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Biomedical subjects

S Kim

Publications and source records attributed to S Kim.

At least 955 records · Page 53Linked to original sources
PubMed1995

Hemorrhagic fever with renal syndrome caused by the Seoul virus.

The Seoul virus is an important etiologic agent in hemorrhagic fever with renal syndrome (HFRS), and infections with the Seoul virus are less severe than those with the Hantaan virus. However, the information on HFRS caused by the Seoul virus is limited in Korea. Retrospective clinical analysis was done on 30 patients with Seoul virus infection who had been diagnosed as having HFRS by clinical features and serologic testing by the plaque reduction neutralization test from 1986 to 1991 at the Seoul National University Hospital. They were compared with 69 patients with Hantaan virus infection. The Seoul virus was the etiologic agent in 25% of Korean HFRS and the major cause of HFRS during the summer season although infections occurred throughout the year. The Seoul virus infection had a milder degree of bleeding and renal derangement but had severer liver dysfunction than the Hantaan virus infection. Renal histopathologic findings revealed a milder degree of hemorrhage and vascular changes than cases involving Hantaan virus infection. The precise mechanisms of vascular dysfunction and organ involvement in Seoul virus infection, however, still remain to be explored.

Adult↗
PubMed1995

Differential gene expression of renin and angiotensinogen in the TGR(mREN-2)27 transgenic rat.

Transgenic rats carrying the murine Ren-2 gene represent a monogenetic model of hypertension characterized by low plasma renin and high extrarenal expression of the transgene. The hypothesis has been raised that stimulated local reninangiotensin systems may be responsible for the development of hypertension in this model. This study analyzes the effects of the converting enzyme inhibitor lisinopril, which specifically interferes with the renin-angiotensin system, and the direct vasodilator dihydralazine on the renal and extrarenal expression of renin and angiotensinogen. A comparison of gene expression between heterozygous and homozygous transgenic and normal Sprague-Dawley rats was also performed. We demonstrate high sensitivity of blood pressure toward converting enzyme inhibition in transgenic TGR(mREN-2)27 rats. In the kidney, expression of the transgene and the endogenous renin gene increased, suggesting that both are modulated by lisinopril in a similar manner. On the other hand, blood pressure reduction by dihydralazine did not abolish renal renin suppression in transgenic rats, indicating that mechanisms different from direct effects of blood pressure account for renin suppression. Homozygosity for the transgene led to increased Ren-2 expression and higher blood pressure and had opposite effects on angiotensinogen expression compared with heterozygous rats. Cardiac hypertrophy was reduced by lisinopril but not dihydralazine and was positively correlated with cardiac angiotensinogen expression. Increased angiotensin II in the adrenal gland of TGR(mREN-2)27 rats, which overexpresses the transgene, provides evidence that this leads to enhanced generation of tissue angiotensin II. We conclude that expression of the mouse transgene, the endogenous rat renin gene, and the angiotensinogen gene is subject to differential tissue-specific regulation. Reversal of cardiovascular damage with the converting enzyme inhibitor but not dihydralazine suggests that angiotensin II generated locally may be involved in the pathogenesis of hypertension and structural changes in TGR(mREN-2)27 rats.

Angiotensin II↗
PubMed1995

Angiotensin II induces cardiac phenotypic modulation and remodeling in vivo in rats.

