Biomedical subjects

W S Shin

Publications and source records attributed to W S Shin.

At least 37 records · Page 2Linked to original sources

PubMed2000

In vitro activities of quinupristin/dalfopristin and eight other antimicrobial agents against 360 clinical isolates from Korea.

The emergence of multi-drug resistant gram-positive cocci such as methicillin-resistant (MR) staphylococci, vancomycin-resistant (VR) enterococci, and vancomycin-intermediate resistant S. aureus (VISA) has given new urgency to the development of new antimicrobial agents. One of these is quinupristin/dalfopristin (Q/D). We decided to determine the susceptibility of gram-positive cocci isolated at two university hospitals in Seoul to Q/D and compare the results with eight other antimicrobial agents. We investigated 120 isolates of S. aureus including 49 MRSAs and one VISA, 120 isolates of coagulase negative staphylococci (CNS), 64 E. faecalis and 56 E. faecium, including seven strains of VR E. faecium. Minimum inhibitory concentrations (MICs) and minimal bactericidal concentrations (MBCs) for several antimicrobials, including vancomycin and Q/D, were determined by broth microdilution. All S. aureus including VISA were susceptible to Q/D. Q/D MIC90 for both methicillin-susceptible S. aureus (MSSA) and MRSA was 0.25 g/mL. 49 (87.5%) of 56 E. faecium including six of seven VR E. faecium were susceptible to Q/D. E. faecalis were not susceptible to Q/D (only 1.5% susceptible), but were inhibited by ampicillin (94% susceptible) or vancomycin (95%). CNS was susceptible to Q/D (96% susceptible) and vancomycin (100% susceptible). One of 38 staphylococci and two of 17 E. faecium were tolerant to Q/D. In conclusion, Q/D showed excellent activity against all species of gram-positive cocci including MRSA, VISA, and VR E. faecium except E. faecalis, and may provide a valuable option for the treatment of infections caused by these emerging nosocomial pathogens of gram-positive cocci.

Anti-Bacterial Agents↗

PubMed2000

Coronary microangiopathy in type 2 diabetic patients: relation to glycemic control, sex, and microvascular angina rather than to coronary artery disease.

UNLABELLED: Coronary microangiopathy is a major complication in diabetics. However, the presence of independent factors in association with coronary microangiopathy in patients with non-insulin-dependent diabetes mellitus (NIDDM) or the difference in coronary microangiopathy between diabetics with coronary artery disease (CAD) and those with microvascular angina is unclear. METHODS: Nineteen patients with NIDDM and microvascular angina, 18 patients with NIDDM and CAD, and 17 age-matched control subjects were studied. Myocardial segments that were perfused by angiographically normal coronary arteries were studied. The baseline myocardial blood flow (MBF) and the MBF during dipyridamole administration were measured using PET and 13N-ammonia, after which the myocardial flow reserve (MFR) was calculated to assess coronary microangiopathy. RESULTS: The baseline MBF was comparable among NIDDM patients with microvascular angina, NIDDM patients with CAD, and control subjects. However, the MBF during dipyridamole administration was significantly lower in NIDDM patients with microvascular angina (126 +/- 42.7 mL/min/100 g) than that in either NIDDM patients with CAD (210 +/- 70.1 mL/min/100 g; P < 0.01) or control subjects (293 +/- 159 mL/min/100 g; P < 0.01), as was the MFR (NIDDM with microvascular angina, 1.90 +/- 0.73; NIDDM with CAD, 2.59 +/- 0.81 [P < 0.01]; control subjects, 3.69 +/- 1.09 [P < 0.01]). Multivariate stepwise regression analysis showed that, among the factors considered, glycemic control was independently related to the MFR (r = 0.838; P < 0.05). CONCLUSION: Glycemic control appears to be essential for coronary microangiopathy in NIDDM.

Adult↗

PubMed2000

[Mitochondrial gene mutation].

Mitochondrial DNA(mtDNA) anomaly was emerging as a cause of idiopathic cardiomyopathy in addition to sarcomeric gene mutation. Meanwhile, several point mutations and deletions in mtDNA initially recognized as major causes of mitochondrial encephalomyopathies are now clarified to share 1% cause of diabetes mellitus. These results indicate that mtDNA mutations will be a significant candidate for cardiomyopathies. Screening of cardiomyopathic patients with mtDNA point mutations revealed that there were at least several % of mtDNA anomaly (MELAS type) among them. They also showed specific findings in ultrastructures of the cardiac muscle.

