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Biomedical subjects

S Kim

Publications and source records attributed to S Kim.

At least 469 records · Page 26Linked to original sources
PubMed2000

Association of coronary risk factors and endothelium-dependent flow-mediated dilatation of the brachial artery.

Impaired endothelial function has been reported to be the initial step in atherosclerosis. Some coronary risk factors independently relate to impaired endothelial function. However, few studies have examined the association between coronary risk factors and endothelial function in patients who have multiple risk factors without clinical atherosclerosis. This study was undertaken to elucidate the relationship between accumulation of coronary risk factors and vascular endothelial dysfunction. We examined 101 subjects with one or more coronary risk factors 56.8 +/- 1.0 years old and 40 age-matched control subjects without coronary risk factors. We measured brachial artery diameter non-invasively using a 7.5-MHz ultrasound machine at rest, during reactive hyperemia caused by endothelium-dependent vasodilatation, and after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. The percentage change in flow-mediated diameter (%FMD; deltaD/D x 100), in subjects with one or more coronary risk factors was significantly lower than that in control subjects(4.8 +/- 0.3% vs. 6.7 +/- 0.5%, p < 0.01). Endothelium-independent vasodilatation by nitroglycerin did not differ between the two groups. Endothelial function was impaired according to the accumulation of coronary risk factors. On multiple regression analysis, the number of risk factors, age, and brachial artery diameter at rest showed significant correlation with %FMD. Our results suggest that an accumulation of coronary risk factors was significantly related to impairment of endothelial function.

Arteriosclerosis↗
PubMed2000

Pericardial constriction due to malignant lymphoma.

We experienced a case of T-cell lymphoma demonstrating diastolic heart failure as an initial manifestation. An 81-year-old Japanese male was admitted to the University of Tokyo Hospital because of progressive dyspnea and general fatigue. Clinical presentation was congestive heart failure and cervical lymphadenopathy. Right heart catheterization revealed "dip and plateau" waveforms in right ventricular pressure, which suggested a constrictive nature of heart failure. Gallium scintigram showed marked uptake in the heart. Biopsy from a cervical lymph node confirmed the diagnosis of malignant lymphoma of T-cell origin. Diastolic heart failure remained after successful chemotherapy. Autopsy revealed pericarditis with severe adhesion of the pericardium and the epicardium.

Aged↗
PubMed2000

Prevention validation and accounting platform: a framework for establishing accountability and performance measures of substance abuse prevention programs.

The field of substance abuse prevention has neither an overarching conceptual framework nor a set of shared terminologies for establishing the accountability and performance outcome measures of substance abuse prevention services rendered. Hence, there is a wide gap between what we currently have as data on one hand and information that are required to meet the performance goals and accountability measures set by the Government Performance and Results Act of 1993 on the other. The task before us is: How can we establish the accountability and performance measures of substance abuse prevention programs and transform the field of prevention into prevention science? The intent of this volume is to serve that purpose and accelerate the processes of this transformation by identifying the requisite components of the transformation (i.e., theory, methodology, convention on terms, and data) and by introducing an open forum called, Prevention Validation and Accounting (PREVA) Platform. The entire PREVA Platform (for short, the Platform) is designed as an analytic framework, which is formulated by a collectivity of common concepts, terminologies, accounting units, protocols for counting the units, data elements, and operationalizations of various constructs, and other summary measures intended to bring about an efficient and effective measurement of process input, program capacity, process output, performance outcome, and societal impact of substance abuse prevention programs. The measurement units and summary data elements are designed to be measured across time and across jurisdictions, i.e., from local to regional to state to national levels. In the Platform, the process input is captured by two dimensions of time and capital. Time is conceptualized in terms of service delivery time and time spent for research and development. Capital is measured by the monies expended for the delivery of program activities during a fiscal or reporting period. Program capacity is captured by fourteen measurement units, tapping into the dimensions of staff resources and community assets. Staff resources are, in turn, operationalized in terms of staff size, staff certification status, staff turnover rate, and the accreditation status of a provider agency. Community assets are operationalized by the number of community centers accessible to the funded agency, number of formalized teams or antidrug coalitions active in the catchment area, and other social/human services providers with whom the prevention agency has formalized networks. The totality of process output from all sources of program activities is reduced to eighteen classes of measures. These are operationalized by thirty-three summary measures. Some of these include: total count of events facilitated; total number of clients served; average number of clients served per event; clients served by single and multiple program sessions; classification of target population in terms of the severity of risk as defined by the Institute of Medicine; age groups and race/ethnicity of clients served; number of program participants retained by recurring programs; number of clients who have completed the program; penetration rates to the target population; client attrition rates; average referral rates per provider per time interval; referral success rates; and so on. All process output measures specified in the Platform are derived from two broad classes of events classified as either products or services. The collectivity of these measures is expected to present a cost-effective, parsimonious, yet comprehensive picture of the entire spectrum of the process output, i.e., "what came out of the program as program activities". For the measurement of performance outcomes, two types of data are incorporated into the Platform: outcome data from individuals and the behavior (or performance) of social indicators from aggregated data bases. Individual data are used to evaluate the outcome of substance abuse programs

