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Biomedical subjects

Y S Yoon

Publications and source records attributed to Y S Yoon.

At least 19 recordsLinked to original sources

The new definition of metabolic syndrome by the international diabetes federation is less likely to identify metabolically abnormal but non-obese individuals than the definition by the revised national cholesterol education program: the Korea NHANES study.

OBJECTIVE: The new definitions for metabolic syndrome (MS) proposed by the IDF and revised NCEP have caused some confusion because patients have emerged that have satisfied the revised NCEP but not the IDF criteria. We performed this study to compare the prevalence of these criteria and to investigate the characteristics of discrepant cases. RESEARCH DESIGN AND METHODS: A total of 7962 individuals aged >or= 20 years (3597 men; 4365 women) who participated in the 1998 Korean NHANES were included. We assessed the agreement between the revised NCEP and IDF criteria and investigated the characteristics of cases satisfying the revised NCEP criteria but not the IDF criteria. RESULTS: The prevalence of MS by the revised NCEP (25.7% of men and 31.9% of women) was higher than that according to the IDF (14.2% of men and 26.6% of women). The IDF criteria failed to identify 44.9% of men and 16.6% of women identified as having MS according to the revised NCEP criteria. The discrepant group showed more adverse metabolic profiles and unfavorable lifestyles despite lower waist circumference as compared with those having MS by both the IDF and revised NCEP criteria. The prevalence of discrepant cases was higher among the elderly. CONCLUSIONS: The IDF criteria were inferior to the revised NCEP criteria in identifying the metabolically abnormal but nonobese groups known to be predisposed to type 2 diabetes and cardiovascular disease. Further research regarding the appropriateness of central obesity as an obligatory criterion proposed by the IDF seems to be warranted.

Adult↗

Impact of fluoroquinolones on the diagnosis of pulmonary tuberculosis initially treated as bacterial pneumonia.

OBJECTIVE: The excellent in vitro activity of fluoroquinolones against Mycobacterium tuberculosis has raised concerns about the delayed diagnosis of pulmonary tuberculosis (PTB) initially misdiagnosed as pneumonia. The aim of this study was to assess the effect of empiric fluoroquinolone therapy on delays in diagnosis in patients with PTB initially misdiagnosed as bacterial pneumonia. DESIGN: Patients with PTB initially treated as having community-acquired pneumonia and treated with fluoroquinolones for more than 5 consecutive days, from January 2000 to December 2004, were enrolled. As a control group, TB patients initially treated with nonfluoroquinolone antibiotics were enrolled. We reviewed the clinical data and compared treatment responses between the two groups. RESULTS: Nine patients in the fluoroquinolone group and 19 patients in the non-fluoroquinolone group were enrolled. In the fluoroquinolone group, eight patients (89%) improved clinically or radiographically, whereas only eight patients (42%) in the non-fluoroquinolone group improved (P = 0.04). The delay in initiation of anti-tuberculosis medication was longer in the fluoroquinolone group than in the non-fluoroquinolone group (43.1 - 40.0 vs. 18.7 +/- 16.9 days, P = 0.04). CONCLUSION: Delay in the initiation of anti-tuberculosis treatment is possible in patients administered fluoroquinolone and initially misdiagnosed as having bacterial pneumonia.

Adult↗

Bone temperature estimation during orthopaedic round bur milling operations.

Heat generation during orthopaedic bone cutting operations may cause thermal bone damage. During the bone cutting, the maximum temperature occurs at the point of contact between the bone and the cutting tool. However, this temperature is difficult to measure. Many researchers have attempted to measure this temperature using a thermocouple; however, limitations of the thermocouple makes it difficult to determine the maximum temperature at the point of contact. In order to solve this problem, in this study, two infrared thermometers are used to measure the fresh-milled surface temperature, and the maximum temperature was extrapolated by a moving plane heat source solution. The estimated maximum temperature increment varied from 49 to 115 degrees C under various cutting conditions. These results showed that the thermal damage may reach up to 1.9 mm in depth during round bur milling. A larger feed rate and a smaller cutting depth decreased the maximum temperature.

Animals↗

Galanin-immunoreactive cells and their relation to calcitonin gene-related peptide-, substance P- and somatostatin-immunoreactive cells in rat lumbar dorsal root ganglia.

