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Biomedical subjects

Y Qiu

Publications and source records attributed to Y Qiu.

At least 199 records · Page 11Linked to original sources
PubMed1995

Chicken ovalbumin upstream promoter transcription factor (COUP-TF): expression during mouse embryogenesis.

Members of the steroid/thyroid hormone receptor superfamily such as TR, RAR, RXR and VDR are known to play important roles in regulation of gene expression during development, differentiation and homeostasis. COUP-TFs are orphan members of this superfamily of nuclear receptors and have been shown to negatively regulate the ability of these nuclear receptors to transactivate target genes. Two different mechanisms are implicated in this repression. First, COUP-TFs bind to AGGTCA direct repeats and palindromes with various spacings, which include response elements for TR, RAR, RXR and VDR, allowing for direct competition of COUP-TFs for the response elements. Second, COUP-TFs can heterodimerize with RXRs, the essential cofactor for effective binding of VDR, TRs and RARs to their cognate response elements. The physiological significance of this negative effect of COUP-TF on the activity of these receptors has been analyzed. Detection of COUP-TF transcripts during mouse development reveal discrete spatial and temporal expression domains consistent with COUP-TFs being involved in regulation of gene expression during embryogenesis. Transcripts are localized within discrete regions of the central and peripheral nervous system including the inner ear. In addition, COUP-TFs are found in many tissues including testes, ovary, prostate, skin, kidney, lung, stomach, intestine, pancreas and salivary gland. Some of these expression domains colocalize with those of TR, RAR, and RXR. The simultaneous expression of these genes raise the possibility that COUP-TFs can act as negative regulatory factors during development and differentiation.

Animals↗
PubMed1995

Protective effect of nicorandil as an additive to the solution for continuous warm cardioplegia.

Experiments were designed to assess whether (1) nicorandil given before global low-flow ischemia or (2) included in low-flow continuous cardioplegia improved the recovery of cardiac function in the isolated rat heart. The first investigated the effect of nicorandil (2, 10, or 100 mumol/L), given for 3 minutes before 30 minutes of normothermic global ischemia, on recovery after 30 minutes of reperfusion. In aerobically perfused hearts, doses of 10 and 100 mumol/L significantly increased coronary flow; the dose of 100 mumol/L exerted a negative inotropic effect. These doses shortened the time to contractile arrest (282 +/- 18 and 276 +/- 22 seconds versus 354 +/- 16 seconds in the control hearts with unmodified ischemia; p < 0.05 in both instances). Nicorandil also improved the postischemic recovery of coronary flow (79.1% +/- 1.7% and 78.0% +/- 1.6%, respectively, versus 71% +/- 1.8%; p < 0.05). However, there was no significant improvement in recovery of contractile function, creatine kinase leakage, or tissue adenosine triphosphate and creatine phosphate contents. Second, pretreatment with nicorandil (10 mumol/L) was shown to increase susceptibility of the hearts to reperfusion-induced ventricular fibrillation from 0% (n = 8) in control hearts to 50% in the drug-treated group (p < 0.05). Third, nicorandil (10 mumol/L) was added to cardioplegic and noncardioplegic solutions infused into the coronary tree throughout 100 minutes of low-flow (0.7 ml/min) ischemia: in eight of nine control hearts electrical activity was maintained throughout, whereas in all nicorandil-treated hearts electrical activity was suppressed for at least part of the time. Nicorandil also reduced the prevalence of ischemic contracture to 0% during continuous infusion of cardioplegic solution (compared with 30% in nicorandil-free control hearts) and improved the recovery of contractile function after 40 minutes of reperfusion. Thus, in the noncardioplegia groups, left ventricular developed pressure recovered to 77.8% +/- 4.0% versus 51.7% +/- 2.6% in control hearts (p < 0.05) and in the cardioplegia groups to 96.2% +/- 4.2% versus 79.7% +/- 5.5% (p < 0.05). Ventricular compliance (the ventricular volume required to achieve a left ventricular end-diastolic pressure of 4 mm Hg) was better preserved in the nicorandil-containing noncardioplegia group (133 +/- 6 microliters) than in the control group (88 +/- 10 microliters; p < 0.05). In conclusion, nicorandil has been shown to (1) reduce ischemic contracture, (2) lessen the effects of ischemic arrest, and (3) improve the postischemic recovery of contractile function. In this species and preparation it may, however, enhance vulnerability to reperfusion-induced arrhythmias.

Animals↗
PubMed1995

Late preconditioning against myocardial stunning. An endogenous protective mechanism that confers resistance to postischemic dysfunction 24 h after brief ischemia in conscious pigs.

