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Biomedical subjects

Ying Wang

Publications and source records attributed to Ying Wang.

At least 289 records · Page 16Linked to original sources
PubMed2005

Genetic basis for conversion of rough-to-smooth colony morphology in Actinobacillus actinomycetemcomitans.

The basis of the rough-to-smooth conversion of Actinobacillus actinomycetemcomitans was examined. Smooth variants often contained mutations at the flp promoter region. Replacing the mutated flp promoter with the wild-type promoter restored the rough phenotype. The expression level of the flp promoter was approximately 100-fold lower in smooth than in rough strains. Mutations of the flp promoter are a cause of the rough-to-smooth conversion.

Aggregatibacter actinomycetemcomitans↗
PubMed2005

Single and combined deletions of the NTAL/LAB and LAT adaptors minimally affect B-cell development and function.

NTAL (non-T-cell activation linker, also called LAB) and LAT (linker for activation of T cells) are evolutionarily related transmembrane adaptor proteins that are phosphorylated upon immunoreceptor engagement. Using quantitative reverse transcription-PCR, both NTAL and LAT were found to be expressed in B cells. However, LAT expression was limited to early B cells, whereas NTAL expression typified mature B cells. To delineate their roles in B-cell development and function, Ntal-deficient mice were generated and crossed with Lat-deficient mice. B cells developed in Lat(-/-) Ntal(-/-) double-deficient mice and in mice lacking either of the two adaptors with the same efficiency as in wild-type mice. Upon B-cell antigen receptor cross-linking, Ntal(-/-) B cells exhibited slightly increased Ca(2+) mobilization and proliferation. In addition, Ntal-deficient mice had increased levels of natural antibodies and slightly increased humoral response to a T-dependent antigen. Normal titers of serum-specific immunoglobulins were produced in response to a T-cell-independent antigen. Although NTAL is also expressed in plasma cells, its absence did not affect the hypergammaglobulinemia E and G1 that developed in mice with a mutation in tyrosine 136 of LAT. Therefore, NTAL does not play a role in B cells symmetric to the role played by LAT in T cells.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Insulin hypersensitivity and resistance to streptozotocin-induced diabetes in mice lacking PTEN in adipose tissue.

In adipose tissue, insulin controls glucose and lipid metabolism through the intracellular mediators phosphatidylinositol 3-kinase and serine-threonine kinase AKT. Phosphatase and a tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of the phosphatidylinositol 3-kinase/AKT pathway, is hypothesized to inhibit the metabolic effects of insulin. Here we report the generation of mice lacking PTEN in adipose tissue. Loss of Pten results in improved systemic glucose tolerance and insulin sensitivity, associated with decreased fasting insulin levels, increased recruitment of the glucose transporter isoform 4 to the cell surface in adipose tissue, and decreased serum resistin levels. Mutant animals also exhibit increased insulin signaling and AMP kinase activity in the liver. Pten mutant mice are resistant to developing streptozotocin-induced diabetes. Adipose-specific Pten deletion, however, does not alter adiposity or plasma fatty acids. Our results demonstrate that in vivo PTEN is a potent negative regulator of insulin signaling and insulin sensitivity in adipose tissue. Furthermore, PTEN may be a promising target for nutritional and/or pharmacological interventions aimed at reversing insulin resistance.

Adipocytes↗
PubMed2005

Systemic lupus erythematosus serum IgG increases CREM binding to the IL-2 promoter and suppresses IL-2 production through CaMKIV.

