(4) Mild anemia is more common with BOC and severe anemia with TVP. (5) Of the patients who achieved SVR, 72.7% in the TVP group were hepatitis C PCR negative at week 4 and 86.5% were negative

at week 8 in the BOC group. SI STRASSER,1 X FORNS,2 M PRIETO,3 M CHARLTON,4 JG MCHUTCHISON,5 WT SYMONDS,5 J DENNING,5 T BRANDT-SARIF,5 P CHANG,5 V KIVETT,5 TF BAUMERT,6 A COILLY,7 L CASTELLS,8 F HABERSETZER6 1Royal Prince Alfred Hospital, Sydney, NSW, 2Liver Unit, IDIBAPS, CIBEREHD, Hospital Clinic, Barcelona, Spain, 3Hepatology Unit, CIBEREHD, Hospital Universitari i Politècnic La Fe, Valencia, Spain, 4Mayo Clinic, Rochester, MN, USA, 5Gilead Sciences, Foster City, CA, USA, 6Hôpitaux Universitaires de Strasbourg, Inserm U 1110, Strasbourg, France, 7Centre Hépato-Bilaire, Hôpital Paul Brousse, Villejuif, France,

8Liver Unit-Internal Medicine Department, CIBEREHD, Hospital Universitari Vall Ivacaftor Hebron, Barcelona, Spain Background: There are no effective treatment options for patients with severe recurrent hepatitis C after liver transplantation (LT). Sofosbuvir (SOF) has demonstrated high efficacy across a broad range of HCV genotypes and patient populations, a high barrier to resistance, no interactions with immunosuppressive agents, and favourable safety profile. Methods: Patients who had exhausted all treatment options and had poor clinical prognoses received compassionate use SOF for severe recurrent hepatitis C following BAY 80-6946 concentration LT. The regimen included SOF 400 mg/day and RBV for up to 48 weeks, with PEG-IFN at the physician’s discretion. Results: 104 patients received a SOF-containing regimen; baseline characteristics are shown in the table. 72 patients completed 24–48 weeks treatment at time of analysis, 7 patients discontinued treatment, 12 patients underwent liver transplantation and 13 patients died. SVR12 was achieved in 53/85

(62%) patients (excluding the LT recipients and patients with missing 上海皓元 data). Of the 104 patients, the clinical outcome of 60 (62%) improved on treatment, 22 (21%) stabilized and 22 (21%) worsened/died, with all deaths attributed to progression of liver disease or associated complications. Fifty (48%) subjects reported SAEs. Baseline Characteristics Overall (n = 104) Male, n (%) 76 (73) Median age, y (range) 55 (16–76) Median HCV RNA, log10 IU/mL (range) 8.4 (1.3–8.9) GT, n 1/1a/1b 8/29/51 2/3/4 1/7/8 Median bilirubin, mg/dL (range) 3.1 (0.4–45) Median albumin, g/dL (range) 3.1 (1.3–12.2) Median INR (range) 1.3 (0.8–4.5) Median ALT, IU/L (range) 71 (8–1162) Median platelets, ×103/μL (range) 78 (19–340) Median MELD (range) 15 (6–43) Median months from LT to treatment, (range) 17 (1–262) Conclusions: In patients with severe HCV recurrence, a compassionate-use regimen containing SOF + RBV (with or without PEG-IFN) was well-tolerated and demonstrated potent antiviral activity, with many patients achieving SVR and clinical improvement.

Critical to individual success is that laboratories participate in EQA surveys and critically assess their own results, and also implement methods which are as close as possible to recommended methods. Inhibitors <0.6 BU detected by FLI and LTA need to be further explored to clarify their clinical significance. The authors stated that they had no interests which might be perceived as posing a conflict or bias. "
“Despite great advances in haemophilia care in the last 20 years, a number of questions on haemophilia therapy remain unanswered. These debated issues primarily involve the choice of the product type (plasma-derived vs. recombinant) for patients with different

characteristics: specifically, if they were infected MI-503 by blood-borne virus infections, and if they bear high or low risk of inhibitor development. In addition, the most appropriate treatment regimen in non-inhibitor and inhibitor patients compel physicians operating at

