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Biomedical subjects

H K Hong

Publications and source records attributed to H K Hong.

At least 19 recordsLinked to original sources
PubMed2002

Expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in human crescentic glomerulonephritis.

AIMS: In glomerulonephritis, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) may play important roles in the formation of crescents. These studies are designed to evaluate the expression patterns of ICAM-1 and VCAM-1 in human crescentic glomerulonephritis and to determine the cellular origin of adhesion molecules in the crescentic lesions. METHODS AND RESULTS: We examined the expression of ICAM-1 and VCAM-1 proteins in renal biopsies with cellular (n=7), fibrocellular (n=9) or fibrous (n=4) crescentic glomerulonephritis, and six controls by immunohistochemistry. mRNA expression of ICAM-1 and VCAM-1 was further evaluated by RNA in-situ hybridization. Cytokeratin or CD68 immunohistochemistry was performed on the same sections, where in-situ hybridization had been carried out. In cellular crescents, ICAM-1 and VCAM-1 proteins were over-expressed to a similar extent. Of the three types of crescents, the extent of ICAM-1 immunopositivity was the greatest in the cellular crescents and decreased towards the fibrous crescents (P < 0.05). Yet the extent of VCAM-1 immunoreactivity was not different between the types. Fibrous crescents still contained some epithelial cells and showed only VCAM-1 expression. In the glomeruli with cellular or fibrocellular crescents, the extent of ICAM-1 immunopositivity in the glomerular tufts was significantly larger than that of VCAM-1 (P < 0.05). In an in-situ hybridization study, the mRNA expression patterns of ICAM-1 and VCAM-1 paralleled their protein expressions. A double-labelling study showed that the signal for ICAM-1 and VCAM-1 mRNAs was mainly present in cytokeratin-positive and CD68-negative cells in the crescentic lesions. CONCLUSIONS: These results suggest that glomerular parietal epithelial cells in cellular crescents up-regulate both ICAM-1 and VCAM-1, and that some epithelial cells retained in fibrous crescents persistently over-express VCAM-1, but not ICAM-1. They also suggest that ICAM-1 is involved in early leucocyte recruitment into glomeruli in crescentic glomerulonephritis.

Endothelium, Vascular↗
PubMed2001

The winged helix/forkhead transcription factor Foxq1 regulates differentiation of hair in satin mice.

Satin (sa) homozygous mice have a silky coat with high sheen arising from structurally abnormal medulla cells and defects in differentiation of the hair shaft. We demonstrate that the winged helix/forkhead transcription factor, Foxq1 (Forkhead box, subclass q, member 1) is mutant in sa mice. An intragenic deletion was identified in the radiation-induced satin mutant of the SB/Le inbred strain; a second allele, identified by an N-ethyl-N-nitrosourea (ENU) mutagenesis screen, has a missense mutation in the conserved winged helix DNA-binding domain. Homozygous mutants of the two alleles are indistinguishable. We show that Foxq1 is expressed during embryogenesis and exhibits a tissue-restricted expression pattern in adult tissues. The hair defects appear to be restricted to the inner structures of the hair; consequently, Foxq1 has a unique and distinct function involved in differentiation and development of the hair shaft. Despite an otherwise healthy appearance, satin mice have been reported to exhibit suppressed NK-cell function and alloimmune cytotoxic T-cell function. We show instead that the immune defects are attributable to genetic background differences.

Amino Acid Sequence↗
PubMed2001

mRNA expression of urokinase and plasminogen activator inhibitor-1 in human crescentic glomerulonephritis.

