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Biomedical subjects

Li Chen

Publications and source records attributed to Li Chen.

At least 199 records · Page 11Linked to original sources
PubMed2004

Molecular mass and antitumor activities of sulfated derivatives of alpha-glucan from Poria cocos mycelia.

Two kinds of water-insoluble (1-->3)-alpha-D-glucan samples, ab-PCM3-I and ac-PCM3-I, isolated from different Poria cocos mycelia were sulfated, to produce two series of water-soluble derivatives ab-PCM3-I-S1-S5 and ac-PCM3-I-S1-S5, respectively. The derivatives having different weight-average molecular mass (Mw) were produced by changing reaction temperature and time as well as molar ratios between chlorosulfonic acid and number of hydroxyl groups in the glucan. The degrees of substitution (DS) of the sulfated derivatives were analyzed by elemental analysis (EA) to be 0.39-0.67 for ab-PCM3-I-S and 0.73-0.96 for ac-PCM3-I-S, respectively. The Mw and the intrinsic viscosity ([eta]) of the samples ab-PCM3-I-S and the ac-PCM3-I-S were measured by size exclusion chromatography combined with laser light scattering (SEC-LLS) and viscometry in phosphate buffer solution (PBS) at 37 degrees C. The results indicated that their Mw ranged from 2.0 to 11.3 x 10(4) for the samples ab-PCM3-I-S, and 4.7 to 40.0 x 10(4) for the samples ac-PCM3-I-S. Moreover, the antitumor activities of the sulfated derivatives ab-PCM3-I-S and ac-PCM3-I-S against Sarcoma 180 tumor cell tested both in vitro and in vivo are significantly higher than those of the native alpha-D-glucans. Therefore, a moderate range of molecular mass from 2.0 x 10(4) to 40.0 x 10(4), relatively high chain stiffness and good water solubility of the sulfated derivatives are beneficial to the enhancement of their antitumor activities.

Animals↗
PubMed2004

The PEX Gene Screen: molecular diagnosis of peroxisome biogenesis disorders in the Zellweger syndrome spectrum.

Peroxisome biogenesis disorders in the Zellweger syndrome spectrum (PBD-ZSS) are caused by defects in at least 12 PEX genes required for normal organelle assembly. Clinical and biochemical features continue to be used reliably to assign patients to this general disease category. Identification of the precise genetic defect is important, however, to permit carrier testing and early prenatal diagnosis. Molecular analysis is likely to expand the clinical spectrum of PBD and may also provide data relevant to prognosis and future therapeutic intervention. However, the large number of genes involved has thus far impeded rapid mutation identification. In response, we developed the PEX Gene Screen, an algorithm for the systematic screening of exons in the six PEX genes most commonly defective in PBD-ZSS. We used PCR amplification of genomic DNA and sequencing to screen 91 unclassified PBD-ZSS patients for mutations in PEX1, PEX26, PEX6, PEX12, PEX10, and PEX2. A maximum of 14 reactions per patient identified pathological mutations in 79% and both mutant alleles in 54%. Twenty-five novel mutations were identified overall. The proportion of patients with different PEX gene defects correlated with frequencies previously identified by complementation analysis. This systematic, hierarchical approach to mutation identification is therefore a valuable tool to identify rapidly the molecular etiology of suspected PBD-ZSS disorders.

Algorithms↗
PubMed2004

Synchronizing strict-feedback chaotic system via a scalar driving signal.

We propose a systematic design procedure to synchronize a class of chaotic system in a so-called strict-feedback form based on back-stepping procedure. This approach needs only a scalar driving signal to realize synchronization no matter how many dimensions the chaotic system contains. Furthermore, the numerical simulation with Chua's chaotic circuit verifies the effectiveness of the method.

Computer Simulation↗
PubMed2004

Cytochrome P4501A1 promotes G1 phase cell cycle progression by controlling aryl hydrocarbon receptor activity.

