We wanted Ribociclib order to test our hypothesis that TNFα plays a dual role in LPS/D-galN-induced liver injury, first acting as a proapoptotic mediator of liver damage, and later as an important hepatoprotective factor. We therefore

injected infliximab 4 hours after LPS/D-galN injection. Interestingly, a late administration of anti-TNFα indeed resulted in a loss of NS3/4A-mediated resistance (Fig. 6). This indicates that the sustained increase in intrahepatic TNFα levels seen in NS3/4A-Tg mice mediates the hepatoprotective effects of TNFα (Fig. 4). LPS is sensed in the liver mainly by TLR4 expressed on the surface of Kupffer cells, which are the liver-specific macrophages, and liver sinusoidal endothelial cells. In response to TLR4, these cells release proinflammatory cytokines such as TNFα. In

human hepatitis, intrahepatic macrophages are the main producers of TNFα. We therefore investigated the expression levels of CCL2 (monocyte chemoattractant protein 1), which represents the main chemokine involved in intrahepatic activation and recruitment of monocytes/macrophages. We found that CCL2 protein levels were enhanced both in untreated and LPS/D-galN-treated livers of NS3/4A-Tg mice as compared to the corresponding WT mice (Fig. 7). This was paralleled by a higher number of F4/80 antigen-positive cells in LPS/D-galN-treated livers of NS3/4A-Tg mice as compared to WT mice (43.70 ± 5.83 versus 28.50 ± 3.37 positive Proteasome inhibitor cells per 10 mm2 of liver, P < 0,0001, Mann-Whitney; Fig. 4B) which may be due to increased CCL2-mediated recruitment of macrophages

to the liver. Thus, the NS3/4A-mediated resistance to LPS/D-galN and TNFα/D-galN in our NS3/4A-Tg mice may be caused by increased CCL2 expression resulting in induction of TNFα production and subsequent NFκB activation, which provokes a paracrine loop with further release of TNFα and check details activation of NFκB. It is well known that patients with chronic HCV infection have increased serum levels of TNFα, a potent proinflammatory factor with a broad spectrum of effects. A major concern in patients with chronic HCV and rheumatoid arthritis has been that the effective block of TNFα conferred by the new class of anti-TNFα agents should have deleterious effects on the HCV infection; however, this has not been the case. On the contrary, when anti-TNFα compounds are added to SOC therapy in patients with chronic HCV, treatment results improve.9 This highly unexpected finding suggests that TNFα has effects that actually promote the viral infection. We therefore used our NS3/4A-Tg mouse model, which we have shown has a reduced sensitivity to TNFα, to elucidate these issues further. We have shown that the NS3/4A complex exerts protective effects toward hepatotoxic stimuli such as LPS/D-galN, TNFα/D-galN, and CCl4 in NS3/4A-Tg mice. All of these compounds induce liver injury, at least in part, through TNFα.

We wanted GDC-0068 molecular weight to test our hypothesis that TNFα plays a dual role in LPS/D-galN-induced liver injury, first acting as a proapoptotic mediator of liver damage, and later as an important hepatoprotective factor. We therefore

injected infliximab 4 hours after LPS/D-galN injection. Interestingly, a late administration of anti-TNFα indeed resulted in a loss of NS3/4A-mediated resistance (Fig. 6). This indicates that the sustained increase in intrahepatic TNFα levels seen in NS3/4A-Tg mice mediates the hepatoprotective effects of TNFα (Fig. 4). LPS is sensed in the liver mainly by TLR4 expressed on the surface of Kupffer cells, which are the liver-specific macrophages, and liver sinusoidal endothelial cells. In response to TLR4, these cells release proinflammatory cytokines such as TNFα. In

human hepatitis, intrahepatic macrophages are the main producers of TNFα. We therefore investigated the expression levels of CCL2 (monocyte chemoattractant protein 1), which represents the main chemokine involved in intrahepatic activation and recruitment of monocytes/macrophages. We found that CCL2 protein levels were enhanced both in untreated and LPS/D-galN-treated livers of NS3/4A-Tg mice as compared to the corresponding WT mice (Fig. 7). This was paralleled by a higher number of F4/80 antigen-positive cells in LPS/D-galN-treated livers of NS3/4A-Tg mice as compared to WT mice (43.70 ± 5.83 versus 28.50 ± 3.37 positive PF-01367338 supplier cells per 10 mm2 of liver, P < 0,0001, Mann-Whitney; Fig. 4B) which may be due to increased CCL2-mediated recruitment of macrophages