AIMS: Weak staining for urokinase-plasminogen activator (uPA), tissue type plasminogen activator (tPA), or plasminogen activator inhibitor-1 (PAI-1) confined to crescents has been described in a few cases of severe crescentic glomerulonephritis. We evaluated the molecular mechanism by which these proteins are increased or induced within crescents. METHODS AND RESULTS: We examined uPA, tPA and PAI-1 mRNA expression in 12 renal biopsies with crescentic glomerulonephritis, and in six control renal biopsies with no detectable abnormalities by RNA in-situ hybridization. The expressions of uPA, tPA and PAI-1 proteins were also assessed by immunofluorescence. To better determine the cellular origin of uPA and PAI-1 transcripts, CD68 protein was studied by immunohistochemistry on the same sections on which in-situ hybridization had been performed. In controls, there were very low level signals of uPA and PAI-1 mRNAs in a few glomerular epithelial cells (GECs). Specific signals of uPA and PAI-1 mRNAs were detected in the cells forming crescents in all the cases with crescentic glomerulonephritis. However, weak expression of mRNA for tPA was detected in two cases only. Immunostaining for uPA and PAI-1 was positive in some but not all, cases of crescentic glomerulonephritis. A double-labelling study showed that the signal for PAI-1 and uPA mRNAs was mainly in CD68- cells. CONCLUSIONS: Local accumulation of uPA or PAI-1 in crescents is associated with enhanced mRNA expression of these proteins. The up-regulation of PAI-1 mRNA by GECs, in particular, could play a major role in the formation of persistent fibrin deposits and progression of the lesions in crescents. Whether up-regulation of uPA is an epiphenomenon or plays a pathogenic role in the formation of crescents remains to be clarified.

Adult↗
PubMed2001

Advanced glycosylation end products stimulate collagen mRNA synthesis in mesangial cells mediated by protein kinase C and transforming growth factor-beta.

Advanced glycosylation end products (AGE) seem to be implicated in the pathogenesis of diabetic nephropathy. The present study has examined the effects of AGE on protein kinase C (PKC) activity and transforming growth factor-beta1 (TGF-beta1) in relation to collagen gene regulation in cultured human mesangial cells (HMCs). Quiescent HMCs were exposed to serum-free media containing bovine serum albumin (BSA), AGE-modified BSA (AGE-BSA), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM). AGE-BSA (200 microg/mL) induced a peak membrane-associated PKC activity, particularly PKC-a, at 4 hours. AGE-BSA stimulated alpha1(I) and alpha1(IV) collagen mRNA expression after 24-hour incubation with HMCs, which remained elevated until hour 60. HMCs incubated with AGE-BSA induced a significant inhibition of cell proliferation compared with cells incubated with BSA. AGE-BSA stimulated TGF-beta mRNA and protein expression in HMCs. The TGF-beta secreted by HMCs was shown by CCL-64 mink lung cell assay to be bioactive. In contrast, BSA-AM did not affect either collagen or TGF-beta mRNA or protein expression in HMCs. The stimulatory effects of AGE-BSA on collagen gene regulation in HMCs could be negated by the pretreatment of HMCs with GF 109203X for 30 minutes or with phorbol myristate acetate for 24 hours before AGE-BSA administration. Neutralizing antibody to TGF-beta inhibited increased collagen mRNA expression by HMCs exposed to AGE-BSA. These results suggest that AGE-BSA stimulates collagen mRNA expression by activating PKC and the transcriptional upregulation of TGF-beta1 in HMCs. Thus, PKC and TGF-beta may function as key signaling intermediaries in the AGE-up-regulated collagen gene expression pathway in HMCs.

Adult↗
PubMed2000

mRNA expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in acute renal allograft rejection.

BACKGROUND: The intercellular adhesion molecule-1 (ICAM-1) and the vascular cell adhesion molecule-1 (VCAM-1) show a form of complementary distribution in normal and grafted kidneys. The molecular mechanism by which ICAM-1 and VCAM-1 are increased or induced on vascular cells during acute renal allograft rejection has not been clearly defined. METHODS: We examined ICAM-1 and VCAM-1 mRNA expression in 17 renal allograft biopsies with (n=12) and without (n=5) features of acute rejection, and four control renal biopsies with no detectable abnormalities by RNA in situ hybridization. The expression of ICAM-1 and VCAM-1 protein was also assessed by immunohistochemical staining of frozen sections. RESULTS: In controls and nonrejecting graft biopsies, the signals of the ICAM-1 and VCAM-1 transcripts in vascular cells were almost negligible. Specific signals of ICAM-1 and VCAM-1 mRNAs were detected on the endothelial cells of small muscular arteries in most cases with acute renal allograft rejection. The messages for ICAM-1 and VCAM-1 were also detected on arterial smooth muscle cells in all the five cases with severe type III rejection. CONCLUSIONS: These results suggest that the induced appearance of ICAM-1 and VCAM-1 on the vascular cells of acutely rejecting renal transplants was related to actual cellular synthesis and that both adhesion molecules could act together in the rejection process. They also suggest that the expression of ICAM-1 and VCAM-1 genes by arterial smooth muscle cells may be an important cause of transmural arteritis in severe acute renal allograft rejection.