Conscious pigs underwent a sequence of 10 2-min coronary occlusions, each separated by 2 min of reperfusion, for three consecutive days (days 1, 2, and 3 of stage I). The recovery of systolic wall thickening (WTh) after the 10th reperfusion was markedly improved on days 2 and 3 compared with day 1, indicating that the myocardium had become preconditioned against "stunning." 10 d after stage I, pigs underwent again a sequence of 10 2-min coronary occlusions for two consecutive days (days 1 and 2 of stage II). On day 1 of stage II, the recovery of WTh after the 10th reperfusion was similar to that noted on day 1 of stage I; on day 2 of stage II, however, the recovery of WTh was again markedly improved compared with day 1. Blockade of adenosine receptors with 8-p-sulfophenyl theophylline failed to prevent the development of preconditioning against stunning. Northern blot analysis demonstrated an increase in heat stress protein (HSP) 70 mRNA 2 h after the preconditioning ischemia; at this same time point, immunohistochemical analysis revealed a concentration of HSP70 in the nucleus and an overall increase in staining for HSP70. 24 h after the preconditioning ischemia, Western dot blot analysis demonstrated an increase in HSP70. This study indicates the existence of a new, previously unrecognized cardioprotective phenomenon. The results demonstrate that a brief ischemic stress induces a powerful, long-lasting (at least 48 h) adaptive response that renders the myocardium relatively resistant to stunning 24 h later (late preconditioning against stunning). This adaptive response disappears within 10 d after the last ischemic stress but can be reinduced by another ischemic stress. Unlike early and late preconditioning against infarction, late preconditioning against stunning is not blocked by adenosine receptor antagonists, and therefore appears to involve a mechanism different from that of other forms of preconditioning currently known. The increase in myocardial HSP70 is compatible with, but does not prove, a role of HSPs in the pathogenesis of this phenomenon.

Adaptation, Physiological↗
PubMed1995

The influenza virus NS1 protein binds to a specific region in human U6 snRNA and inhibits U6-U2 and U6-U4 snRNA interactions during splicing.

The influenza virus NS1 protein is a unique posttranscriptional regulator that has two activities: inhibition of the nuclear export of poly A-containing mRNAs and inhibition of pre-mRNA splicing. Here we demonstrate that this protein binds to a specific region in one of the human spliceosomal snRNAs, U6 snRNA. Using U6 deletion mutations, we show that the binding of the NS1 protein requires both chains of a stem-bulge structure encompassing nucleotides 27-46 and nucleotides 83-101 of human U6 snRNA. A chemical modification/interference assay indicated that the primary binding site is centered around a purine-containing bulge in this stem-bulge structure. These results provide strong evidence that this postulated secondary structure in U6 snRNA actually exists. The NS1 protein also binds to a model U6-U4 snRNA complex, suggesting that the U6 stem-bulge comprising the NS1 protein binding site is also present in natural U6-U4 snRNA complexes. The U6 stem-bulge includes the U6 sequence that forms helix II with U2 snRNA during splicing, an interaction that is essential for mammalian splicing. We demonstrate that the NS1 protein blocks formation of the U6-U2 helix II both in a model system and during in vitro splicing. In addition, we show that the NS1 protein inhibits formation of U6-U4 snRNA complexes during in vitro splicing, presumably because the binding site of the NS1 protein includes the 3'-terminal region of U6 snRNA that has been shown to be important for the formation of U6-U4 complexes. We postulate that the inhibition of U6-U2 and U6-U4 snRNA complex formation is largely responsible for the inhibition of pre-mRNA splicing by the NS1 protein.

Base Sequence↗
PubMed1995

[Prevention of galactose-induced cataractogenesis in rats by salvianolic acid A].

Salvianolic acid A has been demonstrated to have efficient antioxidative and free radical scavenging effects. In the present experiments, the preventive effects of salvianolic acid A on galactose-induced cataract in rats were investigated. Dropping 0.05% salvianolic acid A in the eyes (two times a day) was found to delay the development of cataract. The contents of MDA and H2O2 in the cataract lens were decreased in salvianolic acid A treated rats. The protein and non-protein thiols in the cataract lens of the salvianolic acid A treated rats were higher than those of control rats. In in vitro experiments salvianolic acid A was shown to inhibit aldose reductase activity. These results indicate that salvianolic acid A can prevent galactose-induced cataract by antioxidation and inhibition of aldose reductase.