The aryl hydrocarbon receptor (AhR) transcription factor is increasingly recognized as functioning in cell cycle control. Several recent reports have shown that AhR activity in the absence of exogenous agonists or presence of the prototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin can affect G1 phase progression in cultured cells. Serum release of serum-starved (G0) 5L rat hepatoma cells triggers transient AhR activation and P4501A1 protein expression concomitant with the G0/G1-to-S phase transition. In contrast, sustained AhR activation in response to TCDD treatment increases p27Kip1 expression in addition to P4501A1, resulting in G1 phase cell cycle arrest. Treating serum-released 5L cells with the alkyne metabolism-based P4501A1 inhibitor 1-(1-propynyl)pyrene results in prolonged AhR activation, enhanced p27Kip1 expression, and G1 phase arrest after serum release. The data are consistent with a cell cycle role for P4501A1 because they show that P4501A1 negatively regulates the duration of AhR action through the metabolic removal of the receptor agonist, thereby preventing AhR-mediated G1 phase arrest.

Animals↗
PubMed2004

An overall picture of chemokine receptors: basic research and drug development.

Chemokine receptors belong to the transmembrane G protein coupled receptor (GPCR) family. Although a major physiological role of chemokine receptors is for host defense by recruitment of lymphocytes to inflammatory sites, they are now found to be involved in more processes such as virus infection, tumor genesis and metastasis, and embryologic development. In this review, we show an overall picture of chemokine receptors in structure, signal transduction and modulation, physiological and pathological roles, and applying chemokine receptors for drug discovery.

Animals↗
PubMed2004

The discovery of VLA-4 antagonists.

Starting with a cyclic peptide of moderate potency as a VLA-4 antagonist, highly potent and conformationally defined cyclic peptides were developed incorporating a constrained tyrosine and an achiral Asp-Pro spacer. N-Acyl phenylalanine derivatives were also discovered to have VLA-4 antagonist activity. During the course of development of this series, we found that the active acylphenylalanines mimic the pharmacophores present in the cyclic peptides and hypothesized that they bind to the same site on VLA-4. This insight guided our optimization strategy. Based on the emerging SAR, as well as insights from the recent X-ray crystal structure of the integrin alphavbeta3 bound to a RGD containing cyclic peptide, we propose a binding model for these compounds.

Humans↗
PubMed2004

Validity and reliability of the Wood Motor Success Screening Tool in a special physical education learning laboratory.

The purpose of this study was to estimate the concurrent validity and test-retest reliability of the Wood Motor Success Screening Tool. Participants were 66 children with learning and behavioral disabilities (44 boys and 22 girls; M of age= 7.6 yr.; SD of age= 1.8 yr.). The concurrent validity was checked using the Bruininks-Oseretsky Test of Motor Proficiency-Short Form as the criterion measure. A Pearson product-moment correlation of .84 (p< .01), a sensitivity index of .88, and a specificity index of .64 were found for estimating the concurrent validity. The test-retest reliability was checked using scores on the Wood Motor Success Screening Tool administered twice within a week. An intraclass correlation coefficient of .93 from the one-way analysis of variance was found for estimating the test-retest reliability. These results indicated that this test is valid and reliable for assessing young children.

Child↗
PubMed2004

[Transfection of human hepatic stimulator substance gene could protect BEL-7402 cells against hepatotoxins].

OBJECTIVE: To investigate protective effects of hHSS transfection against CCl4 or H2O2. METHODS: cDNA coding for hHSS was constructed into eukaryotic vector of pcDNA3.1 and transfected into BEL-7402 hepatoma cells. The expression of hHSS was analyzed with Northern blot. RESULTS: The growth of the hepatoma cells was remarkably enhanced 24 to 144h after hHSS gene transfection, which suggesting hHSS gene expression could stimulate cells activity. Meantime, incubation of both wild-type and vector-transfected as well as hHSS-transfected cells with CCl4 or H2O2 resulted in severe damage as marked by cell mortality and the rate of apoptosis. However, it appeared that the transfection of hHSS enabled the hepatoma cells to raise obvious resistance against CCl4 and H2O2 injury. Compared the vector cells to the vector-transfected cells, apoptosis ratio were (32.44+/-0.52)% and (25.60+/-0.66)% in which treated with CCl4, while (47.78+/-0.45)% and (37.40+/-0.69)% in which treated with H2O2, t value is 16.82 and 25.20, P<0.01. MAPK phosphorylation was also activated after HSS transfected. CONCLUSION: The function of hHSS gene expression could be related to proliferation of cell and protection against free radical damage.

