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Y B Kim

Publications and source records attributed to Y B Kim.

At least 145 records · Page 8Linked to original sources

[Levels of thermostable direct hemolysin production by Vibrio parahaemolyticus strains carrying both tdh and trh genes].

One hundred and twenty-five strains of Vibrio parahaemolyticus carrying both the tdh and trh genes were selected from the strains isolated from the travelers with diarrhea by an hybridization test using polynucleotide probes. The levels of TDH produced by these strains and the association between the TDH levels and related characteristics in these strains were analyzed. The TDH level varied greatly from strain to strain, but none of the levels was as high as that of the typical Kanagawa phenomenon-positive strains. The strains were classified into "TDH producer" (18 strains), "Low-level TDH producer" (85 strains), and "No TDH producer" (22 strains) based on the results of a modified Elek test and the hemolysis assay on Wagatsuma agar. The highest TDH level achieved by the "TDH producer" was twofold lower than that of the Kanagawa phenomenon-positive strains as assayed by the RPLA method. All strains possessed the toxR gene. The trh1 and trh2 genes were detected in, respectively, 105 and 20 strains, and no correlation existed between the type of the trh gene and the levels of TDH produced. Considerable restriction fragment length polymorphism was observed with the tdh gene-bearing HindIII DNA fragment in different strains, but it was not related with the TDH level.

Bacterial Toxins↗

Viral loads and E2/NS1 region sequences of hepatitis C virus in hepatocellular carcinoma and surrounding liver.

OBJECTIVES: Numerous epidemiologic data have documented that chronic infection by hepatitis C virus (HCV) is a major risk factor for the development of hepatocellular carcinoma (HCC). But the molecular mechanism underlying these strong epidemiologic associations between HCV and HCC has not be elucidated. We observed the changes of HCV in HCC to investigate the association of HCV with HCC. METHODS: We used competitive and quantitative polymerase chain reaction and dideoxy-nucleotide chain termination method to compare HCV titers and sequences of the hypervariable region of E2/NS1 region of four isolates from the HCC and surrounding cirrhotic liver tissues in tow anti-HCV positive patients. RESULTS: The copy numbers of HCV-RNA were 1 x 10(6) and 4 x 10(6)/gm wet weight of HCC, and 8 x 10(7) and 3.2 x 10(8)/gm wet weight of cirrhotic liver tissues from patient-1 and -2. The sequence differences between HCV RNA in HCC and in cirrhotic liver were two and five nucleotides in patient-1 and in patient-2 respectively. The amino acid sequences were changed in one and two site in each patient. CONCLUSION: These findings may suggest the possible etiological role of HCV in carcinogenesis of HCC, but complete sequence analysis of HCV including multiple isolates in the same patient, should be performed in many cases.

Base Sequence↗

Effects of calmodulin antagonists and anesthetics on the skin lesions induced by 2-chloroethylethyl sulfide.

The effects of calmodulin antagonists and anesthetics on the skin lesions induced by an alkylating vesicant, 2-chloroethylethyl sulfide, were investigated using female hairless mice. 2-Chloroethylethyl sulfide, topically applied (0.6 microliter/5 mm in diameter) on the back skin of hairless mice, induced mild to moderate petechiae on the 1st day, and ulcers with a thick scab after 3 days. The healing process started after 6 days, resulting in shedding of scabs on 9.52 days. Water-soluble ointment bases showed some beneficial effects, whereas oily bases made the skin lesions worse. Trifluoperazine (0.5-1%) and thioridazine (2%), potent calmodulin antagonists, in Pluronic F-127 base substantially prevented the development of 2-chloroethylethyl sulfide-induced skin lesions. A similar effect was achieved with pentamidine (10%), another type of calmodulin antagonist, but not with ketoconazole, a weak calmodulin antagonist. In addition, anesthetics, such as lidocaine and pentobarbital, showed some protection, although at high concentrations (> 5%). As judged by the microscopic appearance, trifluoperazine successfully reduced the hemorrhage and the infiltration of inflammatory cells in early skin lesions, and the formation of thick scabs, which leads to granulomatous scar tissue in late lesions. These results suggest that some calmodulin antagonists and anesthetics in water-soluble bases might be a choice for the treatment of 2-chloroethylethyl sulfide-induced skin burns.