We report upon the distribution of galanin-immunoreactive (GAL-IR) cells in the lumbar dorsal root ganglia (DRG) of the rat, and upon the distribution of GAL-IR cells, which also contain calcitonin gene-related peptide (CGRP)-, substance P (SP)- and somatostatin (SOM)-immunoreactivity. Neuropeptide-immunoreactive lumbar DRG cells were 55.8% for CGRP, 12.7% for SP, and 6.5% for GAL in lumbar DRG cells. There was no significant difference between the right and left DRGs (L1-L6) for any neuropeptide-immunoreactive cell (P < 0.01). In terms of size distribution, CGRP-immunoreactive cells were identified below 1500 microm2, and SP-, and GAL-IR cells below 600 microm2. Neuropeptide immunoreactive cells showed various immunoreactivities in the cytoplasm according to each neuropeptide. CGRP and SP immunoreactive cells were colocalized with GAL immunoreactive cells in the serial sections about 83.3 and 60% respectively, but SOM colocalizing with GAL-IR cells were not in evidence. The current results confirm and extend previous results, and show that neuropeptides can coexist in single sensory neurones of the rat DRG. In addition, our results demonstrate that the normal distribution of some neurotransmitters modulating sensory action in Wistar Kyoto rat, make this model more prone to develop neuropathic pain than Sprague-Dawley rat.

Animals↗

Systematic methodology for the design of a flexible keel for energy-storing prosthetic feet.

An effective design method is suggested for a flexible keel design for energy-storing prosthetic feet (ESPF). The basic, two-dimensional shape of the keel is based on anthropometric data and normal gait analysis available in the literature. Cost function is defined for the performance evaluation of the keel. Five factors and five levels of their effect on the performance of the keel are established. By use of an orthogonal array table, 25 trials of dynamic simulations of prosthetic walking are designed, from among 3,125 possible combinations, dramatically reducing the number of total simulations needed to examine sufficiently the contribution of each factor to cost function. A prosthetic walking model is built, and a dynamic simulation of prosthetic walking is performed using the finite element method. The contribution of each factor to cost function is investigated by an analysis of variance (ANOVA), and the average main effects of factors for cost function are calculated. The optimum combination of factor levels is obtained by minimisation of cost function. To examine the structural safety of the keel, the deformation and stress distribution of the keel are investigated by static analysis, and failure indices are calculated by three failure criteria. Finally, the optimum flexible keel is designed with increased energy storage capacity, without failure, and suitable for more active prosthetic walking; the recoverable strain energy stored in the optimum ESPF keel is 25.8J.

Analysis of Variance↗

Age-related change of neuropeptide Y-immunoreactive neurons in the rat anterior olfactory nucleus.

Neuropeptide Y (NPY) is located in the olfactory system, including the olfactory bulb, and is thought to be one of the main neurotransmitters for olfaction. Thus, we examined age-related changes of NPY-immunoreactive (IR) neurons in the rat anterior olfactory nucleus (AON) at various aging stages over a period of 2 years; postnatal months 1 (PM 1), PM 6, PM 12 and PM 24. NPY-IR neurons in the AON were present in the lateral and medial subdivisions at PM 1 and at PM 6 were distributed in all subdivisions of the AON. Prior to PM 12, the NPY-IR neurons showed a tendency to change from bipolar cells with short processes into multipolar cells with long processes. Moreover, the population of NPY-IR neurons and nerve fibers in the AON increased in proportion to age. In particular, the number of NPY-IR neurons increased about 6-fold between PM 1 and PM 3. At PM 24, the number of NPY-IR neurons was much smaller than that at PM 12 and somal size had decreased. It is therefore suggested that the dramatic increase in the number and size of the NPY-IR neurons between PM 1 and PM 3 may be associated with sexual maturation and that the decrease in the number and cell size of the NPY-IR neurons at PM 24 may underlie age-related changes in the olfactory process.

Aging↗

Carotid artery stenting in patients with symptomatic coronary artery disease.