Systemic lupus erythematosus (SLE) T cells express high levels of cAMP response element modulator (CREM) that binds to the IL-2 promoter and represses the transcription of the IL-2 gene. This study was designed to identify pathways that lead to increased binding of CREM to the IL-2 promoter in SLE T cells. Ca(2+)/calmodulin-dependent kinase IV (CaMKIV) was found to be increased in the nucleus of SLE T cells and to be involved in the overexpression of CREM and its binding to the IL-2 promoter. Treatment of normal T cells with SLE serum resulted in increased expression of CREM protein, increased binding of CREM to the IL-2 promoter, and decreased IL-2 promoter activity and IL-2 production. This process was abolished when a dominant inactive form of CaMKIV was expressed in normal T cells. The effect of SLE serum resided within the IgG fraction and was specifically attributed to anti-TCR/CD3 autoantibodies. This study identifies CaMKIV as being responsible for the increased expression of CREM and the decreased production of IL-2 in SLE T cells and demonstrates that anti-TCR/CD3 antibodies present in SLE sera can account for the increased expression of CREM and the suppression of IL-2 production.

Adult↗
PubMed2005

The cross talk between protein kinase A- and RhoA-mediated signaling in cancer cells.

The cross talk between cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) and RhoA-mediated signal transductions and the effect of this cross talk on biologic features of human prostate and gastric cancer cells were investigated. In the human gastric cancer cell line, SGC-7901, lysophosphatidic acid (LPA) increased RhoA activity in a dose-dependent manner. The cellular permeable cAMP analog, 8-chlorophenylthio-cAMP (CPT-cAMP), inhibited the LPA-induced RhoA activation and caused phosphorylation of RhoA at serine(188). Immunofluorescence microscopy, Western blotting, and green fluorescent protein (GFP)-tagged RhoA location assay in live cells revealed that RhoA was distributed in both the cytoplasm and nucleus of SGC-7901 cells. Treatment with LPA and/or CPT-cAMP did not induce obvious translocation of RhoA in the cells. The LPA treatment caused formation of F-actin in SGC-7901 cells, and CPT-cAMP inhibited the formation. In a modified Boyden chamber assay, LPA stimulated the migration of SGC-7901 cells, and CPT-cAMP dose-dependently inhibited the stimulating effect of LPA. In soft agar assay, LPA stimulated early proliferation of SGC-7901 cells, and CPT-cAMP significantly inhibited the growth of LPA-stimulated cells. In the prostate cancer cell line, PC-3, LPA caused morphologic changes from polygonal to round, and transfection with plasmid DNA encoding constitutively active RhoA(63L) caused a similar change. Treatment with CPT-cAMP inhibited the changes in both cases. However, in PC-3 cells transfected with a plasmid encoding mutant RhoA188A, LPA induced rounding, but CPT-cAMP could not prevent the change. Results of this experiment indicated that cAMP/PKA inhibited RhoA activation, and serine188 phosphorylation on RhoA was necessary for PKA to exert its inhibitory effect on RhoA activation. The cross talk between cAMP/PKA and RhoA-mediated signal transductions had significant affect on biologic features of gastric and prostate cancer cells, such as morphologic and cytoskeletal change, migration, and anchorage-independent growth. The results may be helpful in implementing novel therapeutic strategies for invasive and metastatic prostate and gastric cancers.

Apoptosis Regulatory Proteins↗
PubMed2005

Logistic analysis of veterans' eligibility-status changes.

Currently, the US Department of Veterans Affairs provides medical care to more than four million veterans across the nation. Given the limited resources and increasing demand, the US Department of Veterans Affairs Health Administration (VA) is required by law to ensure that veterans with similar economic status and eligibility priority have similar access to VA health care, regardless of where they reside. This study, using descriptive statistics and logistic regression techniques, examines the factors that affect veterans' eligibility-status changes. This study found that veterans' demographics are correlated with the likelihood of eligibility-status conversion. More importantly, this study concludes that eligibility-status changes have a geographic pattern. These findings are important and useful in planning workload, as well as improving equal access of health care.

Adult↗
PubMed2005

TFAR19 gene changes the biophysical properties of murine erythroleukemia cells.

