BACKGROUND: Lifestyle is an important risk factor for many diseases. We need to educate medical students for advocating health promoting behaviors to their patients. Teaching knowledge, however, was not enough for medical students to change their health-related lifestyle. In this study, we investigated health promoting behaviors of medical students, and the improvement of their health behaviors after competitive lifestyle modification program. METHODS: All sophomores of medical college in Seoul National University were included in this study. We performed lifestyle modification program consisting of lecture, group competition, and feedback. We focused on reforming health behaviors like smoking, drinking, exercise, stress management and eating habits. And we also checked common symptoms of functional diseases, medication frequency for relieving these symptoms and general life satisfaction. RESULTS: After 2 months of lifestyle modification program, the obese (P = 0.0455) and the average value of BMI (P < 0.001) were decreased and two of smokers quitted smoking. Numbers of medical students with health related habits such as regular exerciser (P = 0.027), frequent user of symptom-relief medication (P < 0.001), breakfast skipper (P = 0.005) were signifi cantly changed in positive way, and the average value of general life satisfaction score (P = 0.003) was improved. CONCLUSION: Lifestyle modification program improved medical students' health habits and enhanced general life satisfaction.
Breakfast ; Drinking ; Eating ; Health Behavior ; Humans ; Life Style ; Risk Factors ; Smoke ; Smoking ; Students, Medical

The wide use of lamivudine in chronic hepatitis B has produced a monotonic increase in patients with lamivudine resistance. Therefore, treating lamivudine resistance in chronic hepatitis B is a major concern in clinical practice for the treatment of hepatitis B virus (HBV). There is conflicting evidence on the outcome of pegylated interferon alpha (PEG-IFN alpha) therapy against lamivudine-resistant HBV, which is due to mutations in the YMDD motif. We experienced a patient with chronic hepatitis B who was successfully treated with PEG-IFN alpha-2a after the development of virologic and biochemical breakthrough during lamivudine therapy. Virologic breakthrough was associated with the emergence of YMDD mutants 48 months after starting lamivudine therapy. Treatment with PEG-IFN alpha-2a for 12 months resulted in an undetectable serum level of HBV DNA and the resolution of hepatitis, and the virologic response was maintained over 16 months after cessation of PEG-IFN alpha-2a.
Adult ; Alanine Transaminase/blood ; Antiviral Agents/*therapeutic use ; DNA, Viral/analysis ; Drug Resistance, Viral ; Hepatitis B, Chronic/diagnosis/*drug therapy ; Humans ; Interferon Alfa-2a/*therapeutic use ; Lamivudine/*therapeutic use ; Liver/pathology ; Male ; Polyethylene Glycols/*therapeutic use

Liver cirrhosis is one of the major complications of hepatitis C virus (HCV) infection, but the mechanisms underlying HCV-related fibrogenesis are still not clear. Although the roles of HCV core protein remain poorly understood, it is supposed to play an important role in the regulation of cellular growth and hepatocarcinogenesis. The aim of this study was to examine the role of HCV core protein on the hepatic fibrogenesis. We established an in vitro co-culture system with primary hepatic stellate cell (HSC) isolated from rats, and a stable HepG2-HCV core cell line which had been transfected with HCV core gene. The expressions of fibrosis-related molecules transforming growth factor beta1 (TGF-beta1), transforming growth factor b receptor II (TGF beta RII), alpha-smooth muscle actin (alpha-SMA) and connective tissue growth factor (CTGF) were analyzed via histological or molecular methods. In addition, the expression levels of matrix metaloprotinase-2 (MMP-2) and collagen type I (Col I) from the co-cultured media were measured by zymogram and ELISA, respectively. The expressions of alpha-SMA, TGF-beta1, Col I, TGF beta RII and MMP-2 were significantly increased in the co-culture of stable HepG2-HCV core with HSC. Moreover, the significant increases of CTGF and TGF-beta1 in the HCV core-expressing cells were observed by either Northern or Western blot analysis. These results suggest that HCV core protein may contribute to the hepatic fibrogenesis via up-regulation of CTGF and TGF-beta1.
Actins/metabolism ; Animals ; Cell Line, Tumor ; Cells, Cultured ; Coculture Techniques ; Collagen Type I/metabolism ; Gelatinase A/metabolism ; Immediate-Early Proteins/*biosynthesis ; Intercellular Signaling Peptides and Proteins/*biosynthesis ; Liver/metabolism/*pathology ; Liver Cirrhosis/*metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Transforming Growth Factor beta/metabolism ; Research Support, Non-U.S. Gov't ; Transforming Growth Factor beta/*metabolism ; Up-Regulation ; Viral Core Proteins/genetics/*metabolism

