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Biomedical subjects

Qiang Yu

Publications and source records attributed to Qiang Yu.

51 records · Page 3Linked to original sources
PubMed2003

Leflunomide, a new disease-modifying drug for treating active rheumatoid arthritis in methotrexate-controlled phase II clinical trial.

OBJECTIVE: To evaluate the efficacy and safety of leflunomide in comparison with methotrexate (MTX) on patients with rheumatoid arthritis (RA) in China. METHODS: Five hundred and sixty-six patients with active rheumatoid arthritis were randomly assigned to receive leflunomide at 20 mg once daily or MTX at 15 mg once weekly in a controlled trial. Five hundred and four patients completed the 12-week treatment and some patients continued the treatment for 24 weeks. RESULTS: Both leflunomide and MTX could improve the symptoms, signs, and joint function, but there were no changes in X-ray observations of patients with rheumatoid arthritis. In the leflunomide group, the overall rates of effectiveness at 12 weeks and 24 weeks were 86.94% and 92.31% respectively; the rates of remarkable improvement were 64.95% and 79.81% respectively. In the MTX group, the overall rates of effectiveness at 12 weeks and 24 weeks were 84.04% and 83.15% respectively; the rates of remarkable improvement were 56.81% and 75.28% respectively. According to intent-to-treat analysis, the ACR 20% response rates at 12 weeks and 24 weeks in the leflunomide group were 62.54% and 67.18% respectively, compared with 60.08% and 61.32% respectively in MTX group. No statistical differences were shown in the efficacy between the two groups (P > 0.05). The adverse events in the leflunomide group were gastrointestinal symptoms, skin rash, alopecia, nervous system symptoms, decreased leukocyte count, and elevation of alanine aminotransferase (ALT). Most of these side effects were mild and transient. The incidence of adverse events in the leflunomide group was 16.84%, significantly lower than that in MTX group (28.17%, P = 0.002). CONCLUSIONS: Leflunomide is effective in the treatment of RA with less adverse events than MTX. Its efficacy is similar to MTX, but the incidence of adverse events and the rate of withdrawal due to adverse events were lower in the leflunomide group than in MTX group.

Antirheumatic Agents↗
PubMed2003

[Computed tomography diagnosis of maxillofacial and neck malignant tumors invading carotid artery].

OBJECTIVE: To evaluate the diagnostic value of the carotid artery invasion by the oral-maxillofacial and neck malignant tumors with computed tomography (CT). METHODS: Fifty-three patients (55 tumors) of oral-maxillofacial and neck malignant tumors were examined with enhanced axial CT examination in pre-operation. The CT manifestations of all tumors were retrospectively corresponded with the surgical findings. RESULTS: Oral-maxillofacial and neck malignant tumors with abnormal common carotid artery (CCA) or internal carotid artery (ICA) manifestations were shown on CT as five types: type I, compression and deformation of CCA or ICA in six tumors; type II, displacement of CCA or ICA in 15 tumors; type III, the tumors encompass the carotid vessels more than 180 degrees in 8 tumors; type IV, the segmental deletion of fat or fascia planes between tumor and CCA/ICA in 25 tumors; and type V, ill-defined CCA/ICA wall in 12 tumors. Surgical findings recorded that 20 CCAs or ICAs were adhered by the oral-maxillofacial and neck malignant tumors. Of these 20 lesions, 14 malignant tumors (70%) with more than two abnormal changes of CCA or ICA were shown on CT images. The respective sensitivity, specificity and accuracy were 30.0%, 100.0% and 74.5% for type I, 20.0%, 68.6%, 50.9% for type II, 22.2%, 100.0%, 49.1% for type III, 90.0%, 80.0% and 83.6% for type IV, and 45.0%, 88.6% and 72.7% for type V. CONCLUSIONS: The main CT findings of maxillofacial and neck malignant tumors affecting the carotid artery are different. Comparatively, the signs of type I, type III and type IV may be valuable in evaluating CCA or ICA invasion, although the accurate diagnosis of the CCA or ICA involvement by the maxillofacial and neck malignant tumors remains difficult.

