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Biomedical subjects

W Luo

Publications and source records attributed to W Luo.

At least 73 records · Page 4Linked to original sources
PubMed2000

[Influence of cleftpalate on middle ear conduction and eustachian function].

OBJECTIVE: To explore the influence and its degree of cleftpalate on middle ear conduction and eustachian function. METHOD: 41 cleftpalate patients (82 ears) were performed with otopharyngeal examinations, form of the ostium pharyngeum tubae auditivae observations and acoustic impedance measurements. The results were compared with healthy persons of normal hearing. RESULT: In the cases with cleftpalate, tympanic membrane pathological change incidence was 89.0% (73/82), ostium pharyngeum tubae auditivae of cracked shape was 59.5% (25/42), abnormal tympanogram was 83.1% (64/77), the negative rate of stapedius muscle reflex was 84.4% (65/77). There are significant different in comparison with healthy persons. In synthetic analyses, the rate of secretory otitis media with varied degree in the cleftpalate cases was 74.0% (57/77). CONCLUSION: There was a high incidence of middle ear pathological change and secretory otitis media in the cleftpalate patients. This high incidence was due to susceptivity of the nasopharynx on the infection, weak strength of the dilator tubae eustachii and the deformed shape of the ostium pharyngeum tubae auditivae.

Acoustic Impedance Tests↗
PubMed2000

[Effects of cultivating measures on root rot of Panax notoginseng].

OBJECTIVE: To probe into the effects of cultivating measures on root rot of Panax notoginseng for the integrate control. METHOD: Field investigation on the planting plots was conducted. CONCLUSIONS: Effects of cultural system on root rot are obvious, (1) The rotation period should be more than eight years; (2) Improper fertilizer application is one important fact of the root rot occuring; (3) The light transmitting rate is one important fact; (4) Laying film and using sun-shade shed can reduce the root rot.

Fertilizers↗
PubMed2000

[Expression of inducible nitric oxide synthase in asthmatic rat lung].

OBJECTIVE: In order to study the role of nitric oxide (NO) during the airway inflammation of asthmatic rat, we investigated expression of inducible nitric oxide synthase (iNOS) in the lung tissue of asthmatic rats. METHODS: Animal model of asthmatic Wistar rats was developed by being sensitized and challenged with ovalbumin. Activities of iNOS were measured by using SP immunohistochemical method. RESULTS: In asthmatic rat group (n = 10), lung tissue showed stronger immunostaining (90%) for iNOS than control group (20%) (P < 0.001). Immunostaining was mainly present in the bronchial epithelium, alveolar epithelium, bronchial smooth muscle, vascular endothelial and smooth muscle cells and inflammatory cells such as macrophages and neutrophils. In glucocorticoid treated group (n = 10), there was down regulation of iNOS immunoreactivity (30% positive) compared with control asthmatic rat group (20%). CONCLUSIONS: The increased expression of iNOS in asthmatic rat lung tissue showed NO playing a critical role in asthmatic inflammation, otherwise expression of iNOS was inhibited by glucocorticoid.

Animals↗
PubMed1999

Overexpression of CCAAT displacement protein represses the promiscuously active proximal gp91(phox) promoter.

CCAAT displacement protein (CDP) is a transcriptional repressor that restricts expression of the gp91(phox) gene to mature myeloid cells. CDP interacts with multiple sites within the -450 to +12 bp human gp91(phox) promoter, and down-regulation of CDP DNA-binding activity is required for induction of gp91(phox) transcription in mature phagocytes. Truncation of the gp91(phox) promoter to -102 to +12 bp removes 4 CDP-binding sites and reveals a promiscuous promoter activity that is active in some nonphagocytic cells. A cis-element at -90 bp is required for derepressed transcription and serves as a binding site for multiple transcriptional activators. We now report that this element also serves as a binding site for CDP. The affinity of CDP for this element is relatively weak compared with upstream CDP-binding sites within the promoter, consistent with the promiscuous transcriptional activity exhibited by the -102 to +12 bp gp91(phox) promoter fragment. Further analysis of the proximal promoter reveals an additional weak-affinity CDP-binding site centered at approximately -20 bp. Overexpression of cloned CDP represses the -102 to +12 bp gp91(phox) promoter, indicating that these proximal CDP-binding sites are functionally significant. The constellation of transcriptional activators and a repressor that interacts with the -90 bp cis-element is identical to that observed for a promoter element at -220 bp, reflecting the highly modular organization of the gp91(phox) promoter. These studies illustrate the complex interplay between transcriptional activators and a repressor that contribute to the myeloid-restricted expression of the gp91(phox) gene.