Biliary complications after liver transplantation occur in 13~35% of patients. Biliary cast syndrome, cast formation of biliary sludge along the bile duct, can develop in 4~18% of liver transplant recipients, although the incidence rate is significantly decreasing due to the improvement of graft harvesting and preservation. It is very important that early diagnosis and effective management of biliary cast syndrome be performed when there is a bile duct stricture or dilatation associated with jaundice and cholangitis in the recipient after liver transplantation, due to the possibility of retransplantation and death of the patient from graft loss. We report a case of a biliary cast formed with suppurative cholangitis and extracted incidentally with a plastic biliary stent during an endoscopic procedure after cadaveric liver transplantation, in which the ERCP findings revealed a stricture at the anastomosis site of the common bile duct and cholangitis.
Bile ; Bile Ducts ; Cadaver ; Cholangiopancreatography, Endoscopic Retrograde ; Cholangitis* ; Common Bile Duct ; Constriction, Pathologic* ; Dilatation ; Early Diagnosis ; Humans ; Incidence ; Jaundice ; Liver Transplantation* ; Liver* ; Plastics ; Stents ; Superior Mesenteric Artery Syndrome* ; Transplantation ; Transplants

Successful male germ cell transplantation requires depletion of the host germ cells to allow efficient colonization of the donor spermatogonial stem cells. Although a sterilizing drug, busulfan, is commonly used for the preparation of recipient models before transplantation, the optimal dose of this drug has not yet been defined in dogs. In this study, 1-year-old mongrel dogs were intravenously injected with three different concentrations of busulfan (10, 15, or 17.5 mg/kg). Four weeks after busulfan treatment, no fully matured spermatozoa were detected in any of the busulfan-treated groups. However, small numbers of PGP9.5-positive spermatogonia were detected in all treatment groups, although no synaptonemal complex protein-3-positive spermatocytes were detected. Of note, acrosin-positive spermatids were not detected in the dogs treated with 15 or 17.5 mg/kg busulfan, but were detected in the other group. Eight weeks after busulfan treatment, the dogs treated with 10 mg/kg busulfan fully recovered, but those in the other groups did not. PGP9.5-positive spermatogonia were detected in the 10 mg/kg group, and at a similar level as in the control group, but these cells were rarely detected in the 15 and 17.5 mg/kg groups. These results suggest that a dose of 15-17.5 mg/kg is optimal for ablative treatment with busulfan to prepare the recipient dogs for male germ cell transplantation. At least eight weeks should be allowed for recovery. The results of this study might facilitate the production of recipient dogs for male germ cell transplantation and can also contribute to studies on chemotherapy.
Animals ; Busulfan* ; Colon ; Dogs* ; Drug Therapy ; Germ Cells ; Humans ; Male ; Spermatids ; Spermatocytes ; Spermatogonia ; Spermatozoa ; Stem Cell Transplantation* ; Stem Cells* ; Synaptonemal Complex ; Testis* ; Tissue Donors

BACKGROUND/AIMS: The study of liver fibrogenesis by hepatitis C virus (HCV) has been limited due to the lack of an efficiency in vitro culture systems. In the present study, we investigated whether or not HCV core protein is directly related to liver fibrogenesis through stimulation of hepatic stellate cells (HSC). METHODS: Human and rat HSC were isolated and we established an in vitro co-culture system of a stable HepG2-HCV core cell line which was transfected with HCV core gene and primary HSC. We performed immunocytochemical staining and Western and Northern blot analysis in the stimulated HSC by HCV ocre protein to identify the expression of transforming growth factor beta1 (TGF-beta1), transforming growth factor beta receptor II (TGFbeta R II), alpha-smooth muscle actin (alpha-SMA) and connective tissue growth factor (CTGF). The expression of matrix metaloprotinase-2 (MMP-2) and collagen type I (Col I) in the culture media were measured by zymogram and ELISA, respectively. RESULTS: The expression of TGF-beta1 and CTGF was significantly higher in the stable HepG2-HCV core cell line than in HepG2 cells. Furthermore, the makers related to fibrosis such as alpha-SMA, TGF-beta1, Col I, TGFRII and MMP-2 were highly experssed in the co-culture of stable HepG2-HCV core with HSC. CONCLUSIONS: HCV core protein may play a direct role in the fibrogenesis of chronic liver disease with HCV infection.
Actins/metabolism ; Animals ; Cell Line, Tumor ; Coculture Techniques ; Connective Tissue Growth Factor ; Fibrosis ; Hepatitis C Antigens/*physiology ; Humans ; Immediate-Early Proteins/metabolism ; Immunoblotting ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins/metabolism ; Liver/metabolism/*pathology ; Protein-Serine-Threonine Kinases ; Rats ; Rats, Sprague-Dawley ; Receptors, Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1 ; Viral Core Proteins/*physiology