Cardiac phenotypic modulation and remodeling appear to be involved in the pathophysiology of cardiac hypertrophy and heart failure. We undertook this study to examine whether angiotensin II (Ang II) in vivo, independent of blood pressure, contributes to cardiac phenotypic modulation and remodeling. A low dose (200 ng/kg per minute) of Ang II was continuously infused into rats by osmotic minipump for 24 hours or 3 or 7 days to examine the effects on the expression of cardiac phenotype-related or fibrosis-related genes. This Ang II dose caused a small and gradual increase in blood pressure over 7 days. Left ventricular mRNAs for skeletal alpha-actin, beta-myosin heavy chain, atrial natriuretic polypeptide, and fibronectin were already increased by 6.9-, 1.8-, 4.8-, and 1.5-fold, respectively, after 24 hours of Ang II infusion and by 6.9-, 3.3-, 7.5-, and 2.5-fold, respectively, after 3 days, whereas ventricular alpha-myosin heavy chain and smooth muscle alpha-actin mRNAs were not significantly altered by Ang II infusion. Ventricular transforming growth factor-beta 1 and types I and III collagen mRNA levels did not increase at 24 hours and began to increase by 1.4-, 2.8-, and 2.1-fold, respectively, at 3 days. An increase in left ventricular weight occurred 3 days after Ang II infusion. Treatment with TCV-116 (3 mg/kg per day), a nonpeptide selective angiotensin type 1 receptor antagonist, completely inhibited the above-mentioned Ang II-induced increases in ventricular gene expressions and weight. Hydralazine (10 mg/kg per day), which completely normalized blood pressure, did not block cardiac hypertrophy or increased cardiac gene expressions by Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1995

Transforming growth factor-beta 1 expression and phenotypic modulation in the kidney of hypertensive rats.

We have previously reported that renal mRNA levels for transforming growth factor-beta 1, fibronectin, and collagens were increased in 32-week-old stroke-prone spontaneously hypertensive rats (SHRSP) with severe nephrosclerosis. To elucidate the mechanism of hypertension-induced nephrosclerosis, we examined gene expression and localization of transforming growth factor-beta 1 and cellular phenotype in the kidney of 25-week-old SHRSP with moderate renal damage. Renal mRNA was measured by Northern blot analysis. The localization of transforming growth factor-beta 1 and cellular phenotype was determined by immunohistochemistry. In the kidney of 25-week-old SHRSP, renal transforming growth factor-beta 1 mRNA was elevated compared with Wistar-Kyoto rats (WKY), whereas renal collagen mRNAs of SHRSP were not increased. Immunoreactive transforming growth factor-beta 1 in SHRSP was mainly localized in glomerular cells. Furthermore, alpha-smooth muscle actin and desmin were significantly expressed in SHRSP glomerular cells, in contrast to negligible expression of these proteins in WKY. alpha-Smooth muscle actin staining was also observed in interstitial cells, and vimentin, another phenotypic marker, was expressed in atrophic tubular cells of SHRSP, despite no staining of these proteins in WKY. Furthermore, all these phenotypic changes in SHRSP were associated with increased cell proliferation, as shown by the increased number of proliferating cell nuclear antigen-positive cells. Treatment of SHRSP with cilazapril and nifedipine (from the age of 13 to 25 weeks) prevented the increase in transforming growth factor-beta 1 expression and the cellular phenotypic modulation and was accompanied by a reduction of urinary albumin excretion and inhibition of cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1995

Adhesion receptor phenotypes of murine lung CD4+ T cells during the pulmonary immune response to sheep erythrocytes.

Understanding the molecular mechanisms of pulmonary lymphocyte recruitment is a crucial step toward selective control of immune lung diseases and infections in immunocompromised hosts. To dissect these mechanisms, we are studying the response induced in primed C57BL/6 mice by intratracheal challenge with the T cell-dependent antigen, sheep red blood cells (SRBC). This study used four-parameter flow cytometry to examine expression by CD4+ murine T cells in peripheral blood and lungs of receptors known to be differentially expressed on primed human lymphocytes (CD2, CD11a, CD44, CD45RB, CD49d, and L-selectin). Compared with peripheral blood, more lung CD4+ T cells recovered by bronchoalveolar lavage (BAL) showed a primed phenotype. Judged by low expression of CD45RB or L-selectin, 76 to 90% of BAL CD4+ T cells were primed at all times. Adhesion receptor phenotype of CD4+ T cells in BAL and lung interstitium agreed closely, although BAL contained a greater percentage of primed cells. The percentage of CD4+ T cells with high expression of CD44+ and CD49d increased late in the response. However, when considering only upregulated adhesion receptors which might mediate recruitment, 22 to 52% of CD4+ T cells in BAL did not have increased adhesion receptor expression. Longer duration between priming and challenge did not increase adhesion receptor upregulation. High adhesion receptor expression was least evident during the periods of maximal lymphocyte influx, suggesting that factors other than increased surface density of organ-nonspecific adhesion receptors contribute to lymphocyte recruitment during pulmonary immune responses.