to the liver. Thus, the NS3/4A-mediated resistance to LPS/D-galN and TNFα/D-galN in our NS3/4A-Tg mice may be caused by increased CCL2 expression resulting in induction of TNFα production and subsequent NFκB activation, which provokes a paracrine loop with further release of TNFα and check details activation of NFκB. It is well known that patients with chronic HCV infection have increased serum levels of TNFα, a potent proinflammatory factor with a broad spectrum of effects. A major concern in patients with chronic HCV and rheumatoid arthritis has been that the effective block of TNFα conferred by the new class of anti-TNFα agents should have deleterious effects on the HCV infection; however, this has not been the case. On the contrary, when anti-TNFα compounds are added to SOC therapy in patients with chronic HCV, treatment results improve.9 This highly unexpected finding suggests that TNFα has effects that actually promote the viral infection. We therefore used our NS3/4A-Tg mouse model, which we have shown has a reduced sensitivity to TNFα, to elucidate these issues further. We have shown that the NS3/4A complex exerts protective effects toward hepatotoxic stimuli such as LPS/D-galN, TNFα/D-galN, and CCl4 in NS3/4A-Tg mice. All of these compounds induce liver injury, at least in part, through TNFα.

To prevent postpartum haemorrhage after delivery, women selleck screening library routinely receive oxytocin,

which also causes fluid retention. Administration of DDAVP, combined with litres of fluids and oxytocin, may result in life-threatening hyponatraemia [70]. A single dose of DDAVP immediately prior to epidural catheter placement in labour, however, has not been associated with adverse events [71]. Among the published series of VWD in pregnancy there are multiple cases of postpartum haemorrhage that occurred despite prophylaxis [18]. In a review of published cases of women with VWD who experienced postpartum haemorrhage, Roque et al. [72] determined that the average time of haemorrhage was 15.7 ± 5.2 days after delivery. The implication is that women with bleeding disorders may require more frequent evaluation. Thus, weekly contact is suggested during the postpartum period [73]. Prophylaxis, when indicated, may be required for two or more weeks. More data are required to determine Quizartinib cost optimal length of prophylaxis. Data on the management of women with bleeding disorders are hampered by a lack of randomized trials, case-control studies or even large case series. No one centre sees a large

number of patients. Severe bleeding disorders are rare and women with milder disease may not come to the attention of a haemostasis centre or even be diagnosed. Funding for studies is limited. In the absence of strong evidence to direct

practice, government agencies and haemophilia organizations have developed consensus guidelines. There are at least nine sets of guidelines published by the government agencies or haemophilia organizations that specifically address women with bleeding disorders. The guidelines were reviewed and summarized in 2009 and found to be remarkably congruent [74]. The good news is that there selleckchem is consensus regarding many of the issues pertaining to the management of women with bleeding disorders. “
“Summary.  The development of inhibitors to the infused factor in patients with haemophilia is a serious clinical problem. Recent evidence suggests that alongside the strong genetic contribution to inhibitor formation, there are a number of non-genetic factors – perceived by the immune system as danger signals – which promote formation of inhibitors. This study provides a comprehensive review of clinical studies relating to these factors and also presents a survey of opinion concerning their importance and clinical influence, conducted among the members of the European Haemophilia Treatment Standardisation Board (EHTSB).

To prevent postpartum haemorrhage after delivery, women LDK378 mw routinely receive oxytocin,

which also causes fluid retention. Administration of DDAVP, combined with litres of fluids and oxytocin, may result in life-threatening hyponatraemia [70]. A single dose of DDAVP immediately prior to epidural catheter placement in labour, however, has not been associated with adverse events [71]. Among the published series of VWD in pregnancy there are multiple cases of postpartum haemorrhage that occurred despite prophylaxis [18]. In a review of published cases of women with VWD who experienced postpartum haemorrhage, Roque et al. [72] determined that the average time of haemorrhage was 15.7 ± 5.2 days after delivery. The implication is that women with bleeding disorders may require more frequent evaluation. Thus, weekly contact is suggested during the postpartum period [73]. Prophylaxis, when indicated, may be required for two or more weeks. More data are required to determine Sorafenib nmr optimal length of prophylaxis. Data on the management of women with bleeding disorders are hampered by a lack of randomized trials, case-control studies or even large case series. No one centre sees a large

