Search PubMed⌕ Search

Biomedical subjects

L Qiu

Publications and source records attributed to L Qiu.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Measurement of surfactant in-irrigating fluid from the nasopharynx of patients with secretory otitis media].

OBJECTIVE: Dysfunction of the eustachian tube is believed to play a role in the pathogenesis of secretory otitis media (SOM). In the animal model, previous investigators have found that surfactant in the eustachian tube could decrease the eustachian tube opening pressure and improve eustachian tube functions. Because the nasopharynx is anatomically adjacent to the eustachian tube and the membrane of the nasopharynx continues to the middle ear via the eustachian tube, we hypothesized that the surfactant could also present in the nasopharynx and then designed the following experiment to confirm this hypothesis. METHODS: The concentrations of surfactants in the nasopharyngeal irrigating fluid were measured in normal control and SOM patients. RESULTS: (1) The surfactant from the SOM patients were significantly lower than that from the normal control (8.637 +/- 2.730) mg/L vs. (39.212 +/- 2.437) mg/L. (2) The concentration of surfactant from child SOM was also significantly lower than that of the normal control (8.062 +/- 2.925) mg/L vs. (39.787 +/- 2.557) mg/L. (3) The concentration of surfactant of SOM was not associated with the course of SOM. CONCLUSION: Surfactant reduction in the nasopharynx could indirectly reflect the level of the surfactant in the eustachian tube and the middle ear and influence the eustachian tube function. So surfactant reduction is one of the causative factors in SOM. The strategy of increasing surfactant in the nasopharynx and eustachian tube should be beneficial to reducing persistent secretory otitis media.

Adolescent↗
PubMed1998

Protein prenyl transferase activities of Plasmodium falciparum.

Prenylated proteins have been shown to function in important cellular regulatory processes including signal transduction. The enzymes involved in protein prenylation, farnesyl transferase and geranylgeranyl transferase, have been recent targets for development of cancer chemotherapeutics. We have initiated a systematic study of protein prenyl transferases of the malaria parasite, Plasmodium falciparum, to determine whether these enzymes can be developed as targets for antimalarial chemotherapy. We report here the identification of protein farnesyl transferase and protein geranylgeranyl transferase-I in the malaria parasite, P. falciparum. The farnesyl transferase has been partially purified from the cytosolic fraction through ammonium sulfate precipitation and Mono-Q chromatography. Farnesyl and geranylgeranyl transferase-I activities are present at all stages of P. falciparum intraerythrocytic development with maximum specific activity in the ring stage. Geranylgeranyl transferase-I specific activity is two times that of farnesyl transferase in the ring stage. Peptidomimetics and prenyl analogues of protein farnesyl transferase substrates were tested as in vitro inhibitors of partially purified P. falciparum prenyl transferase and of malaria parasite growth. The peptidomimetics were significantly more potent inhibitors than lipid substrate analogues of both the activity of Mono-Q purified enzyme and parasite growth in intraerythrocytic cultures. Exposure of the parasite to the peptidomimetic L-745,631 also showed significant inhibition of morphological development beyond the trophozoite stage. These studies suggest the potential of designing or identifying differential inhibitors of P. falciparum and mammalian prenyl transferases as an approach to novel malaria therapy.

Alkyl and Aryl Transferases↗
PubMed1998

Constitutive transduction of peptide transporter and HLA genes restores antigen processing function and cytotoxic T cell-mediated immune recognition of human melanoma cells.