Adult↗
PubMed2002

Bcl-2, via its BH4 domain, blocks apoptotic signaling mediated by mitochondrial Ras.

Bcl-2 protects cells against Ras-mediated apoptosis; this protection coincides with its binding to Ras. However, the protection mechanism has remained enigmatic. Here, we demonstrate that, upon apoptotic stimulation, newly synthesized Bcl-2 redistributes to mitochondria, interacts there with activated Ras, and blocks Ras-mediated apoptotic signaling. We also show, by employing bcl-2 mutants, that the BH4 domain of Bcl-2 binds to Ras and regulates its anti-apoptotic activity. Experiments with a C-terminal-truncated Ras or a farnesyltransferase inhibitor demonstrate that the CAAX motif of Ras is essential for apoptotic signaling and Bcl-2 association. The results indicate a potential mechanism by which Bcl-2 protects cells against Ras-mediated apoptotic signaling.

Amino Acid Sequence↗
PubMed2002

Differentially expressed gene profiles between multidrug resistant gastric adenocarcinoma cells and their parental cells.

To better understand the molecular mechanisms of multidrug resistance (MDR) of human cancers, we isolated differentially expressed genes from drug-resistant human gastric adenocarcinoma cell lines using a polymerase chain reaction-based subtractive hybridization technique. Sixty three genes were identified to be differentially expressed in the drug-resistant human gastric adenocarcinoma cell lines. Among the 63 up-regulated genes, 27 were known genes, of which two have been reported to be associated with MDR. The remaining ones were undefined genes or expressed sequenced tags. The results suggest that this strategy is efficient for large-scale cloning of differentially expressed genes in drug-resistant cells. Further characterization of these genes will shed more light on the understanding of molecular mechanisms of MDR of human cancer cells.

Adenocarcinoma↗
PubMed2002

UCN-01 inhibits p53 up-regulation and abrogates gamma-radiation-induced G(2)-M checkpoint independently of p53 by targeting both of the checkpoint kinases, Chk2 and Chk1.

UCN-01 (7-hydroxystaurosporine) is a cell-cycle checkpoint abrogator that sensitizes cells to ionizing radiation (IR) and chemotherapeutic agents. It has been shown previously that UCN-01 abrogates DNA-damage-induced G(2) checkpoint most selectively in p53-defective cells, by primarily targeting Chk1. Here we show that UCN-01 prevented IR-induced p53 up-regulation and p53 phosphorylation on serine 20, a site previously identified for Chk2 (or/and Chk1) kinase. We found that in human colon carcinoma HCT116 cells, IR treatment enhanced Chk2 kinase activity, whereas Chk1 activity remained unchanged, which suggested that UCN-01 may interrupt IR-induced p53 response by inhibiting Chk2 kinase. This conclusion is supported by in vitro kinase assays, showing that UCN-01 inhibits Chk2 immunoprecipitated from HCT116 cells (IC(50), approximately 10 nM). In addition, UCN-01 efficiently abrogated both the initiation and maintenance of IR-induced G(2) arrest in HCT116 cells and their isogenic p53 (-/-) derivative, indicating that G(2) checkpoint abrogation by UCN-01 is p53 independent. In the p53 (-/-) cells, there was no p21(Waf1/Cip1) induction nor UCN-01-induced apoptosis. Taken together, these observations indicate that UCN-01 can modulate both Chk1 and Chk2 in intact cells and enhance IR-induced apoptosis in p53-deficient, and consequently p21-deficient, cells.

Alkaloids↗
PubMed2002

Simulation of rice biomass accumulation by an extended logistic model including influence of meteorological factors.

