Biomedical subjects

R Y Huang

Publications and source records attributed to R Y Huang.

30 records · Page 2Linked to original sources

PubMed1992

Broad-complex function during oogenesis in Drosophila melanogaster.

The Broad-Complex (BR-C) appears to encode factors that mediate ecdysone effects during the larva-adult transition. The main goal of this study was to gain insight into what roles the BR-C might play during oogenesis. The main findings are as follows. First, as determined by heteroallele studies and clonal analysis, de12 is a somatic line mutation that appears to fall into the broad domain of the BR-C. Second, the de12 mutation is associated with the insertion of the gypsy transposon at position 169.5 (Chao and Guild, Embo J, 1986, 5:143-150) in the BR-C domain. In its new context this gypsy element exhibits ovarian-specific activation. Both this gypsy activation and the de12 phenotype are partially suppressible by su(f) and su(Hw). Third, we have identified a set of transcripts that cross-hybridize with BR-C sequence spanning the gypsy insertion site (166-179). There are significant differences in these cross-hybridizing species, both in size and relative abundance, between de12 and its parent strain. Finally we have determined that in de12 there is a premature arrest of chorion gene amplification in the late stages of oogenesis.

Animals↗

PubMed1991

Cloning and structural analysis of MMCP-1, MMCP-4 and MMCP-5, three mouse mast cell-specific serine proteases.

Here we present the cloning of three novel mouse mast cell-specific serine proteases, MMCP-1, MMCP-4 and MMCP-5. A region of approximately 4 kb covering the five exons and 930 bp 5' and 280 bp 3' flanking sequences of the gene for MMCP-1 was characterized by nucleotide sequence analysis. A comparison with the corresponding region of the rat mucosal mast cell-specific protease RMCP-II is presented. cDNA clones for the mast cell proteases MMCP-4 (950 bp) and MMCP-5 (1098 bp) were isolated from a cDNA library of a connective tissue mast cell-like mouse mastocytoma cell line. All three proteases were found to belong to the family of chymotrypic serine proteases as deduced from the absence of the Asp 189 which is characteristic for all serine proteases having cleavage specificities similar to pancreatic trypsin. The active polypeptides, excluding possible post-translational glycosylations, have an Mr of 25-26 kDa. Analysis of the amino acid composition reveals a positive net charge for all three proteases MMCP-1 +3, MMCP-4 +18 and MMCP-5 +12). Based on their high sequence identity (88%) and high positive net charges (+18 and +18, respectively) we assume that the MMCP-4 is the mouse homolog to rat RMCP-I. Probes specific for each of these three highly homologous protease genes have been generated by subcloning of fragments of approximately 100 bp in length, originating from the 3' ends of the mRNA into plasmid vectors. Northern blot analysis of mRNA from a number of murine cell lines shows gene expression of these proteases to be specific for the differentiation stage of the mast cell. The MMCP-1 is expressed only at the mucosal mast cell stage and 5 only in mast cells of the connective tissue mast cell stage. These serine proteases may serve as highly specific markers in the analysis of mast cell heterogeneity, differentiation and function.

Amino Acid Sequence↗

PubMed1990

Cloning and structural analysis of a gene encoding a mouse mastocytoma proteoglycan core protein; analysis of its evolutionary relation to three cross hybridizing regions in the mouse genome.

Serglycin (SGC) is a Ser-Gly-repeat-containing protein, used as a proteoglycan core protein in the parietal yolk sac and in mast cells, where glycosaminoglycan side chains are attached to the serine residues of the repeat region. In this article, the structure of the gene SGC encoding mouse SGC is reported. The gene is divided into three exons, which are all contained within a region of approximately 13 kb. Nucleotide (nt) sequence analysis was carried out on a region of 1.2 kb upstream from the first exon. The region containing the two promoters (active in parietal yolk sac and in mast cells, respectively) was analyzed for the presence of recognition sites for known DNA-binding proteins. A number of sequences closely related to known recognition sites were found in both promoters, and one consensus octamer-binding site could be identified in the putative yolk-sac promoter. Multiple regions in the mouse genome hybridizing with DNA fragments covering the Ser-Gly repeat region have previously been described, and it has been suggested that these loci may represent other proteoglycan core proteins. Analysis of nt sequence was carried out on three out of the more than 15 of these regions present in the mouse genome. However, none of the clones analyzed was found to have any open reading frame in the region of cross-hybridization which possibly could code for a SGC protein. Instead, one of the clones was found to contain an exon encoding a highly basic protein, unrelated to SGC. Hence, no evidence was found for a multigene family of Ser-Gly-repeat-containing proteoglycan-encoding genes.

