No abstract available.
Teratoma*

No abstract available.
Gestational Trophoblastic Disease* ; Sterilization, Tubal*

Brunners gland adenoma is a benign epithelial tumor of the duodenum originating from submucosal Brunners gland. This is an extremely rare entity that account for only 10.6% of benign duodenal tumor, which are themselves relatively rare, representing 0.008% of all surgical and autopsy specimens. The clinical manifestation are nonspecific gastrointestinal complaints, such as bloating or epigastric pain, and the tumor gives rise to melena or anemia, due to the ulceration or erosion of the tumor. The diagnosis is usually made by radiologic studies and gastroduodenal endoscopy which can also provide definitive treatment. The aim of treatment is complete removal of the lesion and exclude malignancy. We report on 4 cases of Brunners gland adenoma which was confirmed by operation or endoscopic polypectomy.
Adenoma* ; Anemia ; Autopsy ; Diagnosis ; Duodenum ; Endoscopy ; Melena ; Ulcer

Postappendectomy bleeding is a rare and occasionally catastrophic phenomenon. Bleed-ing in the gastrointestinal tract may occur early or late. The cause of late bleeding included ulceration, vascular malformation or granuloma. We experienced a case of delayed appen-diceal stump ulceration and bleeding who underwent an appendectomy 1 year ago. The patient was admitted due to melena. A colonoscopy showed a well-circumscribed deep ulcer containing of silk suture material at the base of appendiceal stump. Biopsy revealed only granulation tissue with nonspecific inflammation. The silk was removed by biopsy forcep and sulfasalazine was tried. A repeat colonoscopy showed the complete ulcer heal-ing 3 months later. We report this case with a review of literatures.
Appendectomy* ; Biopsy ; Colonoscopy ; Gastrointestinal Tract ; Granulation Tissue ; Granuloma ; Hemorrhage* ; Humans ; Inflammation ; Melena ; Silk ; Sulfasalazine ; Surgical Instruments ; Sutures ; Ulcer* ; Vascular Malformations

BACKGROUND/AIMS: Unresectable malignant biliary obstruction has usually been treated by placement of a self-expandable metallic stent (SEMS). One of the major complications of SEMS is occlusion of the stent by the ingrowth and overgrowth of tumor. The optimal management of an occluded SEMS is still an unresolved problem. We performed this study to evaluate the usefulness of placing a second stent with using an uncovered SEMS or a covered SEMS in patients with stent occlusion. METHODS: From January 2006 to December 2007, a total of 163 patients were treated with the placement of an uncovered SEMS for treating malignant biliary obstruction, except for the cases with Klatskin's tumor. Thirty four patients were occluded and they underwent a second SEMS insertion. All the patients with an occluded uncovered SEMS were managed with placement of a covered SEMS or an uncovered SEMS by ERCP. RESULTS: The median patent duration after intervention was 98 days (range: 8~300 days) after the second covered SEMS insertion, and the median patent duration after intervention was 90 days (range: 10~643 days) after the second uncovered SEMS insertion. No significant difference in the patent period was observed between the covered SEMS group and the uncovered SEMS group (P=0.832). CONCLUSIONS: The covered SEMS group and the uncovered SEMS group had similar patent periods for the management of occluded uncovered metal stents.
Cholangiopancreatography, Endoscopic Retrograde ; Humans ; Klatskin's Tumor ; Stents

BACKGROUND: Simple ventricular septal defect(VSD) is the most common congenital heart disease. Although closure of VSD is currently associated with a relatively low risk, experience with younger and smaller infants has been variably less satisfactory. We assessed the results of surgical closure of VSD in infant. MATERIALS AND METHODS: Between 1996 and 2000, 45 non-restrictive VSD patients underwent patch repair and retrospective analysis was done. Patients were divided into two groups based on weight: group I infants weighed 5kg or less(n=16), and group II infants weighed more than 5kg(n=29). Both groups had similar variation in sex, VSD location, aortic cross clamp time and total bypass time. But combined diseases (ASD, PDA, MR) were more in group I. We closed VSD with patch and used simple continuous suture method in all patients. RESULTS: There were no operative mortality, no reoperation for hemodynamically significant residual shunt and no surgically induced complete heart block. As a complication, pneumonia(group I: 2 cases, group II: 2 cases), transient seizure(group II: 2), wound infection(group I: 1, group II: 1), urinary tract infection(group I: 1) and chylopericardium(group I: 1) developed, and there was no significant difference between two groups(p>0.05). CONCLUSION: Early primary closure with simple continuous suture method was applicable in all patients with non-restrictive VSD without any serious complications.
Heart Block ; Heart Defects, Congenital ; Heart Septal Defects, Ventricular* ; Humans ; Infant* ; Mortality ; Reoperation ; Retrospective Studies ; Sutures ; Urinary Tract ; Wounds and Injuries