Accounting↗
PubMed2000

Zinc as a paracrine effector in pancreatic islet cell death.

Because of a huge amount of Zn2+ in secretory granules of pancreatic islet beta-cells, Zn2+ released in certain conditions might affect the function or survival of islet cells. We studied potential paracrine effects of endogenous Zn2+ on beta-cell death. Zn2+ induced insulinoma/islet cell death in a dose-dependent manner. Chelation of released endogenous Zn2+ by CaEDTA significantly decreased streptozotocin (STZ)-induced islet cell death in an in vitro culture system simulating in vivo circumstances but not in the conventional culture system. Zn2+ chelation in vivo by continuous CaEDTA infusion significantly decreased the incidence of diabetes after STZ administration. N-(6-methoxy-quinolyl)-para-toluene-sulfonamide staining revealed that Zn2+ was densely deposited in degenerating islet cells 24 h after STZ treatment, which was decreased by CaEDTA infusion. We show here that Zn2+ is not a passive element for insulin storage but an active participant in islet cell death in certain conditions, which in time might contribute to the development of diabetes in aged people.

Biological Transport↗
PubMed2000

Aminoguanidine-induced amelioration of autoimmune encephalomyelitis is mediated by reduced expression of inducible nitric oxide synthase in the spinal cord.

To elucidate whether an inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AMG), affects the expression of iNOS in the spinal cords of rats with experimental autoimmune encephalomyelitis (EAE), we induced EAE in Lewis rats, and treated EAE rats with AMG. AMG (200mg/kg administered intraperitoneally from day 0 to day 7 post-immunization) significantly reduced the clinical severity of EAE paralysis. AMG, however did not prevent the occurrence of EAE. Western blot analysis showed that iNOS expression was significantly reduced in the spinal cords of rats with EAE treated with AMG compared with rats treated with the vehicle. This finding supports the conclusion that the production of nitric oxide by iNOS plays an important role in the induction of EAE. The corollary is that the amelioration of EAE paralysis by the treatment with AMG is associated with the suppression of iNOS expression in the target organ i.e. the spinal cord.

Animals↗
PubMed2000

Aging affects the association between endothelial nitric oxide synthase gene polymorphism and acute myocardial infarction in the Korean male population.

