The situation with plasma-derived products is variable, depending on the nature of the product and

the test systems used. For instance, in a study by Lee et al. [35] Hemofil M was found to give a 20% discrepancy in postinfusion plasmas between one-stage and chromogenic methods, whereas in a study of a similar product performed at CLB, there was no difference between the methods. Equivalence between the methods was also found in a UK NEQAS study on a postinfusion sample VDA chemical from a different type of plasma-derived concentrate. A practical solution to this problem, which has been discussed by the FVIII/FIX Subcommittee of ISTH/SSC, is to regard the postinfusion samples as concentrates ‘diluted’ in a patient’s plasma, which is essentially what they are, and to use a concentrate standard diluted in haemophilic plasma, instead of a plasma standard, to construct the standard curve. This then provides a “like vs like” situation, and hence should provide good agreement on in vivo recoveries of recombinant concentrates when measured by chromogenic and one-stage methods. However, the nature of the concentrate standard needs to be carefully considered; it should be as similar as possible to the injected product. Thus, whereas either of the full-length recombinant concentrates could serve

as a standard for the other, plasma samples following infusion of the B-domain deleted product, ReFacto,

see more would need a Refacto concentrate standard. This approach has been tested in in vivo recovery studies, in which patients’ samples after infusion of Recombinate, Kogenate and Alphanate were assayed against both a plasma standard and a concentrate standard. As shown in Table 1, Mephenoxalone for Recombinate and Kogenate the discrepancy between one-stage and chromogenic methods using the plasma standard was completely abolished with the appropriate concentrate standard. However, in the case of Alphanate, the use of a concentrate standard, in this case not the same as the product infused, made the situation worse. Therefore, the use of concentrate standards needs to be product specific, and should probably be restricted to recombinant and very high-purity plasma-derived products. As indicated in the previous section, this approach will probably be necessary for some of the new modified FVIII and FIX products, particularly the long-lasting pegylated molecules, because of major discrepancies between methods when compared to plasma FVIII and FIX. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“The availability of safe and effective factor replacement therapies, in persons with haemophilia (PWH), has in some countries answered the basic need for treatment of these patients.

Methods: 72 tumor BGJ398 mouse patients undergoing chemotherapy who met the inclusion criteria were randomly divided into control group and experimental group.34 cases were in the control group,and 38 cases the experimental group. We used wrist electric acupuncture apparatus to stimulate PC 6 and PC 5 (1 h,bid)combined with Granisetron(3 mg iv bid) for the experimental group while stimulating false PC 6 and false PC 5 for the control goup. To observe the serum levels of 5-hydroxy

tryptamine and dopamine before and after chemotherapy. Results: There was no difference in serum levels of 5-hydroxy tryptamine and dopamine between the two groups before treatment;serum levels of 5-hydroxy tryptamine and dopamine had no significant differences before and after treatment in the control group,after treatment,they were significantly lower than that before the treatment in the experimental group(p < 0.05). Conclusion: wrist electric acupuncture apparatus stimulating Neiguan point and Jianshi point combined with Granisetron could obviously reduce the nausea of tumor patients undergoing chemotherapy,the mechanism of which may be related to reducing the serum levels of 5-hydroxy tryptamine and dopamine levels. Key Word(s): 1. electric acupuncture; 2. CINV; 3. 5-hydroxy tryptamine; 4. dopamine; Presenting Author:

JING JIANG Additional Authors: XUEYUAN CAO, DONGHUI CAO, LIN MA, RU-MING this website LIU Corresponding Author: XUEYUAN CAO Affiliations: First Hospital of Jilin Fluorometholone Acetate University Objective: 18β-Glycyrrhetinic acid (GRA) was identified as a potent anti-virus, anti-inflammatory compound. It could prevent tumor cell growth. Micro RNAs (miRNA) negatively regulate protein-coding genes at

the posttranscriptional level and are critical in tumorigenesis. MiRNA-7 is considered a tumor suppressor factor in gastric cancer. Expression levels of miRNA-7 significantly decreased in the animal model of gastric carcinogenesis. This study investigated the effects of GRA on the gastric cancer animal model and its molecular mechanisms. Methods: K19-C2mE transgenic animal model of gastric tumor was established by Oshima M. Six-week-old gerbils were randomly divided into two groups: Normal control group (n = 40) and GRA group ((n = 40, drinking water containing 0.05% GRA). Specimens of gastric mucosa were collected after 52 weeks. The incidence of gastric cancer and tumor size were detected. The expression levels of miRNA-7 were detected by real- time quantitive PCR. Results: The survival rate of mice was over 90%. Results show that cancer incidence as the control group 97.6%, the incidence dropped to 73.5% in the GRA group (P < 0.01). Tumor size was significantly reduced in the GRA group (6.0 vs. 4.0 cm; P < 0.01), GRA significant decreased the severity of gastritis in the treatment group.

