Biomedical subjects

W H Kim

Publications and source records attributed to W H Kim.

At least 73 records · Page 4Linked to original sources

PubMed2000

Microsatellite instability and Epstein-Barr virus infection in gastric remnant cancers.

Clinicopathological analysis, microsatellite analysis, detection of Epstein-Barr virus (EBV), and immunohistochemistry on p53 protein were performed in 26 cases of gastric remnant cancer (GRC). They were divided into two groups; Group A (n = 14) who had undergone a primary gastrectomy for benign gastric disease, and Group B (n = 12) who had undergone the same operation for gastric cancer. EBV infection was present in 29% of Group A, 8% of Group B and 6% of the conventional gastric carcinoma (CGC) (Group A vs CGC, P = 0.01). Microsatellite instability (MSI) was found in 7% of Group A, 25% of Group B, and 9% of the CGC (Group B vs CGC; P = 0.08). p53 Overexpression was observed in 46% of the GRC and 33% of the CGC. p53 Overexpression was observed in 90% of the intestinal type of GRC, but in only 20% of the diffuse type of GRC (P = 0.002). The cancer stage was a significant factor in the univariate analysis of survival (P = 0.04). In conclusion, GRC is different from CGC in terms of MSI or EBV association. The pathogenetic differences between the two groups require further investigation. EBV infection may have been involved in the carcinogenesis of Group A. MSI may be an important factor in the carcinogenesis of metachronous multiple gastric cancer (Group B).

Adult↗

PubMed2000

Microsatellite instability and alteration of E2F-4 gene in adenosquamous and squamous cell carcinomas of the stomach.

Microsatellite instability (MSI) due to defective DNA mismatch repair (MMR) is a form of genomic instability underlying the tumorigenesis of various human neoplasms. To evaluate the roles of MSI in the pathogenesis of gastric carcinomas with squamous differentiation, 17 primary stomach cancer patients (15 adenosquamous and two squamous cell carcinomas) were examined for MSI frequency using five microsatellite markers and the criteria for MSI recommended by the National Cancer Institute Workshop. The molecular causes and consequences of MSI in these neoplasms were further researched through the immunohistochemistry of MMR proteins and the mutational analysis of cancer-associated genes targeted by MSI, respectively. Two of the 17 (12%) cases demonstrated MSI at the most examined loci and were classified as having high level MSI (MSI-H). These tumors also exhibited frame-shift mutations at mononucleotide repeats in the target genes, including TGFbetaRII, IGFIIR, BAX, and hMSH6. It is interesting to note that the mutations of the serine (AGC)13 repeats within the E2F-4 gene were found only in the squamous cell carcinoma portions of them, whereas such alterations were not detected in any of the adenocarcinomatous portions. This suggests that E2F-4 might be implicated in the transformation of adenocarcinoma into squamous cell carcinoma and further studies are needed to understand its role in squamous differentiation.

Carcinoma, Adenosquamous↗

PubMed2000

Establishment and characterization of seven human renal cell carcinoma cell lines.

