3A, middle), or nonparenchymal cell fraction (Fig. 3A, right). We photographed 224 different fields and evaluated 3,522 GFP-positive cells. None of them were positive for β-gal. There were 1,737 β-gal-positive cells in the evaluated fields and none of them were GFP-positive. Nonparenchymal cells expressed β-gal upon Ad Cre-mediated excision of the stop codon (Fig. 3B), demonstrating that lack of X-gal staining in nonparenchymal cells was due to persistence of the stop codon, not due to an insufficient level of β-gal expression. This result eliminates the possibility that

some GFP-positive cells were actually derived from hepatocytes but did not express sufficient β-gal to be detected by X-gal staining. The absence of double-positive cells was confirmed at different stages of liver injury: acute phase (single injection with CCl4) and chronic phase (16 times injection with CCl4), in both liver sections Compound Library research buy LEE011 and in cells isolated from the injured liver (Supporting Figs. S4, S5, S6, and S7). Furthermore, GFP-positive cells were sorted

by FACS and none of them (450,000 GFP-positive cells) were positive for β-gal (Fig. 4). These results clearly demonstrate that type I collagen-expressing cells in CCl4-induced liver fibrosis do not originate from hepatocytes. To address if hepatocytes express mesenchymal markers during liver injury we performed immunostaining following X-gal staining. No cells were double-positive for α-SMA and β-gal in CCl4-treated liver of double transgenic mice (Fig. 5A). Similarly, no cells were double-positive for FSP-1, desmin, or vimentin and β-gal in CCl4-treated liver of double transgenic mice (Fig. 5B; Supporting Fig. S8). β-Gal-positive cells in nonparenchymal cell fraction 上海皓元医药股份有限公司 were never positive for α-SMA, FSP-1, desmin, or vimentin and must represent rare contaminating hepatocytes. Immunohistochemical staining and X-gal staining of liver sections supported the absence of hepatocyte-derived

α-SMA or FSP-1 positive cells in CCl4-treated liver (Supporting Fig. S9). Hepatocytes cultured in the presence of TGFβ-1 exhibited fibroblast-like morphological changes (Fig. 6A, upper) and expressed GFP driven by the collagen α1(I) promoter (Fig. 6A, second). Although some α-SMA positive cells were detected in the primary culture of hepatocytes (Fig. 6A, third), they appeared even in the absence of TGFβ-1 (data not shown) and were never positive for β-gal (Fig. 6A, bottom), demonstrating that they were contaminating nonparenchymal cells and did not derive from hepatocytes. Similarly, hepatocytes treated with TGFβ-1 did not express FSP-1 (Fig. 6B, third) or desmin (Supporting Fig. S10, third). A few FSP-1 or desmin-positive cells were present in the primary cultures of hepatocytes, but were never positive for β-gal (Fig. 6B, bottom, and Supporting Fig. S10, bottom). The mRNA level of FSP-1 in hepatocyte culture was neither increased in a time-dependent manner nor enhanced by addition of TGFβ-1 (Supporting Fig. S11).

PNF is characterized clinically by graft function insufficient to sustain life leading to death or re-transplantation in the first week post-operatively. The etiology of PNF is poorly understood but has been associated with prolonged ischemia times as well as several donor factors. “
“See article in J. Gastroenterol. Hepatol. 2011; 26: http://www.selleckchem.com/products/Imatinib-Mesylate.html 1612–1618. Based on the results from the Sorafenib Hepatocellular carcinoma Assessment Randomized Protocol (SHARP) trial and Asia-Pacific

trial, sorafenib, an oral multikinase inhibitor, was globally approved for the treatment of unresectable, advanced hepatocellular carcinoma (HCC).1,2 In the design of both studies, inclusion criteria were advanced stage (vascular invasion or distant metastasis) of HCC and good hepatic reserve function (Child–Pugh A). That is, due to the peculiar characteristic of HCC that malignancy is mostly accompanied by the preneoplastic condition of cirrhosis, which itself affects overall survival,