Aggrecans↗

PubMed1990

[Tardy ulnar palsy treated by anterior subcutaneous transposition].

Twenty cases of tardy ulnar palsy were treated by anterior subcutaneous transposition in the past 6 years at the Veterans General Hospital-Taichung. These cases were followed up for at least 9 months after operation. Mean duration of follow up was 39.5 months. Age distribution was from 40y/o to 72y/o, mean age was 54.5y/o. Duration of symptoms was from 2 months to 72 months, mean was 20.3 months. Eight cases were attributed to the idiopathic type. 16 cases (80%) improved after operation. Four factors were analyzed to evaluate their status as a prognostic guide: age, duration of syndrome, severity before operation and precipitating factors. Only severity before operation correlated with prognosis, but good recovery can be achieved in severe cases. Anterior subcutaneous transposition is a good method for treating tardy ulnar palsy.

Adolescent↗

PubMed1987

Posttreatment with sodium arsenite is coclastogenic in log phase but not in stationary phase.

Posttreatment with sodium arsenite in log phase synergistically increases the chromosomal aberrations induced by ethyl methanesulfonate in Chinese hamster ovary cells, human fibroblasts, and human lymphocytes. However, posttreatment with sodium arsenite in stationary phase has no apparent effect on the clastogenicity of ethyl methanesulfonate. These results indicate that the cycling state of the cell plays a crucial role in the action of arsenite coclastogenicity. One prediction from this finding is that in combined treatment, posttreatment with sodium arsenite should preferentially kill cancer cells.

Animals↗

PubMed1986

Sodium arsenite potentiates the clastogenicity and mutagenicity of DNA crosslinking agents.

To see if sodium arsenite enhances the clastogenicity and the mutagenicity of DNA crosslinking agents, Chinese hamster ovary (CHO) cells and human skin fibroblasts were exposed to cis-diamminedichloroplatinum (II) (cis-Pt(II)) or 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet light (UVA) and then to sodium arsenite. The results indicate that the clastogenicity of cis-Pt(II) and 8-MOP plus UVA are enhanced by the post-treatment with sodium arsenite. Chromatid breaks and exchanges are predominantly increased in doubly treated cells. Furthermore, the mutagenicity of cis-Pt(II) at the hypoxanthine-guanine phosphoribosyl transferase locus is also potentiated by sodium arsenite in CHO cells.

Animals↗

PubMed1986

Cycloheximide suppresses the enhancing effect of sodium arsenite on the clastogenicity of ethyl methanesulphonate.

Post-treatment with sodium arsenite synergistically increases the chromosomal aberrations induced by ethyl methanesulphonate (EMS). We have now provided evidence to show that the enhancing effect of sodium arsenite on the incidence of chromatid breaks and chromatid exchanges induced by EMS in Chinese hamster ovary cells can be suppressed by protein synthesis inhibitors, cycloheximide and puromycin. The most effective time period for cycloheximide or puromycin to suppress the co-clastogenic activity of sodium arsenite was during the middle 6 h in an 18-h incubation time after a 2-h treatment with EMS. The results suggest that the co-clastogenicity of sodium arsenite may require protein synthesis.

Animals↗

PubMed1986

Different modes of action of sodium arsenite, 3-aminobenzamide, and caffeine on the enhancement of ethyl methanesulfonate clastogenicity.

Chromosomal aberrations induced by ethyl methanesulfonate (EMS) in Chinese hamster ovary cells were potentiated by subsequent exposure to sodium arsenite (AS), 3-aminobenzamide (3AB), or caffeine (CAF). The coclastogenicity of AS was most evident when this drug was applied for 3 or 6 h immediately after EMS was removed, whereas caffeine acted primarily after 12-18 h. The coclastogenicity of 3AB was not stage dependent. AS and 3AB increased chromatid exchanges more than chromatid breaks, whereas caffeine mainly increased chromatid breaks. Thus the coclastogenicities of AS, 3AB, and CAF differ in their time of action and the types of aberrations they potentiate.