Adjuvants, Anesthesia↗

Adenosine transport inhibition ameliorates postischemic hypoperfusion in pigs.

Cerebral ischemia is often followed by a period of delayed hypoperfusion that may contribute to tissue injury. We tested the hypothesis that augmentation of interstitial adenosine can improve tissue perfusion under this condition 10 min global ischemia was produced in two groups of isoflurane-anesthetized newborn pigs by occlusion of subclavian and brachiocephalic arteries, and changes in local cortical blood flow and cortical interstitial purine metabolites were measured using the combined hydrogen clearance-microdialysis technique. In one group, the dialysis probe was perfused with artificial cerebrospinal fluid buffer containing nitrobenzyl-thioinosine (NBT1, 100 mumol/l), a competitive inhibitor of adenosine transport. In the untreated group (n = 9), baseline cortical blood flow (39 +/- 3 ml/min/100 g) was depressed by 51 +/- 5% and 42 +/- 6% at 40 and 60 min, respectively, of postischemic reperfusion. NBTI increased baseline interstitial adenosine levels 2.4-fold which increased baseline cortical blood flow 1.5-fold to 60 +/- 4 ml/min/100 g, and increased both absolute adenosine levels as well as adenosine as a percentage of total purine metabolites throughout ischemia and reperfusion. As a result, the extent of postischemic hypoperfusion was significantly lessened in NBTI-treated animals (n = 9), with reductions in cortical blood flow of only 28 +/- 3% and 24 +/- 5% at 40 and 60 min of reperfusion, respectively. These results indicate that inhibition of adenosine transport by NBTI elevates interstitial adenosine concentration during and following cerebral ischemia, and concomitantly improves cortical perfusion in the post-ischemic period. The latter effect may contribute to the documented neuroprotective efficacy of adenosinergic therapy in cerebral ischemia.

Adenosine↗

Enhancement of porcine natural killer cell activity by recombinant human and murine IL-12.

These studies describe the effects of recombinant human (rHu) and recombinant murine (rMu) interleukin 12 (IL-12) in the porcine system. To examine the effects of rHu and rMu IL-12, porcine PBL were cultured with rHu and rMu IL-12, and then used for a NK assay. Significant enhancement of porcine NK cell cytotoxicity was observed, and maximal enhancement was reached after 26 hr culture in nanogram quantities (5 ng/ml = 10 units/ml) of rHu and rMu IL-12. Monoclonal antibody (mAb) specific for human IL-12, C8.6, blocked rHu IL-12 enhanced porcine natural killer (NK) cytotoxicity. It was also shown that rHu IL-12 had additive effects on enhancement of NK cell cytotoxicity with PNK-E/G7 mAbs which react with cytolytic trigger molecules on porcine NK cells. By using purified NK cells, porcine tumor necrosis factor-alpha (TNF-alpha) secretion was measured on rHu IL-12 and PNK-E/G7 mAb-activated NK cells. rHu IL-12 and PNK-E/G7 mAbs synergize to induce TNF-alpha secretion. These data indicate that rHu and rMu IL-12 are cross-reactive in the porcine system and suggest the potential use of the porcine system as an important animal model for further study of rHu IL-12.

Animals↗

Identification of a unique porcine Fc gamma RIIIA alpha molecular complex.

