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Biomedical subjects

Y O Kim

Publications and source records attributed to Y O Kim.

At least 19 recordsLinked to original sources

Influence of calcium hydroxide intracanal medication on apical seal.

AIM: The aim of this study was to determine the influence of calcium hydroxide intracanal medication and various techniques for its removal on the sealing ability of gutta-percha root fillings with a zinc oxide-eugenol sealer. METHODOLOGY: Eighty extracted mature human mandibular molar roots were divided into three groups of similar root-canal configuration. Calcium hydroxide paste was made by mixing calcium hydroxide powder with distilled water at a powder to liquid ratio of 1:1.25. After root canals were prepared and enlarged to a minimum of size 30 with the Profile 0.06 system, calcium hydroxide paste was placed in the canals of two groups, but no medication was placed in the control group. The intracanal calcium hydroxide was removed with two different techniques, 1 week after medication: K-files one size larger than the master apical file (MAF) were used with 2.5% NaOCl and 15% EDTA solutions in one group, whilst K-files the same size as the MAF were used with 2.5% NaOCl solution in another group. Canals were obturated with gutta-percha and Tubli-Seal cement using the lateral condensation technique. The apical sealing-ability was assessed by dye leakage and cross-sections of the specimens were examined under a stereomicroscope. The dye-penetration level was measured and analyzed using Fisher's exact test and Duncan's multiple range test. RESULTS: The calcium hydroxide-medicated groups showed significantly more dye leakage than the non-medicated control group (P < 0.05). However, there was no significant difference between the two calcium hydroxide-medicated groups (P > 0.05). The stereomicroscopic views showed a relatively uneven and thicker layer of sealer in the calcium hydroxide-medicated groups. CONCLUSION: Calcium hydroxide intracanal medication may increase apical leakage of gutta-percha root fillings when a zinc oxide-eugenol sealer is used.

Calcium Hydroxide↗

A membrane-proximal basic domain and cysteine cluster in the C-terminal tail of CCR5 constitute a bipartite motif critical for cell surface expression.

We examined the structural requirements for cell surface expression, signaling, and human immunodeficiency virus co-receptor activity for the chemokine receptor, CCR5. Serial C-terminal truncation of CCR5 resulted in progressive loss of cell surface expression; mutants truncated at the 317th position and shorter were not detected at the cell surface. Alanine substitution of basic residues in the membrane-proximal domain (residues 314-322) in the context of a full-length C-tail resulted in severe reduction in surface expression. C-terminal truncation that excised the three cysteines in this domain reduced surface expression, but further truncation of upstream basic residue(s) abolished surface expression. Substituting the carboxyl-terminal domain of CXCR4 for that of CCR5 failed to rectify the trafficking defect of the tailless CCR5. In contrast, tailless CXCR4 or a CXCR4 chimera that exchanged the native cytoplasmic domain for that of wild type CCR5 was expressed at the cell surface. Deletion mutants that expressed at the cell surface responded to chemokine stimulation and mediated human immunodeficiency virus entry. Substitution of all serine and threonine residues in the C-terminal tail of CCR5 abolished chemokine-mediated receptor phosphorylation but preserved downstream signaling (Ca(2+) flux), while substitutions of tyrosine residues in the C-tail affected neither phenotype. CCR5 mutants that failed to traffic to the plasma membrane did not exhibit obvious changes in metabolic turnover and were retained in the Golgi or pre-Golgi compartments(s). Thus, the basic domain (-KHIAKRF-) and the cysteine cluster (-CKCC-) in the C-terminal tail of CCR5 function cooperatively for optimal surface expression.

Amino Acid Motifs↗

Control of mitochondrial redox balance and cellular defense against oxidative damage by mitochondrial NADP+-dependent isocitrate dehydrogenase.

Mitochondria are the major organelles that produce reactive oxygen species (ROS) and the main target of ROS-induced damage as observed in various pathological states including aging. Production of NADPH required for the regeneration of glutathione in the mitochondria is critical for scavenging mitochondrial ROS through glutathione reductase and peroxidase systems. We investigated the role of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) in controlling the mitochondrial redox balance and subsequent cellular defense against oxidative damage. We demonstrate in this report that IDPm is induced by ROS and that decreased expression of IDPm markedly elevates the ROS generation, DNA fragmentation, lipid peroxidation, and concurrent mitochondrial damage with a significant reduction in ATP level. Conversely, overproduction of IDPm protein efficiently protected the cells from ROS-induced damage. The protective role of IDPm against oxidative damage may be attributed to increased levels of a reducing equivalent, NADPH, needed for regeneration of glutathione in the mitochondria. Our results strongly indicate that IDPm is a major NADPH producer in the mitochondria and thus plays a key role in cellular defense against oxidative stress-induced damage.

