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Biomedical subjects

Gang Li

Publications and source records attributed to Gang Li.

At least 199 records · Page 11Linked to original sources
PubMed2003

Synthesis, crystal structures, and magnetic properties of three novel ferrocenecarboxylato-bridged lanthanide dimers.

Three novel ferrocenecarboxylato-bridged lanthanide dimers [Gd2(mu 2-OOCFc)2(OOCFc)4(MeOH)2(H2O)2].2MeOH.2H2O (1) (Fc = (eta 5-C5H5)Fe(eta 5-C5H4)), [Nd2(mu 2-OOCFc)2(OOCFc)4(H2O)4].2MeOH.H2O (2), and [Y2(mu 2-OOCFc)2-(OOCFc)4(H2O)4].2MeOH (3) have been synthesized and characterized by single-crystal X-ray crystallography. In each complex, two Ln(III) (Ln = Gd, Nd, or Y) ions are bridged by two ferrocenecarboxylate anions as asymmetrically bridging ligands, leading to dimeric cores, [Ln2(mu 2-OOCFc)2]; each Ln(III) ion has an irregular polyhedral coordination environment with nine coordinated oxygen atoms derived from the ferrocenecarboxylate ligands and coordinated solvent molecules. In the solid-state structure of compound 1, [Gd2(mu 2-OOCFc)2(OOCFc)4(MeOH)2(H2O)2] groups are joined together by hydrogen bonds forming a two-dimensional network. Both compounds 2 and 3 show one-dimensional chain structures by hydrogen bonding; they are different from 1. Magnetic measurements show unexpected ferromagnetic coupling between the gadolinium(III) ions; the best fittings to the experimental magnetic susceptibilities gave J = 0.006 cm-1 and g = 2.0 for 1. The magnetic behavior for 2 was also studied in the temperature range of 1.8-300 K.

Journal Article↗
PubMed2003

Tissue-specific regulation of checkpoint kinase 2 expression by p53.

Chk2 (Checkpoint kinase 2) is emerging as a critical mediator of genotoxic stress and diverse cellular responses. Upon ionizing radiation, Chk2 is activated to phosphorylate Cdc25C, leading to G2 phase arrest. p53 has been reported as another substrate of Chk2. Chk2 phosphorylates and stabilizes p53 in response to ionizing radiation. Previous studies found that p53 regulates the Chk2 homologue Chk1 expression both in vitro and in vivo. Using the p53-deficient mouse model, here we demonstrate by immunohistochemistry, Western blot analysis, and RT-PCR that mChk2 expression is reduced in the heart, kidney, lung, and liver of p53(-/-) mice compared to p53(+/+) controls. Similar Chk2 expression was observed in the brain, skin, spleen, and testis in p53(+/+) and p53(-/-) mice. These data indicate that p53 regulates Chk2 expression in a tissue-specific manner.

Animals↗
PubMed2003

Rapid new bone tissue remodeling during distraction osteogenesis is associated with apoptosis.

During the process of distraction osteogenesis new bone forms and undergoes rapid remodeling. Apoptosis may be one of the regulatory mechanisms governing the removal of the redundant callus during distraction osteogenesis. A rabbit tibial lengthening model was used and lengthened at 0.7 mm/day for 3 weeks. The regenerating tissues from the distraction gap were examined for apoptotic changes by transmission electron microscopy (TEM) and the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method. Osteoclastic bone resorption activities were demonstrated by tartrate resistant acid phosphatase (TRAP) staining. The apoptotic cells were mainly present in the transitional regions between the fibrous tissue and the new bone in the mineralization front, and close to or on the new bone surfaces near the center of the regenerate. The TUNEL labeling was greatly reduced in the mature bone near the osteotomied bone ends. TEM examination confirmed the presence of cells with apoptotic changes at various regions of the regenerate. TRAP staining revealed that osteoclastic bone resorption activities in the regenerate were in a similar pattern of distribution to those of the TUNEL labeling. The localization of apoptotic cells at the different regions of the regenerate, accompanied by the osteoclast activities, suggest that apoptosis is closely related to bone formation and remodeling during distraction osteogenesis.