Receptors for the Fc portion of IgG (Fc gamma R) evoke a variety of immune responses upon attachment of the immune complex to this cell surface molecule. Enhancement of tumor cell cytotoxicity is one essential response mediated by Fc gamma Rs. We are studying two mAbs, G7 and PNK-E, which bind to a cytolytic triggering molecular complex on porcine NK cells and phagocytes and function in the enhancement and induction of tumor cell cytotoxicity, respectively. Through biochemical characterization and molecular cloning, we have identified the G7 molecule as the porcine homologue of human Fc gamma RIIIA alpha. The G7 and PNK-E molecules have previously been shown to exist as a complex on the cell surface, suggesting that PNK-E represents an Fc gamma RIIIA alpha-associated molecule in the porcine system. We used the mild detergent Brij 96 to identify associated molecules such as the gamma and zeta subunits. G7 and PNK-E mAbs immunoprecipitate the identical multimolecular complex which includes the gamma subunit on porcine PMN. In addition to the G7 molecule at 40 kDa and the gamma subunit at 7 kDa, Brij 96 immunoprecipitation with G7 mAb, PNK-E mAb, or anti-gamma Ab shows association of unidentified molecules of approximately 15, 20, and 25 kDa on reducing SDS-PAGE, none of which appear to be the zeta subunit. Large-scale immunoprecipitation of the G7 complex from porcine PMN will be performed to isolate sufficient quantities of these unidentified proteins to obtain amino acid sequences. Since these molecules seem to be distinct from Fc gamma R-associated subunits described to date, these studies may lead to the identification of unique Fc gamma R-associated molecules and suggest the presence of a novel Fc gamma RIIIA alpha molecular complex in the porcine system.

Animals↗

What is the role of reassessment laparoscopy in the management of gynecologic cancers in 1995?

One hundred fifty-four patients with a diagnosis of ovarian, primary peritoneal, or fallopian tube carcinoma underwent 181 reassessment procedures to detect persistent or recurrent disease between January 1, 1989 and December 31, 1994 at Cedars-Sinai Medical Center. One hundred four laparoscopic procedures were performed. Eleven of these procedures were converted to laparotomy due to severe adhesions. Therefore, a total of 88 reassessment laparotomies were performed during the study period. Fifty-seven of 93 laparoscopies and 69 of 88 laparotomies were done as second-look procedures. There was no significant difference between the two groups with respect to patient age, tumor histology, degree of primary cytoreduction, and tumor stage or grade. Significant differences were found between laparoscopy and laparotomy groups in the following outcome variables evaluated: estimated blood loss (33.9 ml vs 164.9 ml, P = 0.0001), operative time (81.3 min vs 130.4 min, P = 0.0001), days of hospitalization (0.3 days vs 6.8 days, P = 0.0001), and direct cost/case ($2765 vs $5420, P = 0.0001). Despite obtaining 50% fewer biopsies with laparoscopy than laparotomy, the ability to detect disease was similar between these two groups: 47.3% vs 55.7% for all procedures and 52.6% vs 53.6% in the patients undergoing second-look procedures. Major complications in the laparoscopy group included transverse colon perforation (1), small bowel perforation (2), enterocutaneous fistula (1), and a retroperitoneal hematoma (1). Major complications in the laparotomy group included cystotomy (1), left ureteral injury (1), enterotomy (2), and SBO (4). Laparoscopy, when technically feasible, appears equally as effective as laparotomy in detecting persistent or recurrent malignant disease with less blood loss, less days spent in the hospital, less financial burden, and no increase in patient morbidity.

Evaluation Studies as Topic↗

Vascular endothelial growth factor expression is not regulated by estradiol or medroxyprogesterone acetate in endometrial carcinoma.

OBJECTIVE: To determine whether the expression of vascular endothelial growth factor (VEGF) is altered by treatment in an in vivo tumor with 17 beta-estradiol (E2) or medroxyprogesterone acetate (MPA). METHODS: A well-differentiated endometrial carcinoma tumor was isolated from a patient and explanted into the dorsal skin of ovariectomized nude mice, from which it was serially passaged in vivo. The explanted tumor retained all the properties of the original tumor, including estrogen and progesterone receptor expression and growth promotion and inhibition by E2 and MPA, respectively. The mice were treated with continuous E2 administration followed by treatment with either a single intramuscular administration of 2 mg MPA or weekly administrations of 2 mg MPA. Untreated tumor-bearing mice served as controls. The tumors were harvested at 0 to 21 days from first MPA administration. RNA from the tumors was isolated and VEGF expression was determined by Northern analysis. RESULTS: VEGF was expressed in the absence of treatment with E2 or MPA, and expression was unaltered by continuous treatment with E2. Additional treatment with a single does of MPA did not alter expression at Days 1, 2, 3, 7, 14, and 21, and additional treatment with E2 or E2 + MPA. Regulation of VEGF expression is not a mechanism by which these hormones exert their growth effects on endometrial tumors.