Cell Differentiation↗
PubMed1999

The cytoplasmic domain of C-CAM1 tumor suppressor is necessary and sufficient for suppressing the tumorigenicity of prostate cancer cells.

We have previously shown that C-CAM1 cell adhesion molecule can suppress the growth of prostate cancer cells in vivo. In this study, we determined the minimal domain of C-CAM1 that is required for its tumor-suppressive activity. DU145 prostate cancer cells were infected with recombinant adenoviruses containing various C-CAM1 mutant genes, and the effects of the mutant C-CAM1 proteins on the growth of DU145 cells were assessed in a nude-mice xenograft model. Deletion of C-CAM1's cytoplasmic domain, which is not required for its adhesion activity, abolished the growth-suppressive activity, whereas deletion of the adhesion domain did not. This observation suggests that C-CAM1's extracellular domain may be not essential for its tumor suppressive activity. Indeed, we found that expression of the C-CAM1 cytoplasmic domain alone led to growth suppression of DU145 cells. These results suggest that the cytoplasmic domain of C-CAM1 is necessary and sufficient for its growth-suppressive function.

Adenosine Triphosphatases↗
PubMed1999

Interleukin-10 enhances immune responses to pneumococcal polysaccharides and sheep erythrocytes in young and aged mice.

Antibody responses to pneumococcal polysaccharides are decreased in aged mice. Using a system to measure murine antibody responses to the Pnu-Imune vaccine, here we demonstrate that interleukin-10 (IL-10) has an adjuvant effect in enhancing the vaccine response in the aged. IL-10 increased the vaccine responses of B cells from aged mice in vitro only if either T cells or macrophages were also present. The need for T cells or macrophages could be substituted by cytokines such as IL-1 or IL-5, which are normally made by these accessory cells. Thus, IL-10 appeared to act on B cells directly but it worked in conjunction with other cytokines to induce an antigen specific response. In vivo studies showed that IL-10 administration enhanced antibody responses not only to thymic independent antigens but also to thymic-dependent antigens such as sheep erythrocytes. These data suggest that IL-10 may be useful in enhancing vaccine-specific responses in situations in which the host is immunocompromised.

Aging↗
PubMed1999

HIV-specific cytotoxic T lymphocyte precursors exist in a CD28-CD8+ T cell subset and increase with loss of CD4 T cells.

OBJECTIVES: To determine whether the CD28-CD8+ T cells that develop during HIV infection contain HIV-specific cytotoxic precursor cells. DESIGN: CD8 subpopulations from six asymptomatic HIV-positive adults, with varying degrees of CD4 T cell loss, were sorted by flow cytometry and HIV-specific precursor cytotoxic T lymphocyte frequencies were measured. Three populations of CD8 T cells were tested: CD28+CD5-- T cells, CD28-CD57+ T cells (thought to be memory cells) and CD28-CD57- T cells (function unknown). METHODS: Sorted CD8 subsets were stimulated with antigen presenting cells expressing HIV-1 Gag/Pol molecules. Cytotoxic T cell assays on Gag/Pol expressing 51Cr-labeled Epstein-Barr virus transformed autologous B cells lines or control targets were performed after 2 weeks. Specific lysis and precursor frequencies were calculated. RESULTS: Both CD28 positive and CD28-CD57+ populations contained appreciable numbers of precursors (9-1720 per 10(6) CD8+ T cells). However, the CD28-CD57- population had fewer precursors in five out of six people studied. More CD28 positive HIV-specific cytotoxic T lymphocyte precursors were found in patients with CD4:CD8 ratios > 1, whereas more CD28-CD57+ precursors were found in patients whose CD4:CD8 ratios were < 1 (r2, 0.68). CONCLUSIONS: Memory HIV-specific precursor cytotoxic T lymphocytes are found in both CD28 positive and CD28-CD8+ cells, however, a CD28-CD57- subpopulation had fewer. Because CD28-CD57+ cells are antigen-driven with limited diversity, the loss of CD28 on CD8 T cells during disease progression may reduce the response to new HIV mutations; this requires further testing.

