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Biomedical subjects

K Kim

Publications and source records attributed to K Kim.

At least 523 records · Page 29Linked to original sources

A female case of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor.

The case of a 17-year-old female with a rare form of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor is reported. Laparoscopy showed a tumor 50 mm in diameter in the lower portion of the right lobe of the liver. The tumor was biopsied under ultrasonic guidance, and tentatively diagnosed as adenomatous hyperplasia. The patient was also diagnosed as having type VIII glycogenosis (phosphorylase kinase deficiency).

Adolescent↗

Herpes simplex virus enhances the 7,12-dimethylbenz[a]anthracene (DMBA)-induced carcinogenesis and amplification and overexpression of c-erb-B-1 proto-oncogene in hamster buccal pouch epithelium.

We studied the effects of herpes simplex virus type 1 (HSV-1) inoculation and topical 7,12-dimethylbenz[a]anthracene (DMBA) application, alone or in combination, on the carcinogenesis and on the amplification and expression of various cellular proto-oncogenes in hamster buccal pouch tissue. Topical DMBA treatment produced tumor formation in pouches, but HSV-1 inoculation, alone caused no neoplastic changes. In pouch tissues receiving both DMBA application and HSV-1 inoculation, the development of initial leukoplakia and tumor has hastened and enhanced in comparison with those receiving DMBA alone. Topical DMBA application to pouch tissue induced an amplification and an increase in the expression of cellular erb-B-1 (c-erb-B-1) proto-oncogene in the epithelial tissue, whereas repeated infection with HSV-1 alone did not. Topical DMBA combined with HSV-1 inoculation, however, resulted in greater amplification and expression of c-erb-B-1 proto-oncogene in the pouch epithelial tissue compared to the DMBA alone. These data indicate that HSV-1 inoculation significantly increases the carcinogenic activity of DMBA, in part, by probably enhancing DMBA-induced amplification and expression of c-erb-B-1 proto-oncogene in hamster buccal pouch tissue.

9,10-Dimethyl-1,2-benzanthracene↗

Progesterone increases messenger ribonucleic acid (mRNA) encoding luteinizing hormone releasing hormone (LHRH) level in the hypothalamus of ovariectomized estradiol-primed prepubertal rats.

In order to investigate the mechanism underlying ovarian steroid action on gene expression of hypothalamic luteinizing hormone releasing hormone (LHRH), changes in LHRH mRNA level were determined by RNA-blot hybridization assay. Twenty-eight-day-old female rats were ovariectomized (OVX) and implanted with Silastic capsule containing either 17 beta-estradiol (E) or vehicle (V). Two days later (day 30), OVX + E-primed rats were given s.c. progesterone (P, 1 mg) 6 h prior to decapitation. Four experimental groups were studied: (1) intact, (2) OVX + V, (3) OVX + E, and (4) OVX + E + P-treated rats. Poly(A) RNA fractions from hypothalami (40-50/group) were isolated, blotted onto nitrocellulose paper and hybridized with 32P-end-labeled LHRH oligonucleotides (29 mer) which are complementary to rat LHRH mRNA. The hypothalamic LHRH mRNA signal markedly attenuated 2 days following ovariectomy. E replacement to OVX rats slightly increased LHRH mRNA level, which is lower than that of the intact group. However, a single injection of P to OVX + E-treated rats notably augmented the LHRH mRNA level over that observed in the intact group. In addition, LHRH content and release in vitro were examined to correlate with changes in LHRH gene expression. Ovariectomy and the replacement of E and/or P resulted in a similar fashion of changes in LHRH release and content as compared to alteration of LHRH mRNA level. This study clearly demonstrates that P increases LHRH mRNA level in the hypothalamus of OVX + E-primed immature rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Induction of an antioxidant protein of Saccharomyces cerevisiae by O2, Fe3+, or 2-mercaptoethanol.