the haemophilia treatment centres (HTCs) to take important therapeutic decisions, which are often based on their personal clinical Metformin solubility dmso experience rather than on evidence-based recommendations from published literature data. To know the opinion on the most controversial aspects in haemophilia care of Italian expert physicians, who are responsible for common clinical practice and therapeutic decisions, we have conducted a survey among the Directors of HTCs affiliated to the Italian Association of Haemophilia Centres (AICE). A MCE公司 questionnaire, consisting of 19 questions covering the most important topics related to haemophilia treatment, was sent to the Directors of all 52 Italian HTCs. Forty Directors out of 52 (76.9%) responded, accounting for the large majority of HTCs affiliated to the AICE throughout Italy. The results of this survey provide for the first time a picture of the attitudes towards clotting factor concentrate use and product selection of clinicians working at Italian HTCs. “
“Summary.  N8, a new recombinant

factor VIII (rFVIII) compound developed for the treatment of haemophilia A, is produced in Chinese hamster ovary (CHO) cells and formulated without human- or animal-derived materials. The aim of the present study was to compare the pharmacokinetics (PK) and the procoagulant effect, measured by ex vivo whole blood clot formation, of N8 and a commercial rFVIII in a cross-over study in haemophilia A dogs. N8 and Advate® (100 IU kg−1) were administered intravenously to three haemophilia A dogs. Blood was sampled between 0 and 120 h postdose and FVIII:C analysed. PK parameters maximum plasma concentration, area under the curve, half-life (t½), clearance, mean residence time (MRT) and volume of distribution and incremental recovery were calculated. Whole blood clotting time (WBCT) and thromboelastography (TEG®) were used to determine the haemostatic potential. No adverse reactions were observed with N8 or Advate®.

[23, 24] Recently, studies in B cells have shown that antibody engagement of CD81, a key receptor for HCV infection, induces spleen tyrosine kinase (SYK) phosphorylation of ezrin that recruits F-actin to facilitate cytoskeletal reorganization.[25] In addition, recent studies have found that inhibition of actin and/or microtubule

functions markedly reduced HCV infection in vitro.[10, 26] Taken together, these studies implicate host cytoskeletal proteins in the pathophysiology of HCV infection. Ezrin-moesin-radixin Smad inhibitor (EMR) represents a group of human cytoskeletal proteins that regulate lentiviral infection by modulating stable and dynamic microtubule formation.[8, 9] EMR also function as linkers between the actin cytoskeleton and plasma membrane proteins and as signal transducers in numerous signaling pathways.[27, 28] This family of proteins show >70% sequence homology among members and display a high degree of functional redundancy.[29] Given that EMR proteins regulate human immunodeficiency virus (HIV) infection,[8, 9] it remains unknown Selleck EMD 1214063 if these proteins can regulate other positive sense RNA virus infections including HCV. In the present study we performed a comprehensive molecular analysis to characterize the role of human EMR in HCV infection and replication. Using HCV J6/JFH-1 virus infection

and the HCV Con1 replicon system we demonstrate that HCV infection and replication can be modulated by proteins of the EMR family. We found that chronic HCV infection resulted in a significant decrease in moesin and radixin expression in Huh7.5 cells and HCV-infected patients compared to controls. The significant decrease in moesin and radixin in HCV J6/JFH-1-infected Huh7.5 cells was associated with increased stable microtubule aggregate formation. Overexpression or transient knockdown

of EMR proteins differentially modulated target cell susceptibility to HCV infection and replication. 上海皓元医药股份有限公司 These experiments provided mechanistic insights into modulation of HCV infection by the EMR family of proteins and identified targets for development of new therapies against HCV infection. Huh7.5 and Con1 HCV FL replicon cells were cultured as described[30] Infectious and replication competent HCV J6/JFH-1 virions were generated using pFL-J6/JFH-1 plasmid as described.[31] Detailed protocols are described in the Supporting Materials and Methods. Liver biopsy specimens were obtained from the National Institutes of Health (NIH) liver tissue cell distribution system (LTCDS; Minneapolis, MN; Pittsburgh, PA; Richmond, VA), which was funded by NIH contract # N01-DK-7-004/HHSN26700700004C. Patient samples represented genotypes 1a and 3. Additional methods are included in the Supporting Materials.