number of patients. Severe bleeding disorders are rare and women with milder disease may not come to the attention of a haemostasis centre or even be diagnosed. Funding for studies is limited. In the absence of strong evidence to direct

practice, government agencies and haemophilia organizations have developed consensus guidelines. There are at least nine sets of guidelines published by the government agencies or haemophilia organizations that specifically address women with bleeding disorders. The guidelines were reviewed and summarized in 2009 and found to be remarkably congruent [74]. The good news is that there check details is consensus regarding many of the issues pertaining to the management of women with bleeding disorders. “
“Summary.  The development of inhibitors to the infused factor in patients with haemophilia is a serious clinical problem. Recent evidence suggests that alongside the strong genetic contribution to inhibitor formation, there are a number of non-genetic factors – perceived by the immune system as danger signals – which promote formation of inhibitors. This study provides a comprehensive review of clinical studies relating to these factors and also presents a survey of opinion concerning their importance and clinical influence, conducted among the members of the European Haemophilia Treatment Standardisation Board (EHTSB).

All enrolled participants received comprehensive information about this study, and informed consent

was obtained before any study-related processes began. The study was conducted at Hanyang University Hospital in Korea between March 2011 and August 2011, and was approved by the Clinical Research Ethics Committee of the Hanyang University Hospital of Korea (2010-04-009). After a 2-week run-in period, enrolled patients were randomly assigned to receive either one capsule (500 mg) of LacClean Gold-S (Cell Biotech, Co. Ltd, Gimpo, Korea; a multispecies probiotics) Ixazomib solubility dmso or one capsule (500 mg) of a placebo twice daily (total dosage 1000 mg/day) for 4 weeks (Fig. 1). The patients were instructed to take the study product between meals because the increased gastric pH is more favorable for the ingested bacteria. LacClean Gold-S is a capsule-form probiotics containing six species this website of live bacteria. The six strains of probiotics were Bifidobacterium bifidum (KCTC 12 199BP), Bifidobacterium lactis (KCTC 11 904BP), Bifidobacterium longum (KCTC 12 200BP), Lactobacillus acidophilus (KCTC 11 906BP), Lactobacillus rhamnosus (KCTC 12 202BP), and Streptococcus thermophilus (KCTC 11 870BP). A total of 5 × 109 viable cells in a lyophilized powder form were included in each

capsule and constituted 13.1% (w/w) of the total weight (500 mg/capsule). The amount of probiotics equally consisted in each of the six strains. The dose was determined based on previous studies where the daily doses were see more between 5 × 107 and 3.6 × 1011 colony forming units (CFUs)/day, and ≥ 5 × 109 CFUs/day has been suggested.[9-11] The placebo powder contained the same

“other ingredients” as the active medication and maltodextrin instead of bacteria. OY Lee and KN Lee enrolled the patients for this study. Patients were allocated to the probiotics or placebo group using a computer-generated randomization schedule with a 1 : 1 allocation ratio. Dr. Jun generated the random allocation sequence, and no one but him knew the allocation sequence. The practice nurse gave a questionnaire and explained the protocol to the patients. The nurse did not know the allocation sequence and met the patients in regular sequence. The patient received the medication from the clinical pharmacist. No one could differentiate the two drugs without the sequence information. Stool samples for fecal microflora analysis were obtained immediately before the start of treatment and at the end of the 4 weeks of treatment. Fecal microbiota was analyzed only from patients who agreed to the stool sample collection. IBS symptoms were assessed by examiners and patients at baseline and week 4 using a questionnaire. Global relief of IBS symptoms, drug compliance, and adverse events were evaluated by a questionnaire after the 4 weeks of treatment. The primary efficacy end-point was the proportion of patients who experienced global relief of IBS symptoms after the 4-week treatment.