Carotid artery stenting has been accepted as a potential alternative to carotid endarterectomy in patients with significant carotid artery stenosis. The objective of this study was to evaluate the feasibility, safety and long-term outcome of percutaneous stenting of carotid artery stenosis in patients with coexisting symptomatic coronary disease. Between May 1996 and May 1999, we performed carotid artery stenting at 48 lesions in 36 patients with carotid stenosis of 60% and symptomatic coronary artery stenosis. Twenty-one patients (58%) had neurologic symptoms. Carotid stenting was performed in 43 internal, 2 external and 3 common carotid lesions. We used Wallstent in 46 lesions, Palmaz stent in 2 lesions and Microstent II in 1 lesion. Staged or combined coronary intervention was performed in 18 patients (50%) and staged coronary artery bypass surgery was performed in 6 patients (17%). In the other 12 patients (33%), medical treatments were performed. Carotid stenting was successful in all lesions. Simultaneous bilateral carotid stenting was performed in 11 patients (31%). One major and 1 minor stroke developed during the procedure. There were no deaths during the procedures and within 30 days post-procedure. During the follow-up of 14 +/- 7 (3 to 40) months, there were no deaths or neurological events. On follow-up (6 +/- 1 months) angiography and/or duplex sonography of 44 eligible lesions in 32 patients, there were 2 cases of asymptomatic restenosis (4.5%) which developed in Palmaz stents implanted at the external carotid artery and the common carotid artery, respectively. In conclusion, carotid artery stenting in patients with coexistent carotid and coronary artery disease is feasible, safe and shows favorable follow-up outcomes.

Aged↗

Transseptal approach for stent implantation in right internal carotid artery stenosis.

Carotid artery stenting is emerging as an effective measure to prevent strokes in patients with significant carotid artery stenosis. We report a case of right internal carotid artery stenosis in which we used a transseptal approach for successful carotid artery stenting. This patient had concomitant stenosis at all three coronary arteries, including the left main coronary artery. A transseptal approach was adopted due to the sharply angled take-off of the right brachiocephalic artery from the tortuous aortic arch, where advancement of an extra-stiff wire into the right common carotid artery was not possible by a femoral artery approach.

Aged↗

Morphological structure of accessory spleen in Chinese hamsters.

To attempt a rigorous definition of the structure of the accessory spleen (AS) in the Chinese hamster, we examined twenty-one animals, and found AS in 5 animals (23.8%), which were over 7-month-old. The AS had no connection with the main spleen and was seen as a dark red oval organ (0.7 mm x 1.5 mm), which was embedded in the adipose tissue near the tail of the pancreas. It was demarcated from the adipose tissue and some pancreatic tissue. The organ was encapsulated by thin collagenous connective tissue and smooth muscle fibers, and contained lymphatic nodules, reticular fibers, nodular central arterioles, macrophages and megakaryocytes. Notably the incidence of AS appeared to increase with age in the Chinese hamsters.

Adipose Tissue↗

Regulation of NeuroD expression by activation of the protein kinase-C pathway in Y79 human retinoblastoma cells.

To examine the signals that regulate NeuroD expression, we analyzed the effects of activation of two major signal pathways, the protein kinase A (PKA) pathway and the protein kinase C (PKC) pathway, on the expression of NeuroD in Y79human retinoblastoma cells. Activation of PKC resulted in marked induction of NeuroD mRNA and NeuroD protein. NeuroD mRNA induction was inhibited by calphostin C, an inhibitor of PKC. On the other hand, stimulation of PKA by forskolin had a weak suppressive effect on NeuroD mRNA expression. Induction of NeuroD expression was followed by enhancement of expression of the AK1 gene, one of the target genes of NeuroD, which encodes adenylate kinase isozyme 1, an important enzyme in the cellular adenine nucleotide homeostasis. Our results indicate that NeuroD expression is regulated, at least in part, by the PKC pathway and not by the PKA pathway.

Adenylate Kinase↗

Overexpression of NeuroD in PC12 cells alters morphology and enhances expression of the adenylate kinase isozyme 1 gene.

NeuroD, a basic helix-loop-helix transcription factor, plays an important role in neuronal differentiation. A rat NeuroD cDNA was obtained by the aid of reverse transcription-polymerase chain reaction (RT-PCR) and ligated to an expression vector having a CMV promoter. Transfection of the NeuroD-expression plasmid into PC12 cells, a rat pheochromocytoma cell line, induced morphological changes featured by neurite-like processes and synapse-like structures without a differentiation-inducing reagent such as NGF. In the transfected cells, the overproduced NeuroD was detected by Western blot analysis, and the expression of the gene encoding mid-sized neurofilaments, a neuron-specific marker, was demonstrated by RT-PCR. Adenylate kinase isozyme 1 (AK1) is an enzyme involved in the homeostasis of energy metabolism and appears specifically in neuronal cells during differentiation. The CAT reporter assay of the 5'-flanking region of the AK1 gene suggests that NeuroD activates the AK1 expression through E-boxes in the promoter region. RT-PCR analysis indicated the enhanced level of AK1 mRNA in NeuroD-producing PC12 cells. Electrophoretic mobility shift assays demonstrated that NeuroD was able to interact with a proximal E-box element of the AK1 promoter. The results indicated that NeuroD promoted the PC12 cells to differentiate into neuron-like cells with concomitant activation of the target genes including the AK1 and the neurofilament genes.