Univariate and multivariate Cox regression were used to identify risk factors for prediction of recurrence and death in patients with HCC after initial curative hepatectomy. www.selleckchem.com/products/bay80-6946.html In the univariate analysis, the effect of each variable on the disease recurrence and survival was tested using analysis of variance. If there was a known predominant determinant (e.g., tumor stage versus vascular invasion), bivariate analysis was conducted to detect more detailed correlations independent from the predominant one that might have been unnoticed. Only variables with a P value less than 0.05 were selected for subsequent multivariate analysis. In multivariate analysis, the

selected variables were subjected to a multiple linear model. Hazard ratios (HR) with 95% confidence intervals (CI) were thus obtained. Coefficients were determined via the linear discriminating function of the variables. To examine the potential role of NPM in resistance to anticancer therapies of HCC, HCC cell

lines with different p53 genetic background including HepG2 (wild-type p53), Huh7 (C200Y mutated p53), Mahlavu selleck (R249S mutated p53), and Hep3B (null-genotyped p53),23, 24 were treated with UV-B, mitomycin C, doxorubicin, or cisplatin. Silencing of NPM expression significantly enhanced cellular susceptibility to all MCE kinds of treatments in Huh7, Hep3B, and Mahlavu cells, while the sensitizing effect was minimal in HepG2 cells (Fig. 1A). These findings suggest that an NPM-mediated antideath mechanism is independent of p53 functions in HCC cells, which is different from that found in hematopoietic cells.25 To further inspect the role of p53, we silenced the expression of NPM, p53, or simultaneously NPM and p53 by RNA interference (Fig. 1B). Silencing of p53 expression alone did not significantly change the sensitivity to any of the treatments in Huh7, Hep3B, and Mahlavu cells (Fig. 1B, siTP53 versus siNS). Simultaneous silencing of p53 and NPM did not further

alter the sensitizing effect exerted by silencing of NPM alone (Fig. 1B, siNPM versus [siNPM + siTP53]). Silencing of NPM and p53 expression by RNA interference was confirmed via immunoblotting (Fig. 1C). Interestingly, a negative dominant mutant of p53 converted HepG2 cells from insensitivity to sensitivity to cytotoxic and molecular targeted therapies as NPM silenced (Supporting Fig. 1). NPM apparently executes its death evasion activity independently of p53 function. We further examined the potential role of NPM in resistance to the inhibitors of oncogenic kinases in HCC, such as lapatinib and sorafenib. Silencing of NPM expression significantly sensitized Huh7, Hep3B, and Mahlavu cells to sorafenib and lapatinib (Fig. 2A).

This contention is supported by (1) abrogation by nonabsorbable

antibiotics of the ongoing proinflammatory immune response in MLNs, but not in HLNs or peripheral blood, and (2) direct correlation between HLNs and blood proportions of recently activated Th cells and inflammatory monocytes. Thus, activated immune cells that leave the HLNs and recirculate in peripheral blood preferentially account for the systemic immune activation LY2109761 solubility dmso observed in rats with preascitic cirrhosis. Our detection of passage of bacterial DNA fragments to the MLNs in rats with preascitic cirrhosis is of particular interest. To date, viable (i.e., positive culture) or nonviable (i.e., DNA fragments) bacteria in the MLNs had only been reported in rats with cirrhosis and ascites.6, 11, 16, 27 Similarly, passage of enteric bacterial products to the bloodstream, as shown by increased serum lipopolysaccharide-binding protein or bacterial DNA in serum, has only been demonstrated in patients with cirrhosis and ascites.3, 10, 17, 28 In a setting of cirrhosis with ascites, bacterial translocation results from enteric bacterial overload, deranged intestinal permeability, and probably also impaired intestinal immunity, which is unable to eliminate the translocated

Imatinib chemical structure microorganisms.6, 16, 29 The detection of bacterial genome fragments but not of viable bacteria in the MLNs of our rats with preascitic cirrhosis indicates that the mechanisms leading to passage of enteric bacteria to the MLNs are also operative at the pre-ascitic stage of experimental cirrhosis. However, and in contrast to rats with ascites, a functional intestinal immune system is able to eradicate the accessing bacteria. Interestingly, in our study, bacterial CpG motifs, which are immunologically active components of bacterial DNA,30 were able to elicit an inflammatory response in the MLNs with expansion of activated mononuclear cells and production

of proinflammatory cytokines. Remarkably, the immune system at the MLNs was able to maintain the inflammatory response to bacterial DNA 上海皓元医药股份有限公司 fragments at the local level. This was revealed by a lack of correlation between the expansion of activated immune cells at the systemic level and the presence of bacterial DNA at the MLNs or bowel decontamination with antibiotics. We sought to detect systemic inflammation in rats with CCl4 cirrhosis, given that it is the most widely used and clearly characterized toxin-based experimental model of cirrhosis. This model has been shown to effectively mimic many of the features of human cirrhosis associated with toxic damage.