patients with Child–Pugh A were selected in those trials. Thus, the clinical utility of sorafenib in patients with Child–Pugh B or C remains unknown. In addition, the positioning of sorafenib is still not concrete in nations where the cost of this drug is higher compared to other treatment modalities.3,4 For RXDX-106 price instance, in Korea, reimbursement from the national insurance system is largely restricted. Though the government commenced reimbursement of it from January 2011, the indications are just advanced HCC if patients were not eligible for or had disease progression medchemexpress after surgical or locoregional therapy (transarterial chemoembolization, ethanol injection, or radiofrequency ablation) with all of the following

conditions; (i) Tumor Node Metastasis (TNM) stage III or IV, (ii) Child–Pugh class A, (iii) Eastern Cooperative Oncology Group (ECOG) performance status, 0–2. Rather similar restrictions apply to reimbursement for sorafenib in Australia. Even with this indication, reimbursement in Korea is only partial, with patient copayment being 50%, and the period of reimbursement is only one year. In the USA, the Food and Drug Administration (FDA) authorized the use of sorafenib for patients with “unresectable HCC”, while in Europe, the indication is even extended as sorafenib is indicated for just “HCC”.5 Limited reimbursement policies and high cost of sorafenib in Asia-Pacific countries can lead to physicians treating patients with advanced HCC with other modalities, even though sorafenib is the only drug to show survival benefit in randomized, controlled trials. Under the aforementioned design of clinical trial and reimbursement environment, many physicians want to know the efficacy and safety of sorafenib in real clinical practice, especially in Barcelona Clinic Liver Cancer-C (BCLC-C) stage. In this issue of the Journal, Kim et al.

The only prescription NSAID approved the FDA for the treatment of migraine is Cambia (Depomed, Inc, Newark, CA, USA), a powder form of diclofenac that can be dissolved in water for better

absorption. For those with severe nausea or vomiting, a nasal spray of ketorolac (brand name Sprix [Regency Therapeutics, Shirley, NY, USA]) or injectable ketorolac can be useful options. The formerly known brand name Toradol made by Roche Bioscience (Nutley, NJ, USA) is no longer available in the US, but the generic injectable version remains available. Sometimes an individual’s medical conditions prohibit the use of triptans, DHE, and NSAIDs, or these medicines are ineffective. Medications check details such as metoclopramide and prochlorperazine have a very different mechanism of action by blocking a chemical called dopamine. Prochlorperazine comes as a tablet and as a rectal suppository, so it can be used in migraineurs who vomit. Both medications are helpful in treating the nausea associated with migraines. Either of them can be used with any other acute migraine treatment including triptans, DHE, and NSAIDs. Unfortunately, with long-term continuing use, they can cause a movement disorder, and must be stopped completely in the selleck compound event this occurs. Metoclopramide is rated

pregnancy category B, that is, there is no evidence of fetal harm with its use. This is the only acute migraine intervention discussed that is generally considered safe in pregnancy other than acetaminophen. Acetaminophen is used for migraine pain as a safe alternative treatment. Unfortunately, it is often ineffective, perhaps because of its lesser anti-inflammatory action. It has no specific anti-migraine action. Triptans, NSAIDs, and probably DHE, when taken too frequently, can result in migraineurs getting more frequent headaches, or headaches that are resistant to treatment. This is called medication overuse headache or rebound headache. A good rule of thumb is to use acute medications no

more than 2 days per week. Sometimes, patients believe that if they use one type of medication for 2 days per week, and MCE another type on other days, that rebound can be avoided. Unfortunately, this is not the case. It is safest to remember sticking to 2 days per week of acute medication, and if there is a consistent need to treat more often than that, improved preventive strategies need to be added. Multiple noninvasive devices are undergoing evaluation for the treatment of acute migraine. At this time, only one device has been approved by the FDA for acute treatment, and it is not yet available at the time of this writing. A transcranial magnetic stimulator called Spring TMS, manufactured by eNeura, Baltimore, MD, was approved for acute treatment of migraine with aura.