The biomass (X) of a biological population, described by growth models, depends only on time (t), i.e., X = f(t). Some parameters in these models are frequently taken as constants, but they may vary with growth processes under different ecological conditions. An extended logistic model including changes in the influence of meteorological factors is developed to simulate biomass accumulation processes of rice sown on different dates. The model may be generally described as X = f (p, t), in which p stands for meteorological factors. The model can be used to generalize population growth processes in experiments carried out under different environments. It is shown that the model may account for 96.6% of the variance of rice biomass on the basis of sowing dates, developmental stage, solar radiation and temperature in the Yangtze River valley in China.

Biomass↗
PubMed2002

Identification of Myc-mediated death response pathways by microarray analysis.

To understand the mechanisms of Myc-mediated apoptosis induced by DNA damage, we have characterized the death kinetics of three Rat-1 fibroblast cell lines that either overexpress Myc or lack Myc and their parental wild-type cells following exposure to the DNA-damaging agent VP-16, and we monitored the changes in gene expression using microarray. We have identified three groups of genes whose expressions are distinctly regulated during this process. One cluster (Cluster A) revealed a VP-16-dependent but Myc-independent induction of a set of genes that is not linked to the apoptotic response. Two other gene clusters, however, were associated with VP-16-induced apoptosis. Cluster B, which includes p53-responsive genes, was associated with the temporal onset of apoptosis but accounted for only the basal apoptosis. However, Cluster C, which includes c-jun, was highly regulated by Myc and appeared to be critical to mounting the maximal apoptotic response in Myc-expressing cells. Furthermore, the Myc level dropped sharply following VP-16 exposure, which varied inversely with the induction of Cluster C genes, suggesting Myc normally represses their transcription. Thus, we have proposed that removal of Myc-mediated repression of apoptotic signals, combined with Myc-associated acceleration of the p53 responsive pathway, results in complete and rapid cell death following DNA damage.

Animals↗
PubMed2002

IGF-1 induces Pin1 expression in promoting cell cycle S-phase entry.

Insulin-like growth factor I (IGF-1) is a well-established mitogen to many different cell types and is implicated in progression of a number of human cancers, notably breast cancer. The prolyl isomerase Pin1 plays an important role in cell cycle regulation through its specific interaction with proteins that are phosphorylated at Ser/Thr-Pro motifs. Pin1 knockout mice appear to have relatively normal development yet the Pin1(-/-)mouse embryo fibroblast (MEF) cells are defective in re-entering cell cycle in response to serum stimulation after G0 arrest. Here, we report that Pin1(-/-) MEF cells display a delayed cell cycle S-phase entry in response to IGF stimulation and that IGF-1 induces Pin1 protein expression which correlates with the induction of cyclin D1 and RB phosphorylation in human breast cancer cells. The induction of Pin1 by IGF-1 is mediated via the phosphatidylinositol 3-kinase as well as the MAP kinase pathways. Treatment of PI3K inhibitor LY294002 and the MAP kinase inhibitor PD098059, but not p38 inhibitor SB203580, effectively blocks IGF-1-induced upregulation of Pin1, cyclin D1 and RB phosphorylation. Furthermore, we found that Cyclin D1 expression and RB phosphorylation are dramatically decreased in Pin1(-/-) MEF cells. Reintroducing a recombinant adenovirus encoding Pin1 into Pin1(-/-) MEF cells restores the expression of cyclin D1 and RB phosphorylation. Thus, these data suggest that the mitogenic function of IGF-1 is at least partially linked to the induction of Pin1, which in turn stimulates cyclin D1 expression and RB phosphorylation, therefore contributing to G0/G1-S transition.

Cyclin D1↗
PubMed2002

Anchorage-independent phosphorylation of p130(Cas) protects lung adenocarcinoma cells from anoikis.

