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Biomedical subjects

Hyun-Soo Kim

Publications and source records attributed to Hyun-Soo Kim.

34 records · Page 2Linked to original sources

A prospective, randomized trial comparing mechanical methods of hemostasis plus epinephrine injection to epinephrine injection alone for bleeding peptic ulcer.

BACKGROUND: The hemostatic efficacy of mechanical methods of hemostasis, together with epinephrine injection, was compared with that of epinephrine injection alone in bleeding peptic ulcer. METHODS: Ninety patients with a peptic ulcer with active bleeding or a non-bleeding visible vessel were randomly assigned to undergo a mechanical method of hemostasis (23 hemoclip application, 22 band ligation) plus epinephrine injection, or epinephrine injection alone. RESULTS: The two groups were similar with respect to all background variables. Initial hemostasis was achieved in 44/45 (97.8%) patients in both groups. The mean number of hemoclips and elastic bands applied were 2.8: 95% CI[2.5, 3.1] and 1.1: 95% CI[1.0, 1.2], respectively, and the mean volume of epinephrine injected was 19.9 mL: 95% CI[19.3 mL, 20.5 mL]. The rate of recurrent bleeding in the combination group (2/44, 4.5%) was significantly lower in comparison with the injection group (9/44, 20.5%, p < 0.05). The mean number of therapeutic endoscopic sessions needed to achieve permanent hemostasis in the combination group (1.04: 95% CI[1.01, 1.07]) was significantly lower vs. the injection group (1.22: 95% CI[1.15, 1.30]). CONCLUSIONS: The combination of an endoscopic mechanical method of hemostasis plus epinephrine injection is more effective than epinephrine injection alone for the treatment of bleeding peptic ulcer.

Epinephrine↗

Optimal injection volume of epinephrine for endoscopic prevention of recurrent peptic ulcer bleeding.

BACKGROUND: Although the initial rate of hemostasis achieved by endoscopic epinephrine injection for peptic ulcer bleeding is high, bleeding recurs in 14.6% to 35.5% of patients. The aim of this study was to compare rates of recurrent bleeding after endoscopic injection of two different volumes of epinephrine in patients with peptic ulcer bleeding. METHODS: A total of 72 patients with peptic ulcer with active bleeding or a non-bleeding visible vessel were randomly assigned to 15 to 25 mL or 35 to 45 mL injections of a 1:10,000 solution of epinephrine. RESULTS: The two groups were similar with respect to all background variables. The mean volume of epinephrine injected was 19.4 mL: 95% CI [18.7, 20.1] in the 15 to 25 mL group and 41.1 mL: 95% CI [40.0, 42.2] in the 35 to 45 mL group. Initial hemostasis was achieved in 35 of 36 patients (97.2%) in the 15 to 25 mL group and in all 36 patients in the 35 to 45 mL group. The 35 to 45 mL volume was significantly more effective in preventing recurrent bleeding than the 15 to 25 mL volume (0% vs. 17.1%; p < 0.05). For ulcers in the gastric body, the 35 to 45 mL volume was significantly more effective in preventing recurrent bleeding than the 15 to 25 mL volume (0% vs. 31.6%; p = 0.003). For ulcers in other locations, including the gastric antrum and the duodenum, there were no significant differences in the rate of recurrent bleeding between the two groups. CONCLUSIONS: Injection of 35 to 45 mL of a 1:10,000 solution of epinephrine is more effective than injection of 15 to 25 mL of the same solution for prevention of recurrent bleeding from ulcers in the body of the stomach.

Dose-Response Relationship, Drug↗

Asymmetric multiple-quantum-well laser diodes with wide and flat gain.

Asymmetric multiple-quantum-well laser diodes with wide and flat gain spectra were designed, fabricated, and analyzed. The active layer was composed of three 10-nm, one 8-nm, and two 6-nm 0.5% compressive strained wells and four 10-nm and one 5-nm 0.4% tensile strained barrier layer. Measured spectra of antireflection-coated ridge waveguide laser diodes with such quantum-well structures have shown that -1-dB spectral gain bandwidth can be as large as 90 nm.

Journal Article↗

Modulation of Sp1-dependent transcription by a cis-acting E2F element in dhfr promoter.

The dihydrofolate reductase (dhfr) promoter contains cis-acting elements for Sp1 and E2F. Here we examined the cooperative regulation of dhfr gene transcription by Sp1 and E2F in human osteosarcoma cells, U2OS. Trichostatin A, an inhibitor of histone deacetylases, markedly stimulated dhfr promoter activity, a response that was enhanced by the deletion of an E2F element. In contrast, deletion of the dhfr Sp1 binding sites completely abolished promoter stimulation by trichostatin A. Cotransfection assays showed that activation of dhfr transcription by expression of E2F1/DP1 requires the reiterated Sp1 elements, whereas activation by Sp1 was enhanced by the deletion of the E2F element. Expression of HDAC1 with Sp1 suppressed promoter activity and suppression was not alleviated by coexpression of E2F1/DP1. These results suggest that HDAC1 acts through Sp1 to repress dhfr promoter activity, and that the E2F element modulates the activity of Sp1 at the dhfr promoter through a cis-acting mechanism.

