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Y Oh

Publications and source records attributed to Y Oh.

At least 109 records · Page 6Linked to original sources
PubMed1995

An orphan nuclear receptor, mROR alpha, and its spatial expression in adult mouse brain.

We have cloned cDNA encoding a mouse nuclear receptor mROR alpha which is a homolog of human retinoic acid receptor-related orphan receptor (hROR alpha). Cotransfection experiments revealed that mROR alpha activates transcription through a retinoic acid responsive element of the laminin B1 gene (lamRARE), but not through a RARE of RAR beta gene (beta RARE) or a synthetic palindromic thyroid hormone responsive element (TREpal). The most distal AGGTCA half-site among the three half-sites of lamRARE was sufficient for binding of mROR alpha and consequently for activation of transcription. Transactivation by mROR alpha was dependent on serum in culture medium after transfection, suggesting the presence of a possible ligand. Northern hybridization and in situ hybridization analyses revealed that mROR alpha is expressed in specific areas of the brain including thalamus and olfactory bulb as well as cerebellum where it is present at highest levels in Purkinje cells. In addition to regionally heterogeneous expression in brain, its expression was temporally regulated during differentiation of P19 cells into neural cells, but not into muscle cells. These observations suggest that mROR alpha plays important roles as a transcription factor not only in differentiation of neural cell lineages but also in the mature brain.

Amino Acid Sequence↗
PubMed1995

Antiproliferative actions of insulin-like growth factor binding protein (IGFBP)-3 in human breast cancer cells.

A number of lines of evidence suggest that IGFs are important mitogens in human breast cancer: (1) IGFs are the most potent growth factor in human breast cancer cells; (2) estrogen stimulates expression of IGF-II and the type 1 IGF receptor; and (3) stromal cells express IGFs, which may act in a paracrine manner. Numerous studies have demonstrated that IGFBPs modulate the mitogenic effects of IGFs in the local environment. In particular, we have recently demonstrated that IGFBP-3 inhibits the growth of Hs578T and MDA-MB-231 human breast cancer cells in an IGF-independent manner. Further studies revealed the existence of cell surface-associated IGFBP-3 receptors. Receptor binding and the subsequent antiproliferative action of IGFBP-3 was inhibited by IGFs, owing to the formation of an IGF-IGFBP-3 complex that prevents the binding of IGFBP-3 to its receptors. In addition, exogeneously added soluble heparin or heparan sulfate inhibited the binding of IGFBP-3 to the cell surface in a dose-dependent manner. However, when heparin and heparan sulfate linkages of glycosaminoglycans on the cell surface were enzymatically remove, IGFBP-3 binding was only minimally affected. These data suggest that soluble heparin or heparan sulfate forms a complex with IGFBP-3, thereby inhibiting receptor binding of IGFBP-3, rather than competing with cell-surface glycosaminoglycans for binding of IGFBP-3. Additionally, the role of IGFBP-3 in the antiproliferative effects of transforming growth factor (TGF)-beta and retinoic acid (RA) is supported by our observations that: (1) inhibition of IGFBP-3 gene expression using an IGFNBP-3 antisense oligodeoxynucleotide not only blocks TGF-beta and RA simulation of IGFBP-3 production by up to 90%m but also inhibits their antiproliferative effects by 40-60%; and (2) treatment with IGF-II and IGF-II analogs diminish TGF-beta effects by blocking TGF-beta induced binding of IGFBP-3 to the cell surface. Taken together, our results support the hypothesis that IGFBP-3 is an important antiproliferative factor in human breast cancer, acting in an IGF-independent manner in addition to its ability to modulate the binding of IGF peptides to IGF receptors.

Breast Neoplasms↗
PubMed1995

Characterization of a low molecular mass form of insulin-like growth factor binding protein-3 (17.7 kilodaltons) in urine and serum from healthy children and growth hormone (GH)-deficient patients: relationship with GH therapy.