Animals↗
PubMed1995

Impact of childhood cancer on Korean families.

A health care system that includes institutions such as the home, clinic, or hospital as well as interpersonal relationships between providers and receivers of health care is a part of any culture. Clinical issues are a part of all cultures, and cross-cultural comparisons are useful in understanding health care. With immigration and travel, a better understanding of the situation of families who have a child with cancer in various countries, different health care systems, and different cultures is needed. Understanding the situation for families with a child who has cancer in South Korea will lead one to a better understanding of a Korean family who has immigrated to the west and has a child develop cancer or is in need of treatment.

Adolescent↗
PubMed1995

Health interventions for African American and Latino youth: the potential role of mass media.

Children in Latino and African American families are far more likely to live in urban, high-poverty settings that greatly increase risks to healthy development. During adolescence, these settings are particularly hazardous for their role in the social transmission of risk behavior. Community-wide health promotion using local mass media can counteract these influences by reaching preadolescents and adolescents, their parents, and other adults in urban communities with safe-behavior messages. These messages can be designed to make safer behavior more acceptable and normative in the community, to increase awareness of community resources for adolescents, and to reverse the stereotyping and disregard that characterize media content about impoverished communities. Evidence is reviewed that, despite their poverty status, African American and Latino communities have considerable social resources to which community-wide health promotion can appeal, including strong family bonds, religious attachment, and concern about the community. The influence of these resources is exemplified by relatively low rates of adolescent drug use. Health promotion conducted regularly through local mass media could be an effective strategy to improve the health of adolescents in urban communities.

Adolescent↗
PubMed1995

Control of insulin-like growth factor-II/mannose 6-phosphate receptor gene transcription by proximal promoter elements.

The insulin-like growth factor-II/cation-independent mannose 6-phosphate receptor (IGF-II/MPR) is a multifunctional protein that binds IGF-II and ligands containing a mannose 6-phosphate recognition marker. Recent studies have shown that this receptor plays a critical role in mammalian development, and that its expression is controlled by both epigenetic and tissue-specific factors. Our laboratory has cloned the 93-kilobase mouse gene and characterized its 48 exons. In this report we describe the structure and function of the IGF-II/MPR gene promoter. To study promoter function, a series of chimeric plasmids linking different segments of IGF-II/MPR 5' flanking DNA to the reporter gene, firefly luciferase, were transiently transfected into HepG2 and C3H 10T1/2 cells. Promoter activity was orientation-specific and was maximal (550- to 4250-fold above promoterless control) with a plasmid containing 266 base pairs (bp) of IGF-II/MPR DNA. The fusion gene accurately directed transcription as measured by ribonuclease protection assay using RNA extracted from transfected cells. DNA-protein binding studies by in vitro DNase I footprinting revealed an extended 54-bp footprint within the proximal promoter that contained two E-boxes and potential binding sites for transcription factors Sp1, NGF-IA, and related proteins. Gel mobility shift experiments with double-stranded oligonucleotides containing this region gave rise to several specific DNA-protein complexes, and the addition of specific antibodies indicated that proteins antigenically related to Sp1 and c-Myc were components of one or more of these bands. Deletion of this 54-bp segment led to an 8-fold decline in promoter activity, and its transfer to a heterologous promoter stimulated gene expression by nearly 7-fold. Mutational analyses indicated that each E box contributed to more than half of the enhancer's activity. These results define a strong minimal IGF-II/MPR promoter of no more than 266 bp and identify a 54-bp enhancer within this promoter fragment. Our observations thus represent a first step toward characterizing the developmental, epigenetic, and tissue-specific factors that control IGF-II/MPR gene expression.