3T3 Cells↗

Sonographic evaluation of gallbladder-wall thickening in hemorrhagic fever with renal syndrome: prediction of disease severity.

PURPOSE: Gallbladder-wall thickening (GBWT) frequently occurs in patients with hemorrhagic fever with renal syndrome (HFRS), an acute infectious disease caused by hantaviruses. HFRS is manifested by fever, hemorrhage, renal failure, and in many cases gastrointestinal symptoms, such as abdominal pain and tenderness. The clinical significance of GBWT in HFRS has not been reported. The purpose of this study was to investigate the incidence of GBWT and the relationship between GBWT and the severity of HFRS. METHODS: We retrospectively reviewed the medical records and sonograms of 68 patients with HFRS (47 males and 21 females, with an age range of 10-76 years) who underwent abdominal sonography in the acute stage of the disease. We measured the gallbladder-wall thickness on the sonograms and reviewed other sonographic and radiographic findings. Clinical factors that reflect the severity of HFRS were compared between the patients with GBWT (defined as thickness of 4 mm or more) and those without GBWT. RESULTS: Of the 68 patients, 29 (43%) had GBWT, which was even and diffuse in all cases. The patients with GBWT had a significantly lower mean platelet count and serum albumin level and significantly higher serum aspartate aminotransferase and serum lactate dehydrogenase levels than did the patients without GBWT. In addition, the incidence of renal failure requiring hemodialysis and the incidences of ascites and pleural effusion were higher in the patients with GBWT than in those without GBWT. Five patients died of HFRS; all 5 had GBWT (p = 0.011 for comparison with patients without GBWT). CONCLUSIONS: Our results suggest that the sonographic measurement of gallbladder-wall thickness during the acute stage of HFRS is useful for determining the severity of HFRS.

Adolescent↗

Cytoprotective effect of Scutellaria baicalensis in CA1 hippocampal neurons of rats after global cerebral ischemia.

Based on the use of Scutellaria baicalensis for the treatment of stroke in traditional Oriental medicine, the current study was carried out to evaluate neuroprotective effects of S. baicalensis after transient global ischemia using rat 4-vessel occlusion model. Methanol extracts from the dried roots of S. baicalensis (0.1-10 mg/kg) administered intra-peritoneally significantly protected CA1 neurons against 10 min transient forebrain ischemia as demonstrated by measuring the density of neuronal cells stained with Cresyl violet. Methanol extract of S. baicalensis inhibited microglial tumor necrosis factor-alpha (TNF-alpha) and nitric oxide production, and protected PC12 cells from hydrogen peroxide-induced toxicity in vitro.

Animals↗

Influence of the renin-angiotensin system on epidermal growth factor expression in normal and cyclosporine-treated rat kidney.

BACKGROUND: Epidermal growth factor (EGF) plays an important role in renal tubular regeneration after ischemic injury in kidney. The present study reports the association between the renin-angiotensin system (RAS) and EGF, and the effect of angiotensin II blockade with losartan (LSRT) on EGF expression in an experimental model of chronic cyclosporine (CsA) nephrotoxicity in rats. METHODS: Two separate experiments were performed. In the first experiment, rats on the normal-salt diet (NSD; 0.3%) or low-salt diet (LSD; 0.05%) were treated with or without LSRT for four weeks. In the second experiment, rats on the NSD or LSD were given vehicle (VH group, olive oil, 1 mg/kg per day) or CsA (15 mg/kg per day) or CsA (15 mg/kg per day) plus LSRT (100 mg/L per day). Renal function, histopathology, TUNEL staining, plasma renin activity (PRA), and the expression of renin and EGF were studied. RESULTS: Normal rats on the LSD showed significantly increased EGF expression (cortex, 2.6-fold; medulla, 1.7-fold) and significantly decreased EGF expression with the LSRT treatment compared with the rats treated with the NSD (cortex, 74.8 vs. 10%; medulla, 22.5 vs. 5%). In contrast, the CsA-treated rats on the LSD had a significantly lower EGF expression (cortex, 98 vs. 53%; medulla, 94 vs. 14%); however, concomitant administration of LSRT increased the EGF expression (cortex, 91- vs. 3.8-fold; medulla, 19- vs. 2.4-fold) compared with the rats on the NSD. In the normal and CsA-treated LSD rats, EGF expression was well correlated with PRA. In addition, EGF expression was well correlated with the interstitial fibrosis score (r = 0.664, P < 0.01) or number of TUNEL-positive cells (r = 0.822, P < 0.01) in CsA-treated LSD rats. CONCLUSIONS: These results suggest that angiotensin II blockade with LSRT decreases EGF expression in normal rats on the LSD, but it protects EGF expression in CsA-induced nephrotoxicity. This finding provides a new perspective on the renoprotection of angiotensin II blockade in chronic CsA nephrotoxicity.