A soluble 27-kDa protein from Saccharomyces cerevisiae specifically prevents the inactivation of various enzymes caused by a nonenzymatic Fe3+/O2/thiol mixed-function oxidation system but not by mixed-function oxidation systems in which the thiol component is replaced by another electron donor-e.g., ascorbate. In this report, using a 125I-labeled monospecific antibody against the 27-kDa protein, we measured changes in the 27-kDa protector protein in response to changes in oxidative stress and heat shock. With a shift from an anaerobic (95% N2/5% CO2) to a hyperaerobic (95% O2/5% CO2) atmosphere, a 3-fold increase was observed. This increase was prevented by cycloheximide, indicating that the induction requires new protein synthesis. The antioxidant protein synthesis was also significantly enhanced by the addition of either 2-mercaptoethanol or Fe3+ to the growth medium. Radioimmunoassay results also show that the antioxidant protein is an abundant protein, as it constitutes 0.7% of total soluble protein from yeast grown aerobically. Immunoblotting experiments revealed that rat tissues also contain a 27-kDa protein that can be specifically recognized by antibodies against the yeast protein. These results suggest that in vivo induction in yeast of the 27-kDa protein may represent an adaptive response that evolved to protect cells against damage caused by thiol-dependent mixed-function oxidation systems, and the antioxidant protein is conserved in mammalian tissues. A heat shock applied to yeast did not cause any significant increases in the concentration of the 27-kDa protein.

Aerobiosis↗

Elderly patients admitted to the psychiatric unit of a general hospital.

Elderly psychiatric patients who are cared for in general hospital psychiatric settings have not been clearly characterized in the literature in terms of demographics, primary diagnoses, hospital course, and outcome. The authors reviewed charts of 168 patients over the age of 60 years admitted to a general hospital inpatient psychiatry unit over a 5-year period in order to develop a demographic and clinical profile of this patient population. Results indicated that the large majority of patients had affective syndromes; dementia was the second most common diagnosis. Length of stay correlated with severity of depressive illness, while a diagnosis of dementia was associated with a shorter hospitalization. Outcome measures showed favorable response to treatment in three-fourths of this population of elderly psychiatric patients. These data suggest that the general hospital acute inpatient setting is well suited to care for the combined medical and mental illnesses of elderly psychiatric patients.

Activities of Daily Living↗

Age at onset in late-life delusional depression.

Mean age at onset was not significantly different in 39 delusional and 70 nondelusional unipolar depressed patients over 60 years of age. The finding was unchanged when sex, concurrent dementia, and medical illness were examined.

Age Factors↗

Multiple forms of alkaline phosphatase in mouse preimplantation embryos.

Mouse embryos were extracted with 0.5% Triton X-100 and subjected to cellulose acetate electrophoresis. In fertilized eggs, two forms of alkaline phosphatase (ALP), a slow-moving form and a fast-moving form, were observed. As cleavage proceeded, the fast-moving form disappeared, and the slow-moving form, the mobility of which was similar to that of the slow-moving form of the kidney, became gradually dominant up to the blastocyst stage (named 'embryonic' form). With blastulation, another fast-moving form showing a similar mobility to the lung ALP began to appear in blastocysts and showed a transient dominance in hatched blastocysts. After implantation, both the embryonic form and the fast-moving form gradually faded, and were eventually replaced by the new form, which may be named 'fetal form' in Day 7 embryos. These results clearly demonstrated that ALP activity does exist in embryos at all stages of preimplantation development. Moreover, the changes in multiple forms of ALP correlated with embryonic development may suggest that these multiple forms may have differential roles in the process of early development.

Alkaline Phosphatase↗

Phase II study of cyclophosphamide, doxorubicin, and vincristine (CAV) and etoposide plus cisplatin (EP) alternating chemotherapy combined with radiotherapy in small cell lung cancer.