Actins↗

Successful treatment of neuroendocrine small cell carcinoma of the cervix metastatic to regional lymph nodes.

Neuroendocrine small cell carcinoma of the cervix is an aggressive tumor that is associated with a poor prognosis. No reports have described a patient with metastatic spread who has had long-term survival. A patient with neuroendocrine small cell carcinoma of the cervix metastatic to regional lymph nodes who is free of disease 92 months after multimodality treatment with radiation, surgery, and chemotherapy is described in this paper.

Adult↗

Effect of intravenous immunoglobulin G on natural killer cell cytotoxicity in vitro in women with recurrent spontaneous abortion.

Intravenous immunoglobulin (IVIg) has been used to treat women with recurrent spontaneous abortion (RSA), particularly for women with elevated natural killer (NK) cells. We investigated the effect of IVIg on peripheral blood NK cell activity in vitro in women with RSA. 51Cr-release assays using K562 in the presence of varying concentrations of IVIg were performed using PBL from 16 women with RSA. Antibody dependent cellular cytotoxicity (ADCC) was evaluated using Daudi cells. Effectors and targets were preincubated with IVIg. Binding of IVIg to K562 and Daudi was evaluated by flow cytometry. The effect of K562 absorbed IVIg on NK activity was compared to that of non-absorbed IVIg. NK cytotoxicity and ADCC in the presence of F(ab')2 fragments were compared with those in the presence of intact IVIg. IVIg produced a significant, dose dependent inhibition of NK activity in vitro. Inhibition of NK activity occurred when effectors but not targets were preincubated with IVIg. IVIg binds to K562 and Daudi. IVIg increased ADCC when targets but not effectors were incubated with IVIg. K562 absorbed IVIg produced more inhibition of NK cytotoxicity than non-absorbed IVIg. Suppression of NK cytotoxicity by F(ab')2 was as effective as that of IVIg. However, F(ab')2 did not increase ADCC. IVIg effectively reduces peripheral blood NK cytotoxicity in vitro. Inhibition of NK cytotoxicity is mediated at the effector cell level through the antigen binding portion of the immunoglobulins. Women with RSA and elevated NK cells may benefit from IVIg treatment.

Abortion, Habitual↗

Change in glutathione S-transferase and glyceraldehyde-3-phosphate dehydrogenase activities in the organs of mice treated with 2-chloroethyl ethyl sulfide or its oxidation products.

Various organs or skin from male ICR mice treated intraperitoneally with 2-chloroethyl ethyl sulfide (CEES) or its oxidation derivatives 2-chloroethyl ethyl sulfoxide (CESSO) and 2-chloroethyl ethyl sulfone were analysed for changes in two thiol-containing enzymes, namely glutathione S-transferase (GST) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). CEES was more potent than its oxidation derivatives with respect to the decrease in organ weight and the loss in GAPDH activity, although the reverse was found in GST induction. Whereas the induction of GST was highest in the lung after multiple intraperitoneal intoxication with CEESO (8 and 32 mg/kg), the decrease in GAPDH activity after exposure to CEES (8 mg/kg body weight) was most remarkable in the spleen, the most susceptible organ to toxicity of CEES. GST and GAPDH activities in the skin of male hairless mice exposed subcutaneously to CEES (2 mg/kg body weight) were not altered significantly at 2-hr exposure, but decreased up to 60% of that of controls at 8 hr, when oedema formation was greatest. Taken together, it appears that GAPDH activity is a more sensitive biochemical parameter than GST activity in organs of mice treated with CEES or its oxidation products.