Adenylate Kinase↗

Effect of 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, on parvalbumin immunoreactivity after cerebral ischaemia in the hippocampus of the Mongolian gerbil.

Previous studies have demonstrated that a loss of parvalbumin-immunoreactive (PV-ir) neurones is observed in the hippocampus after transient cerebral ischaemia. However, whether the loss of parvalbumin (PV) immunoreactivity is related to the over-production of nitric oxide (NO) during cerebral ischaemia has not been evaluated. This study was designed to test the effect of 7-nitroindazole pre-treatment (7-NI, 50 mg/kg), a selective neuronal NO synthase inhibitor, on PV immunoreactivity and its cellular activity following forebrain ischaemia. PV-ir neurones in the hippocampus of the control group were widely distributed in the pyramidal cell layer and stratum oriens of CA1 and CA3, and the granular cell layer of dentate gyrus. 7-NI pre-treatment completely suppressed the reduction of PV immunoreactivity in CA1 that was observed in the ischaemia-induced group. Subsequently, 7-NI pre-treatment also protected against the structural loss of microtubule-associated protein 2 (MAP2) immunoreactivity in CA1 after ischaemic insult. In addition, the Fos-defined neuronal activity of PV-ir neurones was slightly increased by the 7-NI pre-treatment 3 h after ischaemia. Based on these data, we conclude that the neuronal toxicity of NO may be involved in the loss of PV-ir neurones after cerebral ischaemia.

Animals↗

Molecular cloning and characterization of the gene encoding human NeuroD.

NeuroD is a basic helix-loop-helix transcription factor that binds to an E-box sequence, CANNTG, in the target gene promoter region. The gene encoding NeuroD is expressed specifically in brain, intestine, and pancreatic cells and plays a pivotal role in tissue-specific differentiation. To investigate the regulation of human NeuroD gene expression, we isolated and sequenced a genomic DNA containing two exons and flanking regions of the NeuroD gene. The sizes of exons 1 and 2 were 168 and 2404 bp, respectively. CAT reporter analysis showed that the elements responsible for basal promoter activity lay in the proximal 408-bp region. Cotransfection of the CAT reporter plasmids with a NeuroD expression plasmid resulted in 5-fold enhancement of the CAT activity, indicating an autoregulatory mechanism is involved in human NeuroD gene expression.

Amino Acid Sequence↗

cDNA cloning and tissue-specific expression of the gene encoding human adenylate kinase isozyme 2.

We isolated two kinds of cDNAs encoding human adenylate kinase (AK) isozyme 2 from a HeLa cell cDNA library using bovine AK2 cDNA as a probe. Nucleotide sequencing revealed that the cDNAs encoded 239- and 232-amino acid proteins with deduced molecular mass of 26.5 (AK2A) and 25.6kDa (AK2B), respectively. Northern blot analysis demonstrated that AK2 mRNA is strongly expressed in liver, heart, skeletal muscle and pancreas, and moderately in kidney, placenta and brain, and weakly in lung. However, Western blot analysis showed that AK2 protein was present in large amounts in liver, heart, kidney, and in a small amount in lung, and undetectable in brain and skeletal muscle. These results suggested the presence of the tissue-specific gene-expression including post-transcriptional regulation in expression of the AK2 gene.

Adenylate Kinase↗

A prospective study of the accuracy of clinical examination evaluated by arthroscopy of the knee.

The diagnostic accuracy of clinical examination for internal derangement of the knee were evaluated by arthroscopy in 195 patients (200 knees). Radiographs were available and 50 patients had magnetic resonance imaging. The clinical diagnosis was correct in 104 knees (52%), incomplete in 70 (35%) and incorrect in 26 (13%). When there was a single abnormality the diagnosis was correct in 70%, but when more than 3 lesions were discovered the figure was 28%. All individual lesions were diagnosed correctly in more than 90%. The lesions most difficult to diagnose were chondral fractures, partial tears of the anterior cruciate ligament and loose bodies. Knees with acute lesions and those with a single diagnosis were significantly easier to diagnose (p < 0.01). Age, sex, MRI and the surgeon were not significant.