Base Sequence↗

Hemobilia caused by liver abscess due to intrahepatic duct stones.

Hemobilia occurs when injury or disease causes communication between intrahepatic blood vessels and the biliary tract. Causes of hemobilia include trauma; gallstones; inflammatory diseases; and vascular disorders such as aneurysm, tumor, and coagulopathy. Recently, with the increasing use of invasive diagnostic and therapeutic procedures involving the hepatobiliary tract, an increasing proportion of the causes of hemobilia have been of iatrogenic origin. Hemobilia may also be associated with liver abscess, but this condition is very rare. Our review of the English-language literature disclosed few cases of liver abscess associated with hemobilia. Here, we present a case of hemobilia caused by liver abscess due to intrahepatic duct stones. Liver abscess should be considered in the causes of hemobilia, especially in areas where hepatobiliary parasitic infection is endemic.

Bile Ducts, Intrahepatic↗

Case of mucinous adenocarcinoma with porcelain gallbladder.

Histologically, the majority of gallbladder cancers are adenocarcinomas. Among the adenocarcinomas, the mucinous adenocarcinoma is relatively uncommon. Porcelain gallbladder is a rare finding and the risk of gallbladder cancer is significantly increased in porcelain gallbladder. We describe a rare case of mucinous adenocarcinoma with porcelain gallbladder. A 46-year-old man was admitted to Chonnam National University Hospital with a 2-week history of right upper quadrant pain. Three and 2 years previously, he had two episodes of cholecystitis with gallstones. An abdominal computed tomography revealed a contracted gallbladder with circumferential mural calcification, and the possibility of gallbladder cancer and porcelain gallbladder were considered. At laparotomy, cholecystectomy, liver wedge resection, and radical lymph node dissection were performed. The resected gallbladder showed thickened wall, luminal narrowing and mucosal irregularity. A histological examination of the resected gallbladder showed a mucinous adenocarcinoma composed of poorly differentiated glandular cells with mucin lakes. Porcelain gallbladder may be an end result of a chronic inflammatory reaction, and this change is associated with the development of gallbladder cancer.

Adenocarcinoma, Mucinous↗

Mammaglobin expression in lymph nodes is an important marker of metastatic breast carcinoma.

CONTEXT: Organ specificity is a desirable property of a tumor marker, especially in metastatic adenocarcinomas of unknown primary origin. Mammaglobin, a mammary-specific member of the uteroglobin family, is known to be overexpressed in human breast cancer. OBJECTIVE: We investigated mammaglobin A expression in metastatic carcinomas of lymph nodes from the breast and various other organs and its usefulness in identifying metastatic carcinoma of the breast. For comparative purposes, we also investigated BRST-1 and BRST-2 expression. DESIGN: We produced recombinant mammaglobin and polyclonal antimammaglobin antibodies. Mammaglobin expression was analyzed by immunohistochemical staining using a tissue microarray and by reverse transcription-polymerase chain reaction in 210 carcinomas, including those of the breast (n = 70), lung (n = 30), stomach (n = 30), colorectum (n = 25), hepatobiliary tract (n = 20), urinary tract (n = 10), thyroid gland (n = 10), ovary and endometrium (n = 10), and salivary gland (n = 5). RESULTS: Mammaglobin expression was observed in 59 cases (84.3%) of breast cancer and in 21 cases (15.0%) of nonbreast cancer. The BRST-1 and BRST-2 expression rates were 75.7% and 44.3% in breast cancer and 26.4% and 2.1% in nonbreast cancer, respectively. Mammaglobin is superior to BRST-1 for both specificity and sensitivity and is superior to BRST-2 for sensitivity. CONCLUSION: Our data suggest that mammaglobin is one of the first relatively mammary-specific and mammary-sensitive markers. Mammaglobin and BRST-2 appear to represent useful markers for breast cancer and should be used as a component of panels evaluating tumors of unknown primary sites.

Biomarkers, Tumor↗

Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes.

We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 microg/ml) and interferon-gamma (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of beta-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS.

Adjuvants, Immunologic↗

Mimosine prevents the death of glucose-deprived immunostimulated astrocytes by scavenging peroxynitrite.

