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Biomedical subjects

G H Kim

Publications and source records attributed to G H Kim.

13 recordsLinked to original sources
PubMed1998

Evaluation of renal tubular functions in convalescent phase of hemorrhagic fever with renal syndrome.

To evaluate renal tubular functions and to investigate the causative factors of urinary-concentrating defects in the late stage of hemorrhagic fever with renal syndrome (HFRS), 11 HFRS patients in the convalescent phase were studied and compared with 8 acute renal failure (ARF) patients in convalescence (disease controls) and 9 healthy adults preparing for kidney donation (normal controls, NC). Minimal urine osmolality induced by water loading was higher (p < 0.05) in HFRS (89.5 +/- 22.1 mosm/kg) and ARF patients (84.8 +/- 14.7 mosm/ kg) than in NC (47.8 +/- 4.6 mosm/kg), but the solute-free water clearance of HFRS patients (9.0 +/- 1.3%), measured at maximal diuresis, was not different from that of ARF patients (6.7 +/- 1.2%) or NC (10.5 +/- 1.4%). After 12-hour water deprivation + vasopressin stimulation, HFRS had lower urine osmolality (433.7 +/- 31.1 versus 850.0 +/- 35.1 mosm/kg; p < 0.05), urine-to-plasma osmolality ratio (1.47 +/- 0.11 versus 2.91 +/- 0.11; p < 0.05), and solute-free water reabsorption (0.53 +/- 0.07 versus 0.91 +/- 0.12%; p < 0.05) than NC. As compared with ARF patients (1.09 +/- 0.16%) or NC (1.49 +/- 0.16%), HFRS patients (0.43 +/- 0.20%) had lower solute-free water reabsorption measured at maximal antidiuresis induced by water deprivation + vasopressin stimulation + hypertonic saline infusion (p < 0.05). In HFRS, the plasma vasopressin level and plasma vasopressin/osmolality ratio increased from 3.9 +/- 0.8 to 6.1 +/- 1.1 pg/ml and from 0.013 +/- 0.003 to 0.020 +/- 0.004 pg/ml/mosm/kg after 12-hour water deprivation, respectively (p < 0.01). However, neither basal nor stimulated values of the plasma vasopressin level or plasma vasopressin/osmolality ratio was different among the 3 groups. HFRS patients were not different from ARF patients or NC in lithium clearance, urinary-acidifying capacity, and fractional excretions of sodium, potassium and bicarbonate. We conclude that in the convalescent phase of HFRS, the urinary-acidifying ability is not disturbed, the urinary-diluting defect is mild, and the urinary-concentrating capacity is obviously impaired. This study suggests that the most important factor contributing to the urinary-concentrating defect in HFRS is the reduced collecting duct responsiveness to vasopressin.

Acute Kidney Injury↗
PubMed1998

Prenatal molecular evaluation of six fetuses in four unrelated Korean families with ornithine transcarbamylase deficiency.

Ornithine transcarbamylase (OTC) deficiency, an X-linked inborn error of the urea cycle, leads to the accumulation of ammonia, causing neurologic deficits. Clinical management for the patients with OTC deficiency is frustrating and requires a burdensome medical regimen, since they may have impairment and recurrent episodes of hyperammonemia in spite of intensive care. Therefore, prenatal diagnosis of the affected fetus is important in genetic counselling for the family at high risk. In this study, mutations in the OTC gene of three obligate heterozygotes and a proband have been identified in four unrelated families: R141Q, R320X, H214Y, M205T. Each mutation altered restriction recognition sites; TaqI for R141Q, NlaIII for M205T, RsaI for H214Y, BclI for R320X. Based on their molecular defects, prenatal diagnoses of 6 fetuses including one set of fraternal twins were successfully made at the ninth to eleventh week of gestation by polymerase chain reaction (PCR)-restriction digestion using genomic DNA from chorionic villus sampling (CVS). We predicted the outcome of all fetuses prenatally. Among six, four were females and two were males, which were determined by PCR amplification of the sex determining region of the Y chromosome (SRY) gene. Each carried a wild type allele for the corresponding mutant allele. They were also tested postnatally for the mutations to be unaffected.

Amino Acid Metabolism, Inborn Errors↗
PubMed1998

Absence of H(+)-ATPase in the intercalated cells of renal tissues in classic distal renal tubular acidosis.

