectomy with null surgical margin for HCC is technically demanding. It would lead to comparable and adequate surgical outcomes in patients with tumors in contact with major vessels, compared to hepatectomy with negative surgical margin. Key Word(s): 1. HCC; 2.

Serum from HCC patients contained higher concentration TGF-β1 than those from cirrhosis and healthy control. Flow cytometry indicated that blocking TGF-β1 stimulated HCC cells proliferation and knockdown it leaded to G1 arrest. Colony formation assay displayed that silencing TGF-β1 affect proliferation of cancer cells. And animal experiments showed that interference TGF-β1 decreased the metastatic nodules in lungs.

Conclusion: Cancer secreted-TGF-β1 is necessary for proliferation of HCC cells. Knockdown selleck products TGF-β1 could inhibit tumor growth and decrease metastases. The findings suggest that TGF-β1 could be a potential therapeutic target for HCC treatment. Key Word(s): 1. HCC; 2. TGF-β1; 3. metastasis; Presenting Author: HIROKI UCHIDA Additional Authors: YUKIO IWASHITA, KIMINORI WATANABE, TAKAHIDE KAWASAKI, YUICHIRO KAWANO, YOKO KOMORI, KAZUHIRO YADA, MASAYUKI OHTA, SEIGO KITANO Corresponding Author: HIROKI UCHIDA Affiliations: Oita university Objective: Surgical resection for hepatocellular carcinoma (HCC) is regarded as a curable treatment. A tumor adhering to the major hepatic vessels sometimes causes a need to perform hepatectomy without surgical margin. The aim of this study was to evaluate the short-term

outcomes Copanlisib nmr of hepatectomy with null surgical margin for HCC. Methods: rom January 2010 to December 2012, 70 patients who underwent curative hepatectomy for HCC in Oita University were analyzed. They were divided into two group with null margin group and negative margin group. These two groups were compared in terms of clinicopathological characteristics, perioperative features, and short-term outcomes. 上海皓元医药股份有限公司 Results: Nineteen patients (27.1%) had been performed hepatectomy with null margin diagnosed pathologically. Mean intraoperative

blood loss was greater and operation time was longer in the null margin group as compared to those in the negative margin group. There were no significant differences in overall survival, disease free survival and other clinicopathological features between the two groups. In the null margin group, 12 patients had recurrence (59.1%) and the recurrence site was liver in all the patients. Four of the 12 patients (33%) had recurrence at the resected stump of the liver and the mean period of recurrence was 10.8 months. Conclusion: Hepatectomy with null surgical margin for HCC is technically demanding. It would lead to comparable and adequate surgical outcomes in patients with tumors in contact with major vessels, compared to hepatectomy with negative surgical margin. Key Word(s): 1. HCC; 2.

Serum from HCC patients contained higher concentration TGF-β1 than those from cirrhosis and healthy control. Flow cytometry indicated that blocking TGF-β1 stimulated HCC cells proliferation and knockdown it leaded to G1 arrest. Colony formation assay displayed that silencing TGF-β1 affect proliferation of cancer cells. And animal experiments showed that interference TGF-β1 decreased the metastatic nodules in lungs.

Conclusion: Cancer secreted-TGF-β1 is necessary for proliferation of HCC cells. Knockdown Trichostatin A mouse TGF-β1 could inhibit tumor growth and decrease metastases. The findings suggest that TGF-β1 could be a potential therapeutic target for HCC treatment. Key Word(s): 1. HCC; 2. TGF-β1; 3. metastasis; Presenting Author: HIROKI UCHIDA Additional Authors: YUKIO IWASHITA, KIMINORI WATANABE, TAKAHIDE KAWASAKI, YUICHIRO KAWANO, YOKO KOMORI, KAZUHIRO YADA, MASAYUKI OHTA, SEIGO KITANO Corresponding Author: HIROKI UCHIDA Affiliations: Oita university Objective: Surgical resection for hepatocellular carcinoma (HCC) is regarded as a curable treatment. A tumor adhering to the major hepatic vessels sometimes causes a need to perform hepatectomy without surgical margin. The aim of this study was to evaluate the short-term

outcomes INCB024360 datasheet of hepatectomy with null surgical margin for HCC. Methods: rom January 2010 to December 2012, 70 patients who underwent curative hepatectomy for HCC in Oita University were analyzed. They were divided into two group with null margin group and negative margin group. These two groups were compared in terms of clinicopathological characteristics, perioperative features, and short-term outcomes. 上海皓元 Results: Nineteen patients (27.1%) had been performed hepatectomy with null margin diagnosed pathologically. Mean intraoperative

blood loss was greater and operation time was longer in the null margin group as compared to those in the negative margin group. There were no significant differences in overall survival, disease free survival and other clinicopathological features between the two groups. In the null margin group, 12 patients had recurrence (59.1%) and the recurrence site was liver in all the patients. Four of the 12 patients (33%) had recurrence at the resected stump of the liver and the mean period of recurrence was 10.8 months. Conclusion: Hepatectomy with null surgical margin for HCC is technically demanding. It would lead to comparable and adequate surgical outcomes in patients with tumors in contact with major vessels, compared to hepatectomy with negative surgical margin. Key Word(s): 1. HCC; 2.