Cardiomyopathies↗

PubMed2000

Necrotizing enterocolitis: experience of 27 cases from a single Korean institution.

Necrotizing enterocolitis (NEC) can involve any site in the gastrointestinal tract and is a fatal complication of immunosuppression. To characterize NEC, clinical and radiological characteristics were analyzed. A total of 27 cases of NEC were identified from January 1993 to August 1998, and medical records were reviewed. NEC was diagnosed by clinical and radiological criteria, and other mimicking conditions were excluded. Of the NEC cases, 22 (81.5%) occurred in patients with underlying hematologic malignancy. All patients complained of abdominal pain and fever at the time of inclusion. Escherichia coli was the most common pathogen identified. The most common finding by computed tomography was single-layered diffuse bowel wall thickening with variable density. Other findings were ascites, fascial thickening, pneumatosis, and mesenteric lymphadenopathy. Of the patients, 25 were treated with antimicrobials with or without recombinant hematopoietic growth factors, and 2 were treated with surgery because of perforation and profound bleeding. Among the 12 patients who died, NEC was the direct cause of death in 7 patients. In conclusion, computed tomography is an effective tool for early diagnosis of NEC. Bowel rest, broad-spectrum antimicrobials, and recombinant hematopoietic growth factors are important aspects of treatment. Surgery should be reserved for complicated cases.

Adolescent↗

PubMed1999

Strain- and age-dependent loss of sarcoglycan complex in cardiomyopathic hamster hearts and its re-expression by delta-sarcoglycan gene transfer in vivo.

The delta-sarcoglycan (SG) gene is deleted in hamsters with hereditary cardiomyopathies. Immunological analyses of heart before, but not after, the progression of cardiomyopathy (CM) revealed that the BIO 14.6 strain, a model of hypertrophic CM, heterogeneously preserved alpha- and gamma-SG with loss of beta- and delta-SG. In contrast, the TO-2 strain, a model of dilated CM, did not show either SG. Furthermore, in vivo transfer of the full length delta-SG gene to TO-2 hearts expressed all four SGs. Thus, this age- and strain-dependent features suggest a more feasible setting for TO-2 than BIO 14.6 to verify both CM progression and the efficacy of gene therapy.

Age Factors↗

PubMed1999

Precise identification of gene products in hearts after in vivo gene transfection, using Sendai virus-coated proteoliposomes.

Both efficient gene transfer and the exact identification of gene product are required for gene therapy. Gene transfection of green fluorescence protein (GFP) might be useful for the reporter. After in vivo cotransfection of GFP and beta-galactosidase (beta-Gal) genes in Sendai virus-coated proteoliposomes to rat hearts, we compared the sensitivity and specificity of three methods: GFP detection, histochemical staining (HC) of beta-Gal activity, and immunostaining (IS) of the beta-Gal protein. Fluorescence microscopy and double staining of HC and IS revealed that both GFP and IS were equally sensitive and fourfold superior to HC at the peak of gene expression. However, different from skeletal muscle, the GFP of transfected cardiomyocytes showed two demerits: the fluorescence quenching due to the intense staining of beta-Gal activity, and nonspecific autofluorescence from myocardium. Thus, specific IS would be so far the most reliable to identify the gene product in heart.

Animals↗

PubMed1999

Morphological onset and early diagnosis in apical hypertrophic cardiomyopathy: a long term analysis with nuclear magnetic resonance imaging.