Adult↗
PubMed1999

Msx2 gene dosage influences the number of proliferative osteogenic cells in growth centers of the developing murine skull: a possible mechanism for MSX2-mediated craniosynostosis in humans.

Throughout its complex morphogenesis, the vertebrate skull must at once protect the brain and expand to accommodate its growth. A key structural adaptation that allows this dual role is the separation of the bony plates of the skull with sutures, fibrous joints that serve as growth centers and allow the calvarial bones to expand as the brain enlarges. Craniosynostosis, the premature fusion of one or more calvarial bones with consequent abnormalities in skull shape, is a common developmental anomaly that disrupts this process. We found previously that a single amino acid substitution in the homeodomain of the human MSX2 gene is associated with the autosomal dominant disorder craniosynostosis, Boston type. This mutation enhances the affinity of Msx2 for its target sequence, suggesting that the mutation acts by a dominant positive mechanism. Consistent with this prediction, we showed that general overexpression of Msx2 under the control of the broadly expressed CMV promoter causes the calvarial bones to invade the sagittal suture. Here we use tissue-specific overexpression of Msx2 within the calvarial sutures to address the developmental mechanisms of craniosynostosis and skull morphogenesis. We demonstrate that a segment of the Msx2 promoter directs reporter gene expression to subsets of cells within the sutures. In late embryonic and neonatal stages, this promoter is expressed in undifferentiated mesenchymal cells medial to the growing bone. By P4, promoter activity is reduced in the suture, exhibiting a punctate pattern in undifferentiated osteoblastic cells in the outer margin of the osteogenic front. Overexpression of Msx2 under the control of this promoter is sufficient to enhance parietal bone growth into the sagittal suture by P6. This phenotype is preceded by an increase in both the number and the BrdU labeling of osteoblastic cells in the osteogenic fronts of the calvarial bones. These findings suggest that an important early event in MSX2-mediated craniosynostosis in humans is a transient retardation of osteogenic cell differentiation in the suture and a consequent increase in the pool of osteogenic cells.

Animals↗
PubMed1999

Activation of Vav by Nef induces cytoskeletal rearrangements and downstream effector functions.

Nef of primate lentiviruses is critical for high levels of viremia and the progression to AIDS. Nef associates with and activates a serine/threonine kinase (Nef-associated kinase [NAK]) via the small GTPases Rac1 and Cdc42. We identified the protooncogene and guanine nucleotide exchange factor Vav as the specific binding partner of Nef proteins from HIV-1 and SIV. The interaction between Nef and Vav led to increased activity of Vav and its downstream effectors. Both cytoskeletal changes and the activation of c-Jun N-terminal kinase (JNK) were observed. Furthermore, a dominant-negative Vav protein inhibited NAK activation and viral replication. Thus, the interaction between Nef and Vav initiates a signaling cascade that changes structural and physiological parameters in the infected cell.

Amino Acid Sequence↗
PubMed1999

Effect of Mg2+ on the thermal inactivation and unfolding of creatine kinase.

The effect of Mg2+ on the thermal inactivation and unfolding of rabbit muscle creatine kinase has been studied for various temperatures and Mg2+ concentrations. Increasing the Mg2+ concentration in the denatured system significantly enhanced the inactivation and unfolding of creatine kinase during thermal denaturation. The analysis of the kinetic course of substrate reaction during thermal inactivation showed that at 47 degrees C the increased free Mg2+ concentration caused the creatine kinase inactivation rate to increase. Increasing the temperature strengthened the effect of Mg2+ on the thermal inactivation. Control experiments showed that treating native creatine kinase with different concentrations of Mg2+ did not change the enzymatic activity. The fluorescence emission spectra showed that the emission maximum for creatine kinase red-shifted from 335 to 337 nm during thermal denaturation at 47 degrees C for 10 min, while the presence of 3 mM Mg2+ caused the enzyme emission maximum to red-shift from 335 to 342.5 nm for the same thermal denaturation conditions. In addition, Mg2+ also enhanced the unfolding of the equilibrium state and decreased the time required to reach the equilibrium state of creatine kinase at 47 degrees C. The potential biological significance of these results are discussed.

Animals↗
PubMed1999

Regulation of complement factor H in a human liver cell line by interferon-gamma.