Animals↗

Gene expression of insulin signal-transduction pathway intermediates is lower in rats fed a beef tallow diet than in rats fed a safflower oil diet.

To elucidate the effects of dietary fatty acid composition on the insulin signaling pathway, we measured the gene expression of the earliest steps in the insulin action pathway in skeletal muscle of rats fed a safflower oil diet or a beef tallow diet. Rats were meal-fed an isoenergetic diet based on either safflower oil or beef tallow for 8 weeks. Both diets provided 45%, 35%, and 20% of energy as fat, carbohydrate, and protein, respectively. Insulin resistance, assessed from the diurnal rhythm of plasma glucose and insulin and the oral glucose tolerance test (OGTT), developed in rats fed a beef tallow diet. Body fat content was greater in rats fed a beef tallow diet versus a safflower oil diet. The level of insulin receptor mRNA, relative expression of the insulin receptor mRNA isoforms, and receptor protein were not affected by the composition of dietary fatty acids. The abundance of insulin receptor substrate-1 (IRS-1) and phosphatidylinositol (PI) 3-kinase mRNA and protein was significantly lower in rats fed a beef tallow diet versus a safflower oil diet. We conclude that long-term feeding of a high-fat diet with saturated fatty acids induces decrease in IRS-1 and PI 3-kinase mRNA and protein levels, causing insulin resistance in skeletal muscle.

Actins↗

Intravenous immunoglobulin inhibits natural killer cell activity in vivo in women with recurrent spontaneous abortion.

We previously reported elevation of natural killer (NK) cells in women with recurrent spontaneous abortion (RSA) of immune etiology. In this study, we investigated the effect of intravenous immunoglobulin G (IVIg) on peripheral blood NK activity in vivo in women with RSA. Blood was drawn prior to and 7-11 days after IVIg therapy in eight women with RSA. NK activity was measured using K562 as target cells for 51Cr-release assays. Serum IgG concentrations were also measured. All received 400 mg/kg/day of IVIg for 3 consecutive days. 1) Seven of eight women became pregnant. Five delivered a live born infant. Three out of five women (60%) who delivered a live born infant showed a significant inhibition of NK cytotoxicity post IVIg and the rest did not show any changes; 2) NK cytotoxicity was significantly increased in a woman who miscarried again; 3) A woman who miscarried a chromosomally abnormal fetus showed a significant inhibition of NK cytotoxicity after IVIg; and 4) Serum IgG concentration increased significantly from 9.3 +/- 3.0 mg/ml to 23.5 +/- 5.1 mg/ml post IVIg therapy. IVIg effectively inhibits peripheral blood NK activity in vivo. These results are consistent with our previous finding showing that IVIg inhibits NK cell activity in vitro. Women with RSA and elevated NK cells may benefit from IVIg treatment.

Abortion, Habitual↗

Cyclin D1 protein expression in lung cancer.

Cyclin D1, a G1 cyclin, has been implicated in the oncogenesis of various types of malignancies via deregulation of cell cycles. Amplification of cyclin D1 as a part of 11q13 amplicon has been reported in lung cancer as well as a subset of carcinomas arising from various organs including breast, head and neck, and esophagus. In addition to its role as an oncogene, several recent studies have suggested that amplification is indicative of poor prognosis. In this study we examined the cyclin D1 protein expression in 102 consecutive cases of lung cancers using the microwave enhanced immunohistochemical staining method and correlated the data with the histologic subtype and grade, Ki-67 (MIB-1) labeling index, and survival. Nuclear positive staining was observed in 18 cases (18 %) of lung cancers. Although squamous cell carcinoma demonstrated a higher rate of expression (12 /58, 21%), three of 33 adenocarcinomas (9%) revealed overexpression and both adenocarcinoma and squamous cell carcinoma components within the adenosquamous carcinoma showed nuclear staining. There was no correlation between cyclin D1 overexpression and histologic grade, Ki-67 (MIB-1) labeling index, and survival. These observations indicate that cyclin D1 protein overexpression might be implicated in the oncogenesis of the various histologic types of non-small cell lung carcinomas but it has no usefulness as a prognostic marker.