Potentiation of immunogenicity of malignant cells by gene transduction provides a unique opportunity for immune targeting of human cancers in vivo. This approach is undoubtedly influenced by the ability of the malignant cells to process and present endogenously target epitopes on their cell surface for immune recognition by cytotoxic T lymphocytes (CTLs). In the present study, we have investigated potential immune-resistance pathways in human malignant melanoma by analyzing the major histocompatibility complex (MHC) gene expression and function in a panel of tumour cell lines. Our analysis showed that a large proportion of these cell lines consistently display a functional defect in the endogenous processing of CTL epitopes and are recognised poorly by specific T cells in spite of high levels of target antigen expression in the tumour cells. Molecular characterisation of this defect revealed that tumour cells under-expressed peptide transporters and surface-assembled MHC class I molecules, which constitute essential components of the class I processing pathway. Induction of peptide transporter and surface class I following treatment of these tumour cells with interferon gamma (IFN-gamma) suggested a transcriptional defect in the expression of antigen-processing genes. Endogenous processing function in these tumour cells was restored completely following simultaneous transduction of cells with peptide transporter and HLA class I genes. Our findings provide a rationale for focussing on strategies designed to improve antigen-processing function in tumour cells and, thus, may strongly influence future strategies for melanoma-specific immunotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Degradation of hammerhead ribozymes by human ribonucleases.

Hammerhead ribozymes were used as substrates to examine endoribonucleolytic activities in cell extracts and cultured human cells. Primer-extension analyses showed that ribozymes directed against tumor necrosis factor-alpha mRNA and human immunodeficiency virus type 1 tat mRNA were cleaved at UA and CA dinucleotides by extracts. Preferred cleavage sites were similar to those observed following digestion with RNase A, and cleavage was blocked by RNasin, an inhibitor of pyrimidine-specific ribonucleases. Removal of UA and CA dinucleotides rendered ribozymes more stable when incubated in cell extracts that were not significantly contaminated by extracellular nucleases. Placement of UA dinucleotides adjacent to a ribozyme in mRNA led to excision of the ribozyme from long transcripts during incubation in extracts. UA dinucleotides also made mRNA more labile than a control RNA when expressed from an endogenous plasmid gene in the human myeloid cell line U937. Similarly, UA and CA dinucleotides caused ribozymes to have a shorter half-life when delivered to U937 cells by lipofectin-mediated transformation. Taken together, these data indicate that one or more members of the pyrimidine-specific ribonuclease family is involved in the intracellular degradation of RNA, and they explain the paucity of UA dinucleotides in eukaryotic mRNA. Judicious manipulation of preferred target sequences of pyrimidine-specific ribonucleases may be useful in designing effective hammerhead ribozymes.

Base Sequence↗
PubMed1998

[Maxillary sinus lifting, bone graft, and simultaneously placement of implants].

OBJECTIVE: To study the effect of maxillary sinus floor lifting by bone graft for immediate implantation. METHODS: 12 maxillary sinus underwent sinus floor bone graft and simultaneously 24 implants olacement. The mean time of follow up was 14 months. RESULTS: There were no implant loose or lost, no clinical complaint of the maxillary sinus area, and X-ray exam showed well osseointegration in 6 months postoperatively. Abnormal sensitivity of chin area were found in 8 patients after bone graft taken from chin, but the sensitivity became normal spontaneously in 3-12 months postoperatively. CONCLUSION: Successful maxillary sinus floor bone graft with simultaneously placement of implant is predictable.

Adult↗
PubMed1998

[Comparative observation on the efficacy of several test/probe systems for detecting schistosome circulating antigen].

AIM: To compare the efficacy of 5 test/probe systems for the detecting of schistosomal circulation antigen (SCA) in sera from infected rabbits. METHODS: Nine rabbits were infected with monosexual cercariae (either male or female), 7 rabbits were infected with bisexual cercariae as controls. Blood samples were collected periodically post infection (p.i). 15 rabbits were infected each with 250 bisexual cercaria and divided into 3 groups, 2 groups were treated with allyl thiourea (295-590 mg/kg) from 19 d or 46 d respectively, to inhibit their egg formation. One untreated group was used as control. Blood samples were collected weekly until 8 wk post infection. SCA detecting methods include (1) dot-ELISA/McAb anti-surface membrane antigen of adult worms (8SE4), (2) dot-ELISA/McAb anti-CCA (3D10), (3) Sandwich dot-ELISA/McAb anti-egg antigen (MG2), (4) Sandwich-ELISA/McAb anti-egg antigen (2H10), (5) Sandwich-ELISA/McAb anti-CAA (1B10). RESULTS: Using method (1) all of the 18 rabbits infected with monosexual cercariae were negative. Using method (2) only 1 rabbit harboured 133 male worms showed positive. Using method (5) no SCA were detected in sera from female cercariae-infected rabbits but 3 out of 9 male cercariae-infected rabbits showed positive reaction. SCA detecting results from rabbits treated with allyl thiourea: both method (1) and (3) showed negative in rabbits treated from 19 d (p.i.) but all gave positive reaction in 6-7 wk in rabbits treated from 46 d (p.i.). There were all negative detected by using method (4) and all positive at 6 wk (p.i.) detected by method (5) in rabbits of 3 groups whether treated or non-treated. CONCLUSION: Various test/probe systems have different efficacy in detecting SCA but (5) of the methods (1)(2) tests/probe systems could not detect SCA in rabbits with single female cercariae infection. From the egg formation inhibition study, the SCA detected by McAb 8SE4 dot-ELISA might be related to egg maturation. Whether the surface membrane antigen of adult worm has common antigenic component with egg antigen remains to be studied.