Aldehyde Reductase↗
PubMed1995

[Protective effect of salvianolic acid a on ischemia-reperfusion induced injury in isolated rat heart].

The protective effect of salvianolic acid A (Sal A) on cardiac ischemia-reperfusion induced injury was studied on the isolated rat heart. The results indicate that Sal A can reduce the occurence of ventricular fibrillation, decrease the cellular LDH leaking and reduce the concentration of lipid peroxidation product-MDA significantly in ischemia-reperfused cardiac tissue. The possible machenism in decreasing ischemia-reperfusion injury of Sal A was discussed.

Animals↗
PubMed1994

Spatiotemporal expression patterns of chicken ovalbumin upstream promoter-transcription factors in the developing mouse central nervous system: evidence for a role in segmental patterning of the diencephalon.

Chicken ovalbumin upstream promoter-transcription factor (COUP-TF) genes encode transcription factors belonging to the orphan subfamily of the steroid/thyroid hormone receptor superfamily. Two COUP-TF counterparts have been cloned from mouse. In an attempt to study the function of these genes in the developing central nervous system (CNS), the spatiotemporal expression patterns of the two mouse genes have been examined by in situ hybridization. Both genes are widely expressed in the developing CNS, with patterns that are overlapping yet distinct from each other. The differential expression of murine COUP-TFI and -II in the diencephalon is striking in that high levels of expression from each gene are confined to specific segmental compartments--the neuromeres. Our results suggest that murine COUP-TFs may play important roles in the development and differentiation of the CNS, including the specification of diencephalic neuromeres.

Amino Acid Sequence↗
PubMed1994

Mutational effects of space flight on Zea mays seeds.

The growth and development of more than 500 Zea mays seeds flown on LDEF were studied. Somatic mutations, including white-yellow stripes on leaves, dwarfing, change of leaf sheath color or seedling color were observed in plants developed from these seeds. When the frequency of white-yellow formation was used as the endpoint and compared with data from ground based studies, the dose to which maize seeds might be exposed during the flight was estimated to be equivalent to 635 cGy of gamma rays. Seeds from one particular holder gave a high mutation frequency and a wide mutation spectrum. White-yellow stripes on leaves were also found in some of the inbred progenies from plants displayed somatic mutation. Electron microscopy studies showed that the damage of chloroplast development in the white-yellow stripe on leaves was similar between seeds flown on LDEF and that irradiated by accelerated heavy ions on ground.

Chloroplasts↗
PubMed1994

Mutagenic effects of heavy ion radiation in plants.

Genetic and developmental effects of heavy ions in maize and rice were investigated. Heavy particles with various charges and energies were accelerated at the BEVALAC. The frequency of occurrence of white-yellow stripes on leaves of plants developed from irradiated maize seeds increased linearly with dose, and high-LET heavy charged particles, e.g., neon, argon, and iron, were 2-12 times as effective as gamma rays in inducing this type of mutation. The effectiveness of high-LET heavy ion in (1) inhibiting rice seedling growth, (2) reducing plant fertility, (3) inducing chromosome aberration and micronuclei in root tip cells and pollen mother cells of the first generation plants developed from exposed seeds, and (4) inducing mutation in the second generation, were greater than that of low-LET gamma rays. All effects observed were dose-dependent; however, there appeared to be an optimal range of doses for inducing certain types of mutation, for example, for argon ions (400 MeV/u) at 90-100 Gy, several valuable mutant lines with favorable characters, such as semidwarf, early maturity and high yield ability, were obtained. Experimental results suggest that the potential application of heavy ions in crop improvement is promising. RFLP analysis of two semidwarf mutants induced by argon particles revealed that large DNA alterations might be involved in these mutants.

Argon↗
PubMed1994

Progress in understanding the Drosophila dnc locus.

The genetic dissection of learning and memory in Drosophila is two decades old. Recently, a great deal of progress has been made towards isolating new mutants as well as towards a better understanding of the originally isolated ones. This paper reviews the recent developments in the understanding of the structure and function of the gene identified by the first and best-characterized of these mutants, the Drosophila dunce mutant.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1994

Separation of subcellular compartments containing distinct functional forms of MHC class II.