Apoptosis↗
PubMed2004

[The three-dimensional nonlinear finite element analysis of force system of the "rocking-chair archwire"].

OBJECTIVE: The purpose of this study was to qualitatively and quantitatively analyze the initial force system of "rocking-chair archwire" on every tooth. METHODS: Three-dimensional finite element model of "rocking-chair archwire" was set up, and nonlinear method was used to analyze the force system. RESULTS: The archwire exerted intruding force, labial force, lingual-root torque and mesial-labial moment on incisors; Extruding force, lingual-root torque and mesial-labial moment were applied on canines and premolars; The archwire also created intruding force, buccal force, buccal-root torque and mesial-labial moment on molars. CONCLUSIONS: "rocking-chair archwire" produced a complicated force system. While intruding incisors, molars and extruding premolars. It has a tendency to induce tooth rotation and tipping.

Dental Stress Analysis↗
PubMed2004

[Changes of carbon monoxide, nitric oxide levels and heme oxygenase system in acute respiratory distress syndrome induced by oleic acid].

OBJECTIVE: To investigate possible role of carbon monoxide (CO) and heme oxygenase (HO) in the pathogenesis of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) and to compared with that induced by nitric oxide (NO). METHODS: ARDS model was established in rats by oleic acid injection and concentrations of CO and NO in pulmonary arterial, carotid jugular blood and bronchoalveolar lavage fluid (BALF) were measured sequentially. Immunohistochemical method was used to determine the expression of HO in the lung. RESULTS: Pulmonary arterial pressure in ARDS rats elevated 10 min after OA injection [(13.80 +/- 1.87) mm Hg to (19.51 +/- 5.02) mm Hg]. At 0.5 h after OA injection, concentration of CO in pulmonary artery began to increase and was markedly higher at 2 h than that in control rats [(0.135 +/- 0.010) g/L versus (0.116 +/- 0.005) g/L] (P < 0.01), also higher than that in carotid artery [(0.117 +/- 0.013) g/L] and in jugular vein [(0.107 +/- 0.018) g/L] in the same group, and maintained at a relatively high level thereafter. Concentration of CO in BALF also increased at 0.5 - 24 h and diminished at 72 h, as compared with that in controls. Concentration of NO in blood of pulmonary and systemic circulation all elevated markedly at 0.5 h and 2 h after OA injection, and then declined to normal at 12 h. Concentration of NO in BALF was significantly higher than that in controls. Arterial blood gas analysis showed that PaO2 markedly decreased in ARDS rats, especially at 2 h after OA injection. HO-2 could be expressed in the lung tissues of normal rats with immunohistochemical method, the strongest in epithelial cells of the bronchi, and HO-1 could only be expressed in pulmonary blood vessel walls, bronchial epithelial cells, alveolar epithelial cells and inflammatory cells of ARDS rats, lasting for 72 h after OA injection, consistent with that of CO level. CONCLUSION: ARDS rats showed a lastecl increase of CO level in pulmonary blood circulation, suggesting CO/HO system might play a more important role in modulation of blood vessel tension than NO might do in pathogenesis of ARDS.

Animals↗
PubMed2004

Different contributions of STAT3, ERK1/2, and PI3-K signaling to cardiomyocyte hypertrophy by cardiotrophin-1.

