Previous Page  21 / 24 Next Page
Information
Show Menu
Previous Page 21 / 24 Next Page
Page Background

Page 96

Gastro 2016

August 11-12, 2016

Volume 6, Issue 4(Suppl)

J Gastrointest Dig Syst 2016

ISSN:2161-069X JGDS, an open access journal

conferenceseries

.com

August 11-12, 2016 Birmingham, UK

6

th

Global Gastroenterologists Meeting

Is there any difference in clinical outcome according to the tumor subsite location within the colon

when performing laparoscopic complete mesocolic excision?

Jun-Gi Kim, Min Ki Kim, Dae Youn Won, In Kyu Lee, Hyeon-Min Cho

and

Bong-Hyeon Kye

Catholic University of Korea, South Korea

Aim:

Procedures of laparoscopic colectomy are different from each other according to the tumor subsite within the colon, and

short-and long-term outcomes of laparoscopic complete mesocolic excision (CME) and central vascular ligation (CVL) for

colon cancer have never been compared based on the tumor location.

Method:

Clinical data of patients who received laparoscopic colectomy for primary colon cancer between April 1995 and

December 2010 from single surgeon were retrospectively reviewed. Data were analyzed and compared among three groups;

patients whose tumor location was between ascending and proximal transverse colon (A, n=142), mid transverse and

descending colon (TD, n=55), and sigmoid and rectosigmoid colon (S, n=214).

Results:

Female patients were more common in group A (53.5% vs. 38.2% vs. 39.3%, p=0.020). Other baseline characteristics

were comparable. Operative time was shorter in group S than another groups [245(145-855) vs. 279(150-485) vs. 295(145-

455) min, p=0.000]. There were no differences among the groups in perioperative complication and patient recovery. Local

recurrence rate was comparable among the groups (4.2% vs. 5.5% vs. 3.3%, p=0.594) for the median follow up period of 73(0-

120) months.

Conclusion:

Laparoscopic CME and CVL for colon cancer can be performed with comparable short- and long-term outcomes

regardless of tumor subsite except for the operative time.

edemiel@cmcnu.or.kr

Computational analysis to detect resistance mutations to direct acting antivirals in hepatitis C virus

Karina Salvatierra

National University of Misiones, Argentina

H

epatitis C virus (HCV) infection is considered as a major public health problem, with an estimate of 200 million people

infected worldwide. HCV infection is the major cause of chronic liver disease, with severe outcomes including cirrhosis

and hepatocellular carcinoma and it is the main cause of liver transplantation. The treatment for HCV chronic infection with

pegylated interferon alpha plus ribavirin inhibitors is unspecific; consequently, the treatment is effective in only 50% of patients

infected. This has prompted the development of direct-acting antivirals agents (DAA’s) that target virus proteins. Unfortunately,

since the virus has a high replication rate and its RNA polymerase lacks proofreading activity, genetic variations might produce

resistance against the DAA’s. These DAA’s have demonstrated a potent effect in vitro and in vivo; however, virus mutations

associated with the development of resistance have been described. The objective of this work is to detect mutations in known

aminoacids to be implicated in resistance to DAA’s in sequences obtained of conventional Sanger and cloning sequencing. We

have designed and developed an online information system named Biomedical Mutation Analysis (BMA), which allows users

to calculate changes in nucleotide and amino acid sequences for each selected sequence from conventional Sanger and cloning

sequencing. BMA allows the computational analysis quickly, easily and effectively. Furthermore, the development of different

visualization techniques allows a proper interpretation and understanding of the results. The data obtained from BMA will be

useful for HCV resistance surveillance, for the design of broad-range inhibitors and rationale therapeutic regimen.

kariales@gmail.com

J Gastrointest Dig Syst 2016, 6:4(Suppl)

http://dx.doi.org/10.4172/2161-069X.C1.035