OBJECTIVE: To establish human renal cell carcinoma (RCC) cell lines, and to investigate the cell phenotypes and molecular characteristics of human RCC cell lines and their corresponding tumour tissues. MATERIALS AND METHODS: Seven human RCC cell lines from pathologically proven RCCs were established. The histopathology of the primary tumours, in vitro growth characteristics and status of tumour suppressor genes, mismatch repair genes and microsatellite instability (MSI) were examined in cell lines and their corresponding tumour tissues. Five of the cell lines were derived from clear cells (SNU-228, -267, -328, -349, and -1272), one from granular cells (SNU-482), and one from mixed clear and granular cell types (SNU-333). The mutational status was compared for von Hippel-Lindau (VHL), p53, TGF-beta type II receptor (TGF-betaRII), hMSH2, and hMLH1 genes in the cell lines and their corresponding tumour tissues. The MSI status of the cell lines was determined by screening for adenine repeat sequences, e.g. BAT-25, BAT-26, and BAT-40. RESULTS: All lines showed different doubling times and were confirmed by DNA fingerprinting analysis to be unique. Contamination by mycoplasma or bacteria was excluded. In two cell lines (SNU-349 and -1272) and their tumour tissues, mutations in the VHL gene were found. The SNU-267 line had a frameshift mutation in the p53 gene. A missense mutation of the TGF-betaRII gene was detected in the SNU-1272 line and the corresponding tissue. Analysis of the repeat sequences showed one cell line (SNU-349) to have MSI and the other six to have microsatellite stability. As MSI is a hallmark of the inactivation of mismatch repair genes, the presence of hMSH2 and hMLH1 mutations was investigated in all seven cell lines. An inactivating homozygous single base-pair deletion of the hMLH1 gene was found only in the SNU-349 cell line and corresponding tissue. Moreover, a frameshift mutation within an 8-bp polyadenine repeat present in the hMSH3 coding region was found only in the MSI cell line and tumour tissue. CONCLUSION: These newly established RCC cell lines should provide a useful in vitro model for studies related to human RCC. The SNU-349 cell line should be especially useful for studies of MSI and mismatch repair-defective RCCs.

Aged↗

PubMed2000

Factors affecting insertion time and patient discomfort during colonoscopy.

BACKGROUND: Successful colonoscopy depends on insertion of the instrument to the cecum, precise observation, and minimal patient discomfort during the procedure. The aim of this prospective study was to determine whether certain variables are associated with insertion time and patient discomfort during colonoscopy. METHODS: Nine hundred nine consecutive colonoscopic examinations performed by a single endoscopist in patients without obstructive disease of the colorectum were analyzed. Four liters of Colonlyte (Taejun, Seoul, Korea) were used for bowel cleansing, and meperidine (25 mg) was administered intramuscularly 10 minutes before the procedure. The degree of patient discomfort was assessed using a 5-level Likert scale. RESULTS: Among 909 study patients, colonoscopy was completed to the cecum in 876 patients (96.4%). The adjusted completion rate was 98% and mean insertion time for complete colonoscopy was 6.9+/-4.2 minutes. Colonoscopy caused less patient discomfort than barium enema or esophagogastroduodenoscopy. Multivariate logistic regression analysis demonstrated that inadequate bowel cleansing, advanced age, and constipation as an indication are independent factors associated with prolonged insertion time (>10 minutes). Female gender was the only independent factor associated with significant discomfort (> or = level 4) during colonoscopy. CONCLUSIONS: Among the factors affecting insertion time and patient discomfort during colonoscopy, unsatisfactory bowel preparation was the only correctable factor.

Adolescent↗

PubMed2000

Histopathologic analysis of in-stent neointimal regression in a porcine coronary model.

BACKGROUND: Animal and clinical studies have demonstrated late regression of in-stent neointima. This study was performed to identify the temporal changes in the in-stent neointimal constituents responsible for late regression. METHODS: NIR stents were implanted in porcine coronary arteries (size of stent (in mm) to size of artery (in mm) approximately equal to 1.1) and harvested at 2 months and 6 months (n = 6 stents/group). Histopathologic analyses included morphometric analysis, smooth muscle cell density, and extracellular matrix contents. RESULTS: Compared with the findings at 2 months, at 6 months there was a significant reduction in area stenosed (from 21 +/- 3% to 14 +/- 1%, P < 0.05) and neointimal thickness (from 0.2 +/- 0.03 mm to 0.03 +/- 0.02 mm, P < 0.05), despite similar injury scores (0.05 +/- 0.06 at 2 months and 0.36 +/- 0.29 at 6 months). This regression was accompanied mainly by a reduction in proteoglycan (from 24 +/- 19% to 5 +/- 8%, P = 0.05), with no change in smooth muscle cell density (71 +/- 7 compared with 76 +/- 23/high power field) or collagen content (25 +/- 19% compared with 25 +/- 19%). CONCLUSIONS: The study confirmed the regression of in-stent neointima, which was mainly attributable to a reduction in proteoglycan content, resembling the natural healing response.