Angiotensin II↗

Influence of melatonin on immunotoxicity of lead.

The results suggested that immunotoxicity induced by lead [Pb, as Pb(NO(3))(2)] was significantly restored or prevented by melatonin (MLT). MLT (10 or 50 mg/kg) was orally administered to ICR mice daily for 28 days, and Pb was also administered at 35 mg/kg in the same way 2 h after the administration of MLT, and the normal mice were given vehicle. Within the Pb plus MLT-treated group, the body weight gains and the relative thymus weights were significantly increased when compared with the treatment of Pb alone. The relative spleen and liver weights were increased by the treatment of Pb alone, and then restored to normal value by MLT treatment. Hemagglutination (HA) titer, plaque-forming cell response to sheep red blood cell (SRBC), and secondary IgG antibody response to BSA were significantly enhanced in the Pb plus MLT-treated mice, as opposed to when compared with the treatment of Pb alone. The mitogenic response of splenic T cell to concanavalin A and that of B cells to lipopolysaccharide was remarkably increased by MLT treatment when compared with treatment of Pb alone. Splenic CD4(+)cells were significantly increased by MLT treatment when compared with treatment of Pb alone. In case of CD8(+) cells, the slight enhancement was observed in MLT treatment. Splenic T and B cells were significantly increased by MLT treatment when compared with the treatment of Pb alone. The natural killer cell, phagocytic activity and the number of peripheral leukocytes were significantly enhanced in Pb plus MLT-treated mice when compared with the treatment of Pb alone.

Animals↗

Effect of biphenyl dimethyl dicarboxylate on the humoral immunosuppression by ethanol.

The present study was undertaken to investigate the effect of biphenyl dimethyl dicarboxylate (PMC) on the humoral immunosuppression by ethanol (EtOH) in ICR mice. PMC at a dose of 6 mg/kg was orally administered to mice daily for 28 consecutive days, and the control mice were given vehicle. Mice treated with EtOH were given freely with 20% EtOH instead of water. The results of this study are summarized as follows; a gain of body weight and the relative weights of spleen and liver were significantly increased by combination of PMC and EtOH, as compared with those in mice treated with EtOH alone. Splenic plaque forming cells (PFC) and hemagglutination (HA) titers to sheep red blood cells (SRBC), and the secondary IgG antibody response to bovine serum albumin (BSA) were decreased by the treatment of EtOH alone, then restored to normal level by PMC treatment. The elevations of serum glutamic-pyruvic transaminase (S-GPT) and total protein levels caused by EtOH were reduced to normal level by the combination of PMC and EtOH. In addition, lower serum albumin and A/G ratio were also increased to normal level. These findings indicate that PMC has a protective effect against EtOH-induced humoral immunosuppression.

Adjuvants, Immunologic↗

Influence of melatonin on immunotoxicity of cadmium.

The results suggested that immunotoxicity induced by Cd was significantly restored or prevented by MLT. MLT (10 or 50 mg/kg) was orally administered to ICR mice daily for 28 consecutive days, and cadmium (Cd, as [Cd(AC)(2)]) was also administered at 25 mg/kg by the same route 2 h after the administration of MLT, and the normal mice were given vehicle. Within the Cd plus MLT-treated group, the body weight gains and relative thymus weights were significantly increased when compared with the treatment of Cd alone. The relative spleen and liver weights were increased by treatment of Cd alone, then restored to normal value by MLT treatment. Hemagglutination (HA) titer, primary IgM antibody response to SRBC, and secondary IgG antibody response to BSA was significantly increased with the Cd plus MLT-treated mice, as opposed to when compared with treatment of Cd alone. The NK cell and phagocytic activity used for evaluation of non-specific immunocompetence was significantly increased in Cd plus MLT-treated mice when compared with the treatment of Cd alone. The number of peripheral leukocytes was significantly increased in Cd plus MLT-treated mice when compared with treatment of Cd alone.