The development of drug resistance is the major limiting factor influencing the survival of patients with small cell lung cancer (SCLC). We have thus examined the activity of cyclophosphamide, doxorubicin and vincristine (CAV) alternating with etoposide and cisplatin (EP) in 35 patients with SCLC. The treatment courses were alternated every 3 or 4 weeks. After induction chemotherapy, patients with limited disease (LD) received thoracic radiotherapy (5000 cGy), prophylactic cranial irradiation (3000 cGy) and maintenance chemotherapy and patients with extensive disease (ED) received maintenance chemotherapy only. In this group of 35 patients, 13 had limited disease (LD) and 22 had extensive disease (ED). After completion of the therapy, 100% of the patients with LD achieved complete plus partial remission (CR + PR) and 68% of the patients with ED achieved CR + PR. The median survival time was 66 weeks (15.3 months) in patients with LD and 44 weeks (10.2 months) in patients with ED. The over all survival for patients with LD was superior to that for patients with ED (p less than 0.05). Also, median response duration for patients with LD (35 wks) was longer than that for patients with ED (17 weeks) (p less than 0.05). The primary site was the most vulnerable site to relapse (18 patients). Toxicity was mild to moderate and acceptable, and there were no treatment-related deaths. These results suggest that the alternation of CAV and EP is effective treatment strategy in the management of SCLC. A randomized controlled study will be required to discriminate the actual effect of this alternating regimen.

Adult↗

Two subunits of mannose permease, II-PMan and II-MMan, of Escherichia coli mediate coliphage N4 infection.

Mutant strains of Escherichia coli that lack one or all of the intact components of mannose permease do not support the growth of phage N4. Complementation experiments using three recombinant plasmids containing DNA fragments coding for the subunits of mannose permease revealed that among the three component subunits, II-PMan and II-MMan alone are sufficient to confer N4 sensitivity.

Coliphages↗

[Three cases of primary malignant lymphoma of the small intestine].

Three cases of a primary malignant lymphoma of the small intestine are reported. Case 1: a 62-year-old male who underwent an emergency operation for a jejunal perforation of a malignant lymphoma (aneurysmal type, Stage III, diffuse small cell type). The patient is still alive 16 months after the operation. Case 2: A 54-year-old female with complaints of an abdominal pain and anemia was found to have three tumors (one in the jejunum, two in the ileum) that were determined as being malignant lymphomas (all of the aneurysmal type, Stage III, diffuse medium-sized cell types). This patient is still alive 11 months after the operation. Case 3: A 40-year-old male with a complaint of an abdominal pain was found to have a malignant lymphoma of the ileum (aneurysmal type, Stage III, a diffuse medium-sized cell type). This patient died on the 60th day after the operation.

Adult↗

Point estimation following group sequential tests.

Kim and DeMets (1987, Biometrics 43, 857-864) described an exact procedure for constructing confidence intervals for a normal mean following group sequential tests when the boundaries were generated based on the notion of use functions proposed by Lan and DeMets (1983, Biometrika 70, 659-663). In this article, three point estimators for a normal mean following group sequential tests are considered, and their properties are investigated by Monte Carlo simulation. Based on the simulation results, some suggestions are made as to the choice of group sequential designs and use function.

Biometry↗

Regulation of tumor-induced myelopoiesis and the associated immune suppressor cells in mice bearing metastatic Lewis lung carcinoma by prostaglandin E2.

The in vitro and in vivo effects of prostaglandin E2 (PGE2) and of its stable analogue, 16,16-dimethyl-PGE2 (dmPGE2), on myelopoiesis and on the myelopoiesis-associated immune suppressor cell activity of mice bearing metastatic variant Lewis lung carcinoma (LLC-C3) tumors are assessed. In vitro studies showed a reduced susceptibility of bone marrow myeloid progenitor cells (CFC) from LLC-C3 tumor bearers versus normal mice to the growth-inhibitory effects of PGE2. When added to cocultures of bone marrow cells with LLC-C3 supernatants, PGE2 lessened the frequency of CFC and slightly reduced the generation of bone marrow immune suppressor cells. In vivo studies showed that 4 daily injections of dmPGE2 into LLC-C3 tumor-bearing mice caused some reduction in femoral bone marrow CFC and had an insignificant effect on bone marrow suppressor cell activity. In contrast to the relative insensitivity of bone marrow cells of tumor bearers to the effects of PGE2, in vitro studies showed that CFC formation by spleen cells of tumor bearers was readily inhibited by PGE2. Likewise, in vivo studies showed that spleen cells of dmPGE2-treated LLC-C3-bearing mice had a reduction in cellularity, CFC, and the level of spontaneous proliferation; a reduction in suppressor cell activity; and an increase in blastogenesis. Thus, short-term dmPGE2 treatment of LLC-C3-bearing mice limited the tumor-induced splenic myelopoiesis and reduced the associated splenic immune suppressor cell activity.