Animals↗
PubMed2003

A reliable externally fixated murine femoral fracture model that accounts for variation in movement between animals.

Fifty-two CFLP mice had an open femoral diaphyseal osteotomy held in compression by a four-pin external fixator. The movement of 34 of the mice in their cages was quantified before and after operation, until sacrifice at 4, 8, 16 or 24 days. Thirty-three specimens underwent histomorphometric analysis and 19 specimens underwent torsional stiffness measurement. The expected combination of intramembranous and endochondral bone formation was observed, and the model was shown to be reliable in that variation in the histological parameters of healing was small between animals at the same time point, compared to the variation between time-points. There was surprisingly large individual variation in the amount of animal movement about the cage, which correlated with both histomorphometric and mechanical measures of healing. Animals that moved more had larger external calluses containing more cartilage and demonstrated lower torsional stiffness at the same time point. Assuming that movement of the whole animal predicts, at least to some extent, movement at the fracture site, this correlation is what would be expected in a model that involves similar processes to those in human fracture healing. Models such as this, employed to determine the effect of experimental interventions, will yield more information if the natural variation in animal motion is measured and included in the analysis.

Animals↗
PubMed2003

Co-C bond dissociation energy and reaction volume change of 2',5'-dideoxyadenosylcobalamin studied by laser-induced time-resolved photoacoustic calorimetry.

Time resolved photoacoustic calorimetry (PAC) was applied to a study of the photolysis of a coenzyme B(12) analog 2',5'-dideoxyadenosylcobalamin, which lacks an -OH group at the 2' position of ribofuranose ring. In aqueous solution, we report for the first time the quantum yield Phi(d) (0.25+/-0.02), Co-C bond dissociation energy (BDE; 31.8+/-2.5 kcal mol(-1)) and reaction volume change deltaV(R) (6.5+/-0.5 ml mol(-1)) due to conformation changes of the corrin ring and its side chains accompanying the cleavage of the Co-C bond. These values for the analog are very similar to those for the natural cofactor. Based our results and previous studies, a possible explanation for the similarity in their structure and properties versus the large difference in their enzymatic activity is discussed.

Calorimetry↗
PubMed2003

Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer.

The murine Pten prostate cancer model described in this study recapitulates the disease progression seen in humans: initiation of prostate cancer with prostatic intraepithelial neoplasia (PIN), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Furthermore, while Pten null prostate cancers regress after androgen ablation, they are capable of proliferating in the absence of androgen. Global assessment of molecular changes caused by homozygous Pten deletion identified key genes known to be relevant to human prostate cancer, including those "signature" genes associated with human cancer metastasis. This murine prostate cancer model provides a unique tool for both exploring the molecular mechanism underlying prostate cancer and for development of new targeted therapies.

Animals↗
PubMed2003

The role of Bcl-2 family members in the progression of cutaneous melanoma.

The overwhelming problem of cutaneous melanoma is chemoresistance. Subversion of the biochemical changes that lead to chemoresistance intersects the apoptosis pathways. The mitochondrion has been a focal point of this intersection for the development of therapeutic strategies aimed at reducing the progression of melanoma. The Bcl-2 family of apoptotic regulators is arguably the most pivotal component to this mitochondrial response. The shear number of studies conducted on the relationship between melanoma and Bcl-2 members prompted us to evaluate the literature available and discern some rational utility of the data. We have found that there are striking inconsistencies for the expression of Bcl-2 family proteins with melanoma progression, particularly for Bcl-2. Roughly one-third of the data suggests an increase in Bcl-2 expression with advancing melanoma, while another third suggests a decrease. Furthermore, the remaining third found on the whole, a detectable level of Bcl-2 in all tissues of melanocytic origin. These discrepancies are difficult to rectify in light of the apparent success of recent clinical trials utilizing Bcl-2 antisense strategies. The general consensus in the literature is that pro-apoptotic Bax is decreased with melanoma progression while anti-apoptotic Bcl-xL and Mcl-1 appear to increase with progression. We suggest that the biochemical techniques being used for analysis present too great of a heterogeneity, which could be mitigated with more standard procedures and reagents. Finally the utility of 'multi-specific' antisense tactics could be a more effective way of targeting advanced melanoma disease.