Proton-secretory defect is thought to be a major pathophysiologic mechanism leading to classic distal renal tubular acidosis (dRTA). However, there have been only two case reports demonstrating the absence of proton pump in renal tissues of the patients with Sjögren's syndrome. This study presents two cases of classic dRTA in which the absence of intact H(+)-ATPase was shown in their renal biopsy tissues by immunohistochemistry using a rabbit polyclonal antibody against the 70 kDa catalytic subunit of H(+)-ATPase from bovine brain clathrin-coated vesicles; one of the cases is diagnosed as subclinical Sjögren's syndrome and the other is idiopathic dRTA. A normal human kidney (NC) and the renal biopsy tissues from a patient with chronic tubulointerstitial nephritus whose proton secretory capacity was intact (DC) were compared as controls. The first patient, a 26-year-old woman, presented with quadriparesis. Her serologic tests revealed positive autoantibodies (ANA, SSA; SSB & RF), and a lower lip biopsy confirmed the diagnosis of Sjögren's syndrome. The second patient, a 43-year-old woman, who initially presented with a pathologic fracture of both femoral necks was referred for an evaluation for hypokalemia by the Department of Orthopedic Surgery. Her renal ultrasonography showed medullary calcification, and no autoantibodies were positive. Serum electrolytes and blood gas analyses of the two patients indicated severe hypokalemia and metabolic acidosis, and proton secretory defects were shown by a failure to lower the urine pH during marked acidemia induced by NH4Cl loading and an abnormally low urine-blood pCO2 difference during bicarbonate administration. While stainings with the anti-H(+)-ATPase antibody in NC and DC were strongly positive in intercalated cells in the connecting tubules and collecting ducts, the tissues from both patients with dRTA were devoid of any anti-H(+)-ATPase staining in the intercalated cells. These results support that the pathophysiologic basis of impaired H+ secretion in idiopathic classic dRTA as well as Sjögren's syndrome is the absence of intact H(+)-ATPase pumps in the intercalated cells.

Acidosis, Renal Tubular↗
PubMed1997

A comparison of the effects of testicular maturation and aging on the stage-specific expression of CP-2/cathepsin L messenger ribonucleic acid by Sertoli cells of the Brown Norway rat.

We have examined the effects of maturation and aging on expression of cyclic protein-2 (CP-2)/cathepsin L mRNA by rat Sertoli cells. During maturation (25-68 days of age) there was a significant, 7.6-fold increase in CP-2/cathepsin L mRNA. There was a significant, 2.9-fold increase in SGP-2 mRNA during the same period. In situ hybridization analysis demonstrated that stage-specific expression of CP-2/cathepsin L mRNA developed between 30 and 35 days. By 64 days of age, this transcript was only detectable in Sertoli cells within stage VI-VII tubules. Northern blot analysis of 23-mo-old testes revealed statistically significant decreases in total testis contents of CP-2/cathepsin L and SGP-2 mRNAs (4- and 3-fold, respectively) in testes that lacked germ cells but not in aged testes with a full complement of germ cells. In situ hybridization analysis revealed high amounts of CP-2/cathepsin L mRNA in all aged tubules that were losing germ cells via apoptosis, regardless of the stage of the cycle. Immunocytochemical analysis demonstrated that in these aged, regressing tubules, CP-2/cathepsin L protein became concentrated in dying or dead germ cells.

Aging↗
PubMed1997

Effect of Ca2+ channel blockers, external Ca2+ and phospholipase A2 inhibitors on t-butylhydroperoxide-induced lipid peroxidation and toxicity in rat liver slices.