16,16-Dimethylprostaglandin E2↗

Expression of cytochrome P450b and P450e genes in small intestinal mucosa of rats following treatment with phenobarbital, polyhalogenated biphenyls, and organochlorine pesticides.

The expression of cytochromes P450b and P450e genes was studied in the small intestinal mucosa of rats using a cDNA which recognizes the mRNAs of both cytochromes as well as oligonucleotide probes which are able to differentiate between the two gene products. Animals were treated with oral and intraperitoneal doses of phenobarbital, gamma-chlordane, trans-non-achlor, and polychlorinated and polybrominated biphenyls. RNA was extracted from small intestinal mucosa and liver. After treatment with each of the compounds, P450b mRNA was markedly induced in small intestinal mucosa and in liver. The greatest degree of induction was found in mucosa of the proximal small intestine where P450b mRNA levels were 4-6-fold higher than levels found in the distal small intestine. This distribution of P450b mRNA was not dependent on the route of administration of inducers. In contrast, although P450e mRNA was induced in the liver after treatment, P450e mRNA in the small intestine did not increase in response to any of the administered inducers. The location of the P450b mRNA within the intestinal mucosa following treatment with inducers was studied by in situ hybridization; the message was induced predominantly in enterocytes located in intestinal villi. These data indicate that the P450b gene is induced in the small intestine following treatment with various xenobiotics and that this induction may be secondary to either transcriptional activation of the gene or to mRNA stabilization in enterocytes located in the villi of the intestinal mucosa. The differential induction of P450b versus P450e genes in the small intestine and liver indicates that the regulation of these closely linked genes is tissue-specific. Furthermore, the marked induction of P450b mRNA in response to the administered xenobiotics indicates that this isoenzyme may have an important biological role in the small intestinal metabolism of environmental toxicants and drugs.

Animals↗

Testosterone stimulates LH-RH-like mRNA level in the rat hypothalamus.

To elucidate whether testosterone (T) replacement to castrated male rats may promote luteinizing hormone-releasing hormone (LH-RH) biosynthesis in the hypothalamus, an RNA-blot hybridization assay was employed. Poly(A) mRNA fractions from hypothalami (40-50) of intact, castrated plus vehicle, and castrated plus T group were isolated, blotted on nitrocellulose paper and hybridized with 32P-end labelled LH-RH oligonucleotides (29 mer) which is complementary to the rat LH-RH mRNA. LH-RH-like mRNA level markedly attenuated 2 weeks following castration and T replacement significantly increased LH-RH-like mRNA level, comparable to about 80% of that observed in intact male rats. In addition, LH-RH contents and release from hypothalami were studied, to examine the correlation with LH-RH gene expression and secretory activity of LH-RH. Castration significantly reduced LH-RH contents and LH-RH release in vitro. T replacement restored LH-RH contents and release comparable to those shown in the intact group. This study demonstrates for the first time that T replacement increases LH-RH-like mRNA level in the hypothalami of castrated rats suggesting that T may act at the pretranslational level. This change in LH-RH gene expression is parallel with alteration of LH-RH content and release.

Animals↗

Methionine modification in cytochrome-c peroxidase.

Hydrogen peroxide oxidizes Met-119, Met-230 and Met-231 to the sulfoxide derivatives with equal initial rates in apocytochrome-c peroxidase at pH 4 in 0.1 M sodium acetate buffer. No detectable oxidation of Met-163 and Met-172 occurs under these conditions. Apoenzyme, in which up to two residues of methionine have been oxidized, binds heme stoichiometrically. Heme-reconstituted modified enzyme has an absorption spectrum with the Soret maximum red-shifted compared to that of the native enzyme, indicating a perturbation of the heme environment in the modified enzyme. Heme-reconstituted modified enzyme can bind cyanide with an affinity nearly identical to that of the native enzyme. The heme-reconstituted enzyme loses its ability to react with hydrogen peroxide to form Compound I. The loss of the ability to form Compound I is correlated with the modification of at least one of the residues in the Met-230/Met-231 pair.

Apoproteins↗