OBJECTIVES: A long-term follow-up study with nuclear magnetic resonance (NMR) imaging was undertaken to detect the morphological onset and to establish the early diagnosis in apical hypertrophic cardiomyopathy (HCM). BACKGROUND: A spadelike configuration on left ventriculogram (LVG) is regarded as a diagnostic criterion for the classical apical HCM. There also exists a segmented hypertrophy at the apical level without indicating the spadelike features (a nonspade configuration). To detect the hypertrophied myocardium of the nonspade configuration, circumferential scrutiny of the apex is required. Although both configurations can be underlying causes of giant negative T waves, etiological relationship between the two is not clarified. METHODS: The criteria for the spadelike configuration defined on left ventricular short-axis NMR images were as follows: (apical maximal thickness > or = 15 mm), (apical anterior thickness over basal anterior thickness > or = 1.3) and (apical posterior thickness over basal posterior thickness > or =1.3). Thirteen patients who had predominant hypertrophy (> or = 15 mm) at the apical level without the spadelike configuration underwent NMR imaging twice before and after 54+/-10 months' follow-up. RESULTS: Apical hypertrophy that had been confined to the lateral wall in four, the anterior-lateral wall in two, and the septal-anterior wall in one developed to become circumferential hypertrophy that fulfilled the criteria for the spadelike configuration after the follow-up period. CONCLUSIONS: The spadelike configuration can begin with the nonspade configuration and therefore, both can constitute a single disease entity of apical HCM. The early diagnosis of apical HCM can be achieved by identifying the hypertrophy frequently confined to the lateral wall at the apical level.

Adult↗

PubMed1999

Application of infrequent-restriction-site PCR to clinical isolates of Acinetobacter baumannii and Serratia marcescens.

We applied infrequent-restriction-site PCR (IRS-PCR) to the investigation of an outbreak caused by 23 isolates of Acinetobacter baumannii in an intensive care unit from November 1996 to May 1997 and a pseudoepidemic caused by 16 isolates of Serratia marcescens in a delivery room from May to September 1996. In the epidemiologic investigation of the outbreak caused by A. baumannii, environmental sampling and screening of all health care workers revealed the same species from the Y piece of a mechanical ventilator and the hands of two health care personnel. IRS-PCR showed that all outbreak-related strains were genotypically identical and that three strains from surveillance cultures were also identical to the outbreak-related strains. In a pseudoepidemic caused by S. marcescens, IRS-PCR identified two different genotypes, and among them one genotype was predominant (15 of 16 [93.8%] isolates). Extensive surveillance failed to find any source of S. marcescens. Validation of the result of IRS-PCR by comparison with that of field inversion gel electrophoresis (FIGE) showed that they were completely concordant. These results suggest that IRS-PCR is comparable to FIGE for molecular epidemiologic studies. In addition, IRS-PCR was less laborious and less time-consuming than FIGE. To our knowledge, this is the first report of the application of IRS-PCR to A. baumannii and S. marcescens.

Acinetobacter↗

PubMed1999

Clinical implication of left precordial T wave inversions in the presence of complete right bundle branch block.

This study was designed to elucidate whether left precordial negative T waves are electrocardiographic indicators for the diagnosis of hypertrophic cardiomyopathy (HCM) even in the presence of complete right bundle branch block (CRBBB). In 7 consecutive patients with CRBBB accompanied by negative T waves in at least one of the left precordial leads (V4, V5, V6, maximal negativity; 1.06 +/- 0.40 mVol) (left precordial negative T wave group) and in 15 randomly selected CRBBB patients without left precordial T wave inversions (control group), echocardiography was performed to rule out underlying diseases causing left ventricular overload and to identify candidates for magnetic resonance (MR) imaging. None had anginal pain indicating ischemic heart disease. When 2-dimensional echocardiography indicated left ventricular hypertrophy with wall thickness > or = 15 mm, the magnitude and distribution of hypertrophy were scrutinized on contiguous left ventricular MR short-axis images. The diagnostic criterion of HCM was the demonstration of hypertrophy with a wall thickness of 20 mm or more on the left ventricular MR short-axis images. All patients in the left precordial negative T wave group had negative T waves in both I (negativity; 0.27 +/- 0.17 mVol) and aVL (negativity; 0.23 +/- 0.14 mVol), whereas none in the control group did. The diagnostic criterion for HCM was fulfilled in six patients in the left precordial negative T wave group. However there were no patients who fulfilled the criterion in the control group. Negative T waves were recorded in the I (negativity; 0.30 +/- 0.17 mVol), aVL (negativity; 0.25 +/- 0.14 mVol), V4 (negativity; 1.03 +/- 0.46 mVol), V5 (negativity; 0.83 +/- 0.37 mVol) and V6 leads (negativity; 0.31 +/- 0.31 mVol) in all patients with HCM, while they were recorded in only 6% of the patients without HCM. In conclusion, the existence of left precordial negative T waves in the presence of CRBBB strongly indicates HCM.