OBJECTIVES: The aging process affects responsiveness and other functions of endothelium and vascular smooth muscle cells, predisposing the old vessels to the development of atherosclerotic lesions. Endothelial nitric oxide synthase (ecNOS) gene polymorphisms were shown to affect the occurrence of acute myocardial infarction (AMI). We hypothesized that aging may affect the association between the ecNOS gene polymorphism and AMI. METHODS: We investigated the age-related distribution of the ecNOS gene a/b polymorphism in 121 male AMI patients and 206 age-matched healthy male controls. RESULTS: The aa, ab and bb genotypes were found in 1, 49 and 156 cases among the control subjects and 5, 23 and 93 cases among the AMI patients, respectively. There was a significant correlation between the ecNOS polymorphism and AMI (p = 0.045). When the correlation was analyzed by age, the significance remained only in the group below the age of 51 (p = 0.009). The proportion of smokers was increased in the young patients when compared to the old patients (p = 0.033), indicating that smoking also has greater effect on the younger population. The incidences of hypertension and diabetes mellitus, however, were similar in both populations. CONCLUSION: Our work provides the first evidence that links ecNOS polymorphism to the risk of AMI in relation to age. Young persons who smoke or have ecNOSaa genotype may have an increased risk of developing AMI. The functional as well as structural changes associated with aging in the vascular endothelium may mask the effect of the ecNOS polymorphism in the development of AMI in old persons.

Adult↗
PubMed2000

Fluorosis risks to resident hispid cotton rats on land-treatment facilities for petrochemical wastes.

Land-treatment of petroleum wastes is a widely used industrial practice, yet there has been no comprehensive evaluation of the long-term risks to human or terrestrial ecosystems from such practices. We evaluated cotton rat (Sigmodon hispidus) populations on three sites in Oklahoma (USA) that historically used land-treatment for disposal of various petroleum wastes (July 1995-March 1997). Average concentrations of fluoride in soil from these sites ranged from 878 to 4317 mg/kg. A census of resident cotton rats on land-treatment sites revealed a high incidence (40% overall) of dental lesions compared to reference populations (<1% dental lesions). During winter there was a 34% to 65% increase compared to summer in frequency of dental lesions in cotton rats on two of the three land-treatment sites. Incidence of dental lesions on two land-treatment sites was greater (9-16%) in female cotton rats compared to males. Cotton rats from land-treatment sites had higher concentrations of fluoride in bone and greater severity of dental lesions compared to reference animals. Dental lesions were considered to be most consistent with dental fluorosis because of elevated fluoride in bone. Neither concentration of fluoride in soil nor level of fluoride in bone was a good predictor of severity of dental lesions in cotton rats on land-treatment sites.

Animals↗
PubMed2000

Involvement of calpains in the destabilization of the acetylcholine receptor clusters in rat myotubes.

The effects of calpain inhibitors on the total number of acetylcholine receptors (AChRs) on cultured rat myotubes and on the stability of AChR clusters in these myotubes were investigated. The degradation rate of total AChRs labeled with (125)I-alpha-bungarotoxin was assessed from radioactivity remaining in the myotubes as a function of time. Treatment with calpain inhibitors resulted in a two- to three-fold increase in the half-life of total AChRs. Incubation with these inhibitors produced 40% increases in intracellular AChRs but no major changes in surface AChRs, indicating that the increased AChR half-life is due to intracellular accumulation. The rate loss of AChRs from the clusters was assessed by measuring the loss of fluorescence intensity in rhodaminated-alpha-bungarotoxin-labeled clusters with time. Treatment with calpain inhibitors resulted in twofold increases in cluster half-life. Thus, there was generally no change in total surface receptors with the calpain inhibitors, whereas cluster half-life was substantially increased. Furthermore, with a low dose of calpeptin there was no change in turnover of total cellular AChRs, whereas cluster half-life was doubled. Taken together, these results suggest that the increased half-life of clusters produced by the calpain inhibitors may be due to retardation of the lateral movement from AChRs in the clusters.

Animals↗
PubMed2000

Molecular and cellular mechanisms of angiotensin II-mediated cardiovascular and renal diseases.

