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Hyung Wook Kim

Publications and source records attributed to Hyung Wook Kim.

9 recordsLinked to original sources
PubMed2005

Calcitriol regresses cardiac hypertrophy and QT dispersion in secondary hyperparathyroidism on hemodialysis.

BACKGROUND: Sudden cardiac death is common in patients on hemodialysis (HD), and its rate is as high as 25% of all cardiac deaths associated with left ventricular hypertrophy (LVH) and secondary hyperparathyroidism. A prolonged QT interval on standard electrocardiography is related to an increase in sudden death in various patient groups. It is also well known that LVH has been noted in uremic patients with high parathyroid hormone levels. METHODS: To evaluate the response of intravenous calcitriol treatment on the QT interval and LVH in HD patients with secondary hyperparathyroidism (intact parathyroid hormone, iPTH, > 450 ng/ml), echocardiographic, electrocardiographic (ECG), and biochemical assessments were performed over a 15-week period in 25 HD patients before and after intravenous calcitriol treatment. We also evaluated 25 age-, sex-, HD duration-, and BMI-matched HD control patients with secondary hyperparathyroidism. RESULTS: In patients receiving intravenous calcitriol, a significant reduction in iPTH levels (p < 0.05) and alkaline phosphatase levels (p < 0.01) was found without changes in values of serum calcium and ionized Ca2+, phosphorus, Na+, K+, Mg2+, hematocrit, blood pressure, or other hemodynamic changes. Echocardiograms showed significant decreases in the thickness of the interventricular septum (p < 0.05), left posterior wall thickness (p < 0.05), and left ventricle mass index (LVMi, p < 0.01). In addition, sequential ECG measurement in patients with calcitriol treatment showed significant reductions in QTcmax (QTmax interval corrected for heart rates, p < 0.01) and QTc dispersion (QT dispersion corrected for heart rates, p < 0.01). However, in the control patients, biochemical, hemodynamic, and ECG changes, as well as myocardial structural and functional changes were not seen. Multiple regression analysis in all patients indicated that iPTH and LVMi levels were independent predictors of QTcmax while the LVMi level was the only independent predictor of QTc dispersion (p < 0.05). CONCLUSIONS: Our study showed a significant correlation between LVMi and QT dispersion in HD patients with secondary hyperparathyroidism. Intravenous calcitriol treatment, to be used for the control of secondary hyperparathyroidism, was found to cause regression of myocardial hypertrophy and a reduction in the QTc interval and dispersion, without biochemical and hemodynamic changes. These findings suggest that an active vitamin D metabolite has a cardioprotective action in HD patients.

Adult↗
PubMed2005

Relationships between the expressions of CDX1 and CDX2 mRNA and clinicopathologic features in colorectal cancers.

BACKGROUND: CDX1 and CDX2 are members of the caudal-type homeobox gene family and control the proliferation and differentiation of intestinal mucosal cells. Their expressions are commonly reduced in colorectal cancer, but reports about the relationships between their expressions and clinicopathologic features are rare. The aim of this study was to examine the expressions of CDX1 and CDX2 mRNAs in colorectal cancers and to assess the relationships between their expressions and clinicopathologic features. METHODS: CDX1 and CDX2 mRNA expressions were analyzed by real-time polymerase chain reaction in 48 colorectal cancers and in adjacent non-tumorous normal mucosal tissue. RESULTS: CDX1 and CDX2 mRNA expressions were significantly reduced in colorectal cancer tissues versus normal mucosal tissues (p=0.001, p=0.042, respectively). As compared with paired normal mucosal tissues, colorectal tissues showed reduced CDX1 mRNA expression in 64.6% (31/48) and reduced CDX2 mRNA expression in 66.7% (32/48) of cases. A statistically significant positive correlation was found between the expressions of CDX1 mRNA and CDX2 mRNA in colorectal cancer (r=0.543, p<0.001). However, the expressions of CDX1 and CDX2 mRNAs were not related to age, sex, cancer location, differentiation, lymphatic or vascular invasion, lymph node metastasis, stage or serum carcinoembryonic antigen level. CONCLUSIONS: CDX1 and CDX2 mRNA expressions were found to be significantly reduced in colorectal cancers but these expressional changes were not found to be related to clinicopathologic features.

CDX2 Transcription Factor↗
PubMed2003

Crystallization and preliminary X-ray crystallographic studies of chorismate synthase from Helicobacter pylori.