However, data about relative effectiveness of opioids and other analgesic/abortive medications Aurora Kinase inhibitor are by no means complete as different members of the opioid class have different properties and potencies, and exhaustive comparative trials have not been done. Opioids have numerous adverse effects,

some life-threatening. There is high risk for tolerance, dependency, and addiction with significant effects on patients, families, and communities. And opioid use seems to make migraines subsequently more frequent and more difficult to treat. However, there are patients for whom opioids on occasion are optimal acute treatments, for example, patients who have contraindications to ergot-type medications because of cardiovascular or cerebrovascular conditions, patients who should not receive neuroleptic medications because of QT prolongation or other contraindications, pregnant women, and patients who cannot tolerate or fail to respond to all other categories of

acute medications. In these situations, both clinician and patient should thoroughly understand the pitfalls in using opioids and make a conscious decision to use them sparingly. This will also apply to cases of secondary head pain expected to be of a time-limited course. As for prophylaxis in patients with refractory CM, regular preventive dosing can seem better than the nightmare of daily or near daily severe pain. medchemexpress And certainly, there are a handful of patients who seem to flourish with a carefully controlled regimen of methadone or long-acting morphine

preparation. Palbociclib But in the experience of most headache medicine specialists, these patients are very few in number, and this observation is borne out by the longitudinal studies. Moreover, the recent trend in overprescribing opioids for chronic non-terminal pain has led to serious individual and societal consequences that must now be addressed conscientiously. On the other hand, this approach, if done in a careful way by skilled practitioners, can be viable for selected cases. (a)  Conception and Design (a)  Drafting the Manuscript (a)  Final Approval of the Completed Manuscript “
“Primary new daily persistent headache is a rare disorder of children and adults defined by the onset of daily and unremitting headaches within 3 days of onset lasting 4 hours or more daily. There may be a link between a preceding flu-like or upper respiratory infection in about 15%, a stressful life event in 10%, or extracranial surgery in 10%. Migraine symptoms may be present in over 50%. The headache is generalized in most but may be unilateral in 11% and may be localized to any head region. The diagnosis is one of exclusion as many secondary etiologies can cause similar headaches. The pathophysiology of the primary type is unknown.

And the

RT in cancerous lesions was significantly longer than in healthy pancreas and non-cancerous lesions. With the use of quantification software, as in our study, this visual impression can thus be detected and measured with a sensitivity that is unachievable with subjective visual impressions alone. Conclusion: Contrast MAPK Inhibitor Library quantification software supplements a subjective visual assessment with objective criteria to facilitate the differential diagnosis of focal lesions in pancreatic cancer and non-cancerous lesions of pancreas, and needs further investigation. Key Word(s): 1. EUS; 2. Pancreatic diseases; 3. CHE; Presenting Author: NERUKAVV RADHAKRISHNAN Additional Authors: RAVIK SHARMA, REGI GEORGE, LAURA QUEST Corresponding Author: NERUKAVV RADHAKRISHNAN

Affiliations: The Acute Pennine Hospitals NHS Trust; The Pennine Acute Hospitals NHS Trust Objective: Buried Bumper Syndrome (BBS) is a rare complication of percutaneous endoscopic gastrostomy/jejunostomy (PEG/J) with an incidence of 1.5–1.9%. Ascertain incidence of BBS and review methods used in the management in our hospital Methods: Details of patients who had new PEG/J placed and those who developed BBS between April 1998–March 2013 were obtained from PEG Register kept in Endoscopy Unit. Results: New PEG/J- 918. 32 patients HM781-36B datasheet with 33 episodes of BBS. Male 23 mean age (MA) 51 (22–80), Female 9 MA 64 (34–87). 20/32 had PEG/J placed at Rochdale giving an incidence of 2.17%. Types of PEG: Fresenius 15 Fr-25, Fresenius 9 Fr-3. PEJ: Wilson Cook 20 Fr- 2, Freka-3. Excluding 8 patients in whom the date of insertion of PEG/J not known mean duration between insertion and BBS diagnosis was 28.4 months (3–65 months). BBS successfully removed at index gastroscopy by: Balloon traction /push technique -in 10/33 cases (in 9 patients), Forceps pull-1, Quill technique-1. In 13 patients 9 Fr and in 1 patient 15 Fr Fresenius gastrostomy tube through the bumper track placed with continuation of feeding. 8/14 of the above (57%) had their

buried flanges gradually 上海皓元 resurfaced and later removed endoscopically after a mean of 4.7 months (1–20 months). Remaining 7 patients – 1-removed by minilap, 4-side by side PEG placed, 1-jejunal tube placement, 1-died from abdominal wall abscess. Conclusion: Incidence of BBS – 2.17%. 31/33 cases associated with Fresenius make. Buried flange successfully removed endoscopically in 20/33 (61%). Balloon method successful at first attempt in 30%. Our experience suggests in difficult patients, placing a 9 or 15 Fr Fresenius gastrostomy tube via buried bumper track may enable release of buried bumper and facilitate its endoscopic removal at a later stage. Key Word(s): 1. Buried Bumper; 2. Gastrostomy; 3. Complication; 4.