Animals↗
PubMed1998

[The experiment research of ginger detoxification to Rhizoma Pinelliae].

The experiment results have shown that Ginger can abate the stimulation of Phizoma Pinelliae on abdominal cavity of mice, reduce the torsion incidence rate of mice because of pain which is resulted to i.p. powder suspension of raw Rhizoma pinelliae. We also observed that Ginger can obviously inhibit the increase of capillary permeatility of abdominal cavity of mice, reduce the PGE2 content of inflammatory foot tissue of mice which is due to inject juice of fresh Pinellia Rhizoma. In addition, Ginger can increase the PGE2 content of mice gastric solution, antegonise the decrease of PGE2 content which is come from administration of raw Pinellia Rhizoma and protect the gastric mucous. Above mentioned results suggested that Ginger have detoxification in vivo. to toxin of Pinellia Rhizoma.

Abdominal Cavity↗
PubMed1997

Identification of a novel member of the TGF-beta superfamily highly expressed in human placenta.

While conducting a gene discovery effort targeted to transcripts of the prevalent and intermediate frequency classes in placenta throughout gestation, we identified a novel member of the TGF-beta superfamily that is expressed at high levels in human placenta. Hence, we named this factor 'Placental Transforming Growth Factor Beta' (PTGFB). The full-length sequence of the 1.2-kb PTGFB mRNA has the potential of encoding a putative pre-pro-PTGFB protein of 295 amino acids and a putative mature PTGFB protein of 112 amino acids. Multiple sequence alignments of PTGFB and representative members of all TGF-beta subfamilies evidenced a number of conserved residues, including the seven cysteines that are almost invariant in all members of the TGF-beta superfamily. The single-copy PTGFB gene was shown to be composed of only two exons of 309 bp and 891 bp, separated by a 2.9-kb intron. The gene was localized to chromosome 19p12-13.1 by fluorescence in-situ hybridization. Northern analyses revealed a complex tissue-specific pattern of expression and a second transcript of 1.9 kb that is predominant in adult skeletal muscle. Most importantly, the 1.2-kb PTGFB transcript was shown to be expressed in placenta at much higher levels than in any other human fetal or adult tissue surveyed.

Adult↗
PubMed1997

Serine protease inhibition and mitochondrial dysfunction associated with cisplatin resistance in human tumor cell lines: targets for therapy.