S. Hepatologie und Gastroenterologie, Charité, Campus Virchow-Klinikum, Universitätsmedizin Berlin, Germany, 4Department of Hepatology, Clinic for Gastroenterology and Rheumatology, University Clinic Leipzig, Leipzig, Germany, 5NIHR Biomedical Research Unit in Gastroenterology see more and the Liver, University of Nottingham, Nottingham, United Kingdom, 6Division of Hepatology, Ospedale Casa Sollievo della Sofferenza, IRCCS, San Giovanni Rotondo, Italy, 7Liver Research Group, Institute of Cellular Medicine, Medical School, Newcastle University, Newcastle upon Tyne, UK, 8Liver Physiopathology Lab, Department

of Internal Medicine, University of Turin, Turin, Italy, Department of Gastroenterology and Hepatology, Nepean Hospital, Sydney, Australia, 10Department of Internal Medicine I, University of Bonn, Sigmund-Freud- Strasse, Bonn, Germany, 11Fremantle hepatitis services, Sydney, Australia, 12Department of Gastroenterology & Hepatology, Royal Perth Hospital, Australia, 13Kirby Institute, The University of New South Wales, Sydney, Australia, 14St Vincent’s Hospital, Sydney, Australia, 15Princess Alexandra Hospital, Department of Gastroenterology and Hepatology, Woolloongabba, 16The University of Queensland, School of Medicine, Princess Alexandra Hospital, Woolloongabba, Queensland,

Australia, 17Gastrointestinal and Liver Unit, Prince of Wales Hospital and University of New South Wales, Sydney, Australia Background and aim: Fibrosis is a common consequence of chronic CRM1 inhibitor liver disease irrespective of etiology. Whether IFNL3 polymorphisms influence hepatic inflammation and fibrosis progression remains unclear, particularly for disease etiologies other than chronic hepatitic C (CHC). We examined MCE公司 the impact of IFNL3 polymorphisms on hepatic inflammation and fibrosis in a large cohort of patients with viral (CHC and chronic hepatitis B [CHB]) and non-viral liver diseases. Methods: 2408 patients were included: CHC (N = 1914), CHB (N = 264),

and NASH (N = 230). Of these, 1214 patients with CHC had an accurate estimate of the date of infection and a liver biopsy, which enabled assessment of the putative fibrosis progression rate (FPR). A further 106 patients with CHC had paired liver biopsies, a median of 5.01 years apart. All patients were genotyped for IFNL3 polymorphisms rs12979860 and rs8099917. Results: CHC: At baseline biopsy, patients with IFNL3 rs12979860 CC and rs8099917 TT had significantly higher portal inflammation (OR: 1.8, 95% CI: 1.42, 2.28, P = 0.001 and OR: 1.49 [1.18–1.88], P = 0.001) and liver fibrosis (OR: 1.63, [1.29–2.07], P = 0.0001 and OR: 1.31 [1.04–1.65], P = 0.02), respectively. For the FPR analysis, by Cox regression, the adjusted hazards ratio for rs12979860 CC and rs8099917 TT with hepatic fibrosis was 1.

1D). In this cluster, miR-UTR2 RG7422 nmr replaced endogenous miR-17 and miR-UTR1 replaced endogenous miR-18. In this orientation, miR-UTR2 was active, inhibiting its target by 72% ± 0.5% (P < 0.01) (Fig. 2C). In contrast, this change resulted in a loss of activity for miR-UTR1, suggesting that mature miRNAs are not processed correctly from the miR-18 scaffold, a finding confirmed by northern analysis (see below). Efficacy of an exogenous polycistronic miRNA has not been previously