The insulin-like growth factor binding proteins (IGFBPs) are the carriers for insulin-like growth factor (IGF0-I and IGF-II. IGFBP-3 is GH-dependent and circulates associated with IGFs and an acid-labile subunit to form a 150-kilodalton (kDa) complex. In human serum, two immunoreactive molecular weight forms of IGFBP-3 have been identified. In human urine, radioimmunoassayable levels of IGFBP-3 have been detected. The objectives of this study were to characterize the molecular weight forms of IGFBP-3 in urine and serum of healthy children and adults and in children with GH deficiency (GHD), to quantify the urinary molecular weight forms of IGFBP-3, and to evaluate the relationship of these forms with GH therapy. Urine and serum were obtained from 12 prepubertal children with GHD, before and after 6 months of GH therapy, from 30 prepubertal healthy children, and from 8 healthy adults. Western immunoblotting (WIB) with IGFBP-3 antiserum (alpha IG-FBP-3g1) showed that in urine the most representative IGFBP-3 was a 17.7-kDa form. The 17.7-kDa IGFBP-3 was high in urine of healthy children compared with healthy adults and was low in children with GHD but increased after GH therapy. Urinary IGFBP-3 immunoreactive profile was determined by neutral-size exclusion chromatography, followed by IGFBP-3 RIA analysis of the fractions. Urine showed a major peak of IGFBP-3 immunoreactivity around 17 kDa. The 17-kDa urinary IGFBP-3 chromatographic peak averaged 8461 +/- 367 ng/12 h.m2 of body surface in healthy children, 3415 +/- 739 in adults (P < 0.001), 2294 +/- 354 in children with GHD before GH therapy (P < 0.001), and 7940 +/- 1874 in children with GHD after GH therapy. Urinary IGFBP-3 was also measured by RIA in unfractionated urine; healthy children showed levels significantly higher (14575 +/- 460 ng/12 h.m2) than adults (7823 +/- 1083, P < 0.001) and higher than children with GHD before GH therapy (4710 +/- 703, P < 0.001). Again, however, immunoreactive IGFBP-3 increased after GH treatment (12294 +/- 3394). In the serum of the healthy children we characterized by specific IGFBP-3 WIB analysis, a 17.7-kDa immunoreactive form of IGFBP-3 that was absent in the serum of healthy adults and low in patients with GHD, increased during GH therapy. Serum samples were subjected to neutral-size exclusion chromatography and the fractions were analyzed by WIB.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Measurement of respiratory acoustic signals. Effect of microphone air cavity width, shape, and venting.

STUDY OBJECTIVE: We have previously investigated the effects of microphone type and coupler air chamber depth on lung sound characteristics. We now report the results of experiments exploring the effects of air chamber width, shape, and venting on lung sounds. DESIGN: We used a single electret microphone with a variety of plastic couplers. The couplers were identical except for the diameter and shape of the air chamber. We used cylindrical chambers of 5, 10, and 15 mm in diameter at the skin and conical chambers of 8, 10, and 15 mm in diameter. We compared the inspiratory lung sound spectra obtained using each of the couplers. We also examined the tendency of various needle vents to transmit ambient noise into the microphone chamber. SETTING: Anechoic chamber. MEASUREMENTS AND RESULTS: The shape and diameter had little important effect on the lung sound spectrum below 500 Hz. From approximately 500 to 1,500 Hz, the 5-mm diameter couplers showed slightly less sensitivity than the 10- and 15-mm diameter couplers. All conical couplers provided approximately 5 to 10 decibel more sensitivity than the cylindrical couplers. All vents allowed some ambient noise to enter the chamber but the amount was trivial using the narrowest, longest vent. CONCLUSIONS: These data suggest that the optimal electret microphone coupler chamber for lung sound acquisition should be conical in shape, between 10 and 15 mm in diameter at the skin, and either not vented or vented with a tube no wider than 23-g or shorter than 20 mm.

Adult↗
PubMed1995

Insulin-like growth factor II overexpression in myoblasts induces phenotypic changes typical of the malignant phenotype.

The objective of this study was to examine the role of insulin-like growth factor II (IGF-II) in the pathogenesis of human rhabdomyosarcomas (RMS). We have demonstrated previously that RMS express high levels of IGF-II mRNA, secrete IGF-II peptide, and express both IGF-I and IGF-II receptors. Moreover, we showed that IGF-II functions as an autocrine growth and motility factor in RMS. Since IGF-II is expressed at high levels in fetal muscle cells and RMS are tumors thought to derive from skeletal myoblasts arrested along the normal myogenic pathway, autocrine production of IGF-II by RMS may be an etiological event in the development of this tumor. We have developed a model system which enabled us to study the effects of endogenous IGF-II overprotection in muscle myoblasts. Human cDNA for pre-prohormone IGF-II was transfected into mouse myoblasts in order to achieve high, constant expression of this growth factor, which is normally down-regulated at the end of the differentiation process. Expression of high IGF-II levels resulted in: (a) an increased proliferative rate; (b) impairment of the ability to differentiate into myoblasts; and (c) acquisition of the capability of anchorage-independent growth. No changes in the expression of IGF-I receptors were noted. We conclude that IGF-II overexpression in muscle myoblasts induces morphological and biological changes typical of the malignant phenotype and represents a fundamental event in the pathogenesis of RMS and possibly of other embryonal tumors.

Animals↗
PubMed1995

Induction of cell death by myristylated death domain of p55 TNF receptor is not abolished by Iprcg-like point mutation in death domain.