01, Table 4) but not depression scores than asymptomatic patients. According to one study, the majority of patients with an acute BPU are asymptomatic until life-threatening severe bleeding occurs. This remains a hitherto unexplained yet potentially important

observation.29 The findings from our current study provide a potential explanation. While we had hypothesized that patients with BPU might be less sensitive as compared to healthy controls, our data suggest that patients with uPUD are actually more sensitive than HC. Using a standardized test of visceral sensation, our findings show that patients with uPUD have an augmented symptom response whilst patients with BPU have a symptom response to a test meal that is not different from NU7441 concentration that in HC. Data on the prevalence of ulcer symptoms prior to ulcer bleeding are few. The proportion of patients

without symptoms has been reported to range from 43% to 87%.11,13,14,29 The systematic survey of our DNA Damage inhibitor patients using validated questionnaires shows that the majority (83%) of patients with BPU are asymptomatic. In contrast, the majority of patients with uPUD usually present with abdominal pain. Our study also shows that after ulcer healing, or treatment that would reasonably be expected to have healed the ulcer, patients with uPUD continued to report symptoms that were more severe than those in patients with BPU. Persistent symptoms after healing of ulcers might be the result of post-inflammatory hyperalgesia, as occurs in an animal model of transient colitis.30 The patients were studied after cessation of PPI therapy and, potentially, rebound acid secretion

might have contributed to the persistence of symptoms.31 However, such effects would not explain the difference between patients with bleeding and uncomplicated ulcer disease. The major finding of this study is that patients with BPU have diminished gastric visceral sensation compared with uPUD. Similarly asymptomatic PUD patients, irrespective of bleeding status, have diminished visceral sensation compared 上海皓元 with patients who experienced peptic ulcer symptoms. These differences were present after ulcer healing, suggesting a fundamental difference in visceral sensitivity between patients with bleeding or asymptomatic ulcers and those with symptomatic or uncomplicated ulcers. Lowered visceral sensitivity and asymptomatic status is a plausible explanation for the presentation of ulcers with complications such as bleeding. Conversely, visceral hyperalgesia, higher degrees of psychological distress, more concomitant bowel symptoms and persistent dyspepsia after medical treatment in patients with uPUD may explain earlier presentation and diagnosis of the ulcers. The augmented symptom response to the test meal and the higher level of background symptoms after ulcer healing suggest that patients with symptomatic but uncomplicated peptic ulcers share similarities with patients with functional dyspepsia.

01, Table 4) but not depression scores than asymptomatic patients. According to one study, the majority of patients with an acute BPU are asymptomatic until life-threatening severe bleeding occurs. This remains a hitherto unexplained yet potentially important

observation.29 The findings from our current study provide a potential explanation. While we had hypothesized that patients with BPU might be less sensitive as compared to healthy controls, our data suggest that patients with uPUD are actually more sensitive than HC. Using a standardized test of visceral sensation, our findings show that patients with uPUD have an augmented symptom response whilst patients with BPU have a symptom response to a test meal that is not different from IWR-1 mw that in HC. Data on the prevalence of ulcer symptoms prior to ulcer bleeding are few. The proportion of patients

without symptoms has been reported to range from 43% to 87%.11,13,14,29 The systematic survey of our 3-MA cell line patients using validated questionnaires shows that the majority (83%) of patients with BPU are asymptomatic. In contrast, the majority of patients with uPUD usually present with abdominal pain. Our study also shows that after ulcer healing, or treatment that would reasonably be expected to have healed the ulcer, patients with uPUD continued to report symptoms that were more severe than those in patients with BPU. Persistent symptoms after healing of ulcers might be the result of post-inflammatory hyperalgesia, as occurs in an animal model of transient colitis.30 The patients were studied after cessation of PPI therapy and, potentially, rebound acid secretion