3%). About half of the patients were associated with a previous history of aspiration pneumonia. The common preoperative nutrition was transnasal nutrition in 155 patients (55.2%), followed by peripheral parenteral nutrition alone and in combination with oral feeding in each 45 (16.0%) and parenteral nutrition in 20 (9.6%). Methods for gastrostomy included an introducer Rapamycin ic50 method in 24 patients and a push method in 257 (bumper-button-type in 221 and bumper-tube-type in 36). Early complications within 30 postoperative

days were noted in 62 patients (22.0%); wound infection in 27 (peritonitis in 7), aspiration pneumonia in 17, and wound bleeding in 8. Early death within 30 postoperative days occurred in 13 patients (4.6%) due to peritonitis (3 patients), aspiration pneumonia (3), underlying diseases (5), and other cases (2). For comparison, the patients were divided into two groups based on a preoperative serum albumin level <3.0 mg/dL (137 patients; A group) or ≥3.0 mg/dL (144; B group). Early postoperative complications were observed in 35 and 27 patients of the A (25.5%) and B groups (18.7%), respectively. This suggests no significant difference but a trend toward more common early postoperative complications for the A group. Early postoperative death occurred in 11 and 2 patients of the A and B groups, respectively, showing a significantly

HDAC inhibitor higher mortality rate for the A group (p < 0. 01). Followed-up were possible for 134 of the patients. The outcomes were survival in 40 patients (29.2%), death in 89 (66.4%), and possible oral feeding resulting in a removal of gastrostomy in 5 (3.7%). The cause of the 89 deaths was primarily underlying diseases (48 patients), followed by aspiration pneumonia (25). The mean survival was 7.5 months. Conclusion: PEG is an invasive procedure where preoperative evaluation of general conditions and nutrition management are important. We

may need to carefully consider whether a patient is indicated for the procedure. Key Word(s): 1. percutaneous endoscopic gastrostomy Presenting Author: XIU QING WEI Additional Authors: JIN TAO, BIN WU Corresponding Author: XIUQING WEI Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University; Third Affiliated Hospital, Sun Yat-Sen University Objective: To introduce an uncommon cause Etomidate of abdominal pain mimicking appendicitis. Methods: The medical course of a rare patient with abdominal pain mimicking appendicitis caused by toothpick perforation of the intestine was presented in brief. Results: We present a case of a 37-year old man who had suffered a sudden right lower abdominal pain for three days. On physical examination, he was afebrile and lower right abdominal tenderness and tender flank on palpation was found. The white blood cell increased dramatically. Acute appendicitis was suspected by ultrasound B examination.

7). These data clearly reveal a role for hepatic leptin signaling in regulating lipase activity in the liver. Similar to mice that have a liver-specific loss

of leptin signaling, Ad-β-gal-treated db/db mice also had a ∼30% decrease in non-LPL activity in the liver compared with C57BL/6 controls (Fig. 6D), and this correlated with a decrease in hepatic HL mRNA (Fig. 5C). When functional leptin receptors were overexpressed in the livers of db/db mice, non-LPL activity increased even beyond levels seen in wild-type mice (Fig. 6D). Furthermore, control db/db mice had a two-fold increase in LPL activity levels, and when db/db mice were treated with Ad-Lepr-b, LPL activity returned to wild-type levels (Fig. 6E). We also observed that in the total lack of leptin signaling, hepatic LPL activity contributed to 60% of total triglyceride lipase

activity in the liver, and when learn more leptin signaling was selectively restored to the liver, hepatic LPL activity contributed only 20% to total triglyceride lipase activity, which is similar to wild-type levels (Fig. 6F). These data from two complementary models reveal a novel role for hepatic leptin signaling in modulating lipase activity in the liver. However, the manner (transcriptional versus posttranscriptional) by which lipase activity in the liver is regulated in mice with a life-long loss of hepatic leptin signaling and mice with an induced gain of hepatic leptin signaling is different (Figs. 5 and 6). Nonetheless, the functional end result is that with

