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Biomedical subjects

B J Kim

Publications and source records attributed to B J Kim.

84 records · Page 5Linked to original sources

Identification of glucocorticoid response element of the rat TRH gene.

OBJECTIVES: It was suggested that glucocorticoid exerts cell-specific effects on thyrotropin-releasing hormone (TRH) gene expression at the transcriptional level. Although there is no typical palindromic glucocorticoid response element (GRE) on the rat TRH gene promoter, a perfect GRE half-site is found between -205 bp and -211 bp. We investigated whether the segment between -242 bp and -200 bp of the rat TRH gene promoter is responsible for glucocorticoid response. METHODS: For the 5' deletion study of the TRH gene, four different plasmid constructs, pTRH(- 554/84), pTRH(-242/84), pTRH(-200/6), pTRH(-113/84) were used for transient transfection study. The plasmid pMAMneo-LUC was used as a positive control and pRSV-GR expression vector, as a co-transfection study. Transfection was performed by the modified calcium precipitation method with 2 micrograms of each lasmid on the HeLa cells. RESULTS: Dexamethasone (DEX) stimulated the transcriptional activity of pTRH(-554/84)-LUC and pTRH(-242/84)-LUC by approximately 3.2 fold at 10(-8) M and 5.4 fold at 10(-8) M. On the contrary, deletion of the region between -242 to -200 bp reduced the basal transcriptional activity by 90% and also completely abolished the DEX-induced transcriptional activation of the luciferase gene. The DEX-induced transcriptional activation of pTRH(-242/84)-LUC was in dose-dependent manner. While the co-transfection of glucocorticoid receptor expression vector (pRSV-GR) did not increase the basal transcriptional activity of pMAMneo-LUC, it increased the basal transcription of pTRH(-242/84)-LUC by 1.8 fold. The pRSV-GR co-transfection and DEX treatment further increased the transcription of pTRH(-242/84)-LUC by 2-4 fold at the concentration of 10(-8) M. CONCLUSION: These findings suggest that a cis-acting element(s) which is important for the basal transcriptional activation and glucocorticoid response of the rat TRH gene is located between -242 bp and -200 bp. The gene has a weak GRE glucocorticoid response and seems to be mediated by an interaction between glucocorticoid receptor and other transcriptional factor (s).

Animals↗

The expression of beta 1 integrin and intercellular adhesion molecule-1 on mesangial cells and its modulation in glomerulonephritis.

OBJECTIVES: This study was performed to observe the effects of conditioned media (CM) of cultured mononuclear cells (MNC) on the expression of beta 1 integrin and intercellular adhesion molecule(ICAM)-1 on mesangial cells and the modulation by TGF-beta, TNF alpha, or hydroxyl radical Also these were examined in anti-Thy mesangial proliferative GN (MsPGN) or puromycin aminonucleoside nephrosis(PAN). METHODS: The expression of beta 1 integrin and ICAM-1 on mesangial cells was examined by ELISA and the modulation by TGF-beta, TNF alpha, or hydroxyl radical was investigated by using neutralizing antibody and dimethylthiourea. [.OH] scavenger. RESULTS: The CM of MNC from Control suppressed the beta 1 integrin expression and thymidine incorporation and increased ICAM-1 expression on mesangial cells, compared to media alone. Especially the significant increase in ICAM-1 expression was reversed by anti-TNF alpha antibody. beta 1 integrin expression on mesangial cells was higher by the addition of CM of MNC in MsPGN than in Control, which was prevented by anti-TGF beta antibody or dimethylthiourea. ICAM-1 expression was not different among groups. Thymidine incorporation by adding CM of MNC was lower in MsPGN and PAN, which was mitigated by anti-TGF beta and anti-TNF alpha. Thus the ratio of the expression of ICAM-1 to thymidine incorporation was higher in MsPGN and PAN. CONCLUSION: The expression of beta 1 integrin and ICAM-1, and the thymidine incorporation on mesangial cells are directly regulated by MNC, maybe through factors such as TGF beta or TNF alpha. In MsPGN, the overexpression of beta 1 integrin induced by MNC through TGF beta or hydroxyl radical on day 3 may be related to the pathogenesis.

Animals↗

Alcoholic pellagra encephalopathy combined with Wernicke disease.

Clinical and postmortem findings of a case that had combined alcoholic pellagra encephalopathy and Wernicke disease are described. This 51-year-old malnourished and chronic alcoholic man presented with progressive mental deterioration, pellagra dermatitis, hypertonus of the neck and other musculatures, myoclonic jerks with bizarre involuntary movements, in addition to total external ophthalmoplegia and gait disturbance. After administration of multivitamins, including thiamine and nicotinamide, these neurologic abnormalities were dramatically improved in a few days. However, the patient died thereafter because of sepsis associated with pneumonia. Postmortem examination revealed marked abnormalities in CNS, characterized by diffuse atrophy of gray matter and widespread neuronal degeneration and characteristic central chromatolysis in pontine nuclei, dentate nuclei, cranial nerve nuclei in the brain stem, Betz cells of the cerebral cortex, and Clarke's column and anterior horn cells of the spinal cord. There were also atrophy and gliosis of the mammillary bodies, degeneration and vascular proliferation of periaqueductal gray matter, and massive gliosis around the third ventricle. These neuropathological changes were compatible with symptoms of both alcoholic pellagra encephalopathy and Wernicke's disease, but they were also strongly suspected on clinical grounds.