Animals↗

PubMed2000

Coadministration of angiopoietin-1 and vascular endothelial growth factor enhances collateral vascularization.

Using growth factors to induce vasculogenesis is a promising approach in the treatment of ischemic legs and myocardium. Because the vasculogenesis requires a cascade of growth factors, their receptors, and intracellular signals, such therapies may require the application of more than a single growth factor. We examined the effect of 2 endothelial cell-specific growth factors, angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF), on primary cultured porcine coronary artery endothelial cells. VEGF, but not Ang1, increased DNA synthesis and cell number. Ang1 or VEGF induced migration and sprouting activity, increased plasmin and matrix metalloproteinase-2 secretion, and decreased tissue inhibitors of metalloproteinase type 2 secretion. A combination of the submaximal doses of Ang1 and VEGF enhanced these effects and was more potent than the maximal dose of either alone. In a rabbit ischemic hindlimb model, a combination of Ang1 and VEGF gene delivery produced an enhanced effect on resting and maximal blood flow and capillary formation that was greater than that of either factor alone. Angiographic analyses revealed that larger blood vessels were formed after gene delivery of Ang1 or Ang1 plus VEGF than after VEGF gene delivery. These results suggest that combined treatment of Ang1 and VEGF could be used to produce therapeutic vascularization.

Angiopoietin-1↗

PubMed2000

Helical CT angiography and three-dimensional reconstruction of total anomalous pulmonary venous connections in neonates and infants.

OBJECTIVE: The objective of this study was to investigate the usefulness of helical CT angiography in the evaluation of total anomalous pulmonary venous connections. MATERIALS AND METHODS: Fourteen patients with total anomalous pulmonary venous connections underwent helical CT angiography and subsequent three-dimensional (3D) reconstruction. They ranged in age from 3 days to 8 months (median age, 2.3 months) and in weight from 2.3 to 7.1 kg (median weight, 4.3 kg). The types of total anomalous pulmonary venous connections and the number of pulmonary veins were evaluated on axial and 3D images. Qualitative evaluations were performed for extent of pulmonary vascular enhancement and contrast- or motion-induced artifacts. RESULTS: In all patients, helical CT angiography correctly depicted total anomalous pulmonary venous connections. Seven cases were the supracardiac type, four cases were the cardiac type, one case was the infracardiac type, and two cases were the mixed type. The detection rate of the pulmonary vein in 3D reconstruction images (95-98%) was slightly lower than that of the pulmonary vein in the axial images (100%), but the difference between axial and 3D reconstruction images was not statistically significant (p > 0.1). No statistically significant differences were noted among 3D reconstruction images in the detection rates of the pulmonary vein (p > 0.1). The extent of contrast enhancement of the pulmonary vein was good or excellent in all patients. In five patients, there were contrast-induced artifacts that made some surrounding vascular distortion but did not interfere with the pulmonary vein analysis, except in one patient. Motion-induced artifacts were observed in nine patients. One of them had an obstacle in pulmonary vein analysis. CONCLUSION: The combination of axial and 3D images in helical CT angiography is helpful in the assessment of a total anomalous pulmonary venous connection containing the individual pulmonary vein, and this combination can be a good diagnostic tool in preoperative evaluation of neonates and infants with a total anomalous pulmonary venous connection.

Angiography↗

PubMed2000

Clinicopathologic study of Castleman's disease in Korea.