Amino Acid Sequence↗
PubMed1995

Cardiac hypertrophy-related gene expression in spontaneously hypertensive rats: crucial role of angiotensin AT1 receptor.

Angiotensin converting-enzyme inhibitors (alacepril and imidapril) or an AT1-receptor antagonist (SC-52458) was administered to 10-week-old spontaneously hypertensive rats (SHR) for 7 days, and cardiac mRNA levels for contractile proteins and atrial natriuretic polypeptide (ANP) were comprehensively measured. The expression of skeletal alpha-actin and ANP was selectively enhanced in the heart of vehicle-treated SHR compared with Wistar-Kyoto rats (WKY), thereby suggesting that the phenotypic modulation of myocytes occurred at the early stage of hypertension. The above-mentioned three drugs similarly suppressed these enhanced gene expressions, nearly to the control levels. In contrast, although the treatment with hydralazine lowered the blood pressure of SHR similarly, hydralazine did not suppress ANP expression at all and only partially suppressed skeletal alpha-actin. Moreover, alacepril did not affect these gene expressions in WKY. Thus, AT1 receptor may be crucial for phenotypic modulation in the heart of SHR.

Angiotensin Receptor Antagonists↗
PubMed1995

Combined pyridostigmine-thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men.

Pyridostigmine (PST), a cholinesterase inhibitor, induces a clear growth hormone (GH) release in man by suppression of hypothalamic somatostatin (SRIH). Somatostatin suppresses thyrotrophin (TSH) release in rats and men. Earlier studies showed that the thryotrophin-releasing hormone (TRH)-induced TSH response was not altered by 60-120 mg of PST. We studied whether a larger dose (180 mg) of PST can increase the TSH response to TRH. Six healthy young men were studied with the following six tests: (Test 1) 200 micrograms of TRH i.v.; (Test 2) 180 mg of PST po; (Test 3) three different doses of PST (60, 120, 180 mg) + TRH; (Test 4) 100 micrograms of octreotide (SMS) i.v.; (Test 5) SMS + TRH; (Test 6) PST + SMS + TRH. A large dose of PST (180 mg) significantly augmented GH, TSH and prolactin responses to TRH, while smaller doses of PST (60 and 120 mg) did not significantly increase the responses of GH and TSH. While the increased TRH-induced prolactin response by PST was not suppressed by SMS, the increased responses of GH and TSH were suppressed remarkably by SMS. Most of the subjects noticed a mild to moderate abdominal pain, nausea and muscular fasciculation after the administration of a large dose of PST administration. These data suggest that suppression of hypothalamic SRIH secretion by 180 mg of PST can augment the TSH response to TRH. However, the considerable side effects should be minimized before clinical application of the combined PST-TRH test.

Adult↗
PubMed1995

Benefit-cost analysis of drug abuse prevention programs: a macroscopic approach.

To date, benefit-cost analysis has rarely been used to justify the drug abuse prevention field. However, there is an increasing demand for this type of analysis as the field of substance abuse prevention enters a new phase--a phase characterized by a competitive marketplace, an increased demand for accountability, and the desire to measure return on the money invested in prevention. In response, an effort is made to stimulate discussion and further research on the topic. This article first determines the overall strategy for initiating benefit-cost analysis (BCA), followed by definitions of BCA and cost-effectiveness analysis (CEA). This is followed by the determination of some of the major variables used in BCA along with the algorithm for determining the benefit-cost efficiency ratio (R) as it applies to the macro level analysis. In estimating a value for the R, a decision has been made to incorporate uncertainty into the BCA. In a macroscopic approach to BCA, four independent variables are identified for computing R. These independent and dependent variables are assumed to be random variables with normal distributions. The population means and standard deviations pertaining to these independent variables are estimated from the existing literature. In order to incorporate uncertainty into the computation of R, ten measurements have been randomly selected for each of the four independent variables. Following this procedure, fifteen benefit-cost efficiency ratios are calculated by selecting one of the ten values at random per variable used in the R equation. In this way, we were able to determine the most likely population benefit-cost efficiency ratio of 15:1, indicating that there is a $15 savings on every dollar spent on drug abuse prevention. The 95 percent confidence level pertaining to the R has an interval from $13.7 to $16.1. This indicates that the population R resides within the range 95 percent of the time.