Apoptosis↗
PubMed2003

Stroma formation and angiogenesis by overexpression of growth factors, cytokines, and proteolytic enzymes in human skin grafted to SCID mice.

Reorganization of skin during wound healing, inflammatory disorders, or cancer growth is the result of expression changes of multiple genes associated with tissue morphogenesis. We wanted to identify proteins involved in skin remodeling and select those that may be targeted for agonistic or antagonist therapeutic approaches in various disease processes. Full-thickness human skin was grafted to severe combined immunodeficient mice and injected intradermally with 38 different adenoviral vectors inserted with 37 different genes coding for growth factors, cytokines, proteolytic enzymes and their inhibitors, adhesion receptors, oncogenes, and tumor suppressor genes. Responses were characterized for infiltration of inflammatory cells, vascular density, matrix formation, fibroblast-like cell proliferation, and epidermal hyperplasia. Of the 17 growth factor vectors, 16 induced histological changes in human skin. Members of the VEGF and angiopoietin families induced neovascularization. PDGFs and TGF-betas stimulated connective tissue formation, and the chemokines IL-8 and MCP-1 attracted inflammatory neutrophils and monocytes, respectively. The serine protease uPA induced a vascular response similar to that of VEGF. Vectors with adhesion receptors, oncogenes and tumor suppressor genes had, with few exceptions, little effects on skin architecture. The overall results suggest that adenoviral vectors can effectively remodel the architecture of human skin for studies in morphogenesis, inflammatory skin disorders, wound healing, and cancer development.

Adenoviridae↗
PubMed2003

Retrograde cardioplegia.

OBJECTIVE: This study was undertaken to compare the efficacy of retrograde cardioplegia for myocardial perfusion with that of antegrade cardioplegia at the same flow rate. METHODS: Colored microspheres were used in rat hearts to assess the capillary flow of cardioplegia solution. Myocardial perfusion was evaluated with magnetic resonance imaging in pig hearts. Phosphorus 31 magnetic resonance spectroscopy was used to determine the efficacies of the cardioplegic techniques in sustaining myocardial energy metabolism. RESULTS: At the same flow rate, the number of colored microspheres delivered to the capillaries by retrograde cardioplegia (15 +/- 1 microspheres/mm2) was significantly lower than that delivered by antegrade cardioplegia (29 +/- 2 microspheres/mm2). Furthermore, only 19% +/- 3% of the colored microspheres delivered to the capillaries by retrograde cardioplegia were found in the arteriolar portions of the capillaries, whereas most (80% +/- 3%) remained in the venular portions. Moreover, magnetic resonance images showed that contrast-enhanced signal-time courses obtained from different regions of the myocardium during retrograde cardioplegia varied significantly. Localized phosphorus 31 spectra showed that retrograde cardioplegia required a higher flow rate than did antegrade cardioplegia to sustain normal myocardial energy metabolism. CONCLUSIONS: We conclude that retrograde cardioplegia provides significantly less capillary flow than does antegrade cardioplegia. Its microvascular perfusion varies significantly among the various small areas of the myocardium. As a result, its efficacy in sustaining normal myocardial energy metabolism is lower than that of antegrade cardioplegia.

Animals↗
PubMed2003

Colocalization and interaction of the porcine arterivirus nucleocapsid protein with the small nucleolar RNA-associated protein fibrillarin.