Acute appendicitis is the most common cause of an acute abdomen. But torsion of the appendix is a rare disorder that causes abdominal symptoms that are indistinguishable from acute appendicitis. So, making the preoperative diagnosis of torsion of the appendix is difficult. In 1918, Payne et al. reported the first case of torsion of the appendix in a 37 years old woman. Since then, more than thirty cases have been reported. Torsion of the appendix can occur at any age & gender. Here, we report on a case of secondary torsion of appendix with mucinous cystadenoma in a 52 year-old woman, which was initially thought to be a right adnexal mass. Abdomen CT showed an 11x5 cm sized intra-abdominal mass growing along the right fallopian tube. On the small bowel series, an extra-luminal mass was found and this was pushing aside the small intestine. We performed diagnostic laparoscopic exploration and found inflammation of appendix with torsion. It was twisted 720degrees in a clockwise direction with ischemic change. The histological result was mucinous cystadenoma.
Abdomen ; Abdomen, Acute ; Appendicitis ; Appendix ; Cystadenoma, Mucinous ; Fallopian Tubes ; Female ; Humans ; Inflammation ; Intestine, Small

BACKGROUND/AIMS: The aims of this study were (1) to identify the useful clinical parameters of noninvasive approach for distinguishing nonalcoholic steatohepatitis (NASH) from nonalcoholic fatty liver disease (NAFLD), and (2) to determine whether the levels of the identified parameters are correlated with the severity of liver injury in patients with NASH. METHODS: One hundred and eight consecutive patients with biopsy-proven NAFLD (age, 39.8+/-13.5 years, mean+/-SD; males, 67.6%) were prospectively enrolled from 10 participating centers across Korea. RESULTS: According to the original criteria for NAFLD subtypes, 67 patients (62.0%) had NASH (defined as steatosis with hepatocellular ballooning and/or Mallory-Denk bodies or fibrosis > or =2). Among those with NAFLD subtype 3 or 4, none had an NAFLD histologic activity score (NAS) below 3 points, 40.3% had a score of 3 or 4 points, and 59.7% had a score >4 points. Fragmented cytokeratin-18 (CK-18) levels were positively correlated with NAS (r=0.401), as well as NAS components such as lobular inflammation (r=0.387) and ballooning (r=0.231). Fragmented CK-18 was also correlated with aspartate aminotransferase (r=0.609), alanine aminotransferase (r=0.588), serum ferritin (r=0.432), and the fibrosis stage (r=0.314). A fragmented CK-18 cutoff level of 235.5 U/L yielded sensitivity, specificity, and positive and negative predictive values of 69.0%, 64.9%, 75.5% (95% CI 62.4-85.1), and 57.1% (95% CI 42.2-70.9), respectively, for the diagnosis of NASH. CONCLUSIONS: Serum fragmented CK-18 levels can be used to distinguish between NASH and NAFL. Further evaluation is required to determine whether the combined measurement of serum CK-18 and ferritin levels improves the diagnostic performance of this distinction.
Adult ; Aged ; Aged, 80 and over ; Alanine Transaminase/blood ; Asian Continental Ancestry Group ; Aspartate Aminotransferases/blood ; Biological Markers/blood ; Fatty Liver/classification/metabolism/*pathology ; Female ; Ferritins/blood ; Fibrosis/complications ; Humans ; Keratin-18/analysis ; Male ; Middle Aged ; Predictive Value of Tests ; Prospective Studies ; Republic of Korea ; Severity of Illness Index ; Young Adult