OBJECTIVES: This study was undertaken to examine the effect of oxidant on lipid peroxidation and lethal cell injury in rat liver slices. METHODS: t-Butylhydroperoxide (t-BHP) was employed as a model of an oxidant. The lipid peroxidation and lethal cell injury were estimated by measuring the formation of malondialdehyde (MDA) and lactate dehydrogenase (LDH) release, respectively. RESULTS: t-BHP increased lipid peroxidation and LDH release in a dose-dependent manner over concentrations of 0.5-10 mM. t-BHP-induced lipid peroxidation was completely prevented by an antioxidant, N,N-diphenyl-p-phenylenediamine (DPPD), but LDH release was partially decreased. Both t-BHP-induced lipid peroxidation and LDH release were significantly protected by iron chelator, deferoxamine, sulfhydryl reducing agent, dithiothreitol and glutathione. Ca2+ channel blockers, verapamil, diltiazem and nifedipine exerted a significant protective effect against t-BHP-induced lipid peroxidation and LDH release. By contrast, addition of external Ca2+ chelator, ethylene glycol bis(b-aminoethyl ether)-N,N-tetraacetic acid (EGTA) did not alter t-BHP-induced lipid peroxidation, whereas t-BHP-induced lethal cell injury was significantly prevented. Phospholipase A2 (PLA2) inhibitors, mepacrine and butacaine produced a partial protective effect. CONCLUSIONS: These results suggest that t-BHP induces cell injury by lipid peroxidation-dependent and -independent mechanisms which can be partially prevented by Ca2+ channel blockers and PLA2 inhibitors.

Animals↗
PubMed1996

Simple procedure for phase identification using convergent beam electron diffraction patterns.

The use of the primitive cell volume and the zero order Laue zone (ZOLZ) pattern is proposed as a means to identify phases in a complex microstructure. A single convergent beam pattern, containing a higher order Laue zone ring, from a nanosized region is sufficient to calculate the primitive cell volume of the phase, while ZOLZ pattern is used to determine the zone axis of the crystal. A computer program is used to screen out possible phases on the basis of the value of measured cell volume. The indexing of the ZOLZ pattern follows in the program to find the zone axis of the identified phase. Combination of these two methods ensures accuracy and reliability of phase identification from a single CBED pattern. An example of the analysis is given from the rapidly solidified Al-Al3Ti system.

Crystallization↗
PubMed1996

Identification of new mutations in the ornithine transcarbamylase (OTC) gene in Korean families.

Ornithine transcarbamylase (OTC) deficiency, an X-linked inborn error of the urea cycle, is known to be heterogeneous genetically as well as phenotypically. Molecular defects of Korean patients with OTC deficiency have not been reported. To investigate molecular lesions resulting in OTC deficiency, the OTC genes of unrelated symptomatic or asymptomatic female heterozygotes were amplified exon by exon and analysed by direct sequencing of double-stranded DNA. Three new mutations, two missense and one nonsense, were detected: (1) a C-to-T transition in codon 44 in exon 2 replacing a threonine by an isoleucine (T44I) was found in a late-onset symptomatic female patient but not in her asymptomatic mother; (2) a C-to-T transition in codon 214 creating a new RsaI recognition site in exon 6 and substituting tyrosine for histidine (H214Y) was identified in an asymptomatic female carrier whose son developed acute neonatal onset of OTC deficiency; (3) a C-to-T transition in codon 320 (arginine) abolishing a TaqI recognition site and creating a new BclI site in exon 9 with generation of a stop codon (R320X) leading to premature termination in the enzyme. This nonsense mutation was found in a symptomatic female patient and her asymptomatic mother whose son died of OTC deficiency during the neonatal period. In addition, we found a G-to-A transition in codon 141 in exon 5 causing substitution of glutamine for arginine (R141Q) in a female obligate heterozygote whose previous three sons succumbed to acute neonatal-onset OTC deficiency. This missense mutation has been described previously and is known to eliminate a TaqI recognition site in exon 5.

Alleles↗
PubMed1996

Evaluation of urine acidification by urine anion gap and urine osmolal gap in chronic metabolic acidosis.