Cyclin D1↗

Adhesion formation after incisional hernia repair: a randomized porcine trial.

Adhesion formation involving intraperitoneal contents is a significant complication of incisional hernia repair. We evaluated the rate of peritoneal adhesion formation following closure of experimentally induced large ventral fascial defects using selected synthetic prosthetic materials in a well standardized porcine model. Sixty 25 kg hogs had a 4 x 6 cm ventral fascial defect induced and were randomized to repair with either interrupted 0-Prolene suture, Marlex surgical mesh (Mx), GoreTex Dual Mesh (Gore-DM), or an experimental version of the latter having multiple 0.4 mm fenestrations (Gore-DMH). Mx mesh induced significantly more adhesions than did Gore-DM when the two materials were placed in a comparable manner (P < 0.001). Those animals whose defects were closed primarily with Prolene suture alone developed significantly fewer adhesions than either Mx or Gore-DM (with or without holes) when these materials were sutured in an overlaying (i.e., extraperitoneal) manner (Mx, P < 0.0001; Gore-DM, P < 0.05; Gore-DMH, P < 0.01). The intraperitoneal placement of the Gore-DM materials (i.e., underlay manner) resulted in a rate of adhesion formation that was not statistically different from that induced by closure with Prolene alone (P = 0.08 for Gore-DM and P = 0.07 for Gore-DMH). Our findings support the use of Gore-DM biomaterial as the preferred material in the repair of large abdominal fascial defects when the use of a synthetic prosthetic material is necessitated by the defect size.

Animals↗

The release of lysosomal arylsulfatase from liver lysosomes exposed to 2-chloroethylethyl sulfide.

Treatment of a lysosome-rich fraction from liver with 2-chloroethylethyl sulfide resulted in a dose-dependent release of arylsulfatase. The inclusion of Ca2+ enhanced the enzyme release by approximately 2.3-fold. The enhancing effect of Ca2+, showing an EC50 value of 30 mM, was mimicked by neither Mg2+ nor Mn2+. Studies on a structural requirement and a time-dependent release suggest that the Ca(2+)-dependent release proceeds via a specific process involving the alkylation of lysosomal membranes by 2-chloroethylethyl sulfide. Furthermore, the Ca(2+)-dependent process was prevented partially by either leupeptin or gentamycin, but neither pepstatin nor PMSF, implying that the enzyme release may be partially mediated by lysosomal cysteine-protease or phospholipase. Meanwhile, the Ca(2+)-independent release seems to be expressed non-specifically by various compounds.

Animals↗

Inactivation of microsomal Ca(2+)-ATPase by 2-chloroethylethyl sulfide.

Exposure of liver microsomes to 2-chloroethylethyl sulfide (CEES) led to a dose-dependent decrease of Ca(2+)-ATPase activity. Studies on a structural requirement and a time dependence suggest that the enzyme inhibition may proceed via an instantaneous process involving an alkylation by an unstable intermediate, presumably a sulfonium form. It is noteworthy that the microsomal Ca(2+)-ATPase was more sensitive to CEES than the Na+/K(+)-ATPase from erythrocyte membranes. The Ca(2+)-ATPase was inhibited non-competitively by CEES, and its inhibitory action was independent of Ca2+ concentrations. The involvement of membrane phospholipid in the enzyme inhibition is excluded, since the temperature dependence of microsomal Ca(2+)-ATPase was not affected by CEES. Moreover, Triton X-100-solubilized Ca(2+)-ATPase was inactivated by the compound to the same extent as the membrane-bound enzyme was. Thus, it is suggested that CEES inactivates Ca(2+)-ATPase by alkylating the enzyme molecule at a region other than the active site.

Adenosine Triphosphate↗