Immunostimulated astrocytes become highly vulnerable to glucose deprivation (Choi and Kim: J Neurosci Res 54:870-875, 1998a). The increased vulnerability is caused by the enhanced level of peroxynitrite endogenously produced in glucose-deprived immunostimulated astrocytes. In the present study, we report that the plant amino acid mimosine can attenuate the increased death by scavenging peroxynitrite. Treatment with mimosine blocked the increase of nitrotyrosine immunoreactivity, a marker of peroxynitrite, in glucose-deprived immunostimulated astrocytes. Furthermore, mimosine directly inhibited the nitration of tyrosine residues of bovine serum albumin and the oxidation of dihydrorhodamine-123 to rhodamine-123 by peroxynitrite. Mimosine has been used experimentally as a cell cycle G1/S phase transition blocker (Lalande: Exp Cell Res 186:332-339, 1990; Hoffman et al.: Cytometry 12:26-32, 1991). Flow cytometry analysis, however, showed that the cytoprotective effect of mimosine was not attributed to its inhibition of cell cycle progression. Furthermore, under our experimental conditions, mimosine did not alter the levels of cell cycle regulatory proteins, including p21(WAF1/CIP1), cyclins D1 and E, and proliferating cell nuclear antigen. In addition, cyclin-dependent kinase inhibitors olomoucine and roscovitine did not block the increased death. These results indicate that mimosine inhibits the augmented death of glucose-deprived immunostimulated astrocytes by scavenging peroxynitrite rather than suppressing the cell cycle progression.

Adjuvants, Immunologic↗

Primary duodenal adenocarcinoma associated with neurofibromatosis type 1.

It is well known that patients with neurofibromatosis have an increased incidence of various neoplasms, most of these being tumors of neural-crest origin, including neurofibromas, leiomyomas, ganglioneuromas, paragangliomas, and carcinoids. However, the occurrence of small-bowel adenocarcinoma is rare. In this article, we report a patient with small-bowel adenocarcinoma, the seventh such reported case. We include a review of the literature and a brief discussion of the implications of this association. We suggest that the association between small-bowel adenocarcinomas and neurofibromatosis may not be fortuitous, and that small-bowel adenocarcinoma should be considered, in particular. in the differential diagnosis of gastrointestinal symptoms in patients with neurofibromatosis. Also, a definite histologic diagnosis must be made, with the employment of special staining techniques, because of the differing prognoses for various cell types.

Adenocarcinoma↗

Inverse relationship between APC gene mutation in gastric adenomas and development of adenocarcinoma.

Gastric cancer is common among the world, but genetic mechanisms of gastric carcinogenesis are not well understood. Gastric polypoid adenomas and flat dysplasias are regarded as precursor lesions. However, a detailed molecular study of these lesions has not been done to determine their role as precancerous lesions. We investigated mutations of the APC, beta-catenin, and K-ras genes, and microsatellite instability (MSI) status in 35 adenomas and 47 flat dysplasias without adenocarcinoma, 35 adenomas/dysplasias associated with adenocarcinomas, and 39 adenocarcinomas (20 diffuse type and 19 intestinal type). Somatic APC gene mutations were identified in 76% (59 of 78) of adenomas or flat dysplasias without associated adenocarcinoma, but in only 3% (1 of 30) of adenomas/dysplasias associated with adenocarcinoma, and in only 4% (3 of 69) of adenocarcinomas (P < 0.000001). No mutations of beta-catenin were found in adenocarcinomas, or adenomas/dysplasia without APC mutation. K-ras mutations were detected in 5% (4 of 82) of gastric adenomas/dysplasia without carcinoma, 3% (1 of 39) of adenocarcinomas without associated adenoma/dysplasia, and not in 32 adenocarcinomas with associated adenoma/dysplasia. High level of MSI (MSI-H) was more frequent in gastric adenoma/dysplasia associated with carcinoma (17%, 6 of 35) than in adenomas/dysplasia without carcinoma (3%, 2 of 75; P = 0.01). MSI-H was also more frequent in intestinal type adenocarcinoma (20%, 11 of 54) than in diffuse type (0%, 0 of 20; P = 0.03). APC gene mutations were present in six of nine (67%) of gastric adenomas/dysplasias with low level of MSI, but in none of the eight adenomas/dysplasia with MSI-H phenotype (P = 0.009). Our results indicate that somatic mutation of the APC gene plays an important role in the pathogenesis of gastric adenoma and dysplasia but has a limited role in neoplastic progression to adenocarcinoma. Gastric adenomas or dysplasias without APC mutations but with or without MSI may have a different biological behavior, and are precursors of intestinal-type of gastric adenocarcinomas.

Adenocarcinoma↗

Expression of cyclooxygenase-2 protein in colorectal carcinomas.

