No abstract available.
46, XY Disorders of Sex Development* ; Humans ; Male*

We have experienced three cases of mucinous ductal ectasia of the pancreas. They showed the characteristic duodenoscopic findings and underlying pathology was hyperplasia in two cases and adenocarcinoma in one case. When endoscopic retrograde pancreatography was performed, bulging ampulla of Vater, patulous ampullary orifice and mucus leakage from papillary orifice were noted. Also cyst-like dilatation of main duct or side branch of the uncinate process were observed.
Adenocarcinoma ; Ampulla of Vater ; Dilatation ; Dilatation, Pathologic* ; Hyperplasia ; Mucins* ; Mucus ; Pancreas* ; Pathology

It hae been well established that, specifi alterations in members of the ras gene family, H-ras, K-ras and N-ras, can convert them into active oncogenes. These alterations are either point mutations occurirg in either codon 12, 13 or 61, or alternatively, a 5- to 50-fold amplification of the wfld-type gene. Activated ras oncogenes have been found in a significant proportion of all turnors, but the incidence varies considerably with the tumor type : it is frequent (20~40%) in colarectal eancer and acute myeloid leukemia, but absent or preaent rarely in breast and atomach cancer. But the role of c-K-ras point mutatio in the development of cancers in the female genital tract has not been extensively studied. Polymerase chain reaction followed by gel electrophoresis was performed respectively using wild-type normal and specific point mutation primers{GGT->GAT, GGT->AGT, GGT->TGT and GGT->GTT) to detect, point, mutation of codon 12 of c-K-ras oncogene. The c-K-ras oncogene point mutation was confirmed by Southern blot hybridization using synthetic oligonucleatide probe. 3'-end Iabelled with digoxigenin -dUTP. With this method, the frequency of point mutation on codon 12 of c-K-ras oncogene was examined the tissues in 37 casea of ovarian cancer, 7 cases of endometrial cancer, 36 cases of the gestational trophoblastic tumor, 60 cases of cervical cancer. The relationship between the presence of a c-K-ras point mutation and clinicopathological characteristics of the female genital tract cancers were also analysed. The results were as follows; 1. The incidence of four point mutations on codon 12 of c-K-ras oncogene in 37 ovarian cancers was 45.9% (17/37) and distribution were 43.2% (16/37), 2.7% (1/37) and 0% (0/37) in GGT-->GAT, GGT-->AGT, GGT-->TGT, and GGT-->GTT, respectively. According to histological type, in ovarian cancers, The point mutation of K-ras oncogene waspositive in 45 % (10/22) of serous cystadenocarcinomas. The incidence of four point mutations on codon 12 among 37 patients with ovarian cancer according to histological type was 45.5 % (10/22) with serous cystadenocarcinoma, 57.1% (4/7) of mucinous cystadenocarcinoma. Comparing the positive rate of point mutations of K-ras oncogen among 37 patients with ovarian cancer with the clinical stage, point mutation was detected in 28.5% (2/7) of patients with stage I, 40.0% (2/5) with stage II, and 52.0% (13/25) with stage III/IV. There was no statistically significant increasement of point mutations with the advance of the clinical stage of ovarian cancer. Comparing the positive rate of point mutations of K-ras oncogen among 37 patients with ovarian cancer according to the histologic grade point mutation was detected in 50.0 % (2/4) 0f patients with grade I, 451.7 % (5/12) with grade II and 47.6 % (10/21) with grade III. 2. The incidence of point mutations of K-ras oncogen among 33 patients with ovarian cancer who were performed pelvic lymph node dissection was 57.1 % (12/21) of the patients with pelvic lymph node metastases and 16.7% (2/12) of the patients without pelvic lymph node metastases. There was statistically significant difference between the positive rate of c-K-ras point mutations and the pelvic lymph nodal status(P<0.05). 3. In 7 cases of endometrial cancer, positive rate of K-ras point was 42.8 % (3/7). Point mutations were also detected in 2 cases from 4 choriocarcinomas, but, the point mutation was only detected in 1 case from 60 cervical carcinomas. From these results, we may suggest that the point mutation on codon 12 c-K-ras oncogene are considered to be one of the important genetic change in the tumor formation and progression of ovarian of c-K-ras oncogene seems to be the one stop in the multistep process of tumor formation in ovarian cancer. Furthermore, the point mutation of c-k-ras gene could occur more frequently in the patients of ovarian cancer with pelvic lymph node metastases than in those without pelvic metastases, suggesting the orle in tumor progression. And we concluded that point mutation on codon 12 is comparable frequent in uterine endometrial carcinomas and have significance as an event that contributes to progrssion of endometrial cancers and choriocarcinoma, but cervical carcinoma do not appear to have c-K-ras point mutation in general. More studies will be necessary, but the detection of c-k-ras point mutation as the possibility of biological tumor marker to predict clinical outcome may be utilized in female malignancies.
Blotting, Southern ; Breast ; Choriocarcinoma ; Codon ; Cystadenocarcinoma, Mucinous ; Cystadenocarcinoma, Serous ; Digoxigenin ; Electrophoresis ; Endometrial Neoplasms ; Female* ; Genes, ras ; Humans ; Incidence ; Leukemia, Myeloid, Acute ; Lymph Node Excision ; Lymph Nodes ; Neoplasm Metastasis ; Oncogenes* ; Ovarian Neoplasms ; Point Mutation* ; Polymerase Chain Reaction ; Pregnancy ; Trophoblastic Neoplasms ; Biomarkers, Tumor ; Uterine Cervical Neoplasms