Castleman's disease represents an atypical lymphoproliferative disorder, infrequently associated with various immunologic abnormalities or subsequent development of malignancy such as Kaposi sarcoma, malignant lymphoma and plasmacytoma. Its clinicopathologic features depend on various etiologic factors such as Kaposi sarcoma herpesvirus (KSHV), oversecretion of IL-6, adhesion molecule and follicular dendritic cell dysplasia, etc. To investigate the relationship of Castleman's disease (CD) and the above factors, we reviewed 22 cases of CD. Four cases of KSHV positive CD were detected, all multicentric, plasma cell type, and these cases displayed prominent vascular proliferation, characteristic 'Kaposi-like lesion'. IL-6 and CD54 positive mononuclear cells were scattered in interfollicular areas of KSHV positive cases. Follicular dendritic cell hyperplasia, vascular proliferation, expression of IL-6 and CD54 did not show any significant difference between solitary vs multicentric type, and plasma cell type vs hyaline vascular type. Our study suggests that KSHV positive CD reveals unique pathologic features, and the probable relationship of KSHV and IL-6 and CD54 is discussed.

Adolescent↗

PubMed2000

Hamartomatous gastric polyposis in a patient with tuberous sclerosis.

A 42-year-old female diagnosed with tuberous sclerosis was found to have multiple polyps in the fundus of stomach. On histologic examination, the lesions were hamartomatous polyps. In tuberous sclerosis, many lesions occur in multiple organs and there are several reports about the frequent association of hamartomatous polyps of the colon. However, gastric manifestation of tuberous sclerosis has not been established probably due to its asymptomatic nature. This is the first report of multiple gastric hamartomatous polyposis in patient with tuberous sclerosis.

Abdominal Pain↗

PubMed2000

Topographic expression of p21WAF1/SDI1/CIP1, bcl2, and p53 is altered at the early stage of colorectal carcinogenesis.

We analyzed the expression of p21, bcl2, and p53 in normal and different pathologic mucosa of the human colorectum using immunohistochemistry and cold polymerase chain reaction-single strand conformation polymorphism. The topography of normal mucosa showed; bcl2 and p53 expression restricted to basal epithelial cells and p21 expressed only in superficial epithelial cells. This topographic expression was altered in hyperplastic polyps and adenomas. Hyperplastic polyps revealed absence of or weak bcl2 expression and strong p21 expression without topography. In adenomas, whereas bcl2 expression increased and extended to parabasal and superficial dysplastic epithelium, the increase of p21 expression was limited to surface dysplastic epithelium. p53 was weakly expressed throughout the full thickness of dysplastic epithelium. Bcl2 expression in adenomas was stronger than in carcinomas; p53 expression was converse and p21 expression was variable. In carcinomas, this topographic expression was largely abrogated but p53 mutation (36%) was more frequent than in adenomas (2%). In carcinomas, p21 and p53 expression correlated inversely, but there was no relationship with bcl2. These results suggest that there is precisely ordered topographic pattern of p21, bcl2, and wild p53 expression in normal colorectal cells, but this becomes disordered during the early stage of colorectal carcinogenesis.

Colorectal Neoplasms↗

PubMed2000

Significance of rectosigmoid polyp as a predictor of proximal colonic polyp.

The association between rectosigmoid polyps and polyps in the more proximal colon is still a matter of debate, and the need for colonoscopy in patients with rectosigmoid polyps that are detected by flexible sigmoidoscopy is controversial. The aim of this study was to determine whether or not certain characteristics of rectosigmoid polyps are associated with the presence and characteristics of proximal colonic polyps. Seven hundred and twenty-eight patients who underwent total colonoscopy between October 1995 and June 1998 and who had colorectal polyps were retrospectively analyzed. Patients with inflammatory bowel diseases, familial adenomatous polyposis, or any advanced cancer were excluded. The odds ratio (OR) and 95% confidence interval (CI) of prevalence of proximal colonic polyps according to the patients age and sex, as well as the characteristics of rectosigmoid polyps, were calculated. Advanced adenoma was defined as an adenoma larger than 10 mm or an adenoma of any size with villous component, high-grade dysplasia or invasive carcinoma. Among 728 patients with colorectal polyps, 356 patients (48.9%) had polyps only in the rectosigmoid region, 193 patients (26.5%) had polyps only in the proximal colon, and 179 patients (24.6%) had polyps in both the rectosigmoid and proximal colon. In 535 patients with rectosigmoid polyps, the prevalence of proximal colonic polyps, neoplastic polyps and advanced adenomas were 33.4%, 27.3% and 2.9%, respectively. The prevalence of proximal colonic polyps in patients with rectosigmoid polyps was found to be significantly related to the male gender and elderly patients, in addition to the neoplastic histology of the rectosigmoid polyps. However, the prevalence of the proximal colonic polyps was not related to the size, number and shape of rectosigmoid polyps. In 179 patients with both rectosigmoid and proximal colonic polyps, the characteristics of proximal colonic polyps such as size, number and shape were similar to those of rectosigmoid polyps. We recommend total colonoscopic examination in all patients with rectosigmoid adenomas, regardless of the size, number, and shape, especially in elderly males.