Indicators of mitochondrial function were studied in two different cell culture models of cis-diamminedichloroplatinum-II (CDDP) resistance: the intrinsically resistant human ovarian cancer cell line CI-80-13S, and resistant clones (HeLa-S1a and HeLa-S1b) generated by stable expression of the serine protease inhibitor-plasminogen activator inhibitor type-2 (PAI-2), in the human cervical cancer cell line HeLa. In both models, CDDP resistance was associated with sensitivity to killing by adriamycin, etoposide, auranofin, bis[1,2-bis(diphenylphosphino)ethane]gold(I) chloride ([Au(DPPE)2]Cl), CdCl2 and the mitochondrial inhibitors rhodamine-123 (Rh123), dequalinium chloride (DeCH), tetraphenylphosphonium (TPP), and ethidium bromide (EtBr) and with lower constitutive levels of ATP. Unlike the HeLa clones, CI-80-13S cells were additionally sensitive to chloramphenicol, 1-methyl-4-phenylpyridinium ion (MPP+), rotenone, thenoyltrifluoroacetone (TTFA), and antimycin A, and showed poor reduction of 1-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT), suggesting a deficiency in NADH dehydrogenase and/or succinate dehydrogenase activities. Total platinum uptake and DNA-bound platinum were slightly lower in CI-80-13S than in sensitive cells. The HeLa-S1a and HeLa-S1b clones, on the other hand, showed poor reduction of triphenyltetrazolium chloride (TTC), indicative of low cytochrome c oxidase activity. Total platinum uptake by HeLa-Sla was similar to HeLa, but DNA-bound platinum was much lower than for the parent cell line. The mitochondria of CI-80-13S and HeLa-S1a showed altered morphology and were fewer in number than those of JAM and HeLa. In both models, CDDP resistance was associated with less platinum accumulation and with mitochondrial and membrane defects, brought about one case with expression of a protease inhibitor which is implicated in tumor progression. Such markers may identify tumors suitable for treatment with gold phosphine complexes or other mitochondrial inhibitors.

Adenosine Triphosphate↗
PubMed1997

Ultraviolet light attenuates heat-inducible gene expression.

Ultraviolet light (UV) induces a stress response mediated through transcription factors such as NF-kB and AP-1, yet little is known about its effect on other transactivators of stress gene expression such as heat shock factor (HSF1). Analysis of UV-treated HeLa cells unexpectedly revealed uncoupling of the heat shock response. UV weakly induced HSF1 into its DNA bound state and markedly attenuated heat-inducible gene expression. HSF1 was further analyzed as a potential target for the uncharacteristic uncoupling of the thermal stress response by another type of stress. Heat-inducible multimerization and nuclear translocation of HSF1 were found to be intact in UV-treated cells; however, the monomeric rather than the multimeric form of HSF1 become hyperphosphorylated by UV. This effect could be partially abolished by the antioxidant N-acetyl cysteine with partial reconstitution of hs gene expression. The reported role of a MAP kinase blockade of HSF1 transactivating properties could not be confirmed by an inhibitor of the MAP kinase pathway. Fibroblasts defective in SAP kinase activity also did not exhibit resistance to UV-inducible phosphorylation of HSF1. Two-dimensional phosphopeptide mapping of HSF1 revealed a single tryptic peptide to be affected by UV, but no new pattern of phosphorylation was evident relative to tryptic phosphopeptide profile observed in control cells. These data suggest that UV uncoupling of the hs response possibly involves steps in addition to those associated with phosphorylation the monomeric form of HSF1.

Acetylcysteine↗
PubMed1997

Distribution of cholinergic neuronal differentiation factor/leukemia inhibitory factor binding sites in the developing and adult rat nervous system in vivo.

Cholinergic neuronal differentiation factor/leukemia inhibitory factor (CDF/LIF) is a multifunctional cytokine that affects neurons as well as many other cell types. Toward elucidating its neural functions in vivo, we previously investigated the distribution of CDF/LIF binding sites with iodinated native CDF/LIF in embryonic to postnatal day 0 (P0) rats. In the present study, we have extended our examination to postnatal ages and find that specific CDF/LIF binding sites are present at defined developmental stages in additional brain regions not previously exhibiting binding by P0. High levels of binding are detected in all P7 sensory and autonomic ganglia examined, but only in restricted postnatal central nervous system structures. Cranial motor and mesencephalic trigeminal neurons maintain high levels throughout, while binding to spinal motor neurons, which decreases to low levels at P0, reappears by P14 and increases with age. Most other structures, which show detectable binding by P0, exhibit higher levels at postnatal ages, including the red, deep, ventral cochlear, trapezoid, superior olivary, vestibular, ventral tegmental, and ventral posterior thalamic nuclei as well as the glomerular layer of the olfactory bulb. High levels are also detected in several structures for the first time after P0, including the cerebellar cortex (molecular and Purkinje cell layers), lateral reticular nucleus of the medulla and reticular formation, as well as the reticulotegmental, medial geniculate, solitary (rostral, dorsomedial, and commissural regions), medial septal, lateral mammillary, and lateral habenular nuclei. These results not only identify regions of potential CDF/LIF-responsive neurons and glia throughout development but suggest new CDF/LIF roles in the nervous system.