Factor H is a regulatory protein of the alternative pathway of complement activation. The liver is the major site of synthesis. We have used the Hep3b human liver cell line as a model for examining its regulation by interferon-gamma (IFN-gamma). The maximal response was achieved at 50 U/ml of IFN-gamma. An increase in H mRNA was observed as early as 2 h after addition of IFN-gamma; the response peaked at 24 h. The half-life of H mRNA in the presence of IFN-gamma was 3.8 +/- 0.8 h. The increase in H mRNA by IFN-gamma was partly dependent on protein synthesis, as cycloheximide (CHX) reduced the response by 40% and the level of H mRNA decreased in a dose-dependent manner with increasing concentrations of CHX. Phosphorylation events were also important in this induction because the kinase inhibitors staurosporine and genistein inhibited the induction of H mRNA by 88% and 68%, respectively. The induction could be inhibited completely when Hep3b cells were treated with CHX and staurosporine. Thus induction of factor H by IFN-gamma apparently involves two factors. One is likely to be Stat1alpha and the other is a CHX-sensitive protein.

Complement Factor H↗
PubMed1999

Differential expression of C-CAM cell adhesion molecule in prostate carcinogenesis in a transgenic mouse model.

PURPOSE: The transgenic adenocarcinoma of mouse prostate (TRAMP) model, in which various grades of prostate intraepithelial neoplasia (PIN) and prostate cancer with metastases can be reproducibly generated, is a paradigm for prostate disease progression. We have previously shown that C-CAM, an adhesion molecule, can suppress the growth of prostate cancer. In this report, we describe immunohistochemical characterization of differential expression of C-CAM at various stages of prostate tumorigenesis in the TRAMP model. MATERIALS AND METHODS: We sampled prostate specimens and periaortic lymph nodes from TRAMP mice. Indirect immunohistochemical staining with a polyclonal anti-C-CAM antibody was performed on the formalin-fixed, paraffin-embedded specimens. After castration at 12 weeks of age, the TRAMP mice developed androgen-independent prostate cancer (AIPC) and lymph node metastasis at 18 to 24 weeks of age. Samples from these castrated mice were also analyzed. RESULTS: C-CAM protein was expressed in the normal prostate epithelia of non-transgenic and TRAMP mice as well as in low-grade PINs in TRAMP mice. Expression was uniform on the luminal surfaces of these epithelia. C-CAM expression was noticeably reduced and the staining pattern heterogeneous in some high-grade PINs. C-CAM staining was generally absent in prostate cancer and metastatic lymph nodes. Androgen independent prostate cancer and its metastatic tumors generated in castrated TRAMP mice were also C-CAM negative. CONCLUSIONS: C-CAM expression correlates with the differentiation states of prostate epithelia and is down regulated early in prostate tumorigenesis in the TRAMP model.

Adenosine Triphosphatases↗
PubMed1999

Analysis of vaginal cell populations during experimental vaginal candidiasis.

Studies with an estrogen-dependent murine model of vaginal candidiasis suggest that local cell-mediated immunity (CMI) is more important than systemic CMI for protection against vaginitis. The present study, however, showed that, compared to uninfected mice, little to no change in the percentage or types of vaginal T cells occurred during a primary vaginal infection or during a secondary vaginal infection where partial protection was observed. Furthermore, depletion of polymorphonuclear leukocytes (PMN) had no effect on infection in the presence or absence of pseudoestrus. These results indicate a lack of demonstrable effects by systemic CMI or PMN against vaginitis and suggest that if local T cells are important, they are functioning without showing significant increases in numbers within the vaginal mucosa during infection.

Animals↗
PubMed1999

Phospholamban deficiency does not compromise exercise capacity.

Deficiency of phospholamban (PLB) results in enhancement of basal murine cardiac function and an attenuated response to beta-adrenergic stimulation. To determine whether the absence of PLB also reduces the reserve capacity of the murine cardiovascular system to respond to stress, we evaluated the heart rate (HR), blood pressure, and metabolic responses of PLB-deficient (PLB-/-) mice to graded treadmill exercise (GTE). PLB-/- mice were hypertensive at rest (125 +/- 19 vs. 109 +/- 16 mmHg, P < 0.05) but had normal tachycardic and hypotensive responses to isoproterenol. The HR response to GTE was normal; however, the hypertension in PLB-/- mice normalized at peak exercise. Their exercise capacities, as measured by duration of exercise and peak oxygen consumption (VO2), were normal. The oxygen pulse (VO2/HR) curve was also normal in PLB-/- mice, suggesting an ability to appropriately increase stroke volume and oxygen extraction during GTE, despite an inability to increase beta-adrenergically stimulated cardiac contractility. Thus deficiency of PLB, although resulting in diminished beta-adrenergic inotropic reserve, does not compromise cardiac performance during exercise.