We transiently expressed the intracellular domains of p55 TNF receptor (TNFR1) as either a cytosolic- or a membrane-associated form and examined their effects on the endogenous receptor-mediated gene expression as well as on cell viability. We found that gene expression as measured by luciferase activity under NF-kappa B-controlling elements was blocked by all forms of the intracellular domain of TNFR1. The blockade of reporter gene expression was due to the cell death induced by the intracellular domain of TNFR1 per se. The killing mechanism of the intracellular domain peptides appeared to be apoptotic. Interestingly, myristylated form of the intracellular domain, consisting of mainly death domain showed the most potent cell-killing activity. Moreover, this myristylated death domain could still induce cell death even if lprcg-like point mutation (Leu351 to Ala), which has been reported to abrogate TNF-induced cytotoxicity, was introduced. This result suggests that the myristylated death domain activates an additional death signaling pathway which is not involved in TNF-induced cell death.

Apoptosis↗
PubMed1994

The beta 1 subunit mRNA of the rat brain Na+ channel is expressed in glial cells.

Although the molecular characteristics of glial Na+ channels are not well understood, recent studies have shown the presence of mRNA for rat brain Na+ channel alpha subunits in astrocytes and Schwann cells. In this study, we asked whether the mRNA for the rat brain Na+ channel beta 1 subunit is expressed in glial cells. We performed in situ hybridization using a complementary RNA probe for the coding regions of the rat brain Na+ channel beta 1 subunit mRNA and detected beta 1 subunit mRNA in cultured rat optic nerve astrocytes and sciatic nerve Schwann cells. The beta 1 subunit was amplified by reverse transcription-polymerase chain reaction in rat optic and sciatic nerves, which lack neuronal somata but contain astrocytes and Schwann cells, respectively. Doublet bands of the beta 1 subunit mRNA were amplified from both optic and sciatic nerves. Through the cloning and sequencing of these bands, we confirmed the amplification of a mRNA highly homologous to the previously cloned rat brain Na+ channel beta 1 subunit (beta 1.1) and a novel form of the beta 1 subunit mRNA (beta 1.2), which is closely homologous to beta 1.1 but contains an additional 86-nucleotide insert in 3' noncoding regions. Two beta 1 subunit mRNAs were also amplified from rat brain and skeletal muscle, but not from rat liver or kidney. These results indicate that rat brain Na+ channel beta 1 subunit mRNAs are expressed in glial cells as well as in neurons.

Animals↗
PubMed1994

Rat brain Na+ channel mRNAs in non-excitable Schwann cells.

The expression of rat brain voltage-sensitive Na+ channel mRNAs in Schwann cells was examined using in situ hybridization cytochemistry and RT-PCR. The mRNAs of rat brain Na+ channel subtype II and III, but not subtype I, were detected in cultured Schwann cells from sciatic nerve and in intact sciatic nerve, which contains Schwann cells but not neuronal cell bodies. These results indicate that rat brain Na+ channel mRNAs, which have been considered as mainly neuronal-type messages, are also expressed in glial cells in vitro and in vivo.

Animals↗
PubMed1994

In situ hybridization localization of the Na+ channel beta 1 subunit mRNA in rat CNS neurons.

Localization of Na+ channel beta 1 subunit (Na beta 1) mRNA was examined in adult rat hippocampus, cerebellum and spinal cord by in situ hybridization histochemistry. In hippocampus, Na beta 1 mRNA was strongly expressed by CA3 followed by CA1 pyramidal cells and dentate granule cells. In cerebellum, strong Na beta 1 mRNA expression was observed in Purkinje cells and moderate expression in granule cells and scattered cells of the molecular layer. In spinal cord, neurons in gray matter exhibited moderate to strong expression of Na beta 1 mRNA. These results provide the first localization study of Na beta 1 mRNA in the CNS, demonstrating a differential expression in different neurons.

Animals↗
PubMed1994

The expression of rat brain voltage-sensitive Na+ channel mRNAs in astrocytes.

Astrocytes from various regions of CNS have been shown to express voltage-activated Na+ currents. To date, three distinct subtypes (I, II and III) of Na+ channels have been cloned from rat brain. We have applied a combined technique of reverse transcription and polymerase chain reaction (RT-PCR) to examine the expression of rat brain Na+ channels in rat astrocytes in vivo and in vitro. Five PCR primer sets were used to amplify coding or 3' non-coding regions of subtype I, II, and III Na+ channels. We were able to amplify all three of these rat brain Na+ channel subtypes from rat optic nerve, which does not have neuronal cell bodies but does contain astrocytes known to express voltage-sensitive Na+ channels. In studies on cultured spinal cord astrocytes, we were also able to amplify all three subtypes of rat brain Na+ channel mRNAs. In control experiments, RT-PCR was performed on RNAs prepared from several rat tissues, including brain, skeletal muscle, and liver. Rat brain was shown to express the three Na+ channel subtypes as expected. In rat skeletal muscle, subtype I and III Na+ channel mRNAs, but not subtype II, were amplified. In rat liver, Na+ channel messages were not detectable. The present study provides the first direct evidence that astrocytes in vivo and in vitro express rat brain voltage-sensitive Na+ channel mRNAs, which have been considered as mainly neuronal-type Na+ channel messages.

