Biomedical subjects

Qiang Dai

Publications and source records attributed to Qiang Dai.

7 recordsLinked to original sources

PubMed2006

A biomechanical comparison between two volar locking plate systems for distal radius fractures.

The biomechanical properties of two distal radius volar locking plate systems were investigated. A cadaveric model simulating distal radius fractures with dorsal comminution was selected. The biomechanical properties of fracture fixation using the Synthes volar locking T-plate and the Hand Innovation DVR plate were characterized. The average stiffness was 137.1 +/- 19.9 N/mm for the DVR group and 119.1 +/- 9.9 N/mm for the Synthes group (P = .49), and the average changes of the opening angle describing plastic deformation were 10.1 degrees +/- 4.0 degrees and 8.6 degrees +/- 13.2 degrees, respectively (P = .23). This study demonstrates that both the Synthes T-plate and Hand Innovations DVR plate fixation systems show comparable biomechanical characteristics.

Biomechanical Phenomena↗

PubMed2004

Mitochondrial ceramide increases in UV-irradiated HeLa cells and is mainly derived from hydrolysis of sphingomyelin.

Sphingolipids are important signaling molecules in many biologic processes, but little is known about their organelle-specific roles. Using HeLa cells, we investigated the effects of UV and etoposide-induced apoptosis on the contents of sphingomyelin (SM) and ceramide in subcellular compartments. UV irradiation of HeLa cells increased the levels of SM in all subcellular fractions, but the change was most dramatic in mitochondria. Using diacylglycerol kinase assays to quantify ceramide, we found that the levels of ceramide in mitochondria increased as early as 2 h after UV irradiation and remained elevated at 6 h. The increase in mitochondrial SM and ceramide was inhibited by D609, an inhibitor of sphingomyelinase and SM synthase. The inhibition of sphingolipid production correlated with protection of the mitochondrial transmembrane potential and prevention of cytochrome c release following UV irradiation. In contrast, myriocin, an inhibitor of the de novo ceramide synthesis pathway, only partially suppressed the production of ceramides in mitochondria and cannot suppress UV-induced apoptosis. Fumonicin B1, an inhibitor of ceramide synthase, can only prevent mitochondrial ceramide synthesis and UV-induced apoptosis in a small degree. These results indicate that mitochondrial ceramide production in UV-irradiated HeLa cells is not mediated by the de novo synthesis pathway, but mainly through SM hydrolysis.

Apoptosis↗

PubMed2004

[Biomass and net primary productivity of secondary evergreen broadleaved forest in Huangmian Forest Farm, Guangxi].

By the methods of sampling plot harvesting method and allometric dimension analysis, we measured the belowground and aboveground standing biomass and net primary productivity (NPP) of the secondary evergreen broadleaved forest in Huangmian Forest farm of Guangxi, southern China, with the location of 24 degrees 51'N and 109 degrees 51'E and an altitude of about 315 m. The total biomass was 99.96 t x hm(-2), aboveground and belowground biomasses accounted for 69.41% and 30.59%, respectively. The leaf area index of trees and undergrowth shrubs was 6.50, and the total annual NPP was 24.65 t x hm(-2) x yr(-1) by estimate, aboveground and belowground NPP accounted for 44.54% and 55.46%, respectively. The NPP of fine roots was 11.79 t x hm(-2) x yr(-1), being 86.24% of the belowground NPP.

Biomass↗

PubMed2003

Phospholipid scramblase 3 is the mitochondrial target of protein kinase C delta-induced apoptosis.

Protein kinase C (PKC) delta translocates to mitochondria during apo-ptosis,but its mitochondrial target remains unclear. We found that PKC-delta physically interacted with and phosphorylated phospholipid scramblase 3 (PLS3) after UV irradiation. PLS3 is a high-affinity substrate for PKC-delta in vitro with the K(m) at 10.5 nM. Cells expressing wild-type PLS3 became apoptotic on phorbol ester stimulation, whereas the control cells did not. Expression of a mitochondrial-targeted PKC-delta enhanced apoptosis more prominently in HeLa-PLS3 cells than control HeLa cells and HeLa cells expressing an inactive PLS3 mutant. These results indicate that PLS3 is a downstream effector of PKC-delta in the mitochondria.