Alcoholism↗

[The relation of pericoronitis to the position of the mandibular third molar].

Pericoronitis is the most commonly encountered pathologic condition involving the mandibular third molar. Because of the dangers associated with mandibular third molar pericoronitis, prophylactic extraction of third molar at high risk has been recommended. We studied 411 patients with mandibular third molar pericoronitis by clinical symptoms and radiographic measurement of mandibular third molar height, wideth and angulation. The results were as follows: 1. Mandibular third molar pericoronitis is frequently seen in third decade and there are no sexual difference significantely. 2. In inflammatory type of mandibular third molar pericoronitis, chronic pericoronitis occured more frequently than acute type. 3. In relation to angulation and height, mandibular third molar most likely to be afflicted with pericoronitis is vertical eruption at occlusal plane of the second molar. 4. In relation to angulation and width, it appears that the position of the mandibular third molar most likely to be afflicted with pericoronitis is in a vertically erupted tooth of which the space between the ramus and the distal side of the second molar is less than the mesiodistal diameter of crown. (Class II). 5. In relation to height and width, it appears that the position of the mandibular third molar most likely to be afflicted with pericoronitis is class II width (described above)at occlusal plane of the second molar.

Adolescent↗

Actuarial analysis of the risk of prosthetic valve endocarditis in 1,598 patients with mechanical and bioprosthetic valves.

We reviewed the charts of 1,598 patients undergoing valve replacement at the National Institutes of Health, Bethesda, Md, from 1956 through 1981. Retrospective analysis disclosed that 43 patients had prosthetic valve endocarditis (PVE). Twelve patients had early (less than 60 days after operation) and 31 patients had late (greater than 60 days after operation) endocarditis. The cumulative risk was 3% at five years and 5% at ten years. We also calculated the interval risk of PVE. The high risk of early PVE development peaked 15 days after operation. The peak risk was 45 episodes per 100,000 patient days. The risk then declined rapidly and from 150 days to 20 years remained stable at approximately one episode per 100,000 patient days. Nine hundred fifty-two patients had valve replacement with a Starr-Edwards prosthesis and 363 patients had valve replacement with a bioprosthetic valve; there was no significant difference in the risk of PVE in either group. Neither the valve make, position, model, nor the number of valves implanted affected the frequency of PVE or the mortality. Actuarial techniques disclosed the high early risk of PVE, the prolonged risk of PVE up to 150 days after operation, and the low but persistent risk late after operation. There was no significant difference in the risk of PVE in patients with bioprosthetic v mechanical valves.

Actuarial Analysis↗

Mediastinal infection after open heart surgery.

Mediastinal infection occurred in 29 of 2031 patients (1.4%) who underwent median sternotomy for cardiac operation at the National Heart, Lung and Blood Institute between 1956 and 1981. Factors associated with the development of mediastinitis included postoperative complications such as low cardiac output, respiratory insufficiency, reoperation for bleeding, repeat median sternotomy, and triple valve replacement. Factors that were not significantly associated with the development of mediastinitis included preoperative functional class, preoperative cardiac index, age, sex, weight, or presence of diabetes mellitus. The mortality rate in patients who developed mediastinitis was 52%. Factors associated with death included preoperative functional class III or IV, type of operation, type of organism involved, and the development of pneumonia. The mortality rate was significantly lower (35% versus 73%) in the patients who underwent mediastinal exploration for treatment. There was no difference in survival whether the wound was closed over drainage tubes or packed open. Hospital stay, however, was significantly prolonged in the patients whose wounds were packed open.

Adolescent↗

Role of Campylobacter jejuni potential virulence genes in cecal colonization.

Campylobacter jejuni, a common commensal in chickens, is one of the leading causes of bacterial gastroenteritis in humans worldwide. The aims of this investigation were twofold. First, we sought to determine whether mutations in the C. jejuni ciaB and pldA virulence-associated genes impaired the organism's ability to colonize chickens. Second, we sought to determine if inoculation of chicks with C. jejuni mutants could confer protection from subsequent challenge with the C. jejuni wild-type strain. The C. jejuni ciaB gene encodes a secreted protein necessary for the maximal invasion of C. jejuni into cultured epithelial cells, and the pldA gene encodes a protein with phospholipase activity. Also included in this study were two additional C. jejuni mutants, one harboring a mutation in cadF and the other in dnaJ, with which we have previously performed colonization studies. In contrast to results with the parental C. jejuni strain, viable organisms were not recovered from any of the chicks inoculated with the C. jejuni mutants. To determine if chicks inoculated with the C. jejuni mutants become resistant to colonization by the C. jejuni parental strain upon subsequent challenge, chicks were inoculated either intraperitoneally (i.p.) or both orally and i.p. with the C. jejuni mutants. Inoculated birds were then orally challenged with the parental strain. Inoculation with the C. jejuni mutants did not provide protection from subsequent challenge with the wild-type strain. In addition, neither the C. jejuni parental nor the mutant strains caused any apparent morbidity or mortality of the chicks. We conclude that mutations in genes cadF, dnaJ, pldA, and ciaB impair the ability of C. jejuni to colonize the cecum, that chicks tolerate massive inoculation with these mutant strains, and that such inoculations do not provide biologically significant protection against colonization by the parental strain.

Administration, Oral↗