Confidence Intervals↗
PubMed1995

Intracerebral infusion of thrombin as a cause of brain edema.

Purified thrombin from an exogenous source is a hemostatic agent commonly used in neurosurgical procedures. The toxicity of thrombin in the brain, however, has not been examined. This study was performed to assess the effect of thrombin on brain parenchyma, using the formation of brain edema as an indicator of injury. Ten microliters of test solution was infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later, and the extent of brain edema and ion content were measured. Concentrations of human thrombin as low as 1 U/microliter resulted in a significant increase in brain water content. Rats receiving 10 U/microliters had a mortality rate of 33% compared to no mortality in the groups receiving smaller doses. Thrombin-induced brain edema was inhibited by a specific and potent thrombin inhibitor, hirudin. A medical grade of bovine thrombin commonly used in surgery also caused brain edema when injected at a concentration of 2 U/microliters. Edema formation was prevented by another highly specific thrombin inhibitor, N alpha-(2-Naphthalenesulfonylglycyl)-4-DL-phenylalaninepiperidid e (alpha-NAPAP). Thrombin-induced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Changes in brain ions were inhibited by both hirudin and alpha-NAPAP, corresponding to the inhibition of brain water accumulation. This study shows that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/microliter, an amount within the range of concentrations used for topical hemostasis in neurosurgery.

Animals↗
PubMed1995

Angiotensin II type I receptor antagonist inhibits the gene expression of transforming growth factor-beta 1 and extracellular matrix in cardiac and vascular tissues of hypertensive rats.

TCV-116 [(+/-)-(cyclohexyloxycarbony-loxy)ethyl2-ethoxy-1-[[2' -(1H- tetrazol-5-yl)biphenyl-4-yl]methyl]-1H-benzimidazole-7-carboxylate ], a nonpeptide selective angiotensin II type I receptor (AT1 receptor) antagonist, at the dose of 0.1, 1 or 10 mg kg-1 day-1, was orally given to 22-week-old stroke-prone spontaneously hypertensive rats (SHRSP) for 10 weeks (from the age of 22-32 weeks) to examine the effects on gene expression of transforming growth factor-beta 1 (TGF-beta 1) and extracellular matrix proteins in the heart and blood vessels. Tissue messenger RNA (mRNA) was measured by northern blot analysis, with a specific complementary DNA probe. In the heart, left ventricular mRNA levels for fibronectin; types I, III and IV collagen; and laminin were significantly higher in SHRSP than control Wistar-Kyoto rats. In the mesenteric artery and aorta of SHRSP, TGF-beta 1 mRNA and the mentioned extracellular matrix protein mRNAs were increased compared with Wistar-Kyoto rats. Thus, the expression of various genes was up-regulated in cardiovascular tissues of SHRSP. Treatment of SHRSP with TCV-116 suppressed the gene expression of the mentioned extracellular matrix proteins and TGF-beta 1 in both heart and blood vessels in a dose-dependent fashion. Furthermore, TCV-116 regressed cardiac hypertrophy and lessened the medial hypertrophy of the aorta in SHRSP. These results show that angiotensin AT1 receptor antagonist in vivo can inhibit the gene expression of TGF-beta 1 and extracellular matrix proteins in hypertensive cardiovascular tissues. These effects may contribute to the beneficial effects of AT1 receptor antagonist on hypertensive cardiac hypertrophy and vascular thickening.