Apoptosis↗

PubMed2003

Capillary electrophoresis of cardiolipin with on-line dye interaction and spectrophotometric detection.

Cardiolipin is an important phospholipid present in the mitochondrial inner membrane. It plays a key function in mitochondrial respiration by interacting with many enzymes or cofactors related to oxidative phosphorylation complexes. We have determined the concentration of cardiolipin using on-line 10-N-nonyl acridine orange (NAO) dye interaction capillary electrophoresis (CE) and spectrophotometric detection with a sample throughput of 3 min. In addition to the presence of 0.1 mM NAO, the background electrolyte (BGE) composition has been set at 80% methanol-10% acetonitrile-10% H(2)O (all v/v) to provide both good solubility and the maximum absorbance enhancement at 497 nm for the NAO-cardiolipin complex as compared to NAO alone. Sample consumption for each injection is about 57 nL. A calibration curve is established from 0.5 microM to 0.1 mM with R (2) = 0.9912 with a detection limit of 0.05 microM for cardiolipin. In a blind study, actual mitochondrial cell membrane samples in the microL range before or after UV light exposure were analyzed using the CE method. Cardiolipin concentration decreased in the different parts of the membrane sample upon UV photolysis of the cells. Support for the theory that UV light can induce cardiolipin translocation from the inner membrane (IM) to the outer membrane (OM) was indicated by a significant percentage increase of cardiolipin (as measured by the cardiolipin in the OM as compared to the sum total in the OM and IM) from 30.7 +/- 2.4% before UV light photolysis to 38.3 +/- 2.2% after UV irradiation.

Cardiolipins↗

PubMed2003

Phospholipid scramblase 3 controls mitochondrial structure, function, and apoptotic response.

Phospholipid scramblase 3 (PLS3) is a newly recognized member of a family of proteins responsible for phospholipid translocation between two lipid compartments. To study PLS3 function in mitochondria, we disrupted its conserved calcium-binding motif yielding an inactive mutant PLS3(F258V). Cells transfected with PLS3(F258V) exhibited reduced proliferative capacity. Mitochondrial analysis revealed that PLS3(F258V)-expressing cells have decreased mitochondrial mass shown by lower cytochrome c and cardiolipin (CL) content, poor mitochondrial respiration, and reduced oxygen consumption and intracellular ATP; whereas wild-type PLS3-transfected cells exhibit increased mitochondrial mass and enhanced respiration. Electron microscopic examination revealed that the mitochondria in PLS3(F258V)-expressing cells have densely packed cristae and are fewer in number and larger than those in control cells. The abnormal mitochondrial metabolism and structure in PLS3(F258V)-expressing cells were associated with decreased sensitivity to UV- and tBid-induced apoptosis and diminished translocation of CL to the mitochondrial outer membrane. In contrast, wild-type PLS3-transfected cells displayed increased sensitivity to apoptosis and enhanced CL translocation. These studies identify PLS3 as a critical regulator of mitochondrial structure and respiration, and CL transport in apoptosis.

Apoptosis↗

PubMed2002

The apoptotic effect of HA14-1, a Bcl-2-interacting small molecular compound, requires Bax translocation and is enhanced by PK11195.

HA14-1 is a small molecular compound that was identified based on the structure of Bcl-2. HA14-1 interacts with Bcl-2 and inhibits the antiapoptotic effect of Bcl-2. We investigated the mechanism of HA14-1-induced apoptosis and found that HA14-1 induces translocation of Bax from cytosols to the mitochondria. Cells deficient in Bax were much more resistant to HA14-1-induced apoptosis, suggesting that Bax is required for this process. A pan-caspase inhibitor failed to inhibit the apoptotic effect of HA14-1, indicating that this is through a caspase-independent pathway. To eliminate the effect of cytosolic Bax, we incubated cell-free mitochondria with HA14-1 to study its effect on cytochrome c release. HA14-1 was ineffective in causing cytochrome c release from the purified mitochondria. However, the combination of HA14-1 and PK11195, an antagonist of peripheral benzodiazepine receptor of the mitochondria, enhanced the cytochrome c release by HA14-1. The combination of PK11195 and HA14-1 could therefore serve as a potentially useful approach to enhance apoptosis in cancer.

Animals↗