Acute Disease↗
PubMed2000

High-level expression of canine parvovirus VP2 using Bombyx mori nucleopolyhedrovirus vector.

For the potential use as recombinant vaccine, canine parvovirus (CPV) major capsid protein VP2 was expressed using Bombyx mori nucleopolyhedrovirus (BmNPV) vector. CPV VP2 gene was introduced into polyhedrin-based BmNPV transfer vector pBmKSK3, and recombinant virus BmK1-Parvo was prepared. When anti-CPV.VP2 monoclonal antibody was employed in immunofluorescence staining, an intense signal was observed within BmK1-Parvo-infected Bm5 cells but not within uninfected cells or cells infected with a wild-type BmNPV-K1. In hemagglutination assay, the expression level of VP2 were 3.2 x 10(3) HA units/ml from infected Bm5 cells, 2.1x 10(5) HA units/larvae from infected larval fat body, and 1.6x 10(6) HA units/ml from infected larval hemolymph. These results suggested that BmNPV vector system using B. mori larva as host could be applied to efficient mass-production of recombinant vaccines.

Animals↗
PubMed2000

Characterization of four isolates of Bombyx mori nucleopolyhedrovirus.

Bombyx mori nucleopolyhedroviruses (BmNPVs), isolated from a sericultural Korean farm, were purified and characterized by their DNA restriction pattern, virus replication, polyhedra production and gene structures. The EcoR I and Sal I fragments showed similar overall patterns with minor difference but distinguishable patterns in each isolate. There was no significant difference in the virus replication pattern, yield of total polyhedra production and polyhedra morphology, but the yield of released polyhedra by BmNPV-K1 in Bm5 cells was 2 to 5 times higher than that of other isolates. In comparative studies of p10 gene, BmNPV-K1 and K3 had same structure and they encoded a protein consisting of 94 amino acids. Although BmNPV-K2 encoded the same length of amino acids with BmNPV-K1 and K3, it had different structure, and BmNPV-K4 had the p10 gene encoding 70 amino acids.

Amino Acid Sequence↗
PubMed1999

mRNA expression of glomerular basement membrane proteins and TGF-beta1 in human membranous nephropathy.

Immunogold densities for the 'classical' and 'novel' alpha chains of type IV collagen, laminin, and fibronectin are increased in the spikes in human membranous nephropathy (MN). To investigate the molecular mechanisms which underlie these changes in glomerular basement membrane (GBM) components, alpha1(IV) collagen, alpha4(IV) collagen, S-laminin, fibronectin, transforming growth factor (TGF)-beta1 and TGF-beta2 mRNA expression was examined in 12 renal biopsy specimens with MN and six renal biopsies with no detectable abnormality by RNA in situ hybridization. In controls, there were relatively low signals of alpha1(IV) collagen, alpha4(IV) collagen, S-laminin, and TGF-beta1 mRNAs, but there were no fibronectin or TGF-beta2 transcripts in glomerular cells. In MN, the number of alpha4(IV) collagen, alpha1(IV) collagen, S-laminin or TGF-beta1 mRNA-expressing cells per glomerular cross-section was significantly larger than in controls (p< 0.05), and fibronectin mRNA was occasionally expressed in glomerular visceral epithelial cells (GECs). No message for TGF-beta2 was seen in MN. The number of TGF-beta1 mRNA-expressing cells per glomerular cross-section significantly correlated with that of alpha1(IV) mRNA-expressing cells (p< 0.01). The MN patients with positivie signal for fibronectin mRNA exhibited more severe GBM thickening than those without (p< 0.05). These results indicate that the increased presence of GBM proteins in spikes of MN is associated with enhanced mRNA expression of these proteins. They also suggest that subepithelial deposits in MN stimulate GECs to produce TGF-beta1, which in turn could mediate the expression of GBM protein genes by GECs.