AIM: To assess the contribution of signal transducer and activator of transcription 3 (JAK-STAT3) pathway, extracellular signal-regulated kinases1/2 (ERK1/2) pathway, and phosphatidylinositol 3-kinase (PI3-K) pathway to cardiomyocytes hypertrophy induced by cardiotrophin-1 (CT-1), a new member of interleukin-6 (IL-6) family of cytokines. METHODS: STAT3, ERK1/2, and PI3-K were assessed by Western blot analysis. Activity of ERK1/2 was also confirmed by in-gel kinase assay. Hypertrophy of cardiomyocyte was evaluated by [3H]leucine incorporation and cellular protein-to-DNA ratio. RESULTS: CT-1 simultaneously activated phosphorylation of STAT3, ERK1/2, and PI3-K in rat cardiomyocytes. Parthenolide, an inhibitor of STAT, suppressed CT-1-induced [3H]leucine incorporation by 88.3 % and protein-to-DNA ratio by 75.0 %. U0126, an MEK1/2 inhibitor, increased CT-1-induced the phosphorylation of STAT3 in a dose-dependent manner and, consistently, augmented CT-1-induced increase in [3H]leucine incorporation and cellular protein-to-DNA ratio by 17.6 % and 16.3 %, respectively. Wortmannin, a PI3-K inhibitor, did not influence CT-1-induced [3H]leucine incorporation and cellular protein-to-DNA ratio. CONCLUSION: The hypertrophic effect of CT-1 was essentially mediated by STAT3, independent of PI3-K, and negatively regulated by ERK1/2 via inhibiting the phosphorylation of STAT3. The interaction between STAT3 and ERK1/2 in CT-1-induced signaling contributes to development of cardiac hypertrophy.

Androstadienes↗
PubMed2004

Crosstalk between ERK1/2 and STAT3 in the modulation of cardiomyocyte hypertrophy induced by cardiotrophin-1.

BACKGROUND: The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway and the extracellular signal-regulated kinases 1/2 (ERK1/2) pathway are the two major independent signal transduction pathways. However, it has recently been found that STAT3 may be negatively regulated by ERK1/2 in gp130-dependent signaling. Cardiotrophin-1 (CT-1), a potent novel hypertrophic cytokine, depends on gp130 to induce signaling and depends on STAT3 to exert hypertrophic effect. In this study, we examined whether STAT3 activity was negatively regulated by ERK1/2 during CT-1-induced signaling in rat cardiomyocytes and, if so, whether such crosstalk interfered with the hypertrophic effect of CT-1 and, furthermore, whether the mechanism underlying the crosstalk involved phosphorylation of serine 727 (S727) in STAT3. METHODS: The activities of ERK1/2 and STAT3 were assessed by in-gel kinase assay and Western blot analysis, respectively. The role of S727 phosphorylation in the crosstalk between ERK1/2 and STAT3 was determined by a transient transfection study using a STAT3S727A mutant. Cardiomyocyte hypertrophy was evaluated by the cellular protein-to-DNA ratio and [(3)H]-leucine incorporation. RESULTS: CT-1 simultaneously activated both ERK1/2 and STAT3 in rat cardiomyocytes. Inhibition of ERK1/2 by U0126 resulted in an increase of CT-1-induced tyrosine phosphorylation of STAT3 and, consequently, the protein-to-DNA ratio and [(3)H]-leucine incorporation. Transient transfection of the cells with STAT3S727A had no significant effect on CT-1-induced tyrosine phosphorylation of STAT3. CONCLUSIONS: STAT3 is activated by CT-1 in rat cardiomyocytes, but full activation is mitigated by the simultaneous activation of ERK1/2. The inhibition of ERK1/2 increases the activity of STAT3, which, in turn, enhances the hypertrophic effect of CT-1. The crosstalk between ERK1/2 and STAT3 is independent of the phosphorylation of the S727 in STAT3. Such crosstalk may contribute to the development of adequate cardiac hypertrophy.

Active Transport, Cell Nucleus↗
PubMed2004

[Testing and analyzing the lung functions in the normal population in Hebei province].