TFAR19 is a novel apoptosis-related gene and can accelerate cell apoptosis in the presence of apoptosis inducements. Here, we studied the effects of TFAR19 on some biophysical properties of mouse erythroleukemia (MEL) cells and their molecular and structural basis. After transfected with TFAR19 and apoptosis inducement, MEL revealed a high cell membrane fluidity, a decrease in resynthesis of phospholipids, an increase in the proteins/nucleic acids ratio, a relatively orderly cytoskeleton network, an impaired deformability, a low integrin aM expression, and a decrease in adhesion to endothelial cells. These findings suggest the potential of TFAR19 for antitumor cell migration, and thus for antitumor gene therapy.

Animals↗
PubMed2005

Identification of a genomic island of Actinobacillus actinomycetemcomitans.

BACKGROUND: Horizontal gene transfer (HGT) is a process by which bacteria acquire genes from organisms of distant taxa. HGT is now recognized as a major driving force in the evolution of bacterial pathogens. Through this process, bacteria may accumulate blocks of DNA such as genomic islands (GEIs) that encode fitness or virulence factors. The periodontal pathogen A. actinomycetemcomitans has been known to exhibit variable virulence potential. It is postulated that GEIs may play a role in modifying the virulence potential of A. actinomycetemcomitans. This study was initiated to identify and determine the distribution of GEIs in A. actinomycetemcomitans. METHODS: Forty-seven A. actinomycetemcomitans strains of serotypes a through f were examined. Strain-specific variant DNA in the genomes of A. actinomycetemcomitans was identified by polymerase chain reaction (PCR) genomic mapping and sequenced to identify GEIs. The distribution of the GEIs among test strains of A. actinomycetemcomitans was determined by PCR analysis and Southern hybridization assays. RESULTS: An approximately 22 kb GEI of A. actinomycetemcomitans, designated AAI-1, was identified in five serotype b strains. The AAI-1 exhibits low %G+C and encodes proteins of phage, restriction modification systems, mobile elements, and other hypothetical proteins of unknown functions. The insertion of AAI-1 was found to cause truncation of A. actinomycetemcomitans genes at the insertion site. CONCLUSIONS: Some A. actinomycetemcomitans strains may harbor GEIs, which were acquired via HGT by the bacteria. The GEIs may increase the gene repertoire of A. actinomycetemcomitans. However, the insertion of the GEIs in A. actinomycetemcomitans may also cause truncation and inactivation of resident genes at the insertion sites. The virulence significance of such gain and loss of genes in A. actinomycetemcomitans remains to be determined.

Aggregatibacter actinomycetemcomitans↗
PubMed2005

Increased glucocorticoid receptor and 11{beta}-hydroxysteroid dehydrogenase type 1 expression in hepatocytes may contribute to the phenotype of type 2 diabetes in db/db mice.

Excess tissue glucocorticoid action may contribute to the hyperglycemia and insulin resistance associated with type 2 diabetes, but the associated mechanisms are poorly understood. 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts inactive 11-dehydrocorticosterone into active corticosterone, thus amplifying glucocorticoid receptor-mediated tissue glucocorticoid action, particularly in the liver. To examine the role of tissue glucocorticoid action in type 2 diabetes, we analyzed expression of glucocorticoid receptor and 11beta-HSD1 and their regulation by endogenous hormones in vivo and in vitro in hepatocytes from db/db mice (a model of type 2 diabetes). We observed positive relations between expression of both glucocorticoid receptor and 11beta-HSD1 in liver and insulin sensitivity and expression of PEPCK mRNA in db/db mice and db/+ controls. Increased expression of glucocorticoid receptor and 11beta-HSD1 in the liver of db/db mice was correlated with elevated circulating levels of corticosterone, insulin, and blood glu-cose. Treatment of db/db mice with glucocorticoid antagonist RU486 reversed the increases in the expression of glucocorticoid receptor and 11beta-HSD1 within the liver and attenuated the phenotype of type 2 diabetes. Addition of corticosterone to db/db mouse primary hepatocytes activated expression of glucocorticoid receptor, 11beta-HSD1, and PEPCK, and these effects were abolished by RU486. Incubation of primary hepatocytes with increasing concentrations of glucose caused dose-dependent increases in glucocorticoid receptor and 11beta-HSD1 expression, whereas insulin did not affect the expression of 11beta-HSD1 and glucocorticoid receptor in primary hepatocytes. These findings suggest that activation of glucocorticoid receptor and 11beta-HSD1 expression within the liver may contribute to the development of type 2 diabetes in db/db mice.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2005