Adolescent↗
PubMed1999

Pleiotropic skeletal and ocular phenotypes of the mouse mutation congenital hydrocephalus (ch/Mf1) arise from a winged helix/forkhead transcriptionfactor gene.

Congenital hydrocephalus is an etiologically diverse, poorly understood, but relatively common birth defect. Most human cases are sporadic with familial forms showing considerable phenotypic and etiologic heterogeneity. We have studied the autosomal recessive mouse mutation congenital hydrocephalus ( ch ) to identify candidate human hydrocephalus genes and their modifiers. ch mice have a congenital, lethal hydrocephalus in association with multiple developmental defects, notably skeletal defects, in tissues derived from the cephalic neural crest. We utilized positional cloning methods to map ch in the vicinity of D13Mit294 and confirm that the ch phenotype is caused by homozygosity for a nonsense mutation in a gene encoding a winged helix/forkhead transcription factor ( Mf1 ). Based on linked genetic markers, we performed detailed phenotypic characterization of mutant homozygotes and heterozygotes to demonstrate the pleiotropic effects of the mutant gene. Surprisingly, ch heterozygotes have the glaucoma-related distinct phenotype of multiple anterior segment defects resembling Axenfeld-Rieger anomaly. We also localized a second member of this gene family ( Hfh1 ), a candidate for other developmental defects, approximately 470 kb proximal to Mf1.

Animals↗
PubMed1999

LDL stimulates collagen mRNA synthesis in mesangial cells through induction of PKC and TGF-beta expression.

Abnormal lipid accumulation in glomeruli could be implicated in the pathogenesis of glomerulosclerosis. Low-density lipoprotein (LDL) stimulates collagen mRNA expression in cultured human mesangial cells (HMC). To explore the possible molecular mechanisms by which LDL promotes collagen gene expression, we examined the effects of LDL on protein kinase C (PKC) activity and transforming growth factor-beta (TGF-beta) expression in relation to collagen gene regulation in HMC. LDL (200 microg/ml) induced an acute increase in PKC activity, particularly PKC-alpha and -delta, within 15 min, which decreased to control value at 2 h. LDL stimulated TGF-beta1, and alpha1(I) and alpha1(IV) collagen mRNA expression within 30 min of incubation with HMC, and levels remained elevated until hour 4. LDL induced the secretion of TGF-beta by HMC. This TGF-beta was shown by CCL-64 mink lung cell assay to be, in part, bioactive. The stimulatory effects of LDL on collagen gene regulation in HMC were blocked by the inhibition of PKC using GF-109203X (GFX) or the downregulation of PKC using phorbol myristate acetate. Neutralizing antibody to TGF-beta inhibited the increased collagen mRNA expression by HMC exposed to LDL. The downregulation or inhibition of PKC did not affect the stimulatory effect of LDL on TGF-beta mRNA or protein expression. These results suggest that in HMC, LDL stimulates collagen mRNA expression through the rapid activation of PKC-alpha and -delta and transcriptional upregulation of TGF-beta. Thus PKC and TGF-beta may function as independent key signaling intermediaries in the pathway by which LDL upregulates collagen gene expression in HMC.

Cells, Cultured↗
PubMed1995

[Seasonal prevalence and behaviour of Aedes togoi].

Ecological studies of Aedes togoi, the vector of malayan filariasis, were carried out at Tolsando, Yosu and Sokcho area in 1991. The adult population of Aedes togoi was continuously appeared from the first week of April to the end of November showing the highest density in July. The larvae of Aedes togoi were found at rock pools from March to December in Sokcho area and the density was highest in July and August, whereas in the southern coastal area (Yosu), the larvae were found throughout the year and the density was the highest in June. The rate of larvae inhabited below 0.5% salinity was 45.7% in Sokcho and 51.7% in Yosu. The feeding activity of Aedes togoi was nocturnal, with the peak period of 01:00-03:00 hours. Indoor feeding activities were slightly higher than outdoors showing the biting ratio of 1:0.8 (indoor: outdoor). The average number of Aedes togoi attracted to CO2 gas was 8.5 whereas 117 Anopheles sinensis was attracted. The result indicates that CO2 is not an effective attractant for host seeking of Aedes togoi compared to Anopheles sinensis. The most common place was bedroom with 54.5% of total collections and next to stock place (18.2%), floor (9.1%) and kitchen (9.1%).