BACKGROUND: Overexpression of cyclooxygenase-2 (COX-2) has been demonstrated in various human cancers, including colorectal cancer. Thus, overexpression of COX-2 may be involved in the growth and progression of cancer, and this may have prognostic significance. AIM: The aim of our study is to evaluate the expression of COX-2 in colorectal cancer tissue, and to examine the relationship of its expression to various clinicopathological parameters and patient survival. METHODS: Formalin-fixed, paraffin-embedded tissue blocks were obtained from 60 patients who underwent surgery for colorectal carcinoma in 1995 at the Chonnam National University Hospital in Gwangju, Korea. We have used an immunohistochemical technique to localize COX-2 in colorectal carcinoma tissues. RESULTS: Immunohistochemical staining of the colorectal cancer specimens demonstrated that COX-2 expression was localized to the carcinoma cells and was not detectable in the stromal compartment of the cancers. The COX-2 immunostaining pattern was predominantly homogenous, and perinuclear cytoplasmic within the tumors. Normal colonic epithelium adjacent to the tumor showed no staining for COX-2. The COX-2 protein was detected in 70% (42/60) of colorectal carcinoma tissues. However, no significant correlation was found between COX-2 expression and various clinicopathological parameters, including histologic grade, tumor size, depth of invasion, lymph node metastasis, distant metastasis, or stage. Furthermore, COX-2 expression did not correlate with patient survival (p = 0.401). CONCLUSION: These results suggest that COX-2 expression may play an important role in the evolution of colon carcinogenesis. However, further studies are needed to determine the prognostic relevance of COX-2.

Adult↗

Seroprevalence of antibody to procine reproductive and respiratory syndrome virus in diagnostic submissions.

During the period from January to December of 2001, a total of 3,391 swine sera were submitted to our laboratory from 256 farms for the diagnosis of porcine reproductive and respiratory syndrome (PRRS). The antibody to porcine reproductive and respiratory syndrome virus (PRRSV) was tested by the indirect immunofluorescent antibody (IFA) test. Of the 256 farms tested, 230 farms (89.8%) were positive for the PRRSV antibody. The overall seroprevalence of the PRRSV antibody was 52.1% (1765/3391). Most of the pigs seemed to be infected with PRRSV at around 50 to 60 days old. The seroprevalence of the antibody became higher with age, and peaked at around 100 days old. More than one-third of the adult pigs, including boars, gilts, and sows, was positive for the PRRSV antibody. The infection of PRRSV was chronic and confined to growers and/or finishers in most farms. However, the antibody was detected in all production phases at some farms.

Age Factors↗

Expression of open reading frame 5 protein of porcine reproductive and respiratory syndrome virus using semliki forest virus expression system.

The ORF5 gene encodes a major envelope glycoprotein (GP5), which is one of the three major proteins of porcine reproductive and respiratory syndrome virus (PRRSV). The GP5 protein has been known to be a 24.5-26 kDa N-glycosylated envelope protein. The GP5 is involved in inducing neutralizing antibodies. For this reason, the GP5 is primary candidate for the PRRSV subunit vaccine. To produce the native form of GP5 in mammalian cells, we have cloned the ORF5 gene from PRRSV CNV-1 into the Semliki Forest virus (SFV)-based expression vector, resulting in recombinant pSFV-ORF5. By the infection with recombinant pSFV-ORF5 to BHK-21 cells, the GP5 expression was confirmed by immunocytochemistry and immunoblotting assay. The recombinant virus particle harboring ORF5 gene was infectious to BHK-21 and MARC-145. The RNA synthesis and expression of GP5 in the infected cell was also confirmed by RT-PCR.

Animals↗

Expression of angiostatin using DNA-based semliki forest virus replicon.

Angiogenesis is recognized as a critical factor in the growth of tumor cells and plays a key role in the tumor metastasis. Recent studies for antiangiogenic substances are getting popular. The angiostatin, one of the antiangiogenic substances, leads to the increased apoptosis of the tumor cells by inhibiting the neovascularization of the tumor. The angiostatin was identified as the internal fragments of the plasminogen which has no antiangiogenic activity. By hydrolysis of the plasminogen, the angiostatin can be produced. In this study, we constructed the SFV-derived DNA vector by employing the cytomegalovirus immediate early enhancer/ promoter (CMV). This vector makes it possible to transfect the cells with DNA without the in vitro transcription process. The C-myc epitope and polyhistidine residue sequences were placed in downstream of the angiostatin gene to make it eligible to detect the expressed protein. The murine Ig k-chain V-J2-C signal sequence was placed in upstream to secrete the expressed protein from the cells. We confirmed the expression of angiostatin in the BHK-21 cells using DNA-based SFV replicon.

Angiostatins↗