evaluated in vivo. We determined the efficacy of the five anti-HCV miRNAs in mouse liver by coinjecting the plasmids expressing the HCV-miR Clusters with the RLuc-HCV reporter plasmids via HDTV injection.20 Two days following the injection, mice were sacrificed, livers were harvested, and dual luciferase assays were performed on liver lysates. Control mice received injections of the same RLuc-HCV reporters MK-2206 mw and a pUC19 plasmid. Four of the five miRNAs expressed from HCV-miR-Cluster 1 + Intron were highly active in inhibiting their individual cognate reporters (Fig. 3A). Furthermore, using the RLuc reporter containing all five HCV targets, 94% ± 2% inhibition was observed (P < 0.01). Similar to what was found in Huh-7 cells, miR-UTR2 was completely inactive. In all cases, higher

silencing activity by the four active miRNAs was observed in vivo, as compared to that seen in vitro. The higher activity 上海皓元 was not due to nonspecific silencing as demonstrated by the failure of HCV-miR-Cluster 1 + Intron to inhibit a reporter lacking HCV sequences (psiCheck2) (Fig. 3A). The lack of inhibition of the RLuc-HCV UTR1 reporter by a plasmid expressing only HCV-miR-Core, also demonstrated that the higher levels of inhibition observed in vivo are not due to nonspecific targeting (data not shown).

As mentioned above, we constructed a second miRNA cluster (HCV-miR-Cluster 2) to evaluate the activity of miR-UTR2 when inserted into endogenous miR-17, rather than miR-18. This change in position resulted in a highly active miR-UTR2, capable of inhibiting its target by 97% ± 0.5% (P < 0.01 relative to pUC19 control) (Fig. 3B). The reciprocal placement of miR-UTR1 into endogenous miR-18 from miR-17 completely abolished its activity (Fig. 3B), again suggesting that mature miRNAs are not processed correctly from a pre-miR-18 scaffold. Similar to HCV-miR-Cluster 1, HCV-miR-Cluster 2 was also able to silence the HCV reporter containing all five targets by 92% ± 2.7% (P < 0.01 relative to pUC19 control) (Fig. 3B). Thus, two separate HCV-miR clusters are able to express four potent miRNAs that target HCV sequences, and mediate gene silencing in vivo. The gene silencing results were corroborated by northern blot analyses, which demonstrated that the mature forms of the four active miRNAs expressed from HCV-miR-Cluster 1 or HCV-miR-Cluster 1 + Intron were produced in mouse liver (Fig. 4A,C-E).

[205, 206] In fact, evaluation of cases of exacerbated hepatitis following cessation of NA therapy revealed significantly lower levels of HBcrAg (3.2 vs 4.9, P = 0.009) in the non-recurrence group compared

to the recurrence group,[207] indicating that HBcrAg is a potential marker for cessation of NA therapy. Similarly to HBcrAg, HBsAg is thought to be little affected by NA transcriptase inhibition, and the retreatment rate after cessation of NA therapy Regorafenib was significantly lower for the group with low HBsAg levels (<1000 IU/mL) at the time of cessation (18% vs 63%, P = 0.049).[208] Based on the above results, the MHLW research group produced a report titled “Studies concerning efficacy of IFN therapy aimed at creation of treatment discontinuation standards and treatment discontinuation in NAs therapy for hepatitis B”, setting out policy regarding cessation of NA therapy.[209, 210] A summary is shown in Table 14. To determine the criteria for Selleckchem Tamoxifen therapy cessation, as shown below in Table 15, HBsAg and HBcrAg levels at therapy cessation were scored, the final score allocated to the following 3 categories of risk of relapse, and the success rate was predicted. Successful cessation was defined as “finally resulting in inactive carrier status, i.e. ALT ≤30 U/L and HBV DNA <4.0 log copies/mL”. Studies have shown that if this inactive carrier status is achieved,

there is no progression of liver disease, and risk of HCC also declines.[34, 211] Group for which cessation may be considered. However, even in the low risk group, recurrence of hepatitis can occur, so vigilance is required. Group for which cessation may be considered depending on circumstances. This group requires further evaluation concerning cessation criteria and methods. Continued treatment is recommended for this group. However, for patients aged <35, the cessation success rate is relatively high at 30∼40%. Recommendations The following 3 patient criteria must be met for cessation of NA therapy: (1) Both the treating physician