Nilotinib is used for treating patients with imatinib-sensitive or -resistant chronic myeloid leukemia (CML); however, nilotinib-resistant cases have been observed in recent years. In addition, a considerable number of patients receiving nilotinib developed diabetes. Metformin is a front-line drug for the treatment of type 2 diabetes, and several studies have shown that diabetes patients treated with metformin have reduced incidence of cancer. This study aimed to define the effect of metformin on CML cells to determine whether metformin overcomes nilotinib resistance, and to identify novel targets for the treatment of nilotinib resistance. Methods: We observed the effects of metformin and nilotinib on K562 and KU812 human CML cell lines. Nilotinib-resistant CML cell lines were generated by exposing cells to gradually increasing doses of nilotinib. Then, we investigated the driving force that makes resistance to nilotinib and the effect of metformin on the driving force. Results: Sub-toxic doses of metformin enhanced nilotinib efficacy by reducing Bcl-xL expression, which induces apoptosis in CML cells. Next, we generated nilotinib-resistant K562 and KU812 cell lines that overexpressed the c-Jun N-terminal kinase (JNK) gene. JNK silencing by a JNK inhibitor restored sensitivity to nilotinib. Furthermore, metformin was effective in decreasing phosphorylated JNK levels, restoring nilotinib sensitivity. Combined treatment with nilotinib and metformin was more effective than combined treatment with nilotinib and a JNK inhibitor in terms of cell proliferation inhibition. Conclusions: This study suggested that combination therapy with metformin and nilotinib may have clinical benefits of enhancing antileukemia efficacy and overcoming resistance to nilotinib.

Polyatreritis nodosa is a rare autoimmune disease (the immune system attacking its own body) characterized by spontaneous inflammation of the arteries (arteritis) of the body. Because arteries are involved, the disease can affect any organ of the body. The most common areas of involvement include the muscles, joints, intestines (bowels), nerves, kidneys, and skin. Gastrointestinal involvement is reported in about 50% of the cases, but bleeding complications are rare and result in a poor prognosis. Polyarteritis nodosa is most common in middle-age persons. Recently, we experienced polyarteritis nodosa which presented as small bowel bleeding and which was diagnosed by angiography, a small-bowel series, and patholgic examination of the surgically removed ileum specimen. We report this case with a brief review of the literature.
Angiography ; Arteries ; Autoimmune Diseases ; Hemorrhage ; Humans ; Ileum ; Immune System ; Inflammation ; Intestines ; Joints ; Kidney ; Muscles ; Polyarteritis Nodosa* ; Prognosis ; Skin

OBJECTIVE: To compare the women who use postmenopausal hormone replacement therapy to never user for the serum leptin level and degree of obesity, then evaluate the precausing factor of postmenopausal obesity. METHOD: We checked the serum leptin level, blood chemistry and body composition in three groups, two groups are postmenopause groups which is HRT user (n=125) and HRT never user (n=194), and the other is premenopause groups(n=82). We used SPSS and Excel for analyzed the difference between the groups. RESULT: BMR is decreased after menopause, body fat ratio, abdominal fat ratio, BMI, leptin, sugar, and cholesterol level are increased after menopause. There is no difference between the postmenopausal HRT group and non-HRT group in body fat composition, abdominal fat ratio, BMI,BMR,AMC and leptin levels. Serum sugar level shows positive correlation with the leptin level in pre and postmenopausal women after exclude the effect of body fat ratio. Serum estradiol and leptin level shows positive correlation.(correlation coefficient 0.68 in postmenopausal non-HRT group and 0.735 in postmenopausal HRT group). CONCLUSION: Serum estradiol and sugar level have some correlation with leptin level and leptin resistance in postmenopausal women, and decreased estradiol level caused obesity through increased leptin resistance.
Abdominal Fat ; Adipose Tissue ; Body Composition* ; Chemistry ; Cholesterol ; Estradiol ; Estrogen Replacement Therapy ; Female ; Humans ; Leptin* ; Menopause ; Obesity ; Postmenopause ; Premenopause

Nonvisualization of left circumflex coronary artery from the left coronary artery is commonly due to anomalous origin of circumflex artery from the right coronary artery or right sinus of Valsalva. However, complete ostial obstruction of circumflex artery, circumflex artery extended from the right coronary artery, anomalous origin of circumflex artery from the pulmonary artery may be the cause. We report two cases of absent left circumflex artery from the left coronary artery, in which the circumflex artery arose as a terminal extension of the right coronary artery. Angiographic features of absent left circumflex artery from the left coronary artery were described.
Arteries* ; Coronary Vessels* ; Pulmonary Artery ; Sinus of Valsalva