Animals↗
PubMed1994

Sodium channel mRNAs in cultured spinal cord astrocytes: in situ hybridization in identified cell types.

The expression of rat brain sodium channel alpha-subunit mRNAs I, II and III and a putative glial cell-specific sodium channel (NaG) mRNA was examined in cultured astrocytes from P-0 rat spinal cord by RNA blot hybridization and by non-isotope in situ hybridization cytochemistry utilizing two independent sets of isoform-specific RNA probes. Sodium channel mRNA I was not detectable in the cultured astrocytes by RNA blot or in situ hybridization. Sodium channel mRNA II showed negligible-to-low levels of expression in flat, fibroblast-like and 'pancake' astrocytes at 4 days in vitro (div), while stellate, process-bearing astrocytes exhibited low-to-moderate levels of mRNA II expression. At 7 div, mRNA II expression ranged from low-to-moderate in flat astrocytes and was moderately high in most process-bearing astrocytes. In RNA blots, a weak band was observed at 9.5 kb. Sodium channel mRNA III expression was negligible in flat astrocytes and was detectable in low-to moderate levels in stellate astrocytes beginning at 4 div; by 7 div, mRNA III was detectable in low levels in flat astrocytes and low-to-moderate levels in stellate astrocytes. RNA blots showed two bands of nearly equal intensity, one at 9.0 kb and one at 7.2 kb. NaG mRNA showed increased expression with time in culture, being detectable in flat and stellate astrocytes at 4 div and becoming very prominent in flat astrocytes at extended times in culture. In RNA blots of cultured astrocytes at 7 div, a strong hybridizing signal with the NaG probe was observed. These observations demonstrate that flat and stellate astrocytes cultured from rat spinal cord express rat brain sodium channel mRNA II and III, and NaG, and suggest that astrocytes in vitro may co-express multiple forms of sodium channel mRNA.

Animals↗
PubMed1994

Risk factors for the development of encapsulated filtering blebs. The role of surgical glove powder and 5-fluorouracil.

PURPOSE: To study risk factors for the development of encapsulated filtering bleb, especially the effect of surgical glove powder and 5-fluorouracil on the development of encapsulated blebs. METHODS: One hundred forty-eight patients who underwent trabeculectomy were prospectively studied. After patient of each surgeon were divided into two subgroups of 5-fluorouracil versus no 5-fluorouracil, each subgroup was then randomized for powder versus powder-free surgical gloves. All patients were followed for at least 2 months (mean, 3.5 months; range, 2-10 months). RESULTS: The overall incidence of encapsulated bleb was 11.2% when an encapsulated bleb was defined by clinical characteristics with a peak intraocular pressure of 26 mmHg or higher. The group that received 5-fluorouracil had a lower incidence of encapsulated blebs despite a higher rate of previous surgeries, whereas the group with powdered gloves had increased incidence. The subgroup in which powder-free gloves were used in conjunction with postoperative injections of 5-fluorouracil had the lowest incidence of encapsulated blebs (2.6%) compared with the other subgroups (12.0%-17.9%) (P = 0.01). CONCLUSION: Combined use of powder-free surgical gloves and 5-fluorouracil may reduce the incidence of encapsulated bleb.

Adult↗
PubMed1994

Developments in mucosal influenza virus vaccines.

Immunogenicity and efficacy of aerosol inactivated split influenza virus vaccines, which are threefold the strength of the vaccines for parenteral use, and cold-adapted reassortant live influenza virus vaccines were evaluated. Mucosal immune responses were evaluated by quantifying specific IgA antibody of the nasal swab solution, and systemic immune responses were evaluated by determining serum haemagglutination inhibition antibody levels. Efficacy of the aerosol inactivated vaccine was evaluated by a challenge test using live vaccine virus. It was concluded that mucosally administered inactivated influenza virus vaccine stimulated systemic and mucosal immune responses more strongly than live influenza virus vaccine and manifested a much stronger booster effect than live vaccine. Mucosal administration of inactivated influenza virus vaccine was effective in preventing infection by live vaccine virus.

Administration, Intranasal↗