and the patient fully understand that after cessation of NA therapy, there is a high incidence of recurrence of hepatitis, possibly severe; (2) Follow-up is possible after treatment cessation, and appropriate treatment is possible even if hepatitis recurs, MCE (3) Even if recurrence of hepatitis occurs, it is unlikely to be severe if the degree of fibrosis is mild and the hepatic reserve is good. The 3 laboratory criteria for cessation of NA therapy are: (1) At least 2 years of administration of NAs; (2) undetectable serum HBV DNA levels (using real time PCR); (3) negative serum HBeAg at the time of treatment cessation. When the above criteria are met, it is possible to predict the risk of relapse from HBsAg and HBcrAg levels at the time of cessation of therapy. NA therapy should be continued in the high risk group.

In 1998, the UK National External Quality Assessment Scheme for Blood Coagulation (UK NEQAS BC) established a pilot quality assurance scheme for molecular genetic testing in haemophilia.

The scheme was designed to assess genotyping, clerical accuracy and the interpretation of genetic analyses in individuals with inherited bleeding disorders. In the original pilot schemes, the presence or Raf inhibitor absence of the F8 intron 22 inversion was examined. Results from three initial surveys highlighted problems with the quality of samples when used to screen for the intron 22 inversion and in part reflected difficulties with these analyses by Southern blot analysis or by long-range PCR at this time. The scheme was re-launched in 2003 and subsequent exercises have included F8 linkage studies as well as mutations within the F8, F9 and VWF genes [37]. The scheme is open to laboratories from all countries and currently 22 laboratories, primarily but not exclusively from Europe, participate. Participants in the scheme are provided with a clinical

PLX4720 scenario (Fig. 1) and either whole blood or DNA isolated from previously established cell lines and asked to seek a familial mutation in a limited part of the relevant gene, to report on the mutation in the patient, its presence/absence in relative(s) and the implications for each individual analysed. Reports are assessed in three areas: clerical accuracy, genotyping and interpretation (Fig. 2). Two exercises

per annum are circulated with a 6-week 上海皓元医药股份有限公司 turnaround time. Reports are assessed by a panel of scientists/clinicians with expertise in this area. To date, 19 exercises have been circulated covering a wide variety of mutations [including inversions events, missense and nonsense mutations, and small deletions] within the F8, F9 and VWF genes. A laboratory report is a summary of any investigations that have been performed and the subsequent interpretation of these results in the light of any phenotypic and family data that were provided. It is important to remember that in many cases, laboratory reports will be read and the contents acted upon by individuals who may not be experts in the field of molecular haemostasis and therefore the reports should be easily interpretable and ‘stand alone.’ Novel mutations should, for example, include an indication as to why they are considered pathogenic, and how the possibility that they could represent polymorphic variants was excluded. In addition, mutations should adhere to conventional methods both for nomenclature and for numbering [36]. In the NEQAS scheme, scoring for each report (Fig. 2) is based on: 1 Clerical accuracy: was the patient correctly identified, was the clinical question, the disorder and its severity clearly stated? The assessment template is similar but slightly different for each exercise and the key points for each exercise are decided in advance of the assessment.

This study adopted short intervals of 2 weeks between banding sessions, according to the guidelines suggested by the American Association for the Study of Liver Diseases.4 A previous report showed that longer interbanding interval (more than 3 weeks) had lower risk of rebleeding in secondary prophylaxis.5 Therefore, whether short intervals between

banding sessions could accelerate eradication of esophageal varices or contradictorily increased the risk of bleeding remained unclear. In summary, carvedilol and VBL are alternative options for primary prophylaxis of esophageal varices. Defining the optimum banding protocol and benefit-to-risk ratio in patients classified as having Child C cirrhosis are needed to improve the efficacy of VBL. Chia-Chi Wang*, Jia-Horng Kao†, * Department of Hepatology, Buddhist Tzu Chi General Hospital, Taipei Branch and School of Medicine, Tzu Chi University, Hualien, Taiwan, Selleckchem CP690550 † Graduate Institute of Clinical Medicine and Hepatitis Research Center, National Taiwan University College of Medicine and Hospital, Taipei, Buparlisib cell line Taiwan. “
“Hou