All enrolled participants received comprehensive information about this study, and informed consent

was obtained before any study-related processes began. The study was conducted at Hanyang University Hospital in Korea between March 2011 and August 2011, and was approved by the Clinical Research Ethics Committee of the Hanyang University Hospital of Korea (2010-04-009). After a 2-week run-in period, enrolled patients were randomly assigned to receive either one capsule (500 mg) of LacClean Gold-S (Cell Biotech, Co. Ltd, Gimpo, Korea; a multispecies probiotics) Everolimus in vivo or one capsule (500 mg) of a placebo twice daily (total dosage 1000 mg/day) for 4 weeks (Fig. 1). The patients were instructed to take the study product between meals because the increased gastric pH is more favorable for the ingested bacteria. LacClean Gold-S is a capsule-form probiotics containing six species selleck chemicals of live bacteria. The six strains of probiotics were Bifidobacterium bifidum (KCTC 12 199BP), Bifidobacterium lactis (KCTC 11 904BP), Bifidobacterium longum (KCTC 12 200BP), Lactobacillus acidophilus (KCTC 11 906BP), Lactobacillus rhamnosus (KCTC 12 202BP), and Streptococcus thermophilus (KCTC 11 870BP). A total of 5 × 109 viable cells in a lyophilized powder form were included in each

capsule and constituted 13.1% (w/w) of the total weight (500 mg/capsule). The amount of probiotics equally consisted in each of the six strains. The dose was determined based on previous studies where the daily doses were learn more between 5 × 107 and 3.6 × 1011 colony forming units (CFUs)/day, and ≥ 5 × 109 CFUs/day has been suggested.[9-11] The placebo powder contained the same

“other ingredients” as the active medication and maltodextrin instead of bacteria. OY Lee and KN Lee enrolled the patients for this study. Patients were allocated to the probiotics or placebo group using a computer-generated randomization schedule with a 1 : 1 allocation ratio. Dr. Jun generated the random allocation sequence, and no one but him knew the allocation sequence. The practice nurse gave a questionnaire and explained the protocol to the patients. The nurse did not know the allocation sequence and met the patients in regular sequence. The patient received the medication from the clinical pharmacist. No one could differentiate the two drugs without the sequence information. Stool samples for fecal microflora analysis were obtained immediately before the start of treatment and at the end of the 4 weeks of treatment. Fecal microbiota was analyzed only from patients who agreed to the stool sample collection. IBS symptoms were assessed by examiners and patients at baseline and week 4 using a questionnaire. Global relief of IBS symptoms, drug compliance, and adverse events were evaluated by a questionnaire after the 4 weeks of treatment. The primary efficacy end-point was the proportion of patients who experienced global relief of IBS symptoms after the 4-week treatment.

All enrolled participants received comprehensive information about this study, and informed consent

was obtained before any study-related processes began. The study was conducted at Hanyang University Hospital in Korea between March 2011 and August 2011, and was approved by the Clinical Research Ethics Committee of the Hanyang University Hospital of Korea (2010-04-009). After a 2-week run-in period, enrolled patients were randomly assigned to receive either one capsule (500 mg) of LacClean Gold-S (Cell Biotech, Co. Ltd, Gimpo, Korea; a multispecies probiotics) Opaganib research buy or one capsule (500 mg) of a placebo twice daily (total dosage 1000 mg/day) for 4 weeks (Fig. 1). The patients were instructed to take the study product between meals because the increased gastric pH is more favorable for the ingested bacteria. LacClean Gold-S is a capsule-form probiotics containing six species selleck products of live bacteria. The six strains of probiotics were Bifidobacterium bifidum (KCTC 12 199BP), Bifidobacterium lactis (KCTC 11 904BP), Bifidobacterium longum (KCTC 12 200BP), Lactobacillus acidophilus (KCTC 11 906BP), Lactobacillus rhamnosus (KCTC 12 202BP), and Streptococcus thermophilus (KCTC 11 870BP). A total of 5 × 109 viable cells in a lyophilized powder form were included in each

capsule and constituted 13.1% (w/w) of the total weight (500 mg/capsule). The amount of probiotics equally consisted in each of the six strains. The dose was determined based on previous studies where the daily doses were check details between 5 × 107 and 3.6 × 1011 colony forming units (CFUs)/day, and ≥ 5 × 109 CFUs/day has been suggested.[9-11] The placebo powder contained the same

“other ingredients” as the active medication and maltodextrin instead of bacteria. OY Lee and KN Lee enrolled the patients for this study. Patients were allocated to the probiotics or placebo group using a computer-generated randomization schedule with a 1 : 1 allocation ratio. Dr. Jun generated the random allocation sequence, and no one but him knew the allocation sequence. The practice nurse gave a questionnaire and explained the protocol to the patients. The nurse did not know the allocation sequence and met the patients in regular sequence. The patient received the medication from the clinical pharmacist. No one could differentiate the two drugs without the sequence information. Stool samples for fecal microflora analysis were obtained immediately before the start of treatment and at the end of the 4 weeks of treatment. Fecal microbiota was analyzed only from patients who agreed to the stool sample collection. IBS symptoms were assessed by examiners and patients at baseline and week 4 using a questionnaire. Global relief of IBS symptoms, drug compliance, and adverse events were evaluated by a questionnaire after the 4 weeks of treatment. The primary efficacy end-point was the proportion of patients who experienced global relief of IBS symptoms after the 4-week treatment.

