Biomedical subjects

Y Luo

Publications and source records attributed to Y Luo.

546 records · Page 31Linked to original sources

PubMedDate not supplied

Glycosaminoglycan hydrogels as supplemental wound dressings for donor sites.

Chemically crosslinked glycosaminoglycan (GAG) hydrogel films were evaluated as biointeractive dressings in a porcine model for donor-site autograft wounds. Multiple 5 x 5 x 0.03 cm wounds were created on the dorsum of pigs. Half of the wounds were treated with a GAG film plus an occlusive dressing (Tegaderm), whereas the other half were treated with Tegaderm alone. At 3, 5, or 7 days after surgery, the partially healed wounds were excised and evaluated histologically for three animals at each time point. By day 3, epithelial cells had proliferated and migrated from wound edges and from epithelial islands associated with residual hair follicles to begin to cover the wound bed. A statistically significant increase in coverage was observed for GAG + Tegaderm-dressed wounds than for those with Tegaderm alone at day 3 and day 5 post-surgery. By day 7, all treatment groups were completely healed. Thus, GAG hydrogels accelerated wound healing by enhancing re-epithelialization.

Animals↗

PubMedDate not supplied

Induction of G1 arrest and differentiation in MDA-MB-231 breast cancer cell by boehmeriasin A, a novel compound from plant.

Boehmeriasin A is a new phenanthroquinolizidine alkaloid recently isolated from the Boehmeria siamensis Craib (Urticaceae). In vitro biological activity assay demonstrated that this novel compound has wide-range, strong antitumor activity. This study is aimed to determine the effects of boehmeriasin A on breast cancer cell (MDA-MB-231 cell line). Proliferation assay and fluorescence activated cell sorter (FACS) showed that cell growth inhibition and G1 phase arrest of cell cycle were caused by boehmeriasin A. The concentrations resulting in total and 50% growth inhibition are 0.007 and 0.0035 microg/mL, respectively. Exposed in 0.007 microg/mL boehmeriasin A for 12 h, the G1 phase cell percent increased from 44.8% pre-drug treatment to 66.3%. Consistent with G1 arrest and cell growth inhibition, cyclin E2 and cyclin D1 messenger RNA expression in the cell was down-regulated with drug treatment. Then, few apoptotic cells were detected, and most other cells underwent differentiation, which is characterized by specific changes in cell morphology, lots of lipid droplet accumulation, and increasing expression of adipocyte differentiation-related protein. The result first demonstrates that boehmeriasin A potently inhibits the proliferation of breast cancer cell MDA-MB-231 via the G1 phase cell cycle arrest and differentiation induction, and as such, may be considered as candidate chemotherapeutic and/or chemopreventive agent for breast cancer.

Apoptosis↗

PubMedDate not supplied

Clinical investigation of two glass-ionomer restoratives used with the atraumatic restorative treatment approach in China: two-years results.

OBJECTIVE: To compare the clinical performance of two glass-ionomer cements, ChemFlex (Dentsply DeTrey) and Fuji IX GP (GC), when used with the atraumatic restorative treatment (ART) approach in China. METHODS: Eighty-nine school children aged between 6 and 14 years who had bilateral matched pairs of carious posterior teeth were included. A split-mouth design was used in which the two materials were randomly placed on contralateral sides. The performance of the restorations was assessed directly and also indirectly from die-stone replicas at baseline and after 6, 12, and 24 months. RESULTS: The 24-month cumulative survival rates of ART restorations in the primary teeth were 93 and 90% for the ChemFlex and Fuji IX GP class I restorations, respectively, while 40 and 46% of class II restorations placed with the respective materials were satisfactory. In the permanent dentition, only class I restorations were involved and the cumulative survival rates were 95 and 96% for ChemFlex and Fuji IX GP. For the primary teeth after 24 months, net mean occlusal wear was 87 microm for ChemFlex and 85 microm for Fuji IX GP. The occlusal wear in the permanent teeth was 75 microm for ChemFlex and 79 microm for Fuji IX GP. CONCLUSION: The clinical performance of both materials over a 24-month period was similar and the survival rates of class I ART restorations in both primary and permanent teeth were high.