Prognostic effect of insertion/deletion polymorphism of the ace gene on renal and cardiovascular clinical outcomes in Chinese patients with type 2 diabetes.

OBJECTIVE: The insertion/deletion (I/D) polymorphism of the ACE gene has been reported to be associated with diabetic microvascular or macrovascular complications. The aim of the present study was to investigate the prognostic effect of I/D polymorphism on renal and cardiovascular clinical outcomes in Chinese patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: A consecutive cohort of 1,281 Chinese patients with type 2 diabetes were followed for 41.3 +/- 21.6 months. Renal end points were defined as renal death and events (need for dialysis, plasma creatinine >/=500 micromol/l, or doubling of plasma creatinine of baseline value >/=150 micromol/l). Cardiovascular end points were defined as cardiovascular death and events, which included ischemic heart disease, heart failure, cerebrovascular accident, and revascularization requiring hospital admission. The I/D polymorphism of the ACE gene was examined by PCR followed by agarose gel electrophoresis. RESULTS: The frequencies of ACE gene I/D polymorphisms were in Hardy-Weinberg equilibrium. Patients who developed a renal end point (n = 98) had higher frequencies of DD genotype (19.4 vs. 10.8%, P = 0.018) and D allele (41.3 vs. 31.8%, P = 0.006) compared with subjects who did not (n = 1,183). The cumulative rates of renal end points were 10.0, 19.2, and 24.4% in the II (n = 595), DI (n = 539), and DD genotype carriers (n = 147), respectively (log rank P = 0.004). In multiple Cox regression analysis, the occurrence of renal end points remained significantly influenced by I/D polymorphism with a dominant deleterious effect of the DD genotype (DD versus II, adjusted hazard ratio 2.80 [95% CI 1.49-5.29]). There was no prognostic effect of I/D polymorphism on cardiovascular end points. CONCLUSIONS: The DD genotype of the ACE I/D polymorphism was an independent risk factor for renal but not cardiovascular end points in Chinese patients with type 2 diabetes.

Aged↗
PubMed2005

Effect of hepatic lipase -514C->T polymorphism and its interactions with apolipoprotein C3 -482C->T and apolipoprotein E exon 4 polymorphisms on the risk of nephropathy in chinese type 2 diabetic patients.

OBJECTIVE: Triglyceride-rich lipoprotein particles may promote the progression of diabetic nephropathy. Patients with diabetic nephropathy have increased plasma triglycerides and reduced activity of hepatic lipase (HL), which hydrolyzes triglycerides. We hypothesized that the HL -514C-->T polymorphism, which reduces HL expression, and its interactions with polymorphisms in apolipoprotein (apo) E and apoC3 increase the risk of diabetic nephropathy. RESEARCH DESIGN AND METHODS: In a case-control study involving 374 Chinese type 2 diabetic patients with and 392 without diabetic nephropathy, we genotyped the HL -514C-->T, apoE exon 4, and apoC3 -482C-->T polymorphisms. RESULTS: HL -514T-containing genotypes (T+) were associated with diabetic nephropathy (OR = 1.7, P = 0.0009). Adjustment by multiple logistic regression for hypertension, triglycerides, sex, non-HDL cholesterol, BMI, smoking, and alcohol intake did not diminish the association (OR = 1.8, P = 0.003). The association between HL T+ genotypes and diabetic nephropathy appeared stronger in diabetic patients with apoC3 -482 non-TT genotypes (OR = 1.9, P = 0.003) or apoE epsilon2 or epsilon4 alleles (OR = 2.2, P = 0.005). Subjects with HL TT exhibited trends toward increased triglyceride and non-HDL cholesterol levels compared with CC carriers. CONCLUSIONS: HL T+ genotypes might increase the risk of developing diabetic nephropathy by slowing clearance of triglyceride-rich remnant lipoproteins. In concert with other risk factors (e.g., hyperglycemia), lipid abnormalities may damage the kidneys and endothelium, where reduced binding sites for lipases may precipitate a vicious cycle of dyslipidemia, proteinuria, and nephropathy.