Animals↗

PubMed1986

Differential effects of pre- and posttreatment of sodium arsenite on the genotoxicity of methyl methanesulfonate in Chinese hamster ovary cells.

Pretreatment of sodium arsenite reduces hypoxanthine-guanine phosphoribosyltransferase mutagenicity and overcomes the inhibition of mitosis and cell proliferation but has no apparent effect on the cytotoxicity and clastogenicity in methyl methanesulfonate (MMS)-treated Chinese hamster ovary cells. Posttreatment of sodium arsenite drastically increases the cytotoxicity, clastogenicity, hypoxanthine-guanine phosphoribosyltransferase mutagenicity, and inhibition of mitosis and cell proliferation induced by MMS. Sodium arsenite either pre- or posttreatment has no apparent effect on the MMS-induced sister chromatid exchanges. The present results indicate that pretreatment of sodium arsenite not only does no harm but may even benefit the MMS-treated cells. On the contrary, posttreatment of sodium arsenite is cogenotoxic.

Animals↗

PubMedDate not supplied

Sodium arsenite enhances the cytotoxicity, clastogenicity, and 6-thioguanine-resistant mutagenicity of ultraviolet light in Chinese hamster ovary cells.

Cytotoxicity, chromosome aberrations, and mutations to 6-thioguanine resistance were synergistically increased by incubating the ultraviolet light (UV)-irradiated Chinese hamster ovary (CHO) cells in medium containing sodium arsenite. However, the frequencies of sister-chromatid exchanges and mutations to ouabain resistance induced by UV were not synergistically increased by sodium arsenite. The synergistic effect of sodium arsenite on UV-induced chromosome aberrations varied with cell-harvesting time and decreased with increasing time intervals between UV and sodium arsenite treatments.

Animals↗

PubMedDate not supplied

Structural airway anomalies in patients with DiGeorge syndrome: a current review.

DiGeorge Syndrome is a genetic disorder characterized by either absence or hypoplasia of the thymus and the parathyroid glands. Patients with this syndrome also have a high incidence of cardiovascular malformations and facial dysmorphism. Structural airway anomalies have also been described, albeit infrequently. Tracheoesophageal fistula, short trachea with reduced numbers of tracheal rings, abnormal thyroid cartilage, laryngomalacia, tracheomalacia, and bronchomalacia have been recognized in these patients. We review all previously reported patients with DiGeorge syndrome and lower airway anomalies. In addition, we present 2 patients with DiGeorge syndrome who were each found to have an aberrant right tracheal bronchus. Structural airway anomalies can be a cause of morbidity and mortality in patients with DiGeorge syndrome. Prompt, thorough evaluation of the upper and lower airway in these patients is essential.

DiGeorge Syndrome↗

PubMedDate not supplied

Endoscopic diagnosis of sarcoidosis in a patient presenting with bilateral exophthalmos and pansinusitis.

Sarcoidosis is a chronic granulomatous disease of unknown etiology. Otolaryngologic and ophthalmologic manifestations occur in 15 to 55% of afflicted individuals, respectively. Neck masses, parotid enlargement, and facial nerve palsy are the most common presenting otolaryngologic complaints, while lacrimal gland enlargement, uveitis, and upper eyelid masses often call the attention of the ophthalmologist. Biopsy reveals non-caseating granulomas, while the angiotensin converting enzyme (ACE) level may be elevated. We report an unusual case of a patient who presented with severe bilateral exophthalmos as the sole initial complaint. A prior workup included a negative conjunctival biopsy. On magnetic resonance imaging (MRI) and computed tomography (CT), the patient had pansinusitis. Endoscopic ethmoidectomies with tissue analysis revealed sarcoidosis. Further evaluation revealed no evidence of systemic disease, and all symptoms resolved with a course of oral steroids. Thus, nasal endoscopy and biopsy of affected paranasal sinus mucosa may prove a useful adjunct to the diagnosis of sarcoidosis, particularly in atypical cases.

Adult↗