The regulation and function of the signaling adaptor protein p130(Cas) in tumor cell anchorage-independent survival, or anoikis resistance, were investigated in human lung adenocarcinoma cells. The tyrosine phosphorylation and function of p130(Cas) during cell detachment were analyzed in tumor cells and compared with that of normal epithelial cells. Cell detachment trigged rapid dephosphorylation of p130(Cas) in the nontumorigenic and anoikis-sensitive normal epithelial cells, but had no effect on the tyrosine phosphorylation of p130(Cas) in the anoikis-resistant lung adenocarcinoma cells. Further analysis revealed that the total tyrosine kinase activities associated with p130(Cas) in the lung tumor cells are anchorage-independent and are significantly higher than that in the normal cells, in which the p130(Cas)-associated tyrosine kinase activities are anchorage-dependent. Analysis of two known p130(Cas)-associated tyrosine kinases FAK and Src indicated that the regulation of tyrosine phosphorylation of FAK and Src are altered in the tumor cells. Inhibition of Src specifically abolished phosphorylation of p130(Cas) and induced anoikis. Furthermore, overexpression of dominant-negative forms of p130(Cas) also induced apoptosis. Taken together, these data suggest that p130(Cas) mediates a cell survival signal from cell-matrix interaction. Alterations in tumor cells that lead to constitutive phosphorylation of p130(Cas) can prevent cells from anoikis, hence contribute to tumor cell anchorage independence and metastasis.

Adenocarcinoma↗
PubMed2002

Multifocal electroretinograms in the early stages of diabetic retinopathy.

OBJECTIVE: To investigate the characteristics of multifocal electroretinograms (mf-ERG) of different phases in diabetic retinopathy (DR) and its clinical significance. METHODS: Multifocal electroretinograms in patients with DR (I - II stage) were tested with VERIS IV system. RESULTS: In I - II stage, the absolute values of N1, P1 and N2 response densities, and the N1-P1 and P1-N2 response densities were attenuated is a field of about 45 degrees in diameter. CONCLUSION: As a new objective and quantitative examination for spatial visual function, multifocal electroretinograms may be valuable in the diagnosis of diabetic retinopathy.

Aged↗
PubMed2002

[The study of the MRI artifacts caused by keepers].

OBJECTIVE: The aim of this research was to observe the extension of MRI artifacts caused by keepers. METHODS: Five samples were imaged in a water phantom and a living human subject by 0.15 Tesla magnetic resonance devices. The maximum diameters of artifacts were measured and compared. RESULTS: The maximal diameters of the artifacts caused by disc-shaped and post-shaped keepers were 95.5mm and 139.4mm. CONCLUSION: Compared with the post-type keeper, the artifacts caused by disc-type keepers diminished significantly, and the difference of the maximal diameter reached statistical significance.

English Abstract↗
PubMed2000

Effects of two epiphyseal-stimulating procedures on local growth of long bones in rabbits.

OBJECTIVE: To study the effects of two epiphyseal stimulating procedures on local growth of long bone in rabbits. METHODS: Osteotomy was performed in the metaphysis near the proximal tibial epiphyseal plate and hemicircumferential periosteal excision was made on the proximal tibial epiphysis. Tibia roentgenography, tetracycline labelling, histological method and electron microscopy were used. RESULTS: The local stimulating effect following the hemicircumferential periosteal excision was more remarkable than the osteotomy. CONCLUSIONS: Periosteal excision is a better treatment for children's knee deformity.

Journal Article↗
PubMedDate not supplied

Restoring p53-mediated apoptosis in cancer cells: new opportunities for cancer therapy.

The p53 gene is the most commonly mutated gene known in human tumors; over half of human tumors contain inactivating mutations in p53. In the past decade, the role of p53 as apoptotic trigger has been well demonstrated both in vitro and in vivo. Many chemotherapeutic agents cause DNA damage and activate the p53 pathway to induce growth arrest and apoptosis. However, the p53 function is often inactivated or suppressed in human cancers. Thus, functional restoration of this pathway is an attractive therapeutic strategy. In recent years, a number of therapeutic approaches aiming at modulation of the p53 pathway have been developed and will be reviewed here. The focus will be on recent developments elucidating a transcription-independent mechanism of p53-mediated apoptosis and the therapeutic opportunities arising from this new mechanism.

Animals↗