Porcine reproductive and respiratory syndrome virus (PRRSV) replicates in the cytoplasm of infected cells, but its nucleocapsid (N) protein localizes specifically to the nucleus and nucleolus. The mechanism of nuclear translocation and whether N associates with particular nucleolar components are unknown. In the present study, we show by confocal microscopy that the PRRSV N protein colocalizes with the small nucleolar RNA (snoRNA)-associated protein fibrillarin. Direct and specific interaction of N with fibrillarin was demonstrated in vivo by the mammalian two-hybrid assay in cells cotransfected with the N and fibrillarin genes and in vitro by the glutathione S-transferase pull-down assay using the expressed fibrillarin protein. Using a series of deletion mutants, the interactive domain of N with fibrillarin was mapped to a region of amino acids 30 to 37. For fibrillarin, the first 80 amino acids, which contain the glycine-arginine-rich region (the GAR domain), was determined to be the domain interactive with N. The N protein was able to bind to the full-length genomic RNA of PRRSV, and the RNA binding domain was identified as the region overlapping with the nuclear localization signal situated at positions 41 to 47. These results suggest that the N protein nuclear transport may be controlled by the binding of RNA to N. The PRRSV N protein was also able to bind to both 28S and 18S ribosomal RNAs. The protein-protein interaction between N and fibrillarin was RNA dependent but independent of N protein phosphorylation. Taken together, our studies demonstrate a specific interaction of the PRRSV nucleocapsid protein with the host cell protein fibrillarin in the nucleolus, and they imply a potential linkage of viral strategies for the modulation of host cell functions, possibly through rRNA precursor processing and ribosome biogenesis.

Animals↗
PubMed2003

Central pro-opiomelanocortin gene delivery results in hypophagia, reduced visceral adiposity, and improved insulin sensitivity in genetically obese Zucker rats.

Zucker (fa/fa) rats with defective leptin receptors are obese, hyperphagic, and hyperinsulinemic. For testing whether chronic activation of the central melanocortin pathway can bypass the defective leptin signaling and normalize altered energy homeostasis in these rats, recombinant adeno-associated virus encoding pro-opiomelanocortin (rAAV-POMC) or control vector was delivered bilaterally into the basal hypothalamus with coordinates targeting the arcuate nucleus. Thirty-eight days after POMC gene delivery, hypothalamic POMC expression increased fourfold and melanocortin signaling (indicated by phosphorylation of CREB) increased by 62% with respect to controls. There was a sustained reduction in food intake, a moderate but significant attenuation of weight gain, and a 24% decrease in visceral adiposity in rAAV-POMC rats. POMC gene delivery enhanced uncoupling protein 1 in brown adipose tissue (BAT) by more than fourfold. Fasting serum leptin, insulin, and cholesterol levels were also significantly reduced by rAAV-POMC treatment. This study demonstrates that targeted POMC gene delivery in the hypothalamus suppresses food intake and weight gain and reduces visceral adiposity and hyperinsulinemia in leptin-resistant obese Zucker rats. The mechanisms may involve the sustained hypophagia and the augmentation of thermogenesis in BAT.

Adipose Tissue, Brown↗
PubMed2003

A new cytokine: the possible effect pathway of methionine enkephalin.

AIM: To investigate experimentally the effects of methionine enkephalin on signal transduction of mouse myeloma NS-1 cells. METHODS: The antigen determinate of delta opioid receptor was designed in this lab and the polypeptide fragment of antigen determinate with 12 amino acids residues was synthesized. Monoclonal antibody against this peptide fragment was prepared. Proliferation of Mouse NS-1 cells treated with methionine enkephalin of 1 x 10(-6) mol x L(-1) was observed. The activities of protein kinase A (PKA) and protein kinase C (PKC) were measured and thereby the mechanism of effect of methionine enkephalin was postulated. RESULTS: The results demonstrated that methionine enkephalin could enhance the proliferation of NS-1 cells and the effect of methionine enkephalin could be particularly blocked by monoclonal antibody. The activity of PKA was increased in both cytosol and cell membrane. With reference to PKC, the intracellular activity of PKC in NS-1 cells was elevated at 1 x 10(-7) mol x L(-1) and then declined gradually as the concentration of methionine enkephalin was raised. The effects of methionine enkephalin might be reversed by both naloxone and monoclonal antibody. CONCLUSION: Coupled with the findings, it indicates that the signal transduction systems via PKA and PKC are involved in the effects of methionine enkephalin by binding with the traditional opioid receptors,and therefore resulting in different biological effects.

Animals↗
PubMed2003

Analyses of the tumour suppressor ING1 expression and gene mutation in human basal cell carcinoma.