J, Lin L, Zhou W, Wang Z, Ding G, Dong Q, et al. Identification of miRNomes in human liver and hepatocellular carcinoma reveals miR-199a/b-3p as therapeutic target for hepatocellular cancer. Cancer Cell 2011;19:232-243. The full scale of human miRNome in specific cell or tissue, especially in cancers, remains to be determined. An in-depth analysis of miRNomes in human normal liver, hepatitis liver, and hepatocellular carcinoma (HCC) was carried out in this study. We found nine miRNAs accounted for 88.2% of the miRNome in human liver. The third most highly expressed miR-199a/b-3p is consistently decreased in HCC, and its decrement significantly correlates with poor survival of HCC patients. Moreover, miR-199a/b-3p can target tumorpromoting PAK4 to suppress HCC growth through inhibiting PAK4/Raf/MEK/ERK pathway both in vitro and in vivo.

Our study provides miRNomes of human liver and HCC and contributes to better understanding of medchemexpress the important deregulated miRNAs in HCC and liver diseases. MicroRNAs (miRNAs) are small RNAs of 22 nucleotides length that do not hold the sequential information to transcribe proteins, but function as critical regulators of gene expression in multicellular and some unicellular eukaryotes.1 Pre-miRNAs undergo sequential processing by the ribonuclease III endonucleases Drosha and Dicer, leading to the mature 20- to 23-nucleotide species.2 These in turn are integrated into the RNA-induced silencing complex (RISC) and recognize their target genes by interacting with complementary sequences in the 3′ untranslated region of their messenger RNAs (mRNAs). In the case of perfect or nearly perfect pairing, the target mRNA becomes degraded, whereas imperfect pairing leads to translational repression of the latter.

Unfortunately, no single agent or combination of agents administered systemically provided beneficial effects on survival rate.9,10 Recently, with the advances in understanding the molecular biology of HCC, new therapeutic strategies to treat HCC have emerged.11 For instance, the clinical efficiency of sorafenib, an oral multi-kinase inhibitor of several kinases (vascular

endothelial growth factor [VEGF], platelet-derived growth factor [PDGF], c-kit receptor, BVD-523 purchase Raf) with antiproliferative and anti-angiogenesis prosperities in HCC, has been studied in clinical trials. Although sorafenib could benefit advanced-HCC patients, the effect is rather limited.12 Vitamin D, identified as a hormone to maintain blood calcium homeostasis and promote skeletal mineralization, has been demonstrated to Epigenetics Compound Library screening exert additional functions, including antiproliferative, pro-differentiation, pro-apoptotic,

anti-angiogenesis and anti-invasive characteristics in many cancer cell systems during the past two decades. These antitumor activities have led to several clinical trials. Regarding HCC, vitamin D has also been investigated from in vitro, pre-clinical animal studies to clinical trials. In this review, we discussed the source and metabolism of vitamin D, a new emerging aspect of the genomic and non-genomic actions of vitamin D, vitamin D receptor (VDR) polymorphism, clinical trials and the latest development of 上海皓元医药股份有限公司 vitamin D analogs for potential HCC therapy. There are two common forms of vitamin D: vitamin D2 and vitamin D3. They originate from two distinct sources. Vitamin D2 (ergocalciferol) is synthesized from ergosterol of yeast and vitamin D3 (cholecalciferol) is produced from 7-dehydrocholesterol (7-DHC) of lanolin. (Fig. 1). Vitamin D (representing D2 and D3) is rare in foods, only few foods contain sufficient vitamin D naturally.13 Therefore, fortification of vitamin D in foods or taking a supplement is gaining popularity