a loss of hepatic leptin signaling, Omipalisib ic50 non-LPL lipase activity is decreased and LPL activity is Farnesyltransferase increased. To determine whether these effects of leptin on apoB transcription and lipase activity in the liver are due to direct or indirect actions of leptin, we treated ob/ob mice with acute leptin injections as well as chronic leptin infusions, which restored leptin signaling to all tissues. Acute leptin injections increased apoB mRNA in the liver by nearly 60%, but chronic low-dose leptin treatment had no effect (Supporting Fig. 3A). Further, while liver-selective restoration of leptin signaling in db/db mice decreased hepatic LPL expression back toward wild-type levels (Fig. 5D), acute leptin injections into ob/ob mice increased hepatic LPL mRNA (Supporting Fig. 3C). Therefore, the increase in hepatic LPL mRNA in ob/ob mice after acute leptin treatment is likely a result of leptin action outside of the liver. Interestingly, we previously observed that a whole body loss of leptin signaling has distinct effects, in fact opposite, from a liver specific loss of leptin signaling with respect to glucose homeostasis.13 Notably, chronic low-dose leptin did not change hepatic LPL mRNA expression in ob/ob mice (Supporting Fig.

5%) or tegobuvir/GS-9256/Peg-IFN/RBV arm (26.7%). Patients in all treatment arms had an initial sharp decline in plasma HCV RNA levels during the first 48 hours of therapy (Fig. 1). In the tegobuvir/GS-9256 arm, this decrease was generally maintained through day 7, after which HCV RNA levels began to rebound, associated with the emergence (i.e., detection) of resistance-associated variants. The addition of RBV to the treatment regimen increased the magnitude, extent, and duration of viral reduction; in the tegobuvir/GS-9256/RBV

arm, reductions in HCV RNA levels were observed through day 14 and were generally maintained through day 28. The addition of Peg-IFN alpha-2a had selleck chemical a similar additive effect; in the tegobuvir/GS-9256/Peg-IFN/RBV arm, reductions in HCV RNA levels were observed through day 28. The association of IL28B genotype

and initial antiviral response was variable, with a trend toward a greater magnitude of HCV RNA reductions in IL28B CC patients. No differences in mean maximal HCV RNA reduction by HCV subtype (i.e., 1a or 1b) were observed. Virologic responses in the 4 patients infected with other HCV-1 subtypes are presented in the Supporting Table. In each case, HCV RNA reductions from baseline during randomized therapy ranged from −0.75 to −2.84 log10 IU/mL. After the switch to Peg-IFN/RBV, RXDX-106 continued VL reductions were observed, ranging from −2.98 to −5.23 log10 IU/mL from baseline by week 6. In the primary efficacy analysis, a greater percentage of patients achieved RVR after receiving tegobuvir/GS-9256 in combination with RBV (38%), compared with tegobuvir/GS-9256 alone (7%) (Table 3). All patients (14 of 14) receiving tegobuvir/GS-9256 in combination with Peg-IFN/RBV achieved RVR. Excluding data points after the early introduction of Peg-IFN/RBV, the median

(i.e., Q1 and Q3) maximal reduction in HCV RNA was highest for patients receiving tegobuvir/GS-9256/Peg-IFN/RBV, −5.7 (−5.9, −5.5) log10 IU/mL, versus Fenbendazole −5.1 (−5.3, −4.4) for tegobuvir/GS-9256/RBV, and −4.1 (−4.4, −2.9) for tegobuvir/GS-9256 alone. Viral breakthrough was most common in the tegobuvir/GS-9256 arm, where the majority of patients (80%) started standard of care with Peg-IFN and RBV before day 28. Although RBV decreased and delayed breakthrough, in the tegobuvir/GS-9256/RBV arm, 31% started standard of care early because of the observed increases in HCV RNA at or before day 28. None of the patients receiving tegobuvir/GS-9256/Peg-IFN/RBV experienced viral plateau or rebound through day 28. For patients in the tegobuvir/GS-9256 arm who had an increase in HCV RNA levels observed at days 14 or 21, HCV RNA levels declined again by day 28 after initiating Peg-IFN and RBV. Among the patients who either did not experience early response or had viral rebound, several achieved RVR after starting either Peg-IFN or Peg-IFN and RBV early.