The incidence of basal cell carcinoma is the highest among all human malignancies. Epidemiological evidence indicates that ultraviolet radiation is the primary environmental cause for the pathogenesis of basal cell carcinoma. However, the genetic changes caused by ultraviolet radiation that lead to basal cell carcinoma formation remain unclear. We and others have demonstrated that the ING1 (inhibitor of growth 1) tumour suppressor plays an important role in cellular stress response to ultraviolet irradiation, such as DNA repair and apoptosis. This study was designed to investigate whether ING1 is overexpressed and/or mutated in human basal cell carcinoma. Immunohistochemistry, single-strand conformation polymorphism, and DNA sequencing were used to determine the expression and mutational status of the ING1 gene in 54 basal cell carcinoma biopsies. Immunohistochemical staining demonstrated that ING1 is overexpressed in 25% (6/24) human basal cell carcinomas. Single-strand conformation polymorphism and DNA sequencing revealed that only 1 in 54 (1.8%) basal cell carcinoma primaries contained a missense mutation in the ING1 gene. The mutation is located in exon 2 and could thus potentially interfere with the structure of every ING1 isoforms and the functions of the PHD zinc finger motif. Our data indicate that overexpression and mutation of the ING1 gene are infrequent in human basal cell carcinoma.

Adult↗
PubMed2003

[Endoscope-assisted supraorbital keyhole approach for excision of suprasellar region tumor].

OBJECTIVE: To study endoscope-assisted microsurgical technique with supraorbital keyhole approach for the treatment of suprasellar region tumor so as to maximize tumor removal and minimize operative-trauma. METHODS: According to high resolution CT and MR images before operation, individual operation schemes were worked out. Skin incision was made in the eyebrow, and the diameter of supraorbital craniotomy was approximately 2 cm. Endoscope-assisted microsurgical technique was used to resect lesions in 16 consecutive patients. RESULTS: Total Tumors were removed in all of the 16 patients via the supraorbital keyhole approach. No postoperative complications occurred. CONCLUSIONS: Supraorbital keyhole approach may diminish tissue injury considerably and has proven to provide sufficient operating space in the suprasellar region for tumor removal.

Adolescent↗
PubMed2003

[The study of biological properties of gliomas].

In order to explore the new methods of biological treatment of human gliomas, this project is to study the biological properties of gliomas from four different aspects, the results show that there is a IL-6 autocrine loop in human gliomas and the growth of gliomas will be inhibited when the autocrine loop is broken. There is a magnificent predominant expression of Th2 cytokines in human gliomas and human glioma cells, the switching of Th2 to Th1 can inhibit the proliferation of glioma cells. The dosage of 100 micrograms/ml of erythromycin is the best of therapeutic effect. Angiostatin can not only inhibit the vascular endothelial growth, but also have the inhibitory role on the growth of glioma cells in vivo. The above studies have provided some new ideas and will be very helpful for the treatment of glioma patients.

Angiostatins↗
PubMed2003

[Age-dependent alternations in beta-adrenoceptor function in human detrusor and possible mechanism].

OBJECTIVE: To study the age-dependent alternations in beta-adrenergic response and possible mechanism. METHODS: The response to beta-adrenergic agonists isoprenaline and BRL37344, forskolin and dibutyryl cyclic AMP (DBcAMP) of samples from senile people in 10 cases were examined by cellular functional test. Radioligand binding assay was also performed using non-selective beta-adrenergic receptors ligand [(3)H]-dihydroalprenolol ([(3)H]-DHA), the specimens of young men in 10 cases as the control group. RESULTS: There was no age-dependent change in the contractile response to potassium chloride. The relaxing responses to isoprenaline, BRL37344 and forskolin decreased by 15.0%, 17.6% and 12.6% respectively (P < 0.01). The pD(2) values of the isoprenaline and BRL37344 also declined significantly. There was no difference in the responses to DBcAMP between the two groups. The maximum binding site decreased significantly with increasing age, but the equilibrium-dissociation constant did not change. CONCLUSIONS: There is an age-related decline in beta-adrenergic responsiveness, which might be one of the causative factors of the reduced bladder compliance of the elderly. The decrease of cAMP level caused by the reduced receptor density and adenyl cyclase activity might be the molecular mechanisms underlying the changes of beta-adrenergic responsiveness.

Adult↗