Adrenergic beta-Agonists↗
PubMed1999

Stable expression of activated Ki-Ras does not constitutively activate the mitogen-activated protein kinase pathway but attenuates epidermal growth factor receptor activation in human astrocytoma cells.

Mutation in the ras oncogene is one of the most commonly reported genetic aberrations in human cancer. Activated ras mutants are thought to play a major role in promoting the growth and malignancy of tumor cells. Ras protein plays a central role in transmitting mitogenic signals from cell surface-to-nucleus by activating signaling pathways in response to receptor activation. Ras protein by recruiting c-Raf-1 kinase to the plasma membrane activates the mitogen-activated protein (MAP) kinase pathway. Expression of activated ras mutants in rodent fibroblast has been reported to constitutively activate the MAP kinase pathway, suggesting that constitutive activation of this pathway contributes to Ras influence on proliferation and transformation. In this study, we investigated whether stable expression of an activated Ki-Ras oncogenic mutant (G12V) in human astrocytoma cells leads to constitutive activation of the MAP kinase pathway and how this may influence cellular proliferation and signaling by epidermal growth factor (EGF) receptor. We discovered that Ki-Ras stable expression does not lead to constitutive activation of the MAP kinase pathway, rather expression of Ki-Ras plays a role in attenuating the activation of this pathway in response to EGF stimulation. Furthermore, we provide evidence that stable Ki-Ras expression attenuates the ability of EGF receptor to activate the MAP kinase pathway by interfering with the receptor ability to autophosphorylate at tyrosine residues and not by down regulating receptor expression.

Astrocytoma↗
PubMed1999

Growth inhibition of Candida albicans by vaginal cells from naïve mice.

Recurrent vulvovaginal candidiasis (RVVC) is a common idiopathic mucosal infection caused by Candida albicans. Current data suggests that local immunity is more important than that in the peripheral circulation for protection against infection. In the present study, anti-Candida innate resistance at the vaginal mucosa was investigated using a murine model. For this, splenic and vaginal cells were assessed for in vitro growth inhibition (GI) of C. albicans and cytotoxicity of natural killer (NK) cell-sensitive tumour targets (YAC-1). As expected, significant GI of C. albicans by splenic cells was mediated predominantly by polymorphonuclear leucocytes (PMNL) at effector to target (E:T) ratios of 100 and 50:1. From the vaginal mucosa, naïve unfractionated, but not nylon wool non-adherent (NWN), cells extracted from whole vaginal tissue showed significant GI of C. albicans at E:T ratios as low as 1:1, but only modest killing of YAC-1 targets at all E:T ratios. Subsequent experiments showed significant GI of C. albicans by vaginal epithelioid-enriched cells and with several epithelial cell lines, but not in supernatants collected from the co-cultures. In contrast, lymphoid cell lines had no anti-Candida activity. These results suggest that anti-Candida activity is present at the vaginal mucosa, but unlike that from the spleen, the vaginal activity appears to be predominantly mediated by epithelial cells.

Animals↗
PubMed1999

DNA-binding properties of CCAAT displacement protein cut repeats.

CCAAT displacement protein (CDP) is a transcriptional repressor that contains four distinct DNA-binding domains; a homeodomain and three cut repeats. Each DNA-binding domain of CDP was expressed as a glutathione S-transferase (GST)-fusion protein and analyzed for relative binding affinity to five CDP-binding sites within the gp91phox promoter. Each cut repeat exhibits a unique pattern of DNA-binding affinities for the five binding sites in the gp91phox promoter, suggesting that each may make a distinct contribution to the DNA-binding behavior of native CDP. Although measurement of DNA/protein complex mass indicates that an isolated cut repeat can bind DNA as a monomer, mixing of GST-cut repeat and GST-homeodomain fusion proteins enhances DNA-binding activity. Far-Western blot and two-hybrid analyses indicate, however, that the CDP domains do not directly interact. We hypothesize that GST-mediated dimerization leads to spatial juxtaposition of these DNA-binding domains, and that the resulting enhanced DNA-binding activity mimics cooperative interactions that occur between these domains in native CDP.

Binding Sites↗