OBJECTIVE: To investigate the lung function of the normal subjects living in Hebei province and its correlative factors such as living circumstance, age, height, and body weight. METHODS: The lung volumes and breath capacities of 1,587 normal subjects were tested by portable spirometers (Scope Rotry) from August to October in 2002. The influences of living circumstance, age, gender, height, and body weight on lung functions were observed and analyzed. RESULTS: No significant difference was found between urban and rural areas in all indexes (P > 0.05); however, significant difference existed between male and female subjects (P = 0.000). The change trends of lung function in male and female subjects were similar. Growth spurt appeared at the age of 12-16 years in male subjects and 12-14 years in female subjects. Vital capacity (VC), forced vital capacity (FVC), and forced expiratory volume in one second (FEV1) reached their peaks at the age of 26-34 years and then decreased with age. Peak expiratory flow (PEF), 25% forced expiratory flow (FEF50%), and 75% forced expiratory flow (FEF75%) appeared at the age of 18 and then went down with age. Both height and weight had a correlation with all the indexes of lung functions, although the influence of height is stronger than weight. CONCLUSIONS: All the indexes of lung function have correlations with age, height, and weight. Lung function changes with aging, therefore different expected values shall be available for the adolescence, young adults, and middle-aged and old people. This study provides reference values of lung function for normal population.

Adolescent↗
PubMed2004

[Establishment of K562 cell lines resistant to STI571 and a preliminary biological study].

To produce leukemic STI571-resistant cell lines and to explore the molecular mechanism of STI571-resistance, cell lines K562-n and K562-n/VCR were induced by exposing cells to gradually increasing STI571 concentration of culture medium to have STI571-resistance and major biological characteristics between these subclones and the parent cells were compared. The results showed that a STI571-resistant cell line based on multidrug-resistance was established, which exhibited 23.41-fold resistance to STI571, 662.26-fold resistance to VCR and cross-resistance to HHT. K562-n/STI was generated from K562-n and had some characteristics of MDR. The intracellular accumulation of DNR in K562-n/STI and K562-n/VCR/STI were 33.24 and 18.76 respectively. Transcription of mdr-1 gene in both K562-n/STI and K562-n/VCR/STI was positive. Cell doubling time of K562-n/STI and K562-n/VCR/STI was significantly longer than that in their parent cells (P <0.05). And proliferation index was also higher than that in parent cells (P <0.05). It is conclusion that the tolerance of K562-n cells to STI571 can be augmented by adding low-dose of STI571 into the culture medium repeatedly. K562-n/STIs expressed MDR at some extent, and transcription of mdr-1 gene in K562-n/STIs was positive. As K562-n is a cell line used to develop human leukemia in nude mice, K562-n/STI and K562-n/VCR/STI 571 will contribute to the study of mechanism of STI571-resistance as in vitro and in vivo experimental models.

Antineoplastic Agents↗
PubMed2004

[Relationship between expression of vimentin, type IV collagen and fibronectin in human placenta and pregnancy induced hypertension].

OBJECTIVE: To elucidate the possible relationship between pregnancy-induced hypertension syndrome (PIH) and expression of vimentin, type IV collagen and fibronectin in human placenta. METHODS: Nineteen pregnant women (PIH group) and 15 normal pregnant women (control group) matched for age and gestation were recruited. The expression of vimentin, type IV collagen and fibronectin in the placenta of PIH patients and normal subjects was investigated using immunohistochemical perioxidase-antiperoxidase (PAP) staining technique combined with an analysis through a computer-aided microphotographic system and compared between the two groups. RESULTS: The average grey value difference (GVD) which indicated positive staining of vimentin was 30 +/- 7 in section images of the moderate and severe PIH group, significantly lower than that of normal control group, 42 +/- 6 and mild PIH group, 42 +/- 9 (P < 0.01). The average GVD of type IV collagen in moderate and severe PIH group was 70 +/- 6, significantly higher than 29 +/- 4 of control group and 30 +/- 5 of mild PIH group (P < 0.001). The average GVD of fibronectin in moderate and severe PIH group was 37 +/- 4, significantly higher than that in control group, 31 +/- 4 and mild PIH group, 32 +/- 6 (P < 0. 05). CONCLUSIONS: There is tight relationship between abnormal expression of placental vimentin, type IV collagen, fibronectin and pathogenesis of PIH. Furthermore, the severity of PIH is positively correlated with the abnormal expression levels of those proteins.

Adult↗