Adolescent↗

PubMedDate not supplied

All trans-retinoic acid suppresses in vitro growth and down-regulates LIF gene expression as well as telomerase activity of human medulloblastoma cells.

Leukemia inhibitory factor (LIF) is prevalently expressed in human medulloblastomas in vivo and in vitro. Blockage of LIF expression or biological function can inhibit in vitro growth and induce differentiation-like phenotypes of medulloblastoma cells (Med-3), suggesting a redifferentiation potential of Med-3 cells when intrinsic dedifferentiation factor(s) is suppressed or external differentiation element(s) is exerted. All-trans retinoic acid (RA) can induce differentiation in some types of cancers but its effect on medulloblastoma cells has not yet been described. To address the above issues, three dosages (5, 8 and 10 mumol/L) of RA were used to treat Med-3 cells and their effects on the target cells were evaluated by multiple approaches. It was found that, in addition to induction of morphological changes and growth inhibition, RA could repress LIF expression as well as the telomerase activity of Med-3 cells in time- and dose-related fashions. Our data thus suggest that the growth inhibitory effect of RA on Med-3 cells may be correlated with the LIF down-regulation. Reduction of telomerase activity by RA indicates that this enzymatic activity is a potential differentiation indicator of medulloblastoma cells.

Antineoplastic Agents↗

PubMedDate not supplied

Abrogation of G2 checkpoint specifically sensitize p53 defective cells to cancer chemotherapeutic agents.

BACKGROUND: Chkl is a checkpoint gene that is activated after DNA damage. It phosphorylates and inactivates Cdc25C at the late G2 phase. The inactivation of Cdc25C and consequently, the inactivation of Cdc2, are required for the G2 arrest induced by DNA damage. METHODS: We treated 184B5 cell line and its E6 transformed cell lines with adriamycin in the presence of staurosporine or UCNO1 and examined G2 arrest and cell death. RESULTS: We found that adriamycin induced a p53 and p21 response as well as a G1 arrest in 184B5 cells, but not in its E6 transformed cells. Staurosporine or UCNO1 abrogated the G2 arrest induced by adriamycin in both cell lines. In addition, staurosporine or UCNO1 specifically sensitized p53 incompetent cells to adriamycin. CONCLUSION: G2/M checkpoint abrogators can potentially enhance the cytotoxic effect of conventional chemotherapeutic reagents specifically to tumor cells.

Alkaloids↗

PubMedDate not supplied

Chkl binds and phosphorylates BAD protein.

Chk1 (checkpoint kinase 1) is a serine-threonine kinase that is critical for G2/M arrest in response to DNA damage. Chk1 phosphorylates Cdc25C at serine-216, a major regulatory site, in response to DNA damage. Furthermore, Chk1 also phosphorylates Cdc25A on serine 123 which accelerates its degradation through the ubiquitin-proteasome pathway and arrests cells in late G2-phase after DNA damage. In the present study, we demonstrated that Chk1 phosphorylates pro-apoptotic protein BAD (Bcl-2/Bcl-XL-Antagonist, causing cell Death) in vitro. In vitro phosphorylation analysis with various mouse BAD peptides has revealed two phosphorylation sites for Chk1 at serine-155 and serine-170. When wild-type and mutant BAD (S155A) constructs were transfected into 293T cells, an association between BAD and Chk1 was observed by co-immunoprecipitation. In addition, there was an increase in the phosphorylation of serine-155 following DNA damage by adriamycin treatment. Our results suggest that Chk1 associates with BAD and phosphorylates the BAD protein at serine-155. Taken together, our results suggest that Chk1 may inactivate BAD by associating with and phosphorylating residues critical for BAD function in response to DNA damage.

Amino Acid Sequence↗