might have contributed to the persistence of symptoms.31 However, such effects would not explain the difference between patients with bleeding and uncomplicated ulcer disease. The major finding of this study is that patients with BPU have diminished gastric visceral sensation compared with uPUD. Similarly asymptomatic PUD patients, irrespective of bleeding status, have diminished visceral sensation compared MCE with patients who experienced peptic ulcer symptoms. These differences were present after ulcer healing, suggesting a fundamental difference in visceral sensitivity between patients with bleeding or asymptomatic ulcers and those with symptomatic or uncomplicated ulcers. Lowered visceral sensitivity and asymptomatic status is a plausible explanation for the presentation of ulcers with complications such as bleeding. Conversely, visceral hyperalgesia, higher degrees of psychological distress, more concomitant bowel symptoms and persistent dyspepsia after medical treatment in patients with uPUD may explain earlier presentation and diagnosis of the ulcers. The augmented symptom response to the test meal and the higher level of background symptoms after ulcer healing suggest that patients with symptomatic but uncomplicated peptic ulcers share similarities with patients with functional dyspepsia.

Prior to testing, frozen plasmas should be thawed rapidly at 37°C (to prevent denaturing fibrinogen) and tested immediately; however, it is acceptable to hold at 4°C for a maximum of 2 h. One of the screening tests particularly sensitive to pre-analytical variables is the APTT which is activated and then recalcified with phospholipids under controlled conditions and these Nutlin-3a supplier can very easily be disrupted during the pre-analytical phase. The test is used to detect various bleeding disorders caused by deficiencies in the intrinsic clotting system, i.e. fibrinogen, prothrombin, FV, FVIII, FIX, FX and FXI. It is invariably prolonged if one or more of these components

are reduced to very low concentrations. It is important to note that deficiencies of any of the contact activation factors, i.e. high molecular weight kininogen (HMWK), prekallikrein or FXII, also leads to a prolongation of the APTT but is not linked to a bleeding diathesis. To detect less obvious bleeding disorders caused by mild to moderate CP-868596 research buy factor deficiencies, it is important to choose a reliable and sensitive APTT reagent. Ideally,

it should have a proven capacity to generate a prolonged APTT if a single or combined deficiency may lead to clinically important bleeding complications. The APTT reagent is also the test base for one-stage factor assays and the variable responsiveness is also propagated to these assays. The importance of choosing the correct APTT reagents for FVIII:C and FIX:C activity assays was recently shown by two investigations that illustrate how the diagnostic value can differ between reagents [14,15]. The laboratory phenotype known as discrepant mild haemophilia A is

another example where the APTT-based one-stage FVIII:C assay may be poorly correlated to the bleeding phenotype. Specialized MCE coagulation laboratories usually have insight about the variability of APTT reagents and can choose between reagents depending on the application. However, it is important to remember that in some patients, a normal APTT may not exclude the possibility of a mild bleeding disorder and further testing may be warranted. As the APTT reflects the sum activity of several clotting factors it can happen that a transient elevated level of one factor may mask a mild deficiency of another under certain conditions. In the case of a prolonged APTT, it is likewise important that an appropriate interpretation is made that may guide any further investigation, particularly in the absence of an obvious explanation for the prolongation. Therefore, every laboratory that performs APTT (and other screening assays) should be aware of their reagent characteristics and have defined a practical approach how to evaluate test results. The APTT is a test to determine the intrinsic coagulation time and was first developed as the partial thromboplastin time test by Langdell et al. [16].

TheICG fluorescence of the patient injected 50 µg/mL intraoperatively was too intense and too many ICG fluorescence-positive lymph nodes existed (Fig. 4a). In this case, sentinel lymphatic basins could be observed, that is, they were along the right gastroepiploic artery (No. 4d–No. 6) and the left gastric artery (No. 3–No. 7) (Fig. 4b). ICG fluorescence was not observed in the lymphatic vessels along the right

gastric artery (No. 5) and the left gastroepiploic artery (No. 4sb). 3 50 µg/mL, the day before operation. Ten patients were enrolled in the group. Sentinel lymph nodes were detected in all cases (Fig. 5) and number of sentinel lymph nodes per patient was 3.6 ± 2.1. Metastasis was observed in one case. In this case, 12 out of 37 lymph nodes were positive for the metastasis. ICG fluorescence-positive sentinel find more nodes VX-770 mw were found along right gastroepiploic