Apolipoprotein C-III↗
PubMed2005

[Construction of an eukaryotic expression plasmid for short peptides used in DNA immunization].

AIM: To construct a plasmid which efficiently express short peptides in DNA immunization. METHODS: The plasmid containing peptide-expressing cassette (PEC) was constructed and its effect in DNA immunization was investigated, using a DHBV B cell epitope as the short peptide. The peptide in vitro was detected by DOT-EIA. The BALB/c mice were immunized with the empty plasmid or the recombinant plasmid, and the specific antibodies against the epitope in the sera of the mice were determined by ELISA. RESULTS: The plasmid containing peptide-expressing cassette (PEC) was successfully constructed. Recombinant epitope-based plasmid could efficiently express the short peptide in vitro and induce immune response against it in DNA immunization. CONCLUSION: The constructed vector provides highly efficient short peptide expression in DNA immunization.

Animals↗
PubMed2005

[Effect of early nutritional support on plasma superoxide dismutase, malondialdehyde and nitric oxide in rats with burns in a hot and humid environment].

OBJECTIVE: To observe the changes of plasma superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) in rats with combined stress of burn injury and hot and humid environment. METHODS: The rats with superficial second-degree scald were subjected to intragastric administration of double-distilled water for one week (control group) or treated with ascorbic acid and L-arginine mixed with a-Tocopherol for one week (treatment group). All the rats were exposed to the same hot and humid environment of Td 37+/-0.5 degrees C with relative humidity of 65%+/-5% for 1-2 h. Observation was performed at 1, 2, 4, and 10 h after the heat exposure, respectively. RESULTS: SOD and MDA changes were significantly different between the two groups (P<0.01, P<0.05). In the control group, NO levels at 1 h were significantly different from those measured at 2 and 6 h after the exposure (P<0.01, P<0.05). CONCLUSION: Early nutritional support can significantly reduce the stress organ injuries, and prevent complications following injury in a hot and humid environment.

Animals↗
PubMed2005

[Expression of FasL gene in porcine chondrocytes].

AIM: To express the Fas ligand(FasL) gene in porcine chondrocytes. METHODS: The porcine FasL gene fragment was amplified by RT-PCR and then inserted into the pGCEN retroviral vector. The recombinant vector was transfected into packaging cells PA317 which were then screened with G418. Supernatant of screened PA317 cells containing high titer recombinant virus was used to infect porcine chondrocytes. Expression of FasL in chondrocytes was analyzed by FACS and Western blot. RESULTS: The recombinant pGCEN-FasL retroviral expression vector was successfully constructed as shown by restriction enzyme digestion analysis and DNA sequencing. FasL was expressed in 57% of infected chondrocytes. Western blot analysis also confirmed the expression of FasL in chondrocytes. The expressed FasL could induce apoptosis of Fas+ cells. CONCLUSION: The recombinant pGCEN-FasL retroviral vector has been successfully constructed and FasL with biological activity was highly expressed in porcine chondrocytes, which lays the foundation for allogenic chondrocytes transplantation.

Animals↗
PubMed2005

[Identification of a novel HLA-A2-restrictive CTL epitope of an ovary cancer-associated antigen OVA66].