Animals↗

Crystal structures of a novel, thermostable phytase in partially and fully calcium-loaded states.

Phytases hydrolyze phytic acid to less phosphorylated myo-inositol derivatives and inorganic phosphate. A thermostable phytase is of great value in applications for improving phosphate and metal ion availability in animal feed, and thereby reducing phosphate pollution to the environment. Here, we report a new folding architecture of a six-bladed propeller for phosphatase activity revealed by the 2.1 A crystal structures of a novel, thermostable phytase determined in both the partially and fully Ca2+-loaded states. Binding of two calcium ions to high-affinity calcium binding sites results in a dramatic increase in thermostability (by as much as approximately 30 degrees C in melting temperature) by joining loop segments remote in the amino acid sequence. Binding of three additional calcium ions to low-affinity calcium binding sites at the top of the molecule turns on the catalytic activity of the enzyme by converting the highly negatively charged cleft into a favorable environment for the binding of phytate.

6-Phytase↗

Intestinal protein loss in patients with haemorrhagic fever with renal syndrome.

BACKGROUND: In haemorrhagic fever with renal syndrome (HFRS) vascular dysfunction has been observed in various organs, but the involvement of the intestine has not yet been reported. This study was performed to evaluate the association of intestinal protein loss in this disease with other clinical parameters reflecting vascular permeability or disease severity. METHODS: Twenty patients with HFRS were included in this study. Intestinal protein loss was measured by (99m)Tc-human serum albumin ((99m)Tc-HSA) scintigraphy in the acute stage, and quantitative analysis of protein loss was measured by the faecal clearance of alpha 1-antitrypsin (C(AT)) in the acute and the recovery stages. C(AT) was then compared with clinical parameters reflecting disease activity and vascular permeability. RESULTS: (99m)Tc-HSA scintigraphy was positive in 13 (65%) patients, and C(AT) in the acute stage was significantly increased as compared with C(AT) in the recovery stage (40.5+/-24.1 vs 9.2+/-4.2 ml/day, P<0.001). C(AT) was associated with serum albumin levels, frequency of hypotensive episodes, severity of acute renal failure, and degree of thrombocytopenia. CONCLUSIONS: Our data suggest that the increased vascular permeability of HFRS is associated with the increased intestinal loss of plasma proteins, which might represent one of the parameters of disease severity in HFRS.

Adult↗

Quantification of osseous facial dysmorphology in untreated unilateral coronal synostosis.

Unilateral coronal synostosis results in dysmorphology of the midface in addition to well-characterized cranial and orbital deformities. Because most American infants with this problem have undergone cranio-orbital surgery within their first year of life for the past 25 years, a paucity of data exist regarding the natural history of untreated unilateral coronal synostosis. In an attempt to remedy this void, an international search was conducted to identify computed tomography data sets of living individuals with untreated unilateral coronal synostosis; data were obtained from two European centers and one center in the United States. Results limited to the study of the midface are presented here. Digital data from high-resolution head computed tomography scans of 11 living, white individuals with untreated unilateral coronal synostosis were obtained from three craniofacial centers (in Denmark, The Netherlands, and the United States). Image volumes were constructed from each scan using ANALYZE biomedical imaging software. Fourteen pairs of three-dimensional distances were calculated on the ipsilateral (the side of the synostosis) and the contralateral (the side opposite to the synostosis) hemifaces using 11 osseous landmarks. The resulting measurements were expressed as a ratio of the ipsilateral: contralateral sides. Descriptive statistics were derived for the untreated unilateral coronal synostosis population and compared with analogous measurements performed on dried skulls. Age at computed tomography ranged from 1.1 to 21.1 years (mean, 6.6 years; median, 4.1 years). Twelve of the 14 measured distances differed by greater than 5 percent on the ipsilateral side, and all but one of these measurements were decreased on the ipsilateral side when compared with contralateral values. The results of this study support the following conclusions: (1) There are discrete and measurable differences in the facial morphology between patients with untreated unilateral coronal synostosis and normal skulls. (2) Intercenter and international collaboration can provide a sufficient number of individuals with rare craniofacial anomalies to quantitatively determine group characteristics. (3) Quantitative documentation of rare anomaly natural history is necessary for quantitative outcome assessment of treated patients.