Bundle-Branch Block↗

PubMed1999

The presumptive identification of Candida albicans with germ tube induced by high temperature.

For direct identification of Candida albicans from other Candida species, the chlamydospore formation and the mycelial transition induced by high temperature and by sera were examined in 198 Candida isolates. The germ tubes of C. albicans developed early at 30 min in high temperature-induction, but at 60 min in serum-induction. C. albicans generated germ tubes well at concentrations lower than 2 x 10(7) cells/ml, but the germ tube formation was markedly restrained at concentrations higher than 4 x 10(7) cells/ml. In a serum-free, yeast extract-peptone-dextrose (YEPD) medium, C. albicans grew as a yeast form at 30 degrees C and as a mycelial form at 35-42 degrees C. Mycelial development was maximal at 37 degrees C in serum and at 39 degrees C in YEPD. Germ tubes were formed within 30 min in YEPD at 39 degrees C, but after 60 min in serum at 37 degrees C. Our examination showed that the 39 degrees C-induced germ tube formation tests were very reliable (sensitivity 100%, specificity 100%) at discerning C. albicans from other Candida species. These results suggest that the high temperature-induced germ tube formation testing could be a useful identification method of C. albicans in clinical laboratories.

Candida albicans↗

PubMed1998

A hypertensive father, but not hypertensive mother, determines blood pressure in normotensive male offspring through body mass index.

This investigation was to assess the role of genetic loading of hypertensive parents in the determination of blood pressure (BP) in their normotensive offspring. The medical check-up data from 7279 Japanese university students aged 19.22 +/- 0.01 years were analysed of which 641 students had only one hypertensive parent with or without hypertensive grandparents, and from this number 609 cases were available for the present analysis. The BP in the students having only one hypertensive parent were in the normotensive range, but was significantly higher than in those students without hypertensive relatives. Analyses of the data from the students having only one hypertensive parent revealed that systolic BP (SBP) and body mass index (BMI) were higher in the male than in the female students. In addition, there were no differences in BP and BMI between the male students with a hypertensive father and the male students having a normotensive father. However, multivariate analyses revealed that BMI was an independent predictor of SBP solely in the male students having a hypertensive father, but not in the male students having a normotensive father. Such a relationship between BMI and BP determination was not observed in the female students with one hypertensive parent. It is suggested that there are different mechanisms for the determination of BP in normotensive offspring of hypertensive parents, and genetic loading of a hypertensive father plays a critical role in the determination of BP through BMI.

Adolescent↗

PubMed1998

Measuring the diameter of coronary arteries on MR angiograms using spatial profile curves.

OBJECTIVE: The spatial profile curve of the nuclear MR intensity across the short axis of a coronary artery in an MR angiogram results in a gradual up-and-down slope lacking sharp definition, which indicates that display parameters may influence edge recognition. Therefore, our study was designed to determine the appropriate window setting and to devise a method of accurately measuring the diameter or width of the artery independent of window parameters. CONCLUSION: The diameter of a coronary artery measured on MR coronary arteriography significantly varied with experimentally selected display parameters. When compared with the diameter on contrast-enhanced coronary arteriograms, the window center on MR angiograms at the midpoint between the peak intensity of the intravascular lumen and the background intensity and the window width of a quarter or a half of the intensity difference between the two were proven to be appropriate. The angiographic diameter corresponded to the diameter obtained at 65% +/- 9% of the peak intensity on the spatial profile curve across the short-axis MR coronary angiogram. Accordingly, 65% of the peak intensity indicates the diameter of the coronary artery. Thus, the intensity profile curve independent of the window setting provided a new method for measurement of the diameter of the coronary artery.

Adult↗

PubMed1998

Vector analysis of the hemodynamics of atherogenesis in the human thoracic aorta using MR velocity mapping.