Chorismate synthase (EC 4.6.1.4) catalyzes the transformation of 5-enolpyruvylshikimate 3-phosphate to chorismate in the last step of the shikimate pathway. Chorismate synthase from Helicobacter pylori fused with an eight-residue C-terminal tag was overexpressed in soluble form in Escherichia coli. It was crystallized at 296 K using polyethylene glycol 400 as a precipitant. A set of X-ray diffraction data was collected to 2.5 A resolution using synchrotron radiation. The crystals belong to the tetragonal space group I4, with unit-cell parameters a = b = 145.79, c = 130.98 A. The asymmetric unit contains a tetramer, giving a crystal Volume per protein mass (V(M)) of 2.13 A(3) Da(-1) and a solvent content of 42.3%.

Crystallization↗
PubMed2003

Crystallization and preliminary X-ray crystallographic studies of phosphopantetheine adenylyltransferase from Helicobacter pylori.

Phosphopantetheine adenylyltransferase (PPAT; EC 2.7.7.3) is an essential enzyme in the coenzyme A (CoA) biosynthetic pathway and catalyzes the reversible transfer of an adenylyl group from ATP to 4'-phosphopantetheine to form 3'-dephospho-CoA. PPAT from Helicobacter pylori has been overexpressed in Escherichia coli and crystallized at 296 K using sodium chloride as a precipitant by the hanging-drop vapour-diffusion method. X-ray diffraction data have been collected to 2.00 A resolution at 100 K using synchrotron radiation. The crystals belong to the trigonal space group P3(1)21 or P3(2)21, with unit-cell parameters a = b = 80.50, c = 143.05 A, alpha = beta = 90, gamma = 120 degrees. Six monomers of PPAT are likely to be present in the asymmetric unit, giving a V(M) of 2.39 A(3) Da(-1) and a solvent content of 49%.

Crystallization↗
PubMed2003

Preconditioning with cyclosporine A or FK506 differentially regulates mitogen-activated protein kinase expression in rat kidneys with ischemia/reperfusion injury.

BACKGROUND: The signaling pathways of mitogen-activated protein kinases (MAPKs) are important molecular components responsible for ischemia/reperfusion (I/R) injury in the kidneys. Preconditioning with cyclosporine A (CsA) or FK506 reduces subsequent I/R injury. We studied the effect of preconditioning with CsA or FK506 on MAPK expression in ischemic rat kidneys. METHODS: Two separate studies were performed using Sprague-Dawley rats. First, MAPK (extracellular signal-regulated kinase [ERK], jun N-terminal kinase [JNK], p38) expressions were observed at 0, 10, 20, 30, 60, 120, and 1,440 min after I/R injury. Second, the effects of preconditioning with CsA or FK506 on MAPK expressions were observed in rat kidneys with I/R injury. I/R injury was induced by clamping both renal arteries for 45 min. Rats were pretreated with intravenous (IV) CsA (3 mg/kg) or IV FK506 (0.3 mg/kg) 6 hr before I/R injury and killed 30 min later. Expression of MAPK was measured using immunoblot and immunohistochemistry. RESULTS: MAPK (ERK, JNK, p38) expressions were significantly increased in kidneys with I/R injury compared with sham-operated controls, and immunohistochemistry revealed increased MAPK immunoreactivity in renal tubules of the outer medulla. Kidneys preconditioned with low-dose CsA or FK506 showed significantly increased ERK expression compared with kidneys with I/R injury alone (CsA, 9.5- vs. 4.5-fold; FK506 10.4- vs. 4.5-fold: P<0.05) but showed decreased JNK (CsA, 3.8- vs. 5.3-fold; FK506, 3.4- vs. 5.3-fold: P<0.05) and p38 expression (CsA, 2.5- vs. 3.7-fold; FK506, 2.1- vs. 3.7-fold: P<0.05). CONCLUSIONS: Preconditioning with CsA or FK506 differentially regulates the expression of MAPK in rat kidneys with I/R injury, and this may explain the remarkable protective effects of these agents.

Animals↗
PubMed2003

Severe renal tubular acidosis in a renal transplant recipient with repeated acute rejections and chronic allograft nephropathy.

Renal tubular acidosis in renal transplant recipients usually is asymptomatic and subclinical. The authors report a case of severe renal tubular acidosis manifested as muscle weakness in a renal transplant recipient. The patient received a renal transplant 30 months ago and had a history of successive episodes of acute rejection during the past 2 months. On admission, arterial blood (arterial blood pH, 7.11; pco(2), 12.8 mm Hg; and bicarbonate, 4 mEq/L [4 mmol/L]) and urine gas analysis were compatible with distal renal tubular acidosis. The graft biopsy findings showed superimposed acute rejection on chronic allograft nephropathy, and immunohistochemical staining and electron microscopic findings showed the reduced immunoactivity of H(+)ATPase pump and anion exchanger 1. The patient was treated successfully with intravenous bicarbonate and oral steroid pulse therapy. This finding suggests that rejection-related renal tubular acidosis should be considered a cause of severely affected metabolic acidosis in renal transplant recipients.

