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Biomedical subjects

B K Bang

Publications and source records attributed to B K Bang.

At least 19 recordsLinked to original sources
PubMed2002

Identification of two new alleles in a single Korean individual, HLA-B*1568 and HLA-DRB1*1208.

We have identified a new HLA-B*15 allele and a new HLA-DRB1*12 allele, named B*1568 and DRB1*1208, respectively. The alleles were identified using a combination of sequence specific primers, reverse line sequence specific oligonucleotide probing and sequence-based typing. Both alleles were identified in a single individual of Korean origin. HLA-B*1568 appears to be an HLA-B*4801/B*1507 hybrid combining the exon 2 sequence of B*4801 and the exon 3 and 4 sequences of B*1507. Exon 2 of DRB1*1208 was most similar to DRB1*1201 or 1206, with a single mismatch at nucleotide position 165 (A to C). At the protein level, this substitution results in a phenylalanine substitution at position 26 that creates an identical amino acid sequence to DRB3*0202 between amino acid positions 17 and 36.

Amino Acid Sequence↗
PubMed2001

Pharmacological preconditioning with low-dose cyclosporine or FK506 reduces subsequent ischemia/reperfusion injury in rat kidney.

BACKGROUND: Ischemia/reperfusion (I/R) injury in the early posttransplant period is closely associated with delayed recovery of graft function, increased acute rejection, and late allograft dysfunction. Pharmacological preconditioning with low-dose cyclosporine (CsA) or FK506 was performed to induce ischemic tolerance in rat kidney with I/R injury. METHODS: Low-dose CsA (3 mg/kg, administered i.v.) or FK506 (0.3 mg/kg i.v.) were used to induce ischemic tolerance in Sprague-Dawley rats, and the induction of heat shock protein (hsp) 70 by CsA or FK506 was evaluated overtime. Rats were pretreated with CsA or FK506 6 hr before I/R injury when hsp70 was maximally expressed, and were killed 24 hr later. The effect of pharmacological preconditioning on subsequent I/R injury was evaluated in terms of renal function, histopathology score, assays for apoptosis (DNA fragmentation analysis, TUNEL staining, expressions of pro-apoptotic genes, and caspase activity), and the expression of inflammatory cytokine genes (interleukin-1 and tumor necrosis factor-alpha). RESULTS: Preconditioning with low-dose CsA or FK506 significantly improved renal function and renal histology, compared to rats with I/R injury. Apoptotic cell death (typical DNA laddering and increased TUNEL-positive cells) in rat kidneys with I/R injury, was decreased by pretreatment with low-dose CsA or FK506. Increased expression of pro-apoptotic genes (Fas, Fas-ligand, caspase 1 and 3) and activated caspases in ischemic rat kidneys were decreased after CsA or FK506 pretreatment. CONCLUSIONS: Pretreatment with low-dose CsA or FK506 prevents subsequent I/R injury, and this effect may be related to the induction of hsp70. Pretreatment of renal donors with low-dose CsA or FK506 may result in an improvement in immediate posttransplant function.

Animals↗
PubMed2001

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↗
PubMed2001

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↗
PubMed2001

Serum cystatin C is an independent predictor of total homocysteine levels in stable Korean renal transplant recipients with normal serum creatinine.

OBJECTIVES: To examine the determinants of fasting plasma total homocysteine (tHcy) levels such as cystatin C, serum creatinine (SCr), estimated glomerular filtration rate (GFR) from Cockroft-Gault equation, albumin, plasma folate, vitamin B12, and pyridoxal-5'-phosphate (PLP) among Korean renal transplant recipients (RTR) with normal SCr levels (< or =1.4 mg/dL). DESIGN: Cross-sectional study. SETTING: Nephrology and Transplant Service, Catholic University Kangnam St. Mary's Hospital, Seoul, Korea. PARTICIPANTS: Fifty-one chronic stable Korean RTR with normal SCr levels (< or =1.4 mg/dL) 6 months or more following transplantation. MEASURES: Medical record review, anthropometric measurements, and overnight (10 to 14 hours) fasting blood samples for measurement of plasma tHcy, folate, vitamin B12, PLP, SCr, albumin, and cystatin C. RESULTS: General linear regression model including age, gender, vitamin status, and measurements of renal function showed that cystatin C and folate were independent predictors of tHcy levels. The partial regression coefficient for folate was -0.444 (P <.01) and for cystatin C, it was +0.334 (P <.05). SCr, estimated GFR, vitamin B12, PLP, age, and gender were not independent predictors of tHcy levels in this model. CONCLUSION: Both cystatin C and folate status were major independent determinants of fasting tHcy levels in the subgroup of Korean RTR with normal SCr.

Adult↗
PubMed2001

Thyroxine treatment induces upregulation of renin-angiotensin-aldosterone system due to decreasing effective plasma volume in patients with primary myxoedema.