OBJECTIVE: Our study was designed to assess the applicability of MR velocity mapping for vector analysis of the hemodynamics of atherogenesis. SUBJECTS AND METHODS: MR velocity mapping was used to measure axial and nonaxial elements and the length of the wall shear rate (a spatial gradient of near-wall flow velocity parallel to the vessel wall) vector at 16 time points per cardiac cycle at eight anatomic locations of the thoracic aorta in six healthy subjects. An oscillatory shear index (a ratio of blood flow volume in the recessive direction divided by the sum of blood flow volume in both dominant and recessive directions) was introduced for analysis of the degree of oscillation. RESULTS: The time-averaged length, axial element, and nonaxial element of the wall shear rate vector were 118+/-53 sec(-1), 106+/-55 sec(-1), and 33+/-23 sec(-1), respectively. The oscillatory shear index in the axial direction was 0.06+/-0.10 and that in the nonaxial direction was 0.07+/-0.13. At the inner wall of the distal portion of the aortic arch, the length of the wall shear rate was smallest (74+/-32 sec(-1)) and oscillation in the axial direction was largest (0.16+/-0.19). CONCLUSION: Vector analysis of the wall shear rate in the thoracic aorta was successfully done with MR velocity mapping in humans. MR velocity mapping can noninvasively evaluate the hemodynamics of atherogenesis induced by the complicated blood flow.

Adult↗

PubMed1998

Molecular analysis of fluoroquinolone-resistance in Escherichia coli on the aspect of gyrase and multiple antibiotic resistance (mar) genes.

We analyzed the fluoroquinolone resistance mechanism of 28 isolates of ciprofloxacin-resistant E. coli from patients who received ciprofloxacin as a regimen of a selective gut decontamination. Isolates distinctive by infrequent restriction site polymerase chain reaction (IRS-PCR) were subjected to Hinf I restriction fragment length polymorphism analysis, single-stranded conformation polymorphism (SSCP), and nucleotide sequencing of the quinolone resistance determining region (QRDR) in gyrA. Double mutations in QRDR of gyrA (Ser83 Leu and Asp87Asn) were found from most of the strains. Nucleotide sequencing of the marR locus showed that 18 out of 28 (64%) ciprofloxacin-resistant E. coli strains had three types of base change in marR loci: a double-base change at nucleotides 1628 and 1751, or 1629 and 1751: and a single-base change at 1751. However, all the mutated strains showed no tolerance to cyclohexane test, suggesting the mutation in the marR region had no influence on overexpression of the MarA protein. In conclusion, mutation in gyrA was the main mechanism of ciporfloxacin resistance in E. coli from patients with selective gut decontamination. Therefore, mutation in the mar region did not influence the levels of ciprofloxacin resistance in our isolates.

Ciprofloxacin↗

PubMed1997

Effects of extracellular pH on receptor-mediated Ca2+ influx in A7r5 rat smooth muscle cells: involvement of two different types of channel.

1. The effects of extracellular pH (pHo) on receptor (vasopressin or endothelin-1)-mediated Ca2- entry and Ca(2+)-permeable channels were investigated in aortic smooth muscle cells (A7r5) from rat embryonic thoracic aorta. Intracellular Ca2+ ([Ca2+]i) was measured using fura-2 AM and whole-cell voltage clamp techniques were employed. 2. Vasopressin and endothelin-1 (100 nM) in the presence of nicardipine (10 microM) evoked a sustained rise in [Ca2+]i due to calcium entry. Extracellular acidosis decreased receptor (vasopressin or endothelin-1)-mediated Ca2+ entry, while extracellular alkalosis potentiated it. 3. Depletion of intracellular Ca2+ stores with thapsigargin (1 microM) also evoked Ca2+ entry activated by emptying of intracellular Ca2+ stores (capacitative Ca2+ entry). Extracellular acidosis decreased this capacitative Ca2+ entry, while extracellular alkalosis potentiated it. 4. Under voltage-clamp conditions with Ca+ internal solution, vasopressin and endothelin-1 activated non-selective cation currents (ICAT). Ba2+ or Ca2+ were also charge carriers of ICAT. Reducing the pHo inhibited ICAT, while increasing pHo potentiated it in a reversible manner. 5. Intracellular pH (pHi) changes did not cause the same marked effects as pHo changes, and a high concentration of Hepes (50 mM) in the patch pipette did not inhibit the effects of pHo on ICAT. 6. Similar results were obtained when ICAT was activated by GTP gamma S (1 mM) applied through the patch pipette, even in the absence of agonists, probably because of direct activation of GTP-binding proteins coupled to the receptors. 7. In cells treated with thapsigargin, addition of Ca2+ to the bath solution induced Ca(2+)-dependent K+ currents activated by capacitative Ca2+ entry. However, no measurable ionic currents activated by capacitative Ca2+ entry (ICRAC) were observed under conditions with Cs+ internal solution and EGTA (5 mM), although vasopressin still activated ICAT. 8. These results suggest that the contractile agonists vasopressin and endothelin-1 evoked Ca2+ entry through two different types of Ca(2+)-permeable channel (ICAT and ICRAC) and pHo affects these channels, which may modulate receptor-mediated Ca2+ influx in A7r5 cells. Thus, pH-induced changes of these channels may play a pathophysiological role in the control of receptor-mediated contractions.