Animals↗
PubMed1997

Attenuated stress responses in young and old human lymphocytes.

Aging generally is understood to be a period defined by altered responses to physiological stress. At the molecular level, several stress responses involving specific gene expression have been revealed, and thermal stress has been tightly linked to induction of the heat shock gene family (D.A. Jurivich. In E. Bittar (ed.), Principles of Medical Biology, Vol. 4, JAI press, San Diego, 1996, pp. 411-462). Perturbations in heat shock gene transcription consistently have been noted in senescent cells from all species examined thus far. Because heat shock proteins serve several vital functions in the immune system, changes in the thermal stress response could potentially contribute to immunosenescence. Inadequate promoter priming by the transactivator or heat shock genes, heat shock factor 1 (HSF1), is thought to account for age-dependent diminution in expression of these genes, although the exact mechanism for this loss is not clearly understood. We have found that human lymphocytes exhibit an age-dependent loss in HSF1-DNA binding, although a range of binding has been observed in both young and old donor cells. This report characterizes a subset of young and old human donor lymphocytes that are non-responders to thermal stress defined by the absence of HSF1-DNA binding after a 42 degrees C heat shock. Whole cell extracts from these donor cells have the capacity to inhibit HSF1-DNA binding when mixed with pre-activated HSF1 from HeLa cells. This inhibitory activity is lost upon heat denaturation and does not appear to be protease mediated. Serial passage of lymphoblasts recapitulates loss of heat inducible HSF1-DNA observed in old donor lymphocytes, thus suggesting that loss of replicative potential and aging lead to altered stress responses. Uncoupling of the thermal response and its potential relevance to apoptosis and aging are discussed.

Adult↗
PubMed1997

Transplantation of adenovirally transduced allogeneic chondrocytes into articular cartilage defects in vivo.

Gene transfer to chondrocytes followed by intra-articular transplantation may allow for functional modulation of chondrocyte biology and enhanced repair of damaged articular cartilage. We chose to examine the loss of chondrocytes transduced with a recombinant adenovirus containing the gene for Escherichia coli beta-galactosidase (Ad.RSVntlacZ), followed by transplantation into deep and shallow articular cartilage defects using New Zealand White rabbits as an animal model. A type I collagen matrix was used as a carrier for the growth of the transduced chondrocytes and to retain the cells within the surgically created articular defects. Histochemical analysis of matrices recovered from the animals 1, 3 and 10 days after implantation showed the continued loss of lacZ positive chondrocytes. The number of cells recovered from the matrices was also compared with the initial innoculum of transduced cells present within the matrices at the time of implantation. The greatest loss of transduced cells was observed in the first 24 h after implantation. The numbers of transduced cells present within the matrices were relatively constant between 1 and 3 days postimplantation, but had progressively declined by 10 days postimplantation. These results suggest that transduction of chondrocytes followed by intra-articular transplantation in this rabbit model may enable us to examine the biological effects of focal transgenic overexpression of proteins involved in cartilage homeostasis and repair.

Adenoviridae↗
PubMed1997

Role of metalloproteinases in the development and healing of acetic acid-induced gastric ulcer in rats.