Antigen processing in B lymphocytes entails initial binding of antigen to the surface Ig and internalization of the antigen into acidic compartments where the antigen is degraded, releasing peptides for binding to major histocompatibility complex class II molecules. Using subcellular fractionation techniques we show that functional, processed antigen-class II complexes capable of activating antigen-specific T cells in vitro are first formed in dense vesicles cosedimenting with lysosomes which are distinct from early endosomes and the bulk of late endosomes. With time, processed antigen-class II complexes appear in vesicles sedimenting with early endosomes and finally cofractionate with plasma membrane. A separate compartment is identified which contains major histocompatibility complex class II receptive to peptide binding but which does not have access to processed antigen in the B cell. These class II molecules are in the so-called "floppy" form in contrast to the class II molecules in the very dense vesicles which are in the "compact" form. These results demonstrate a correlation between the floppy and compact forms of class II molecules and their association with processed antigen and show that floppy and compact forms of class II reside in distinct and physically separable subcellular compartments.

Amino Acid Sequence↗
PubMed1994

PBP74, a new member of the mammalian 70-kDa heat shock protein family, is a mitochondrial protein.

The cloning of a cDNA encoding a new member of the highly conserved mammalian 70-kDa heat shock protein (hsp 70) family termed PBP74 was recently reported. Critical to an understanding of the function of this new hsp 70 is delineating its subcellular localization. Here we use a variety of immunological and biochemical approaches both in vitro and in vivo to demonstrate that PBP74 is imported into and resides in mitochondria. By confocal immunofluorescence microscopy PBP74 is detected in mitochondria, colocalizing with the mitochondrial 60-kDa heat shock protein. To address the inherent problem of serological cross-reactivity among the hsp70 family members, an influenza virus hemagglutinin epitope tag was introduced into the PBP74 cDNA. The epitope-tagged PBP74 protein transiently expressed in L cells localized to mitochondria. Moreover, deletion of the N-terminal 46-amino acid presequence results in a cytosolic localization of the epitope-tagged protein. Cell fractionation studies demonstrated PBP74 in purified mitochondria in a protease-protected location. After coupled transcription-translation the precursor of PBP74 is imported into isolated yeast mitochondria, where it becomes processed to the mature protein. According to a subfractionation of the mitochondria, the imported protein was found to be localized in the matrix space. Import in vitro is time- and temperature-dependent, requires matrix ATP, and is abolished upon depletion of the membrane potential across the mitochondrial inner membrane. Similarly, in mammalian cells PBP74 is synthesized as a pre-protein that requires membrane potential-dependent import into mitochondria for its maturation. Taken together, our data demonstrate that PBP74 is a mammalian mitochondrial hsp70.

Amino Acid Sequence↗
PubMed1994

The influenza virus NS1 protein is a poly(A)-binding protein that inhibits nuclear export of mRNAs containing poly(A).

The influenza virus NS1 protein inhibits the nuclear export of a spliced viral mRNA, NS2 mRNA (F. V. Alonso-Caplen, M. E. Nemeroff, Y. Qiu, and R. M. Krug, Genes Dev. 6:255-267, 1992). To identify the sequence in NS2 mRNA that is recognized by the NS1 protein, we developed a gel shift assay for the formation of specific RNA-protein complexes. With this assay, it was established that the NS1 protein binds to the poly(A) sequence at the 3' end of NS2 mRNA and of other mRNAs. In addition, the NS1 protein was shown to bind to poly(A) itself. This specificity was also observed in vivo. The NS1 protein inhibited the nuclear export of every poly(A)-containing mRNA that was tested. In contrast, the NS1 protein failed to inhibit the nuclear export of an mRNA whose 3' end was generated by cleavage without subsequent addition of poly(A). Addition of poly(A) to this mRNA enabled the NS1 protein to inhibit mRNA export. The implications of these results for the role of the NS1 protein during virus infection are discussed.

Binding, Competitive↗
PubMed1994

[Submucous implantation with pedicel auto-flap of cheek muscle for atrophic rhinitis].

This paper described a method of submucous implantation for 32 patients with atrophic rhinitis by using pedicel auto-flap of cheek muscle and maxillary periosteum of piriform aperture. The results indicated that the total effective rate was 100% and the evident effective rate was 90.6% after 1 to 3 year postoperatively. The cilia beat of nasal mucosa, blood flow, osmotaxis of blood vessel. P substance and the resistance of nasal airflow were all improved. The flap survived and grew well due to autogenuous graft tissues and its original blood supply. No complications have been found. The clinical efficiency was obvious for a short term and was stable for a long term.

Adolescent↗
PubMed1994

[Synthesis of new fluorescent reagent and its application in solution fluorescence analysis].

In our laboratory we have designed and synthesized a new fluorescent CGE(N), which has a fluo-rigen and can react with active hydrogen in chemical compounds. We have studied its application in solution fluorescence, thin-layer fluorescence and solid fluorescence analysis. The results have indicated that CGE (N) is a good reagent in analysis. And the example of its application in solution fluorescence analysis is given in this paper.