33 Additionally,

we report an increase in the expression of IL-12 in OffOb-OD, which is of pathogenic relevance because it has been shown to promote NKT cell death.32 Ablation of NKT cell-mediated anti-inflammatory cytokine responses may therefore potentiate EPZ6438 NAFLD progression. In conclusion, we have shown that maternal obesity, in the context of a postweaning obesogenic diet, leads to heightened dysmetabolic and obesity-related liver sequelae, of greater severity than that induced by the obesogenic diet alone. Therefore, maternal obesity through developmental programming, by changes induced during gestation and lactation, may be compounding the effects of excess calories consumed as an adult to lead to a worsening obesogenic and liver phenotype. Novel findings of heightened disturbance

of the hepatic innate immune system with reduced NKT cell populations and increased KC numbers, which have perturbed phagocytic function, is reported in adversely exposed offspring. Several lines of experimental evidence suggest a mechanistic role for the innate immune system in NAFLD pathogenesis, which is currently implicated in programmed NAFLD. The programming effect of maternal obesity may be at the cellular, subcellular, or epigenetic level and understanding learn more these will form the target of future studies. A by-product of our current study is the development of a novel, comprehensive, and pathophysiologically relevant model of NAFLD, which should translate readily

to epidemiological investigation. The authors thank Jahm Persaud (Department of Clinical Biochemistry). “
“Extra pancreatic necrosis (EPN) alone represents a subgroup of pancreatitis with better outcome than patients with pancreatic parenchymal necrosis (PN). However, data on clinical significance of EPN is limited and significance of extent of EPN is not known. 213 patients (136 Silibinin (63.8%) males; mean age: 39.8 ± 13.2 years) with acute pancreatitis (AP) were prospectively enrolled and followed up till recovery or death. Contrast enhanced computed tomography (CECT) of each patient was retrospectively evaluated for presence of PN and EPN, pleural effusion and ascites. EPN was termed extensive if it extended to paracolic gutters or pelvis. 21 (9.9%) patients had interstitial pancreatitis, 7 (3.3%) patients had PN alone, 48 (22.5%) patients had EPN alone and 137 (64.3%) patients had combined PN & EPN. Patients with EPN alone had significantly higher frequency of organ failure than patients with interstitial pancreatitis. Compared with patients with EPN alone, the patients with combined necrosis had significantly higher frequency of pleural effusion (88.2% versus 75%), ascites (41% versus 20.8%), and need for intervention (32.6% versus 14.6%).

Changes in WPAI:UC scores across acute phase visits (baseline, Week 3, and acute endpoint), and changes in scores across visits of both phases (baseline, Week 3, acute endpoint, and maintenance endpoint) were tested using repeated-measures analysis of variance models. Post-hoc tests, using Bonferroni-adjusted P-values, tested for pairwise

differences in WPAI:UC scores between visits. Results: Significant differences in mean scores were observed for all WPAI:UC domains across the 3 acute phase visits (sample size range [SSR]: 200–404) and across the 4 acute and maintenance phase visits (SSR: 94–226; all P < 0.001). Post-hoc comparisons among the acute phase visits found significant decreases (improvement) in all domains from baseline to Week 3 and from baseline to acute endpoint (all P < 0.001). Further decreases were observed for presenteeism, OWI, and AI domains from Week 3 to acute endpoint (all P < 0.001). Post-hoc comparisons buy GS-1101 MK 2206 across all acute and maintenance phase visits found significant decreases in all domains from baseline to both Week 3 and acute endpoint visits (all P < 0.05), and in presenteeism, OWI, and AI domains from baseline to maintenance endpoint (all P < 0.05). Post-hoc comparisons between acute endpoint and maintenance endpoint visits found significant increases (worsening) for

presenteeism and AI (both P < 0.05), but no significant changes in absenteeism or OWI (both P > 0.05). Conclusion: Patients with active mild-to-moderate UC receiving multimatrix mesalazine demonstrated significant improvements in all measured domains of WRO within 3 weeks of treatment initiation, with continued improvement in most domains through 8 weeks. Patients in this sample who achieved partial or complete remission after 8 weeks and continued Mirabegron on multimatrix mesalazine treatment maintained these improvements for