vessels (No. 4d in JCGC) and all of them were positive for the metastasis. The present study shows that submucosal injection of 0.5 mL × 4 of 50 µg/mL ICG on the day before operation is the adequate administration for detecting sentinel nodes using HEMS in the gastric cancer surgery. Sentinel nodes was detected in all of the patients studied, and mean number of sentinel nodes was 3.6 per patient and similar to that of dual tracer method. Mean number of sentinel nodes per patient by dye method was reported as about 2–2.8.7,16 That was 3.3–4.1 per case1,17 by dual tracer method. In this concentration and timing of ICG injection, clinical case will be accumulated and sensitivity and accuracy of sentinel node mapping will be examined using color fluorescence camera, HEMS, in the laparoscopy-assisted gastrectomy. The present study also shows that HEMS-guided abdominal surgery is quite feasible. As it is written in introduction, HEMS is the novel system for detecting both color image and near-infrared rays under room light. After the experiments in swine,13 it was decided to use HEMS in the clinical surgery for digestive diseases. In the clinical appreciation of HEMS, medchemexpress the operation

can be continued, simultaneously, under the guidance of ICG fluorescence. Sampling of the sentinel lymph nodes can be performed on a back table in the same operating room under the room light. Lymph node metastasis was found in a case injected 50 µg/mL of ICG on the day before operation. All of four sentinel lymph nodes were positive for metastasis. This case encouraged us to continue the study and accumulate patients to prove the sensitivity and accuracy of the sentinel node mapping. More than half of patients underwent laparoscopy-assisted pylorus preserving gastrectomy in the present study. In our operation, the infrapyloric lymph nodes (No. 6 in JCGC) were dissected while the infrapyloric artery was preserved. We also preserve the right gastric artery and the suprapylolric lymph nodes (No. 5 in JCGC).

TheICG fluorescence of the patient injected 50 µg/mL intraoperatively was too intense and too many ICG fluorescence-positive lymph nodes existed (Fig. 4a). In this case, sentinel lymphatic basins could be observed, that is, they were along the right gastroepiploic artery (No. 4d–No. 6) and the left gastric artery (No. 3–No. 7) (Fig. 4b). ICG fluorescence was not observed in the lymphatic vessels along the right

gastric artery (No. 5) and the left gastroepiploic artery (No. 4sb). 3 50 µg/mL, the day before operation. Ten patients were enrolled in the group. Sentinel lymph nodes were detected in all cases (Fig. 5) and number of sentinel lymph nodes per patient was 3.6 ± 2.1. Metastasis was observed in one case. In this case, 12 out of 37 lymph nodes were positive for the metastasis. ICG fluorescence-positive sentinel GSK126 nodes PD-0332991 nmr were found along right gastroepiploic

vessels (No. 4d in JCGC) and all of them were positive for the metastasis. The present study shows that submucosal injection of 0.5 mL × 4 of 50 µg/mL ICG on the day before operation is the adequate administration for detecting sentinel nodes using HEMS in the gastric cancer surgery. Sentinel nodes was detected in all of the patients studied, and mean number of sentinel nodes was 3.6 per patient and similar to that of dual tracer method. Mean number of sentinel nodes per patient by dye method was reported as about 2–2.8.7,16 That was 3.3–4.1 per case1,17 by dual tracer method. In this concentration and timing of ICG injection, clinical case will be accumulated and sensitivity and accuracy of sentinel node mapping will be examined using color fluorescence camera, HEMS, in the laparoscopy-assisted gastrectomy. The present study also shows that HEMS-guided abdominal surgery is quite feasible. As it is written in introduction, HEMS is the novel system for detecting both color image and near-infrared rays under room light. After the experiments in swine,13 it was decided to use HEMS in the clinical surgery for digestive diseases. In the clinical appreciation of HEMS, 上海皓元 the operation

can be continued, simultaneously, under the guidance of ICG fluorescence. Sampling of the sentinel lymph nodes can be performed on a back table in the same operating room under the room light. Lymph node metastasis was found in a case injected 50 µg/mL of ICG on the day before operation. All of four sentinel lymph nodes were positive for metastasis. This case encouraged us to continue the study and accumulate patients to prove the sensitivity and accuracy of the sentinel node mapping. More than half of patients underwent laparoscopy-assisted pylorus preserving gastrectomy in the present study. In our operation, the infrapyloric lymph nodes (No. 6 in JCGC) were dissected while the infrapyloric artery was preserved. We also preserve the right gastric artery and the suprapylolric lymph nodes (No. 5 in JCGC).