Animals↗
PubMed1995

[Effects of nutrient and salinity in egg and larval development of Aedes togoi].

The study made an observation on periodicity of oviposition, and the effects of nutrient and salinity in egg and larval development of Aedes togoi, and the results are summarized as follows: The 53.9% mosquitoes of one feeding laid eggs once, 26.9% laid twice and 19.2% laid three times. Autogenous rate of Aedes togoi reared in three different nutrient groups in larval sage was 6.9% in 0.8 mg/larva, 22.5% in 1.6 mg/larva and 44.4% in 2.4 mg/larva. The oviposition rate according to different salinity of the oviposition sites (0%, 0.5%, 1.0%, 2.0% and 4.0%) was 25.2% in distilled water, 36.2% in 0.5% salinity, 23.5% in 1.0% salinity and 14.6% in 2.0% salinity. Developing period of the aquatic stage of male Aedes togoi in 25 degrees C were shorter (10.73 days) than females (11.85 days). The most effective concentration of salinity for the developing period was 1.0% which took 9.25 days in males and 10.44 days in females. In the developmental status of the follicles according to nutrition in the larval stage, the numbers of follicles of groups fed 0.8 mg, 1.6 mg and 2.4 mg per larva were 180.7, 197.5 and 202 respectively. The result of ovary dissection on the 10th day after emergence, three different nutrition groups were in Christopher's stage IIa mostly; each 71.0%, 61.1% and 39.9% of the total follicles and autogenous females observed.

Animal Nutritional Physiological Phenomena↗
PubMed1995

Infestation rate of head lice in primary school children in Inchon, Korea.

The survey of the head louse infestation of primary school children in Inchon city was carried out in May 26-27, 1995. Total number of the children surveyed were 1,530. Four (0.5%) out of 768 boys were infested with nits or adults/nymphs of lice and 72 (9.4%) out of 762 girls were positive with those of lice. The infestation rate of lice for girls was 19 times higher than that of boys.

Child↗
PubMed1994

Clinical diversity and chromosomal localization of X-linked cone dystrophy (COD1).

X-linked progressive cone dystrophy (COD1) causes progressive deterioration of visual acuity, deepening of central scotomas, macular changes, and bull's-eye lesions. The cone electroretinography (ERG) is variably abnormal in affected males, and the rod ERG may also be abnormal. The clinical picture of heterozygous females ranges from asymptomatic to a widespread spectrum of cone-mediated dysfunction. A prior linkage study demonstrated linkage between the COD1 locus and the marker locus DXS84, assigned to Xp21.1, with no recombination. In the present study, we have clinically characterized a large four-generation family with COD1 and have performed a linkage analysis using seven polymorphic markers on the short arm of the X chromosome. No recombination was observed between the disease and the marker loci DXS7 and MAOA, suggesting that the location of COD1 is in the region Xp11.3, distal to DXS84 and proximal to ARAF1.

Child↗
PubMed1991

The COL6A1 and COL6A2 genes exist as a gene cluster and detect highly informative DNA polymorphisms in the telomeric region of human chromosome 21q.

The genes that encode the alpha 1 (VI) and alpha 2 (VI) collagen chains, designated COL6A1 and COL6A2, map to human chromosomal band 21q22.3. Using pulsed-field gel electrophoresis and somatic cell hybrids, we found that COL6A1 and COL6A2 form a gene cluster on the most distal part of chromosome 21. Furthermore, we detected several DNA polymorphisms (both restriction site and VNTRs) associated with these loci. These polymorphisms make the COL6A1 and COL6A2 genes among the most informative markers on human chromosome 21.

Blotting, Southern↗