infestans; the cultivars included in this study with their respective foliar and tuber ratings in parentheses were Jacqueline Lee [resistant (R), moderately resistant (MR); (Douches et al. 2001)] and Missaukee [R, intermediate (I); (Douches et al. 2010)]. Other cultivars used in this study were FL1879 [susceptible (S,S)], Russet Burbank

[moderately susceptible (MS),S], Red Norland find more (S,S) and Monticello (S,S) (Douches et al. 1997; Porter et al. 2004). Potato tubers were stored at 3°C in the dark at 90% relative humidity (RH) until used. Tubers were warmed to 15°C in incremental steps of 2°C for 7 days before inoculation. Tubers for the experiments were within the size grade range 50–150 mm diameter (any plane). Visual examination of a random sample of tubers from each entry for disease symptoms indicated that tubers were free from late blight. The samples were further tested with an ELISA immunodiagnostic for Phytophthora sp. (Alert Multiwell kit – Phytophthora sp. Neogen Corporation, Lansing, MI, USA) according to the manufacturer’s instructions; P. infestans was not detected in any of the see more tubers. Prior to inoculation, all tubers were washed with water to remove soil. The tubers were surface-disinfested by soaking in a 2% sodium hypochlorite solution for 30 min. Tubers were dried in a controlled environment chamber with continuous

airflow at 15°C in dry air (30% RH) for 4 h prior to inoculation. After inoculation, tubers were stored at 10°C and maintained for 30 days in the dark in a controlled environment chamber at 90% RH. Characteristics of the twelve different P. infestans isolates used in this study are summarized in Table 1. The selected Michigan

isolates were from the collection of W.W. Kirk (MSU, USA), US-8 and US-22 reference isolates were provided by Dr. W.E. Fry (Cornell University, USA), Colombian isolates were provided by Dr. Silvia Restrepo (LAMFU, Los Andes University, Colombia), and UK isolates were provided by Dr. David Cooke (The James Hutton Institute, Scotland, UK). For learn more lenticel infection experiment, isolates US-8F and Pi10-012 were selected due to their virulence on tuber tissue. The isolates were re-activated on inoculated leaf tissue and transferred into rye B media for 14 days in the dark at 18°C for sporangia production and transferred to the light for 2 days to encourage sporulation. Sporangia and mycelium were harvested by flooding with cold sterile water (4°C) and gentle scraping of the surface of the culture using a rubber policeman. The mycelium/sporangia suspension was stirred with a magnetic stirrer for 1 h. The suspension was strained through four layers of sterile cheesecloth, and the sporangia concentration was measured with a hemocytometer and adjusted to approximately 1 × 104 total sporangia/ml (discharged and non-discharged).

infestans; the cultivars included in this study with their respective foliar and tuber ratings in parentheses were Jacqueline Lee [resistant (R), moderately resistant (MR); (Douches et al. 2001)] and Missaukee [R, intermediate (I); (Douches et al. 2010)]. Other cultivars used in this study were FL1879 [susceptible (S,S)], Russet Burbank

[moderately susceptible (MS),S], Red Norland Sirolimus cost (S,S) and Monticello (S,S) (Douches et al. 1997; Porter et al. 2004). Potato tubers were stored at 3°C in the dark at 90% relative humidity (RH) until used. Tubers were warmed to 15°C in incremental steps of 2°C for 7 days before inoculation. Tubers for the experiments were within the size grade range 50–150 mm diameter (any plane). Visual examination of a random sample of tubers from each entry for disease symptoms indicated that tubers were free from late blight. The samples were further tested with an ELISA immunodiagnostic for Phytophthora sp. (Alert Multiwell kit – Phytophthora sp. Neogen Corporation, Lansing, MI, USA) according to the manufacturer’s instructions; P. infestans was not detected in any of the ABT-263 cell line tubers. Prior to inoculation, all tubers were washed with water to remove soil. The tubers were surface-disinfested by soaking in a 2% sodium hypochlorite solution for 30 min. Tubers were dried in a controlled environment chamber with continuous