Acidosis, Renal Tubular↗
PubMed2002

Cyclosporine withdrawal and mycophenolate mofetil treatment effects on the progression of chronic cyclosporine nephrotoxicity.

BACKGROUND: Recent clinical trials of mycophenolate mofetil (MMF) in chronic allograft nephropathy (CAN) demonstrated that the dose of cyclosporine A (CsA) is one of the critical factors in determining graft function in CAN, but the effect of MMF on chronic CsA nephropathy is undetermined. We undertook this study to evaluate the effect of MMF on CsA-induced nephrotoxicity in an animal model of chronic CsA nephropathy. METHODS: In the first experiment, Sprague-Dawley rats on a low-salt diet were treated with CsA (7.5 mg/kg per day) for 10 weeks, or were treated with CsA for five weeks and then MMF (20 mg/kg per day) was administered five weeks later. In the second experiment, rats were treated with CsA for five weeks, and CsA was then withdrawn for five weeks with or without MMF treatment. Renal function, histologic parameters (tubulointerstitial fibrosis, arteriolopathy, ED-1-positive cells, renin-positive glomeruli, TUNEL-positive cells) and the expression of osteopontin and transforming growth factor (TGF)-beta1 mRNA expressions were compared for different treatment groups. RESULTS: CsA-treated rats showed decreased renal function and increased histologic parameters compared with the vehicle (VH)-treated rats. The addition of MMF did not improve these parameters compared with the CsA-treated rats. With CsA withdrawal, renal function and histologic parameters were significantly improved compared with the CsA-treated rats, and MMF treatment after CsA withdrawal further improved the histologic parameters. At the molecular level, the addition of MMF did not decrease the expression of osteopontin and transforming growth factor-beta1 (TGF-beta1) mRNAs, which were increased in the CsA-treated rat kidney. With CsA withdrawal, the expression of both mRNAs was significantly decreased compared with the CsA group, and a further decrease was observed with MMF treatment after CsA was withdrawn. CONCLUSION: The combined treatment of CsA and MMF does not prevent the development of chronic CsA nephrotoxicity, but MMF treatment after CsA withdrawal does improve chronic CsA nephrotoxicity. This finding provides a rationale for MMF treatment in chronic CsA nephrotoxicity.

Animals↗
PubMed2002

Cyclosporine or FK506 decrease mature epidermal growth factor protein expression and renal tubular regeneration in rat kidneys with ischemia/reperfusion injury.

BACKGROUND: Epidermal growth factor (EGF) plays an important role in tubular regeneration in kidneys with ischemia/reperfusion (I/R) injury. This study was undertaken to evaluate the influence of cyclosporine A (CsA) or FK506 on mature EGF expression and tubular regeneration in rat kidneys with I/R injury. METHODS: Two separate studies were performed. First, the expression of EGF and tubular regeneration was observed in rat kidneys with I/R injury on days 1, 2, 3, 5, and 7. Second, the dose-dependent response of EGF expression and tubular regeneration to CsA (5, 10, and 20 mg/kg) or FK506 (0.25, 0.5, and 1.0 mg/kg) was observed in rat kidneys with I/R injury. I/R injury was induced by clamping both renal arteries for 45 min, and CsA or FK506 was injected just after release of vascular clamps. Rats were sacrificed on day 1 for evaluation of EGF expression, and on day 2 for evaluation of BudU-positive cells. Renal function, tubular injury score, EGF expression assessed by immunoblotting, levels of CsA and FK506 in whole blood, and immunostaining for BrdU was studied. RESULTS: EGF expression was maximal on day 1 (cortex, 29-fold; medulla, 31-fold compared with sham-operated controls), and renal tubular regeneration measured with the number of BrdU-positive cells was maximal on days 2 and 3 in kidney with I/R injury, and thereafter the level of EGF and the number of BrdU-positive cells decreased progressively. CsA or FK506 treatment to ischemic rat kidneys reduced the expression of EGF and the number of BrdU-positive cells in a dose-dependent manner. CONCLUSIONS: CsA or FK506 treatment delays recovery from acute tubular necrosis, and this may be associated with decreased EGF expression by CsA or FK506.

Animals↗