AIM: To identify a novel HLA-A2-restrictive CTL epitope of an ovary cancer-associated antigen OVA66. METHODS: Dendritic cells (DCs), induced from peripheral blood mononuclear cells(PBMCs) by cytokines, were confirmed by morphological observation and FACS. Mature DCs were pulsed with each of the two synthesized peptides which were selected as possible CTL epitopes by software analysis. The pulsed DCs were used to stimulate autologous CD8+ T cells from an HLA-A2+ healthy donor. One week later, the peptides-pulsed autologous PBMCs were used to stimulate the CD8+ T cells for another 3 times at weekly intervals. The stimulated CD8+ T cells were used as CTLs. The cytotoxicity of CTLs to target cells was detected by lactate dehydrogenase (LDH) release assay and the number of T cells secreting antigen-specific IFN-gamma in CTLs was analyzed by enzyme-linked immunospot assay (ELISPOT). RESULTS: The results of morphology observation and FACS indicated that mature DCs were induced from PBMCs. Of the two peptides, peptide L235(FLPDHINIV) induced peptide-specific CD8+ T cells that lysed HLA-A2+ T2 cells pulsed with L235 and OVA66+/HLA-A2+ SW480 cells. Compared with control peptide, L235 increased the number of IFN-gamma producing T cells. CONCLUSION: This novel OVA66-derived CTL epitope L235 can induce HLA-A2-restrictive CTL response, which lays the foundation for preparation of tumor-specific peptide vaccine.

Amino Acid Sequence↗
PubMed2005

[Chemical constituents from marine alga Chaetomorpha basiretorsa].

OBJECTIVE: To investigate the chemical constituents of marine alga Chaetomorpha basiretorsa. METHOD: Compounds were isolated by normal phase silica gel and Sephadex LH-20 gel colum chromatography, reverse phase MPLC, reverse phase HPLC and recrystallization. Their structures were elucidated by spectroscopic methods including MS, IR, NMR, and X-ray crystalography. Cytotoxicity of the compounds were screened by using standard MTT method. RESULT: Nine compounds were isolated from C. basiretorsa and their structures were identified as N-phenyl-2-naphthalenamine( I ), dibutyl phthalate( II ), diisobutyl phthalate( III ), 1-phenyl-ethane-1, 2-diol( IV ), 2-hydrox-gamma-benzaldehyde( V ), diethyleneglycol monobenzoate( VI ), uracil( VII ), thymine( VIII ) and thymidine( IX ). CONCLUSION: All these compounds were obtained from this genus for the first time, N-phenyl-2-naphthalenamine and diethyleneglycol monobenzoate were first reported from the marine organisms. Compound I and VII showed moderate activity against KB cell(IC50 10.15 microg x mL(-1) for I and 3.79 microg x mL(-1) for VII ) and MCF-7 cell(IC50 3.24 microg x mL(-1) for VII).

1-Naphthylamine↗
PubMed2005

[A new de-noising technique for spectra based on Mexican hat wavelet].

Signals in spectral analysis often have random noise, which has negative influence on the accuracy and detection limit of analysis. A new chemometrics method named Mexican Hat Wavelet De-noising Arithmetic (MWDA) is presented, which can be used to remove noise in analytical chemical signals. In this method, Mexican Hat wavelet is chosen to construct de-noising function because of its excellent properties, then the de-noising function is used to extract useful information from noisy signals. MWDA is effective for signals with either wide peaks or very sharp peaks. Many processing results of simulated and experimental signals indicate that MWDA is a simple and powerful de-noising method, even when the signal has very high noise (whose signal to noise ratio is 1). After processed, the relative errors of peak position, peak height and peak area are less than 0.2%, 3.2% and 1.1% respectively. When it is applied to experimental spectra, the results are also satisfactory. This new method can increase the accuracy of spectral analysis, and the result is credible and satisfying.

Algorithms↗