BACKGROUND: In experimental animals and humans, hypothyroidism is associated with fluid retention and generalized oedema, increased antidiuretic hormone (ADH), decreased atrial natriuretic hormone (ANH), and decreased renin-angiotensin-aldosterone system (RAAS), which subsequently can be corrected by thyroid hormone replacement. The purpose of this study was to determine the effect of thyroxine therapy on RAAS and neurohormones affecting water and electrolyte metabolism and the reason for these changes in patients with primary myxoedema. METHODS: We measured changes in the plasma renin activity (PRA), serum aldosterone (Aldo), ADH, ANH levels, serum and 24 h urinary electrolytes and osmolalities, and cardiac function in 22 female patients with primary myxoedema before and after correction of hypothyroidism. We also evaluated age-, sex-, and BMI-matched 15 healthy control subjects (Cont). RESULTS: It took an average of 4.3 months (range, 3-9 months) to normalize thyroid function. The mean reductions of body weight and estimated plasma volume were 1.8+/-1.0 kg (P=0.002) and 8.5% (P<0.001), respectively. In addition, serum Na+ and osmolality and the haematocrit were significantly elevated after correction of hypothyroidism (P<0.01 and P<0.001, respectively). Increased F(E)Na and C(OSM) (P<0.05) levels in patients with hypothyroidism (Ho) compared with those in Cont did not change after thyroxine therapy (Eu). However, C(H(2)O), U(E)K, F(E)K, and TTKG levels as well as creatinine clearance (Ccr) were markedly increased in Eu compared with Ho and Cont (P<0.01, respectively). Increased plasma ADH concentration and decreased plasma ANH concentration were normalized compared to Cont after thyroxine therapy (P<0.001 and P<0.01, respectively). Low PRA and serum Aldo concentration in Ho were significantly increased in Eu (P<0.001 and P<0.01, respectively). In addition, increased left ventricular mass index and decreased cardiac output in Ho were normalized compared to Cont after thyroxine therapy (P<0.01, respectively) CONCLUSIONS: These findings suggest that the exaggerated upregulation of RAAS after correction of hypothyroidism in patients with primary myxoedema is associated with an increase in Ccr and a decrease in plasma volume resulting from water diuresis, natriuresis, osmotic diuresis and inappropriate changes in plasma ADH and ANH levels. The improved renal function coincided with an amelioration of cardiac function. These changes seem to be an adaptive response for preventing excessive plasma volume and weight loss after thyroxine therapy.

Adult↗
PubMed2001

Preconditioning with sodium arsenite inhibits apoptotic cell death in rat kidney with ischemia/reperfusion or cyclosporine-induced Injuries. The possible role of heat-shock protein 70 as a mediator of ischemic tolerance.

This study was performed to evaluate the effect of heat-shock protein (HSP)70 induction with sodium arsenite (SA) on ischemia/reperfusion (I/R) or cyclosporin A (CsA)-induced injuries in rat kidney. Rats were classified into five groups (sham, I/R, SA+I/R, I/R+CsA and SA+I/R+CsA groups) according to both the status of SA pretreatment and treatment with CsA. SA (6 mg/kg, i.v.) pretreatment was accomplished 12 h before I/R injury, and CsA (20 mg/kg, s.c.) was given subsequent to I/R injury. The effect of SA pretreatment on I/R injury was evaluated using measurements of renal function, the histopathology score, and assays for apoptosis (DNA fragmentation analysis, TUNEL staining, mRNA expressions of the pro-apoptotic genes and caspase activities). In addition, mitochondrial morphology was examined by electron microscopy. Induction of HSP70 with SA improved both renal function and the histopathology score as compared to the group without HSP70 induction. The assays for apoptosis revealed that SA pretreatment decreased the DNA laddering pattern, TUNEL-positive cells, mRNAs expression of pro-apoptotic genes and caspase activities as compared with the group without SA pretreatment. In addition, the mitochondrial morphology was well preserved in the groups with SA pretreatment. In conclusion, SA pretreatment prevents subsequent I/R or CsA-induced injuries in the rat kidney, and this renoprotective effect appears to be mediated by induction of HSP70.

Animals↗
PubMed2001

Juxtaglomerular cell tumor of the kidney: a case report.

We report a case of renin-secreting juxtaglomerular cell tumor which developed in a hypertensive 47-yr-old Korean man. Presumptive clinical diagnosis was made before surgery based on the high level of plasma renin and the radiologic evidence of renal mass. Grossly, a round, bulging, well-encapsulated mass of 3 x 3 cm was located in the mid-portion of the right kidney. On microscopic examination, the tumor was composed of ovoid to polyhedral cells with bland nuclei, indistinct nucleoli and light eosinophilic cytoplasm. The immunostaining for renin showed strong positivity in the cytoplasm of tumor cells. The characteristic rhomboid shaped renin protogranules were observed in ultrastructural analysis.