some domains (absenteeism and OWI), although not others (presenteeism and AI), for up to 12 months. OMAR ELNAWSRA,1 IAN FOK,2 SUSAN CONNOR,3 MILES SPARROW,4 PETER GIBSON,5 JANE ANDREWS6 1Liverpool hospital, NSW; 2Department of Colorectal Medicine and Genetics at Royal Melbourne Hospital; 3Department of Gastroenterology & Hepatology, Liverpool Hospital. NSW; 4Alfred Health and Monash University; 5Alfred Health and Monash University; 6IBD Service Dept of G&H and SChool of Med, Uni Of Adelaide at RAH Background: Fecal calprotectin (FC) has emerged as a reliable means of distinguishing between irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) and as a measure for activity of IBD. However colonoscopy is still the predominant test used by gastroenterologists in these settings. This preference may be influenced by funding and availability of each of these two techniques. The aim of this study was to investigate the current & desired use of FC by Australian gastroenterologists (GEs), and to elicit factors which reportedly affect physicians’ choices.

AQP-1 overexpression increased both Pf and Jv (1.77-fold and 3.29-fold, respectively), an effect that was inhibited with AQP-1 siRNA (Fig. 7D, E). Coupled with the changes seen in bleb dynamics and invasion, these results strongly support a role for AQP-1-mediated water transport as a biophysical component of the forces driving dynamic membrane blebs, thereby facilitating FGF-induced amoeboid invasion in LECs. An understanding of the precise mechanisms controlling endothelial cell invasion and angiogenesis in liver, especially in a pathophysiological context, is an important

area of Ceritinib concentration investigation given recent implications of anti-angiogenic therapies on the treatment of liver disease.3, 4, 8, 10 In this regard, the current study provides the following novel observations: (1) AQP-1 expression is increased in the neovasculature within cirrhotic liver in vivo; (2) FGF promotes mode-switching toward an invasive, amoeboid phenotype that is sufficient to drive endothelial cell invasion

through ECM; (3) AQP-1 overexpression enhances both dynamic membrane blebbing and invasion capacity in LEC; MK-2206 cost and (4) AQP-1 localizes to plasma membrane blebs, where it allows for the rapid, trans-membrane flux of water. This data provide several conceptual advances across disciplines. First, we have elucidated a new mechanism for endothelial cell invasion in the cirrhotic liver involving FGF, an understanding of which might ultimately allow for more refined targeting of anti-angiogenic therapy in cirrhosis. Second, although amoeboid motility is increasingly recognized as an important form of invasion in the contexts of embryology, immunology, and malignancy, there are surprisingly few studies in endothelial cells.38,

39 Indeed, to our knowledge, this is the first study to demonstrate amoeboid motility in the context of angiogenic invasion. Third, our data implicate channel-mediated water transport across dynamic membrane blebs, a concept that could substantially alter our understanding of these structures and their role in liver relevant processes. Considerable controversy exists in the literature regarding stiripentol the causal relationship between hepatic fibrosis and pathological liver angiogenesis. There is evidence of the anti-angiogenic compound, Sunitinib, reducing hepatic fibrosis in experimental animals.3 In contrast, the integrin αvB3 inhibitor, Cilengitide, worsens fibrosis in similar models.8 What appears congruent is that angiogenesis and fibrosis occur together, are closely intertwined, and that there is considerable molecular and paracrine crosstalk in the signals driving each process. Less apparent are the precise mechanisms by which one process perpetuates the other and the therapeutic implications of inhibition of either pathway.

We diagnosed autoimmune fulminant liver failure based on the criteria, and discussed the etiology of fulminant hepatitis (FH) and late onset hepatic failure (LOHF), and the characteristics of autoimmune fulminant liver failure. Methods:  We investigated the etiology of 95 consecutive adult patients with FH or LOHF admitted to our liver unit between 1990 and 2009. Clinical and biochemical features, therapies and outcomes were examined in patients with AIH after 2000. Results:  Of 95 patients, 85 were FH and 10 LOHF. The

etiology was due to viral infections in 51.6% (hepatitis A virus in 7.4%, hepatitis B virus in 43.2% and hepatitis E virus in 1.1%), Selleck RG7204 AIH in 15.8%, drug allergy-induced in 12.6%, and unknown causes in 20.0%. The rate of patients with AIH increased significantly between 2000 and 2009 compared to the rate between 1990 and 1999 (P = 0.002). In recovered patients with AIH without