No abstract available.
Ultrasonics*

Organ transplantation has become a' widely accepted treatment modality for end-stage organ disease. The shortage of allogenic donors for organ transplantation has brought about the necessity of xenotransplantation as an unlimited source of organ donation. However, organ transplantation between different species have never been successful because of hyperacute rejection. Although the mechanism of this phenomenon is not fully understood, many researchers believe that the natural antibodies present in the recipient's serum may bind to the graft and induce the activation of complement cascade triggering the process of hyperacute rejection. ...continue...
Antibodies ; Complement System Proteins ; Heterografts ; Humans ; Organ Transplantation ; Tissue and Organ Procurement ; Tissue Donors ; Transplantation, Heterologous ; Transplants

No abstract available.
Polyarteritis Nodosa*

Fungal peritonitis is one of the leading causes of patient dropout from continuous ambulatory peritoneal dialysis (CAPD) therapy. Although the most causative agents of peritonitis associated with CAPD are bacteria, fungi are implicated in up to 10% of cases. The most common organism of fungal peritonitis is Candida specises, but Trichosporon beigelii was reported as a rare causative agent of fungal peritonitis. We experienced a case of CAPD peritonitis by Trichosporon beigelii, which was treated with CAPD catheter removal, and antifungal agents with amphotericin B and fluconazole. Thus, we report our experience of CAPD peritonitis caused by Trichosporon beigelii and review of the literature.
Amphotericin B ; Antifungal Agents ; Bacteria ; Candida ; Catheters ; Fluconazole ; Fungi ; Humans ; Patient Dropouts ; Peritoneal Dialysis, Continuous Ambulatory* ; Peritonitis* ; Trichosporon*

Purpose: The purpose of this study was to examine the psychological distress related to quality of life (QoL) of patients with colorectal cancer receiving 5-fluorouracil (5-FU) chemotherapy at home with disposable Elastomeric infusion pumps. Methods: In this study, 179 colorectal outpatients were recruited between September 2019 and January 2021. National Cancer Center Psychological Symptom Inventory scores, general self-efficacy, and the EORTC QLQ-C30 scores were measured. Data were analyzed using Independent t-test, One-way ANOVA with Bonferroni post hoc analysis, and hierarchical multiple linear regression with the SPSS/WIN 26.0 programs. Results: The overall prevalence of psychological distress was 52.0% in colorectal patients. In multiple regression, psychological distress (β=-.20, p=.005), appetite loss (β=-.20, p=.001), chemotherapy cycles (β= .19, p=.002), fatigue (β=-.16, p=.035), physical functioning (β=-.16, p=.024), and emotional functioning (β=-.15, p=.025) were significant factors of QoL, and the final model explained 45.0% of the total variance of QoL. Conclusion Supporting patients toward decreased psychological distress and increased physical and emotional functioning, especially in the first or second cycle of chemotherapy, could be used to improve their QoL. To consider the thresholds for clinical importance, it is necessary to increase the interpretation of psychological distress in clinical practice and further research.

OBJECTIVE: Ovarian cancer represents a relatively chemosensitive solid tumor, with responsiveness to a range of agents. Cisplatin is the mainstay of drug treatment and is one of the most active single agent. However, the overall outcome for patients remains unsatisfactory and the emergence of drug resistance is a major factor in treatment failure. Loss of DNA mismatch repair is a common finding in many types of sporadic cancer as well as in patients with hereditary nonpolyposis colon cancer. Cells that lack DNA mismatch repair are resistant to commonly used chemotherapeutic agents. Selection of cells for resistance to cisplatin, a well-recognized mutagen, could result in mutation in genes involved in DNA mismatch repair. METHODS: This study evaluated the mutation of hMLH1 and hMSH2, and its relation to the Taxol and Topotecan chemosensitivity in the clones from the ovarian cancer cell line 2008 and cisplatin-resistant cell line 2008/ C13*5.25. RESULTS: 1. Cells from 2008 and 2008/C13*5.25 expressed both hMLH1 and hMSH2 when analysed with immunoblotting. 2. Twenty two out of 100 single-cell clones from 2008 and 27 of clones from 2008/C13*5.25 expressed no hMLH1. hMSH2 was expressed in all clones. 3. There was no difference of Taxol chemosensitivity between 2008 and 2008/C13*5.25 cell lines. In the 2008/C13*5.25 cell line, the hMLH1-deficient clones were more sensitive to Taxol than the hMLH1-proficient clones(P=0.049), but in 2008 cell lines hMLH1-proficient clones were more sesitive to Taxol(P=0.003). 4. There was no difference in Topotecan chemosensitivity between 2008 and 2008/C13*5.25 cell lines. In the 2008/C13*5.25 cell line, the hMLH1- deficient clones were not more sensitive to Topotecan than the hMLH1-proficient clones. In the 2008 cell lines hMLH1-deficient clones were more sesitive to Topotecan(P=0.001). Overall, hMLH1-deficient clones from both 2008 and 2008/C13*5.25 cell lines were significantly more sensitive to Topotecan(P=0.001). 5. Microsatellite instability was not demonstrated in all 4 types of single-cell clones from 2008 and 2008/C13*5.25 cell lines. CONCLUSIONS: The present results indicate that there is no relation between mutation of mismatch repair gene and cisplatin resistance. But hMLH1-deficient ovarian cancer cells are more sensitive to Taxol or Topotecan in this study. The latter finding mandates the examination to assess the mutation of hMLH1 in tumor cells before treatment or at the time clinical resistance to cisplatin develops in ovarian cancer.
Cell Line* ; Cisplatin ; Clone Cells* ; Colorectal Neoplasms, Hereditary Nonpolyposis ; DNA Mismatch Repair* ; DNA* ; Drug Resistance ; Humans ; Immunoblotting ; Microsatellite Instability ; Ovarian Neoplasms* ; Paclitaxel* ; Topotecan* ; Treatment Failure