Adult↗

PubMed2000

Restoration of P-glycoprotein function is involved in the increase of natural killer activity with exogenous interleukin-15 in human immunodeficiency virus-infected individuals.

A depressed level of natural killer (NK) activity is one of the various immunologic abnormalities in human immunodeficiency virus (HIV) infection. Interleukin-15 (IL-15), an immunotherapeutic candidate in HIV infection, increases NK activity and induces the excretion of CC-chemokines from divergent immune cells, but the mechanisms of NK activity enhancement by IL-15 stimulation is not clearly established in HIV infection. This study examined whether CC-chemokines, which are known to increase NK activity, are secreted adequately in HIV-infected individuals, and also investigated whether P-glycoprotein is involved in NK activity enhancement after IL-15 administration. NK activity increased with IL-15 stimulation in NK cells of HIV-infected individuals, as it does in normal NK cells. IL-15 stimulates NK cells to secrete CC-chemokines, such as, macrophage inflammatory protein-1alpha (MIP-1alpha), macrophage chemotactic protein-1alpha (MCP-1alpha) and regulated upon activation, normal T cells expressed and secreted (RANTES) in both HIV-infected individuals and controls with no significant difference. P-glycoprotein expression and function is decreased in HIV-infected individuals and restored only in NK cells of HIV-infected individuals after IL-15 stimulation. P-glycoprotein may play a role in the mechanism of increased NK cell activity in HIV-infected individuals after IL-15 stimulation.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2000

Clinicopathologic characteristics of early gastric cancer in Korea.

Gastric cancer is the most common cause of cancer related death in Korea. Early gastric cancer (EGC), confined to mucosa or submucosa, regardless of lymph node metastasis, is known to have a favorable prognosis. From 1976 to 1995, four thousand nine hundred and twenty eight gastric cancer patients underwent operation at the Severance Hospital, Yonsei University, College of Medicine, Seoul, Korea. Of these, 1,117 patients (22.6%) were diagnosed as EGC and underwent curative operation. Clinicopathologic characteristics were reviewed and survival data was analyzed. The proportion of EGC has increased during the last two decades, from 14.9% during 1976-1985 to 25.8% for 1986-1995. EGC has a wide age distribution range from the thirties to the sixties, with highest incidence in the sixties. The male to female ratio is 1.8:1, without any significant change in last two decades. Most lesions are located in the lower third of stomach (52.3%), and the lesser curvature (52.2%) was the most frequent site in the transverse axis. Macroscopically, the depressed type was the most common (66.1%) followed by the elevated, flat and mixed types, in that order. Tumor confined to the mucosa layer was seen in 52.5%, and lymph node involvement in 11.7%. The depth of tumor invasion correlated with tumor size and regional lymph node involvement. On histopathologic examination, signet ring cell type accounted for 29.6% of all EGCs. Overall 5-year survival rate was 92.7% and the presence of lymph node metastasis significantly affected survival (84.6% versus 96.2%) (p<0.05). In conclusion, the proportion of EGC, in terms of the gastric cancers operated upon, has been increasing in Korea over the last two decades. The introduction of active diagnostic approaches and diagnostic modalities could improve early diagnosis and the cure rate of gastric cancer in Korea.