Colchicine↗
PubMed1993

Structure and function of C-CAM1. The first immunoglobulin domain is required for intercellular adhesion.

Cell-CAM105 proteins (also called C-CAM) are epithelial cell adhesion molecules of the immunoglobulin (Ig) superfamily. The sequences of C-CAM are highly homologous to those of human carcinoembryonic antigen (CEA)-family proteins. In previous studies using baculoviral vectors, we showed that expression of the L-form cell-CAM105 (also called C-CAM1) in insect cells resulted in cell aggregation (Cheung, P. H., Thompson, N. L., Earley, K., Culic, O., Hixson, D., and Lin, S. H. (1993) J. Biol. Chem. 268, 6139-6146). This result indicates that the insect-cell system is suitable for studying the adhesion function of C-CAM. Since C-CAM1 contains four extracellular Ig-domains, the structural features directly responsible for C-CAM1 adhesion function were investigated by site-directed deletion and expression in the baculovirus/insect cell system. Results from these studies indicated that the first Ig domain located in the NH2-terminal of C-CAM plays a crucial role in intercellular adhesion. Site-directed deletion producing mutants lacking the second, third, or fourth Ig domains had no effect on the adhesion function. In addition, adhesion function was retained when both the third and fourth Ig domains were deleted, although the adhesion activity was reduced to half that in control cells. However, simultaneous deletion of the second, third, and fourth domains abolished adhesion, suggesting that these domains affect the accessibility of the binding site localized in the first domain. In our previous studies, we showed that the cytoplasmic domains of C-CAM play a significant role in the isoforms' adhesion activity since expression of a C-CAM isoform containing only 6 instead of 71 amino acids intracellularly failed to show the adhesion phenotype (Cheung, P. H., Culic, O., Qiu, Y., Earley, K., Thompson, N., Hixson, D. C., and Lin, S.-H. (1993) Biochem. J. 295, in press). These results together suggest that both the cytoplasmic domain and the first N-terminal Ig-like domain are required for C-CAM-mediated cell adhesion activity.

Adenosine Triphosphatases↗
PubMed1993

The cytoplasmic domain of C-CAM is required for C-CAM-mediated adhesion function: studies of a C-CAM transcript containing an unspliced intron.

Cell-CAM105 (also named C-CAM) is a cell surface glycoprotein involved in intercellular adhesion of rat hepatocytes. It has four extracellular immunoglobulin (Ig) domains, a transmembrane domain and a cytoplasmic domain and therefore is a member of the Ig supergene family. We have characterized multiple cDNAs of the C-CAM genes in rat intestine. Sequence analyses showed that rat intestine contained not only the previously reported L-form and S-form C-CAMs (renamed C-CAM1 and C-CAM2 respectively) but also a new isoform, C-CAM3. The C-CAM3 transcript codes for a polypeptide with a truncated C-terminus that lacks 65 amino acids from the previously reported C-CAM1 cytoplasmic domain. Unlike C-CAM1, C-CAM3 did not mediate cell adhesion when expressed in insect cells using the baculoviral expression system. Thus the extra 65 amino acids in the cytoplasmic domain of C-CAM1 are important for adhesion phenotype when expressed in insect cells. Although C-CAM1 and C-CAM2 are encoded by different genes, sequence analysis suggests that C-CAM3 is probably derived from alternative splicing of the C-CAM1 gene. To examine this possibility, we have determined the exon organization of the C-CAM1 gene. C-CAM3 differed from C-CAM1 by the presence of a single unspliced intron which contained a stop codon immediately after the regular splice junction. As a result, translation of C-CAM3 terminates at the point where C-CAM1 and C-CAM3 sequences diverge. To investigate the expression of C-CAM1, C-CAM2 and C-CAM3 in different tissues, we used an RNAase-protection assay to simultaneously assess the levels of expression of these transcripts. Using total RNA prepared from various tissues, we showed that expression of C-CAM3 was tissue-specific, and the C-CAM3 transcript accounted for about 25% of the transcripts derived from the C-CAM1 gene. However, further analysis revealed that C-CAM3 transcript was not present in cytosolic RNA, rather it was enriched in nuclear RNA prepared from hepatocytes. Although C-CAM3 cDNA contains the polyadenylation signal and is polyadenylated, these results indicate that C-CAM3 is probably an incomplete spliced product of C-CAM1 gene.

Adenosine Triphosphatases↗