Angiotensin II↗
PubMed1995

Characterization of 5-lipoxygenase inhibitors in biochemical and functional in vivo assays.

Several potent and selective inhibitors of 5-lipoxygenase (5-LO) have been recently developed with excellent activity in certain in vivo assays of leukotriene production. The efficacy of three such inhibitors that have been in clinical trials (zileuton, A-78773 and ZD2138) were evaluated in: 1) ex vivo whole blood assay, 2) dermal Arthus reaction, and 3) functional airway response. In addition, a model of eicosanoid production in rat lung was developed that provides a simple assay for evaluation of the biochemical efficacy of 5-LO inhibitors in the lung. Bronchoalveolar lavage of rat lung with calcium ionophore A23187 resulted in rapid and robust production of PGE2, 6-keto-PGF1 alpha, thromboxane (TxB2), and leukotriene B4 (LTB4). Supplementation of lavage fluid with archidonic acid markedly augmented production of all eicosanoids except LTB4. All three inhibitors were potent and selective blockers of LTB4 production in the ex vivo whole blood assay and in the dermal Arthus reaction. In contrast, higher doses of inhibitor were needed to block LTB4 production in the rat lung lavage model than were needed to block ex vivo whole blood LTB4 production when both end points were measured in the same animal. Similarly, zileuton and A-78733 were less effective in suppressing the functional airway response to antigen in sensitized guinea pigs, whereas both inhibitors were effective in suppressing LTB4 production in the ex vivo whole blood assay. These results demonstrate that different 5-LO inhibitors have markedly distinct efficacy for inhibition of leukotriene production, depending on the animal model.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Measurement of pulpal blood flow in humans using laser Doppler flowmetry: a technique allowing stability and repeatability of pulpal blood flow measurement during surgical manipulations.

This study was undertaken to validate the repeatability of pulpal blood flow in human teeth with the laser Doppler flowmetry technique using a repeatable method of attachment of the laser Doppler probe. The variation in laser Doppler flowmetry measurements was evaluated over time periods that ranged from hours to days. In a prospective study, the pulpal blood flow was recorded from a maxillary central incisor (randomly selected) at a site directly gingival to the orthodontic bracket of three subjects. Measurements were made eight times over a 2-week period and every 30 minutes over 4 hours for eight recordings. The results indicated that there was only a slight difference between the temporal variability of the laser Doppler measurements over the course of 4 hours (intraday variability) or 2 weeks (interday variability). Furthermore, it appeared that subjects varied in their mean value recordings and may have varied widely in their respective signal-to-noise ratios.

Adult↗
PubMed1994

Topological studies of spinach 22 kDa protein of Photosystem II.

An intrinsic 22 kDa polypeptide is associated with the O2-evolving Photosystem II core complex in a variety of green plants, although it does not appear to be required for O2 evolution. Digestion of thylakoid membranes and isolated Photosystem II preparations with trypsin, followed by immunoblotting using spinach anti-22 kDa antibodies, leads to two observations: (1) the domain between the 2nd and 3rd transmembrane helices of the 22 kDa protein is stromally exposed, and (2) only in a reaction center complex preparation, lacking the chlorophyll a/b-light harvesting complex II, is there extensive proteolytic cleavage of the 22 kDa protein. We also found that after, but not prior to, selective extraction of the 22 and 10 kDa proteins from Photosystem II membranes, the chlorophyll a/b-light harvesting complex II can be separated from the Photosystem II reaction center core by precipitation with MgCl2. This result suggests that the 22 kDa polypeptide is located between the Photosystem II reaction center polypeptides and light-harvesting complex II; it is possible that the protein serves as a link between the two protein complexes. The presence of the 22 kDa protein in several species was also examined by immunoblotting with polyclonal spinach anti-22 kDa antibodies.

Amino Acid Sequence↗