Adolescent↗

A case of Goodpasture's syndrome with massive pulmonary hemorrhage.

We present a typical case of Goodpasture's syndrome with massive pulmonary hemorrhage and acute deterioration of renal function. A 20-year-old male was admitted due to severe azotemia (blood urea nitrogen 214.7 mg/dL, serum creatinine 30.2 mg/dL) and was treated with emergency hemodialysis. On the 4th hospital day, a sudden onset of pulmonary hemorrhage developed. The circulating level of anti-glomerular basement membrane antibody was then elevated highly, and the kidney biopsy showed crescentic glomerulonephritis and linear deposition of IgG along the glomerular capillary. The patient was treated with intravenous high dose-steroid, oral cyclophosphamide and plasma exchanges. The pulmonary hemorrhage improved with the therapy, however, his renal function did not improve. He is currently on a regular schedule of hemodialysis.

Adult↗

Comparison of acquired cystic kidney disease between hemodialysis and continuous ambulatory peritoneal dialysis.

OBJECTIVES: ACKD has been described mainly in patients treated with hemodialysis(HD), and there are only a few reports about the prevalence of ACKD in continuous ambulatory peritoneal dialysis (CAPD) patients. Therefore, we compared the prevalence of ACKD in patients receiving HD and CAPD, and evaluated the possible factors which may affect the development of ACKD. METHODS: Forty nine HD and 49 CAPD patients who had received dialysis therapy for at least 12 months were enrolled in this cross-sectional study. Patients who had a past history of polycystic kidney disease and had acquired cystic kidney disease on predialysis sonographic exam were excluded. Detection of ACKD was made by ultrasonography and ACKD was defined as 3 or more cysts in each kidney. RESULTS: The prevalence of ACKD was about 31% (30/98) and there was no significant difference between HD and CAPD patients(27% vs. 34%, p > 0.05). The prevalence of ACKD was not associated with age, sex, primary renal disease, the levels of hemoglobin, BUN, and serum creatinine. However, the duration of dialysis was significantly related to the development of ACKD (presence of ACKD, 74.4 +/- 42.4 months vs. absence of ACKD, 37.8 +/- 24.1 months, p < 0.05). CONCLUSION: The prevalence of ACKD is not different according to the mode of dialysis, and the major determinant of acquired cyst formation is duration of dialysis.

Adolescent↗

Identification and functional characterization of a novel, tissue-specific NAD(+)-dependent isocitrate dehydrogenase beta subunit isoform.

To understand the interactions and functional role of each of the three mitochondrial NAD(+)-dependent isocitrate dehydrogenase (IDH) subunits (alpha, beta, and gamma), we have characterized human cDNAs encoding two beta isoforms (beta(1) and beta(2)) and the gamma subunit. Analysis of deduced amino acid sequences revealed that beta(1) and beta(2) encode 349 and 354 amino acids, respectively, and the two isoforms only differ in the most carboxyl 28 amino acids. The gamma cDNA encodes 354 amino acids and is almost identical to monkey IDHgamma. Northern analyses revealed that the smaller beta(2) transcript (1.3 kilobases) is primarily expressed in heart and skeletal muscle, whereas the larger beta(1) mRNA (1.6 kilobases) is prevalent in nonmuscle tissues. Sequence analysis of the IDHbeta gene indicates that the difference in the C-terminal 28 amino acids between beta(1) and beta(2) proteins results from alternative splicing of a single transcript. Among the various combinations of human IDH subunits co-expressed in bacteria, alphabetagamma, alphabeta, and alphagamma combinations exhibited significant amounts of IDH activity, whereas subunits produced alone and betagamma showed no detectable activity. These data suggest that the alpha is the catalytic subunit and that at least one of the other two subunits plays an essential supporting role for activity. Substitution of beta(1) with beta(2) in the co-expression system lowered the pH optimum for IDH activity from 8.0 to 7.6. This difference in optimal pH was analogous to what was observed in mouse kidney and brain (beta(1) prevalent; optimal pH 8.0) versus heart (beta(2) prevalent; pH 7.6) mitochondria. Experiments with a specially designed splicing reporter construct stably transfected into HT1080 cells indicate that acidic conditions favor a splicing pattern responsible for the muscle- and heart-specific beta(2) isoform. Taken together, these data indicate a regulatory role of IDHbeta isoforms in determining the pH optimum for IDH activity through the tissue-specific alternative splicing.

Alternative Splicing↗