To investigate the clinical significance of urine anion gap and urine osmolal gap as indirect markers of urine acidification in chronic metabolic acidosis, we evaluated urine ammonium (NH4+), net acid excretion (NAE), urine anion gap (Na(+) + K(+) - Cl-), and urine osmolal gap (urine osmolality - [2(Na(+) + K(+)) + urea]) in 24 patients with chronic renal failure (CRF), eight patients with classic distal renal tubular acidosis (dRTA), and eight NH4Cl-loaded normal controls (NCs). Urine NH4+ excretion was lower (P < 0.001) in the CRF (5.4 +/- 0.6 mmol/d) and dRTA (19.2 +/- 2.7 mmol/d) patients than in the NCs (52.6 +/- 3.7 mmol/d); NAE was also lower (P < 0.001) in the CRF (9.8 +/- 1.6 mmol/d) and dRTA (16.7 +/- 4.7 mmol/d) patients than in the NCs (79.4 +/- 4.7 mmol/d). Urine anion gap was higher (P < 0.001) in the CRF (24.7 +/- 2.2 mmol/L) and dRTA (36.7 +/- 7.7 mmol/L) patients than in the NCs (-16.2 +/- 5.5 mmol/L). Urine osmolal gap was lower (P < 0.05) in the dRTA patients (129.7 +/- 17.0 mmol/L) than in the NCs (319.7 +/- 58.4 mmol/L). When the data from all subjects were pooled, urine anion gap correlated inversely with urine NH4+ (r = -0.70, P < 0.001) and with NAE (r = -0.83, P < 0.001), and urine osmolal gap correlated positively with urine NH4+ (r = 0.69, P < 0.01) and with NAE (r = 0.71, P < 0.05). We conclude that impaired urine acidification in CRF and dRTA patients is associated with an increase in urine anion gap and a decrease in urine osmolal gap, and that both urine anion gap and urine osmolal gap correlate well with NAE as well as with urine NH4+.

Acid-Base Equilibrium↗
PubMed1995

Intracellular signal transduction of PBAN action in lepidopteran insects: inhibition of sex pheromone production by compactin, an HMG CoA reductase inhibitor.

Pheromone biosynthesis activating neuropeptide (PBAN) regulates sex pheromone production in the pheromone glands of many species of female moths. In order to probe the biochemical steps as well as underlying mechanisms regulated by PBAN, we have tested the effect of chemicals on sex pheromone production by using an in vitro assay. Among the chemicals we tested here, compactin, a specific 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor, clearly inhibited the pheromone biosynthesis in the silkworm, Bombyx mori, and the common cutworm, Spodoptera litura. Since the activation of HMG CoA reductase occurs by dephosphorylation mediated by a specific phosphatase and the biochemical step regulated by PBAN in bombykol biosynthesis is similar to the one catalyzed by HMG-CoA reductase in cholesterol biosynthesis, the present results support the idea that phosphoprotein phosphatase has a significant role to regulate bombykol production in the intracellular transduction of PBAN action in B. mori.

Amino Acid Sequence↗
PubMed1995

Intracellular transduction in the regulation of pheromone biosynthesis of the silkworm, Bombyx mori: suggested involvement of calmodulin and phosphoprotein phosphatase.

We have tested the effects of chemicals on bombykol production in vitro in the silkworm, Bombyx mori, to probe the biochemical steps as well as underlying mechanisms regulated by PBAN. These results suggest the involvement of calmodulin and phosphoprotein phosphatase in the intracellular signal transduction of PBAN action.

Amino Acid Sequence↗
PubMed1992

Intestinal neurofibromatosis in von Recklinghausen's disease: presenting as chronic anemia due to recurrent intestinal hemorrhage.

Neurofibromatosis (von Recklinghausen's disease) is a neuroectodermal disorder characterized by pigmentary changes of the skin (café-au-lait spots), cutaneous and visceral tumors (neurofibromas) and systemic abnormalities. The involvement of gastrointestinal tract in neurofibromatosis is not common. The most common symptoms, refer able to lesions in the gut, are hematemesis, melena and abdominal pain. We experienced a case of intestinal neurofibroma in von Recklinghausen's disease. The patient was a 39 year-old female who had suffered from chronic iron deficiency anemia and recurrent gastrointestinal hemorrhage due to two neurofibromas of jejunum for 3 years, which was diagnosed by superior mesenteric and ileal arteriogram and 99mTc pertechnetate-labelled RBC scan, and treated by segmental resection of jejunum with end to end anastomosis.

Adult↗
PubMed1988

Reduction of the blocking effect in block-coded images using a model of early human vision.

We propose a method, based on lowpass and bandpass components of Granrath's early human vision model, which reduces the blocking effect in block-coded images. The method consists of a lowpass filtering stage to smooth out the blocking effect and a contrast-enhancement stage to increase contrast in the restored image. Experimental results of the method show better performance than that of conventional methods for reducing blocking effects.

Algorithms↗