Adolescent↗

Modulation of protein kinase C activity in NIH 3T3 cells by plant glycosides from Panax ginseng.

The involvement of ginsenosides in the signal cascade that stimulates cellular growth was investigated. It was found that ginsenosides Rh1 and Rh2 extracted from the root of Panax ginseng inhibited cellular proliferation in NIH 3T3 fibroblasts. Both ginsenosides Rh1 and Rh2 effectively reduced phospholipase C activity resulting in a decrease in the intracellular level of diacylglycerol, an endogenous activator of protein kinase C. The treatment of cells with Rh1 or Rh2 was thus found to reduce intracellular protein kinase C activity. We also observed that the phosphorylation of myristoylated alanine-rich C kinase substrate, one of the major substrates of protein kinase C in cells, was inhibited by the ginsenosides. Data suggest that the ginsenoside Rh1 or Rh2 exerts antiproliferative effects by inhibiting phospholipase C, which produces second messengers necessary for the activation of protein kinase C.

3T3 Cells↗

Poly(ADP-ribosyl)ation of histone H1 correlates with internucleosomal DNA fragmentation during apoptosis.

The biochemical role of poly(ADP-ribosyl)ation on internucleosomal DNA fragmentation associated with apoptosis was investigated in HL 60 human premyelocytic leukemia cells. It was found that UV light and chemotherapeutic drugs including adriamycin, mitomycin C, and cisplatin increased poly(ADP-ribosyl)ation of nuclear proteins, particularly histone H1. A poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide, prevented both internucleosomal DNA fragmentation and histone H1 poly(ADP-ribosyl)ation in cells treated with the apoptosis inducers. When nuclear chromatin was made accessible to the exogenous nuclease in a permeabilized cell system, chromatin of UV-treated cells was more susceptible to micrococcal nuclease than the chromatin of control cells. Suppression of histone H1 poly(ADP-ribosyl)ation by 3-aminobenzamide reduced the micrococcal nuclease digestibility of internucleosomal chromatin in UV-treated cells. These results suggest that the poly(ADP-ribosyl)ation of histone H1 correlates with the internucleosomal DNA fragmentation during apoptosis mediated by DNA damaging agents. This suggestion is supported by the finding that xeroderma pigmentosum cells which are defective in introducing incision at the site of DNA damage, failed to induce DNA fragmentation as well as histone H1 poly(ADP-ribosyl)ation after UV irradiation. We propose that poly(ADP-ribosyl)ation of histone H1 protein in the early stage of apoptosis facilitates internucleosomal DNA fragmentation by increasing the susceptibility of chromatin to cellular endonuclease.

Adenosine Diphosphate Ribose↗

Calcium-free hemodialysis for the management of hypercalcemia.

The drug therapies for hypercalcemia of malignancy have been known to be associated with either limited efficacy or cumulative toxicity in patients with advanced renal failure. To establish the guidelines for the use of dialysis and to determine its optimal prescription for hypercalcemia, calcium-free hemodialysis was performed in 6 hypercalcemic patients with renal failure not responding enough to forced saline diuresis. Calcium-free dialysate contained sodium 135, potassium 2.5, chloride 108, magnesium 0.75, bicarbonate 30 mmol/l. Mean hemodialysis time was 160 +/- 27 min and mean Kt/V urea was 0.75 +/- 0.2. Plasma calcium concentrations fell from a mean value of 2.92 +/- 0.21 mmol/l (range 2.55-3.25) to 2.58 +/- 0.16 mmol/l at 1 h of hemodialysis and to 2.16 +/- 0.33 mmol/l (range 1.63-2.53) following 2-3 h of hemodialysis. The ionized calcium (n = 4) decreased from 1.44 +/- 0.14 mmol/l to 0.99 +/- 0.2 mmol/l. No patient showed any hypocalcemic symptoms and signs during hemodialysis. The rate of decrease in plasma calcium did not appear to produce adverse effects in any of the patients. There was a significant positive correlation between the decrease in plasma calcium concentration and the Kt/V urea (y = 1.4x - 0.29, r = 0.92, p < 0.01). We conclude that calcium-free hemodialysis is indicated when the presence of severe renal failure prevents the administration of large volumes of intravenous fluids to hypercalcemic patients. The amount of dialysis (Kt/V urea) can be used to predict the decrease in plasma calcium concentration during calcium-free hemodialysis.

Adult↗