A growing body of evidence supports the notion that angiotensin II (Ang II), the central product of the renin-angiotensin system, may play a central role not only in the etiology of hypertension but also in the pathophysiology of cardiovascular and renal diseases in humans. In this review, we focus on the role of Ang II in cardiovascular and renal diseases at the molecular and cellular levels and discuss up-to-date evidence concerning the in vitro and in vivo actions of Ang II and the pharmacological effects of angiotensin receptor antagonists in comparison with angiotensin-converting enzyme inhibitors. Ang II, via AT(1) receptor, directly causes cellular phenotypic changes and cell growth, regulates the gene expression of various bioactive substances (vasoactive hormones, growth factors, extracellular matrix components, cytokines, etc.), and activates multiple intracellular signaling cascades (mitogen-activated protein kinase cascades, tyrosine kinases, various transcription factors, etc.) in cardiac myocytes and fibroblasts, vascular endothelial and smooth muscle cells, and renal mesangial cells. These actions are supposed to participate in the pathophysiology of cardiac hypertrophy and remodeling, heart failure, vascular thickening, atherosclerosis, and glomerulosclerosis. Furthermore, in vivo recent evidence suggest that the activation of mitogen-activated protein kinases and activator protein-1 by Ang II may play the key role in cardiovascular and renal diseases. However, there are still unresolved questions and controversies on the mechanism of Ang II-mediated cardiovascular and renal diseases.

Angiotensin II↗
PubMed2000

Detection of Hantaan and Seoul viruses by reverse transcriptase-polymerase chain reaction (RT-PCR) and restriction fragment length polymorphism (RFLP) in renal syndrome patients with hemorrhagic fever.

BACKGROUND: Hemorrhagic fever with renal syndrome (HFRS), also called Korean hemorrhagic fever (KHF), is the most common cause of acute renal failure in the Far East. Two serotypes of hantavirus, Hantaan and Seoul viruses are known pathogens for HFRS in Korea. PURPOSE: To elucidate the diagnostic applicability for the serotype diagnosis in HFRS patients, we used nested reverse transcriptase-PCR and restriction fragment length polymorphism (nRT-PCR/RFLP) to screen 2 prototype viruses, 11 virus isolates from HFRS patients, and 69 specimens obtained from 31 HFRS patients. METHODS: The nRT-PCR was performed using primers specific for the G1 segments of the Hantaan (HF3 1140-1163, HB14 1363-1342) and Seoul (SF2 809-832, SB3 1200-1177) viruses. The initial PCR products were then further amplified using nested primers for the Hantaan (HF4 1141-1164, HB13 1360-1339) and Seoul (SF7 863-884, SB1 1165-1142 ) viruses. Amplified segments were then digested with restriction enzymes specific for either Hantaan (C1a I) or Seoul (Sac I) virus sequences. RESULTS: In all cultured viruses, the serotypes identified by nRT-PCR/RFLP were consistent with those of PRNT. nRT-PCR/RFLP results indicated the presence of Hantaan virus in 10 patients and of Seoul virus in 15 patients. In 3 patients, both Hantaan- and Seoul-specific amplified bands were visualized in serially collected samples, and in 4 patients no amplicon was detected. Among 69 specimens, 55 were positive; these positive specimens were obtained between days 3 and days 33 of illness. The positive rate was not affected by the clinical phase, day of illness, or severity of HFRS. CONCLUSIONS: nRT-PCR/RFLP is a rapid and convenient method for serotype diagnosis in most HFRS patients. It could also allow detection of genetic variation of hantavirus within the same serotype.

Adult↗
PubMed2000

Toward development of an in vitro model of methamphetamine-induced dopamine nerve terminal toxicity.

To develop an in vitro model of methamphetamine (METH)-induced dopamine (DA) neurotoxicity, striatal synaptosomes were incubated at 37 degrees C with METH for different periods of time (10-80 min), washed once, then tested for DA transporter function at 37 degrees C. METH produced time- and dose-dependent reductions in the V(max) of DA uptake, without producing any change in K(m). Incubation of synaptosomes with the DA neurotoxins 1-methyl-4-phenyl-pyridinium ion, 6-hydroxydopamine, and amphetamine under similar conditions produced comparable effects. In contrast, incubation with fenfluramine, a serotonin neurotoxin, did not. METH-induced decreases in DA uptake were selective, insofar as striatal glutamate uptake was unaffected. Various DA transporter blockers (cocaine, methylphenidate, and bupropion) afforded complete protection against METH-induced decreases in DA uptake, without producing any effect themselves. METH's effects were also temperature dependent, with greater decreases in DA uptake occurring at higher temperatures. Tests for residual drug revealed small amounts (0.1-0.2 microM) of remaining METH, but kinetic studies indicated that decreases in DA uptake were not likely to be due to METH acting as a competitive inhibitor of DA uptake. Decreases in the V(max) of DA uptake were not accompanied by decreases in B(max) of [(3)H]WIN 35,428 binding, possibly because there is no mechanism for removing damaged DA nerve endings from the in vitro preparation Collectively, these results give good support to the development of a valid in vitro model that may prove helpful for elucidating the mechanisms underlying METH-induced DA neurotoxicity.