Humans↗
PubMed2001

Clinical significance of anti-endothelial cell antibody in renal transplant recipients.

In order to evaluate the role of anti-endothelial cell antibody (AECA) in acute rejection in renal transplantation, serum AECA IgG titers were measured in 68 healthy controls, 111 chronic hemodialysis (HD) patients and 58 first renal transplant recipients. The AECA titer in hemodialysis patients was higher than in healthy controls (13.9 +/- 5.0 vs. 4.8 +/- 2.3 U/mL, p < 0.01). In transplant recipients, AECA titers were not affected by dialysis mode (HD vs. CAPD vs. non-dialysis; 9.6 +/- 7.6 vs. 7.9 +/- 3.9 vs. 11.9 +/- 3.1 U/mL, p > 0.05). After renal transplantation, AECA titer was decreased significantly (vs. 4.7 +/- 3.6 U/mL. p < 0.01). The serum AECA IgG titers increased significantly in recipients with acute rejection (6.9 +/- 3.1 vs. 13.5 +/- 9.9 U/mL, p < 0.01), but decreased to 5.6 +/- 3.0 U/mL (p < 0.01) after formal rejection therapy. In the recipients with acute rejection (n = 27), the pre-renal transplant AECA titer was higher than in that without acute rejection (14.0 +/- 8.6 vs. 7.7 +/- 3.8 U/mL, p < 0.01). The results of this study lead us to conclude that pre- and post-renal transplant AECA titer might be a useful predictor for acute rejection and useful for monitoring acute rejection in renal transplant recipients.

Adult↗
PubMed2000

High glucose-induced intercellular adhesion molecule-1 (ICAM-1) expression through an osmotic effect in rat mesangial cells is PKC-NF-kappa B-dependent.

AIMS/HYPOTHESIS: Infiltration of mononuclear cells and glomerular enlargement accompanied by glomerular cell proliferation are very early characteristics of the pathophysiology of diabetes. To clarify the mechanism of early diabetic nephropathy, we measured [3H]-thymidine incorporation and cell numbers to show the influence of a high ambient glucose concentration and the osmotic effect on rat mesangial cell proliferation. We also measured the effect of high glucose on the expression of intercellular adhesion molecule-1 and vascular adhesion molecule-1 by flow cytometry and semiquantitative RT-PCR in mesangial cells and the adhesion of leukocytes to mesangial cells. METHODS/RESULTS: Cells exposed to high D-glucose (30 mmol/l) caused an increase in [3H]-thymidine incorporation and cell numbers at 24 and 48 h and normalized at 72 h (p < 0.05), whereas these changes were not found in high mannitol (30 mmol/l), IL-1 beta, or TNF alpha-stimulated mesangial cells. Cells exposed to high-glucose (15, 30, or 60 mmol/l) or osmotic agents (L-glucose, raffinose and mannitol) showed that intercellular adhesion molecule-1 expression began to increase after 24 h, reached its maximum at 24 and 48 h and gradually decreased afterwards. The stimulatory effects of high glucose and high mannitol on mRNA expression were observed as early as 6 h and reached its maximum at 12 h. Up-regulation of ICAM-1 protein and mRNA was also found in IL-1-beta and TNF-alpha-stimulated mesangial cells. Neither vascular adhesion molecule-1 protein nor mRNA expression was, however, affected by high glucose and high mannitol. Notably, the protein kinase C inhibitors calphostin C and staurosporine reduced high glucose- or high mannitol-induced intercellular adhesion molecule-1 mRNA expression and high glucose-induced proliferation. Furthermore, the NF-kappa B inhibitor N-tosyl-L-phenylalanine chloromethyl ketone reduced high glucose- or high mannitol-induced intercellular adhesion molecule-1 mRNA expression and high glucose-induced proliferation. Results showed that high glucose (15, 30 mmol/l) or high concentrations of osmotic agents remarkably increased the number of adherent leukocytes to mesangial cells (p < 0.01) compared with control cells (5 mmol/l D-glucose). Functional blocking of intercellular adhesion molecule-1 on mesangial cells with rat intercellular adhesion molecule-1 monoclonal antibody, calphostin C, staurosporine, or N-tosyl-L-phenylalanine chloromethyl ketone significantly inhibited high glucose- or high mannitol-induced increase in leukocyte adhesion (p << 0.05). CONCLUSION/INTERPRETATION: These results suggest that high glucose can upregulate intercellular adhesion molecule-1 protein and mRNA expression but not vascular adhesion molecule-1 expression in mesangial cells and promote leukocyte adhesion through up-regulation of intercellular adhesion molecule-1 through osmotic effect, possibly depending on the protein kinase C nuclear factor-kappa B (PKC-NF-kappa B) pathway. High glucose itself can also promote mesangial cell proliferation through the PKC-NF-kappa B pathways. We conclude that hyperglycaemia in itself seems to be an important factor in the development of early diabetic nephropathy.

Animals↗