Adult↗

PubMed2000

Induction of p53-independent p21 during ceramide-induced G1 arrest in human hepatocarcinoma cells.

Ceramide is known to induce pRb (retinoblastoma gene product) dephosphorylation through the activation of ceramide-activated protein phosphatase (CAPP) during G1 arrest, but other molecular mechanisms linked to regulation of pRb dephosphorylation during ceramide-induced G1 arrest are poorly understood. In this paper, we investigated whether p21, a cdk (cyclin-dependent kinase) inhibitor, is involved in the induction of pRb dephosphorylation during ceramide-induced G1 arrest. In SK-Hep-1 cells, the addition of ceramide resulted in pRb dephosphorylation and G1 arrest. The activity of cdk2 was inhibited in response to ceramide during this process. p21 protein and mRNA were remarkably induced, while the protein level of p53, known as a transcriptional activator of p21, was not elevated at the same condition. p21 induction was also observed in the Hep3B cells lacking a functional p53 after exposure to ceramide. Although p21 is induced in ceramide-treated Hep3B cells, Hep3B cells do not induce G1 arrest, because Hep3B cells are deficient in a functional pRb protein. To confirm that pRb is a critical target for the induction of G1 arrest by inhibiting cdk2 activity through p53-independent p21, pRb-expressing vector was transfected into Hep3B cells. After treatment with ceramide, pRb-expressing cells (pRb+/+), but not pRb-/- cells, were arrested in G1 phase. In pRb+/+ cells, ceramide-mediated G1 arrest was accompanied by the accumulation of hypophosphorylated pRb and p21 associated with cdk2. Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells.

Blotting, Northern↗

PubMed1999

p21 promotes ceramide-induced apoptosis and antagonizes the antideath effect of Bcl-2 in human hepatocarcinoma cells.

p21, a potent cyclin-dependent kinase inhibitor, has been known to induce cell cycle arrest in response to DNA-damaging agents. Although p21 has been reported to play an important role in the regulation of apoptosis, the postulated role for p21 in apoptosis is still controversial. Previously, we reported that p21 was induced in a p53-independent manner during ceramide-induced apoptosis in human hepatocarcinoma cell lines. In the present study, we investigated the precise role of p21 in ceramide-induced apoptosis in human hepatocarcinoma cells by using a tetracycline-inducible expression system. Overexpression of p21 by itself did not induce apoptosis in p53-deficient Hep3B cells. However, Hep3B/p21 cells were more sensitive to ceramide-induced apoptosis. In these cells, p21 overexpression did not result in G1 arrest. The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition. Overexpression of Bax induced apoptosis in Hep3B cells. On the other hand, the levels of p21 and Bax protein were increased by ceramide in another hepatocarcinoma cell line, SK-Hep-1, while the Bcl-2 protein level was not changed. Overexpression of Bcl-2 not only suppressed apoptosis but also completely prevented induction of p21 and Bax caused by ceramide in SK-Hep-1 cells. Furthermore, overexpression of p21 antagonized the death-protective function of Bcl-2 and upregulated expression of Bax protein. These results suggest that p21 promotes ceramide-induced apoptosis by enhancing the expression of Bax, thereby modulating the molecular ratio of Bcl-2:Bax in human hepatocarcinoma cells.

Apoptosis↗

PubMed1999

Establishment and characterization of 12 human colorectal-carcinoma cell lines.