airflow at 15°C in dry air (30% RH) for 4 h prior to inoculation. After inoculation, tubers were stored at 10°C and maintained for 30 days in the dark in a controlled environment chamber at 90% RH. Characteristics of the twelve different P. infestans isolates used in this study are summarized in Table 1. The selected Michigan

isolates were from the collection of W.W. Kirk (MSU, USA), US-8 and US-22 reference isolates were provided by Dr. W.E. Fry (Cornell University, USA), Colombian isolates were provided by Dr. Silvia Restrepo (LAMFU, Los Andes University, Colombia), and UK isolates were provided by Dr. David Cooke (The James Hutton Institute, Scotland, UK). For find more lenticel infection experiment, isolates US-8F and Pi10-012 were selected due to their virulence on tuber tissue. The isolates were re-activated on inoculated leaf tissue and transferred into rye B media for 14 days in the dark at 18°C for sporangia production and transferred to the light for 2 days to encourage sporulation. Sporangia and mycelium were harvested by flooding with cold sterile water (4°C) and gentle scraping of the surface of the culture using a rubber policeman. The mycelium/sporangia suspension was stirred with a magnetic stirrer for 1 h. The suspension was strained through four layers of sterile cheesecloth, and the sporangia concentration was measured with a hemocytometer and adjusted to approximately 1 × 104 total sporangia/ml (discharged and non-discharged).

Methods: Subjects were 83 patients with ampullary tumor (62 patients: endoscopic snare papillectomy; 21 patients: surgical resection). EUS and IDUS were performed preoperatively to evaluate focal extension as possible. Outcome was also evaluated who were treated by endoscopic snare papillectomy. Results: The final pathological diagnosis was adenoma in 36 patients, carcinoma in adenoma in 10 patients, adenocarcinoma in 27 patients, neuroendocrine tumor in 4 patients, regenerative change or hyperplasia in 6 patients. The accuracy of preoperative biopsy was 71%. EUS had diagnostic accuracy of 88% for duodenal invasion, 92% for extension into bile duct and 98% for extension

into pancreatic duct. IDUS had diagnostic accuracy of 88% for duodenal SCH727965 invasion, 86% into bile duct and 94% into pancreatic duct. Success rate of endoscopic snare papillectomy was 89%. Follow-up endoscopy revealed recurrent/residual adenoma in 2 patients, carcinoma in adenoma in 1 GPCR Compound Library manufacturer patient and adenocarcinoma in 1 patient. 1 patient in carcinoma in adenoma

and 1 patient in adenocarcinoma were resected endoscopically, 2 patients in adenoma and 1 patient in adenocarcinoma were resected surgically. Conclusion: Endoscopic snare papillectomy is useful as complete biopsy. EUS and IDUS are highly capable of evaluating tumors of the major duodenal papilla preoperatively. However, these techniques are not sufficient to evaluate focal extension preoperatively for carcinoma. At the current point in time, endoscopic snare papillectomy is adequate at treating adenoma and carcinoma in adenoma. Key Word(s): 1. Ampullary Tumor; 2. EUS; 3. IDUS; Presenting Author: XUEFENG LU Corresponding Author: XUEFENG LU Affiliations: Qilu hospital of Shandong university Objective: Endoscopic submucosal dissection (ESD) which is a kind of minimally invasive technology is to use all kinds of electric knives to resect gastrointestinal lesions under

endoscopy. It is reported that ESD is a safe and effective method for gastrointestinal lesions with low recurrence rate, few complications, less pain and short hospitalization days. But recently it has developed a new kind of minimally invasive treatment technology this website – Endoscopic Submucosal Tunnel Dissection (ESTD) on the basis of ESD. The purpose of the study is to explore the clinical value of ESTD by comparing the ESTD and ESD in the treatment of the esophageal submucosal protrusion lesions. Methods: From Jan. 2011 to Feb. 2013, 42 patients with 44 lesions in gastroesophageal submucosa were treated with ESE in Qilu Hospital of Shandong University. Efficacy and safety were evaluated based on their status. Results: 27 of the 42 patients were male. Of all the 44 lesions, 17 originated from the esophagus. The mean tumor size was 1.52 (0.5∼3.0) cm. Media age of patients were 53 (18∼67) yrs. The mean hospital stay was 8.2 (6∼12) days. Complications were evaluated in post-ESE hemorrhage and perforation.