Animals↗

PubMed1997

Direct action of nitric oxide on osteoblastic differentiation.

The effect of nitric oxide (NO) on osteoblastic differentiation was examined in cultured mouse osteoblasts. Interleukin-1beta and tumor necrosis factor-alpha expressed inducible NO synthase gene with little effect on constitutive NO synthase gene. These cytokines increased NO production, which was inhibited by L-NMMA pretreatment, and decreased alkaline phosphatase (AIPase) activity, which was not restored by L-NMMA. Furthermore, NO donors, sodium nitroprusside and NONOate dose-dependently elevated AIPase activity and expression of osteocalcin gene. These results suggest that NO directly facilitates osteoblastic differentiation and the cytokine-induced inhibition of AIPase activity is mediated via mechanism other than NO.

Alkaline Phosphatase↗

PubMed1997

In vivo gene transfection of human endothelial cell nitric oxide synthase in cardiomyocytes causes apoptosis-like cell death. Identification using Sendai virus-coated liposomes.

BACKGROUND: Nitric oxide (NO) has various actions on the cardiovascular system, although its pathophysiological significance in myocardial cells remains obscure. The aim of the present study was to identify direct NO actions on cardiomyocytes by gene transfection in vivo using a newly developed vector under physiological conditions. METHODS AND RESULTS: Liposomes containing the beta-galactosidase (beta-gal) gene alone or with the human endothelial cell nitric oxide synthase (ecNOS) gene were coated with UV-inactivated Sendai virus and injected into the left ventricular wall of rat heart in vivo. Histological examination confirmed that the transfection efficiency was comparable to adenovirus-mediated transfection and that the new vector per se caused no inflammation. beta-Gal expression was confined to cardiomyocytes between two intercalated discs, suggesting that the transfected gene did not permeate the discs. An immunohistochemical study showed that cotransfection of the ecNOS gene induced massive myocardial cell shrinkage in both transfected cells and the adjacent myocytes in a time- and dose-dependent manner. Histochemical findings in shrunk cells coincided with apoptosis as identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling. Electron microscopy of the lesion revealed myofibrillar degradation and accumulation of mitochondria but no apoptotic bodies. Pre-treatment with the NOS inhibitor N omega-nitro-L-arginine methyl ester abolished these morphological alterations. CONCLUSIONS: The efficient expression of the human ecNOS gene in vivo suggests that NO or its toxic metabolite caused myocardial degradation, a part of which was compatible with apoptosis of the transfected cardiomyocytes themselves and the adjacent cells as a paracrine effect. These morphological features mimicked acute myocarditis or ischemic injury.

Animals↗

PubMed1997

Esophageal aspergillosis after bone marrow transplant.

The prolonged immune suppression associated with bone marrow transplants predisposes to fungal infections including Aspergillus. Disseminated aspergillosis occurs in up to 60% of patients with invasive pulmonary aspergillosis; sites of involvement include the brain, gastrointestinal tract, kidney, liver, thyroid, heart, and spleen. There is only one report of isolated esophageal aspergillosis. A recent acute myelogenous leukemia patient had isolated esophageal aspergillosis after bone marrow transplantation which was successfully treated with amphotericin B.

Adult↗