In this article, we describe the characteristics of 12 human colorectal-carcinoma cell lines established from 6 primary tumors and 6 metastatic sites of 11 Korean colorectal-carcinoma patients, including the morphology in vivo and in vitro and mutations of K-ras2, p15, p16, p53, APC, beta-catenin, hMLH1 and hMSH2 genes in vitro. No lines were contaminated with Mycoplasma or bacteria. All lines were proven to be unique by DNA-fingerprinting analysis. All lines expressed the surface carcino-embryonic antigen and secreted it into the supernatant fluid. The morphological correlation between the original tumors and cultured cells suggested that the original tumors showing mucinous adenocarcinoma correlated with floating aggregates in culture, and degree of desmoplasia in the original tumor correlated with attached growth in culture. Five of the cell lines showed mutations in the K-ras2 gene, and 6 of the cell lines showed mutations in the p53 gene. The p15 gene was deleted in 2 cell lines, and the p16 gene was hypermethylated in 3 cell lines. The mutation of mismatch-repair genes (hMLH1 and hMSH2) was found in 4 lines, the APC gene and beta-catenin gene were mutated in 9 and 2 lines respectively. These well-characterized colorectal-cancer cell lines should serve as useful tools for investigating the biological characteristics of colorectal cancer.

Adaptor Proteins, Signal Transducing↗

PubMed1999

Significant correlation between serum level of hepatocyte growth factor and progression of gastric carcinoma.

Hepatocyte growth factor (HGF) can promote proliferation of many types of tumor cells including gastric cancer cells. To study the role of HGF in the progression of gastric carcinoma, HGF levels were measured by an enzyme immunoassay (EIA) system in sera of gastric cancer patients and followed up the levels after the operation. The mean serum HGF level in 212 healthy control subjects, 140 patients with primary gastric cancer, and 13 patients with recurrent gastric cancer were 0.199 +/- 0.073, 0.325 +/- 0.209, and 0.578 +/- 0.258 ng/ml, respectively. The increase of the levels was significantly correlated with the progression of tumor stage. The levels decreased to normal levels 1 month after curative resection of the tumors. However, the levels did not decrease significantly in nonresected cases. During the follow-up of the patients for several months, the level was significantly increased in recurrent gastric cancer patients, whereas there was no increase in nonrecurrent patients. In conclusion, the serum HGF levels significantly correlated with the aggressiveness of the tumors, suggesting an important role of HGF in the progression of gastric carcinoma.

Adenocarcinoma↗

PubMed1999

Quality of life in Korean patients with inflammatory bowel diseases: ulcerative colitis, Crohn's disease and intestinal Behçet's disease.

Health-related quality of life (HRQOL) is an important outcome factor in chronic diseases such as inflammatory bowel disease (IBD). This study used the Korean translation of the disease-specific, self-administered Inflammatory Bowel Disease Questionnaire (IBDQ) to compare HRQOL in ulcerative colitis (UC; n = 98), Crohn's disease (CD; n = 49), and intestinal Behçet's disease (BD; n = 34). In addition to the current status, patients were asked retrospectively to recall their symptoms at the beginning and during the worst period of their disease. Disease activity was measured by St. Mark's Activity Index, Crohn's disease Activity Index (CDAI), and the Harvey-Bradshaw Index (HBI). In all IBD patients, including those with BD, the IBDQ total score during the worst period was significantly lower than that at present and that at the beginning of the disease. However, there were no significant differences between groups regarding the total IBDQ score or its various dimensions. In UC a strong correlation between IBDQ scores and St. Mark's Activity Index was observed (r = -0.708, P < 0.001). IBDQ scores were also highly correlated with CDAI and HBI in both CD (r = -0.506, P < 0.001 for CDAI; r = -0.600, P < 0.001 for HBI) and BD (r = -0.687, P < 0.001 for CDAI; r = -0.531, P < 0.001 for HBI). However, the current IBDQ score was not related to demographic parameters such as gender, age, educational status, economic status, and marital status as well as disease factors such as duration of disease, history of operation or hospital admission, extent of disease in UC, involved region in CD, and clinical type in BD. We conclude that the Korean IBDQ is a responsive and promising instrument for measuring HRQOL of IBD patients in clinical trials. In addition, the IBDQ can be helpful in developing a disease-specific activity index in BD.

Adolescent↗