Animals↗
PubMed2000

Detection of the cholera toxin-binding activity of kappa-casein macropeptide and optimization of its production by the response surface methodology.

The cholera toxin (CT)-binding activity of purified kappa-casein macropeptide (CMP) from bovine kappa-casein was detected. In addition, a statistical model was developed to optimize the production of CMP. CMP was prepared by chymosin hydrolysis of kappa-casein and a subsequent 3% trichloroacetic acid treatment. CMP was further fractionated in an ion-exchange column by FPLC. CT binding activity was eluted at 0.18 M NaCl and was a single 8.9 kDa peptide without tyrosine and arginine residues. The CT binding activity was rapidly lost by a carbohydrase treatment. The conditions for CMP production with chymosin were optimized by using the response surface methodology (RSM). The estimated optimum levels of the factors were as follows: reaction temperature, 38.5 degrees C; pH, 6.44; and time, 35.9 min. A validation experiment was performed in which CMP was prepared under the predicted parameters, and it was ascertained that the estimated optimum conditions gave better production of CMP than any other conditions.

Animals↗
PubMed2000

Peroxisome proliferator-activated receptor-gamma ligands inhibit choroidal neovascularization.

PURPOSE: To determine the antiangiogenic effects of peroxisome proliferator-activated receptor (PPAR)-gamma agonists on ocular cells involved in the pathogenesis of choroidal neovascularization (CNV) in vitro and on experimental laser photocoagulation-induced CNV in vivo. METHODS: PPAR-gamma expression in human retinal pigment epithelial (RPE) cells and bovine choroidal endothelial cells (CECs) was determined using an RNase protection assay and Western blot analysis. Two PPAR-gamma ligands, troglitazone (TRO) and rosiglitazone (RSG; 0.1-20 microM), were used to assess effects on RPE and CEC proliferation and migration and CEC tube formation in response to vascular endothelial growth factor (VEGF). The effects of intravitreal injection of TRO on laser photocoagulation-induced CNV lesions in rat eyes (15 experimental, 15 control, nine burns per eye) and cynomolgus monkey eyes (two experimental, two control, seven paramacular burns per eye) was assessed by fluorescein angiography and histologic evaluation. RESULTS. PPAR-gamma1 was expressed in both RPE and CEC. PPAR-gamma ligands significantly inhibited VEGF-induced migration and proliferation in both cell types and tube formation of CEC in a dose-response manner. CNV in rats was markedly inhibited by intravitreous injection of TRO (P < 0.001). Lesions showed significantly less fluorescein leakage and were histologically thinner in the TRO-treated animals. Similar findings were present in the TRO-treated lesions in two monkey eyes. The drug showed no apparent adverse effects in the adjacent retina or in control eyes. CONCLUSIONS: The inhibition of VEGF-induced choroidal angiogenesis in vitro, and CNV in vivo by PPAR-gamma ligands suggests the potential application of these agents in the large group of patients with age-related macular degeneration complicated by CNV.

Animals↗
PubMed2000

Severe necrotizing mastopathy caused by calciphylaxis alleviated by total parathyroidectomy.

Calciphylaxis is a complication caused by secondary hyperparathyroidism in patients with chronic renal failure. These patients may present with clinical findings of ischemic necrosis involving the skin and muscle resulting in subsequent gangrene and vascular calcifications. We report a rare case of necrotizing mastopathy caused by calciphylaxis in a 70-year-old female with end-stage renal disease whose symptoms resolved with a total parathyroidectomy.

Aged↗