transplantation after 2000, coma grade was lower, alanine aminotransferase level, prothrombin time activity and alfa-fetoprotein level were higher than in the others with statistical significance. Conclusion:  AIH is not a rare cause of FH and LOHF, and the number of patients with unknown causes would surely decrease in concert with JAK inhibitor the precise diagnosis of AIH. “
“Nonalcoholic fatty liver disease (NAFLD) is characterized by triglyceride (TG) accumulation and endoplasmic reticulum (ER) stress. Because fatty aminophylline acids (FAs) may trigger ER stress, we hypothesized that the absence of adipose triglyceride lipase (ATGL/PNPLA2)–the main enzyme for intracellular lipolysis, releasing FAs, and closest homolog to adiponutrin (PNPLA3) recently implicated in the pathogenesis of NAFLD–protects against hepatic ER stress. Wild-type (WT) and ATGL knockout (KO) mice were challenged with tunicamycin (TM) to induce ER stress. Serum biochemistry, hepatic TG and FA profiles, liver histology, and gene expression for markers of hepatic lipid

metabolism, ER stress, and inflammation were explored. Moreover, cell-culture experiments were performed in Hepa1.6 cells after the knockdown of ATGL before FA and TM treatment. TM increased hepatic TG accumulation in ATGL KO, but not in WT, mice. Lipogenesis and β-oxidation were repressed at the gene-expression level (sterol regulatory element-binding transcription factor 1c, fatty acid synthase, acetyl coenzyme A carboxylase 2, and carnitine palmitoyltransferase 1 alpha) in both WT and ATGL KO mice. Genes for very-low-density lipoprotein (VLDL) synthesis (microsomal triglyceride transfer protein and apolipoprotein B) were down-regulated by TM in WT and even more in ATGL KO mice, which displayed strongly reduced serum VLDL cholesterol levels.

The median diameter of CD-tract was

www.selleckchem.com/products/chir-99021-ct99021-hcl.html 2.87 (2.54–3.14) mm, and was negatively correlated with electric output. In vertical section, the tract seemed to be covered with coagulated tissue in CD-case with low output, though coagulation was intermittently observed in high output cases. 2) Leakage of water was not observed in MD-tract, but it was observed in 2/10 (20%) of 3 cm segment and 10/10 (100%) of 1 cm segment in CD-tract. Conclusion: The influence of CD was larger than that of MD. They have to be selected in different procedures. Key Word(s): 1. cautery dilator; 2. EUS-guided biliary drainage Presenting Author: YUKINORI YOSHII Additional Authors: YU TAKAHASHI, YUUKI IWATA, MINORU TAKEDA, YASUSHI MATSUMOTO, NOBUMITSU MIYASAKA, TAKASHI OKAZAKI, MASAAKI NOMURA, TAKAYUKI MATSUMOTO Corresponding Author: YU TAKAHASHI Affiliations: Kayashimaikuno Hospital, Saiseikai Izuo Hospital, Saiseikai Izuo Hospital, Saiseikai Izuo Hospital, Saiseikai Izuo Hospital, Kayashimaikuno Hospital, Saiseikai Izuo Hospital, Saiseikai Izuo Hospital Objective: We have often experienced a situation that effective counter traction is required for Endoscopic Submucosal Dissection. If you

can pull the target lesion, good counter traction can be made. The “clip with line” method is a simple and useful method to make counter traction during ESD. This method was ABT-737 reported in 2002. We have also used it for gastric Non-specific serine/threonine protein kinase carcinoma. Especially, it is useful for the greater curvature or posterior wall of the middle body of the stomach. We could carried out more safety and effective ESD, by applying good counter traction to use it. Methods: We showed two typical

cases used this method, to compare which side of the lesion is effective position to put a clip for treating ESD of gastric cancer at the greater curvature posterior wall of the middle body of the stomach. Case 1- we put a clip at the anal side of the lesion by look up operation. Case 2, we put a clip at the oral side by look down operation. Results: In case 1, the approach toward the submucosal layer got easier. However, this caused excessive tension of pulling the string. We have often experienced the clip comes off. In case 2, this method led visibility of the layer more clear significantly, and easier to complete the submucosal dissection than case 1. We could smoothly operate, because the counter traction was more stable. By comparing case1 and case 2, the method of putting the clip at the oral side was more effective. Case 2 makes ESD more safety and the duration of procedure shorter. Conclusion: We present the two cases, and show the “clip with line” method for treating early gastric corpus cancer. Key Word(s): 1. ESD; 2. stomach; 3.