BACKGROUND/AIMS: Matrix metalloproteinases (MMPs) are believed to be active in connective tissue remodeling associated with various physiological processes and in pathological conditions such as cancer and arthritis. However, the role of MMPs in gastrointestinal ulceration has not been clearly established. Therefore, the aim of this study was to examine the role of collagenase and gelatinases A and B in the development and healing of acetic acid-induced gastric ulcer in rats. METHODS: Gastric ulcer was induced by injecting 20 microliters glacial acetic acid into gastric wall of rat stomachs. To examine whether changes in the ulcer formation and healing phase correlate with MMP activity, Triton X-100/CaCl2 and Tris/CaCl2 (60 degrees C) extracts of stomachs were prepared from controls and animals killed 24 h (formation phase) and 7 days (healing phase) after acetic acid administration. Total collagenase and gelatinase activities were measured using (H3)labeled-acetylated type I collagen or gelatin as substrate, respectively, prepared from rat skin. RESULTS: Twenty-four hours after administration of acetic acid, the mean area of ulcer crater was 51.2 mm2. By day 7, the mean size of ulcer crater was reduced to 35.9 mm2. The mean activity of collagenase in gastric tissue from controls animals was 0.007 U/g tissue. In acetic acid-treated rats, this activity increased to 2.18 U/g at 24 h and declined to 0.69 U/g by day 7. Similarly, total gelatinase activity increased from 20.5 U/g tissue (controls) to 28.8 U/g at 24 h and declined to 23.9 U/g at day 7. Gelatinzymography revealed that gelatinase B levels were greatly increased at 24 h and declined by day 7, whereas the gelatinase A levels remained constant. CONCLUSIONS: The data showed that the formation of acetic acid-induced ulcer in rats is accompanied by an elevation of collagenase and gelatinase B that gradually tend to return to control values during the healing phase.

Acetic Acid↗
PubMed1997

A 120 kilobase resolution contig map of the rice genome.

92% of the rice genome (4.3 x 10(8) bp, 2n = 24) was covered by 631 contigs of various length, which were generated by fingerprinting from a representative and genetically stable bacterial artificial chromosome (BAC) library of the Guang Lu Ai 4 (a O. Sativa variety) genome with the average insert of 120 kb in length. To form the contig map, 565 molecular markers of RFLP, STS, cDNA and anchor set derived from two O. Sativa varieties were by colony hybridization mapped to the contigs, which were then assigned to and ordered along the particular chromosomes according to the marker colinearity. Being highly conserved DNA sequences shared among the genomes of rice, barley, wheat, oat, maize, sorghum and sugar cane, 89 anchor markers mapped help to identify the rice genes through the information provided by the maps of relative genomes, and vice versa. Numerous repeated DNA sequences of various length were identified and mapped to the chromosomes. Physical distances have been determined for hundreds pairs of adjacent markers, which would facilitate the identification by map-based cloning the rice genes of interest. The accuracy of clone overlaps in contigs was further confirmed by the existence in contigs of well fit stacks of marker-lodged clones independently identified by hybridization. Large scale DNA sequencing of individual chromosomes could now be initiated simply by selecting and sequencing the minimally overlapped BAC clones of the contigs.

Alkyl and Aryl Transferases↗
PubMed1997

[Comparison of changes of bone mass, parathyroid hormone and calcitonin between two animal models of bone loss].

The changes in bone mass, blood parathyroid hormone (PTH) and calcitonin (CT) between rats suspended for 14 and 21 days, simulated weightlessness, and rats ovariectomized (OVX) for 30 and 60 days were observed. The results revealed that mineral density of T6 and L3 was significantly increased in rats suspended for 14 days. T6 mineral density was also significantly increased in rats suspended for 21 days, but L3 mineral density was significantly decreased. T6 mineral density had no change in OVX rats, but L3 mineral density was significantly decreased in them both for 30 and 60 days. Mineral content at proximal 1/3 of femur shaft was significantly decreased in rats suspended for 14 and 21 days, and in rats OVX for 60 days. Bone biomechanical properties of suspended rats were more seriously deteriorated than that in OVX rats. There was no change in blood PTH, but CT was significantly increased in rats suspended for 14 and 21 days. Blood PTH and CT were significantly decreased in rats OVX for 30 and 60 days. The results indicate that the mineral redistribution and bone loss are presented in trabecular bone of suspended rats, but not in OVX rats. The deterioration of bone quality was more seriously in suspended rats than that in OVX rats. Both the cortical and trabecular bone in the two models were affected.

Animals↗