in some countries. To most humans, exposure to sunlight accounts for about 90% of vitamin D requirements.13 Vitamin D is inert biologically. Vitamin D is first hydroxylated in the liver by vitamin D-25-hydroxylase (25-OHase)14 to form 25-hydroxyvitamin D [25(OH)D], the circulating form of vitamin D. 25(OH)D is considered as the most reliable index of human vitamin D status. 25(OH)D circulates as a vitamin-D-binding-protein (DBP)-bound form in the blood stream. Upon entering the kidneys, 25(OH)D is further hydroxylated mainly in the proximal tubules at the C-1 position to form 1α,25-dihydroxyvitamin D [1α,25(OH)2D], catalyzed by 25(OH)D-1α-hydroxylase (1α-OHase or CYP27B1). Among all of the vitamin D metabolites, 1α,25(OH)2D is the most active form. Another renal enzyme that also plays a crucial role is 25(OH)D-24-hydroxylase (24-OHase or CYP24A1).

A perforation score helps stratify patients into different risk groups. Key Word(s): 1. esophagus; 2. perforation; 3. Boerhaave’s; 4. perforation score; Presenting Author: FAN FENG Additional Authors: HONGWEI ZHANG Corresponding Author: FAN FENG Affiliations: Xijing Hospital Objective: Dissection of subcarinal

lymph nodes is technically difficult in that it may cause main bronchus injury and prolong operation time. The aim of the present study was to evaluate the clinical outcomes of clinical T1N0 esophageal squamous cell carcinoma (ESCC) patients with or without subcarinal lymph nodes dissection. Methods: A total of 283 patients with ESCC had undergone three stage esophagectomy. The clinical and pathological features were collected and correlations Copanlisib molecular weight with subcarinal lymph nodes metastasis were BMS-354825 research buy analyzed. The survival of patients was analyzed. Results: Tumor length, clinical

T, N and TNM stage, pathological T, N, and TNM stage were associated with subcarinal lymph node metastasis. The survival of T1N0 patients with subcarinal lymph nodes clearance was comparable to that without subcarinal lymph nodes clearance. No significant difference was found between the patients with subcarinal lymph nodes metastasis and patients without metastasis and had less than 4 subcarinal lymph nodes dissection (P > 0.05). The survival of patients without metastasis and had 4–6 subcarinal lymph nodes dissection was significantly higher than that of the patients MCE without metastasis and had less than 4 nodes dissection (P < 0.05), while patients without metastasis and had more than 6 subcarinal lymph nodes dissection had no survival benefit compared to that of the patients had 4–6 nodes dissection (P > 0.05). Conclusion: For clinical T1N0 ESCC patients, subcarinal lymph nodes clearance may be unnecessary. For the rest ESCC patients, we recommend that at least 4 subcarinal lymph nodes should be removed in order to improve patients’ survival. Key Word(s): 1. Esophageal cancer; 2. Subcarinal lymphnode; Presenting Author: RAVINDRA SATARASINGHE Additional

Authors: SATHYAJITH AMBAWATTE, NAYOMISHERMILA JAYASINGHE, JAYEWARDENE RATHNAYAKE, RAVI WIJESINGHE, PUBUDU DE SILVA, NARTHANIRASENDRANRASENDRAN RASENDRAN Corresponding Author: RAVINDRA SATARASINGHE, NAYOMISHERMILA JAYASINGHE Affiliations: Sri Jayewardenepura General Hospital Objective: To study the prevalence and demographics of peptic ulcer disease in a cohort of adult Sri Lankans presented to a tertiary referral centre. Methods: Case notes of 2728 patients who had undergone upper gastrointestinal endoscopy for various reasons in the principle author’s unit at Sri Jayewardenepura General Hospital, Kotte, Sri Lanka from 15th of February 2002 to 15th February 2013 were retrospectively analyzed to obtain the required information. Results: There were178 patients having peptic ulcer disease with an age range of 24 to 92 years with a mean age of 62.3 ±13.5 SD years.