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Articles by G Gao
Total Records ( 3 ) for G Gao
  W Wu , W Zhang , R Qiao , D Chen , H Wang , Y Wang , S Zhang , G Gao , A Gu , J Shen , J Qian , W Fan , L Jin , B Han and D. Lu

Purpose: Platinum agents cause DNA cross-linking and adducts. Xeroderma pigmentosum group D (XPD) plays a key role in the nucleotide excision repair pathway of DNA repair. Genetic polymorphisms of XPD may affect the capacity to remove the deleterious DNA lesions in normal tissues and lead to greater treatment-related toxicity. This study aimed to investigate the association of three polymorphisms of XPD at codons 156, 312, and 711, with the occurrence of grade 3 or 4 toxicity in advanced non–small cell lung cancer patients.

Experimental Design: We used matrix-assisted laser desorption/ionization time-of-flight mass spectrometry to genotype the three polymorphisms in 209 stage III and IV non–small cell lung cancer patients treated with platinum-based chemotherapy.

Results: The variant homozygotes of XPD p.Arg156Arg (rs238406) polymorphism were associated with a significantly increased risk of grade 3 or 4 hematologic toxicity (adjusted odds ratios, 3.24; 95% confidence interval, 1.35-7.78; P for trend = 0.009), and, more specifically, severe leukopenia toxicity (P for trend = 0.005). No statistically significant association was found for the three polymorphisms and grade 3 or 4 gastrointestinal toxicity. Consistent with these results of single-locus analysis, both the haplotype and the diplotype analyses revealed a protective effect of the haplotype "CG" (in the order of p.Arg156Arg-p.Asp312Asn) on the risk of grade 3 or 4 hematologic toxicity.

Conclusions: This investigation, for the first time, provides suggestive evidence of an effect of XPD p.Arg156Arg polymorphism on severe toxicity variability among platinum-treated non–small cell lung cancer patients.

  X Wang , B Qin , G Gao and H. W. Paerl

An experiment was conducted with a natural freshwater phytoplankton community from a eutrophic pond to investigate the combined effects of phytoplankton community competitive interactions, nutrient enrichment and zooplankton on Microcystis bloom formation. The pond water initially had a very low concentration of Microcystis, but the total phytoplankton biomass as chlorophyll a reached ~110 µg L–1 in summer. The pond water was incubated outdoors at natural temperature and light with a 2 x 2 factorial manipulation of nutrient (nutrient additions versus no additions) with and without zooplankton. The interaction of a two-phase nutrient addition (a net increase in concentrations of 250.0 µM N and 16.1 µM P each time) and the presence of zooplankton significantly altered phytoplankton community composition. When the water initially contained zooplankton, nitrogen and phosphorus enrichment promoted a surface Microcystis bloom. However, when the zooplankton was removed from the water at the start of the experiment, no surface Microcystis bloom formed, regardless of nutrient additions. Chlorophyta dominated in the absence of zooplankton, when the same nutrient was provided. Our results demonstrate that Microcystis bloom formation in this eutrophic water body at a mean temperature of about 36°C at 14:00 h was closely related to the initial presence of zooplankton and a sufficient supply of nitrogen and phosphorus. We believe this is one of the first demonstrations of zooplankton controlling Microcystis bloom formation in a water body previously free of surface cyanobacterial blooms.

  K Guo , X Wang , G Gao , C Huang , K. S Elmslie and B. Z. Peterson

We have found that phospholemman (PLM) associates with and modulates the gating of cardiac L-type calcium channels (Wang et al., Biophys J 98: 1149–1159, 2010). The short 17 amino acid extracellular NH2-terminal domain of PLM contains a highly conserved PFTYD sequence that defines it as a member of the FXYD family of ion transport regulators. Although we have learned a great deal about PLM-dependent changes in calcium channel gating, little is known regarding the molecular mechanisms underlying the observed changes. Therefore, we investigated the role of the PFTYD segment in the modulation of cardiac calcium channels by individually replacing Pro-8, Phe-9, Thr-10, Tyr-11, and Asp-12 with alanine (P8A, F9A, T10A, Y11A, D12A). In addition, Asp-12 was changed to lysine (D12K) and cysteine (D12C). As expected, wild-type PLM significantly slows channel activation and deactivation and enhances voltage-dependent inactivation (VDI). We were surprised to find that amino acid substitutions at Thr-10 and Asp-12 significantly enhanced the ability of PLM to modulate CaV1.2 gating. T10A exhibited a twofold enhancement of PLM-induced slowing of activation, whereas D12K and D12C dramatically enhanced PLM-induced increase of VDI. The PLM-induced slowing of channel closing was abrogated by D12A and D12C, whereas D12K and T10A failed to impact this effect. These studies demonstrate that the PFXYD motif is not necessary for the association of PLM with CaV1.2. Instead, since altering the chemical and/or physical properties of the PFXYD segment alters the relative magnitudes of opposing PLM-induced effects on CaV1.2 channel gating, PLM appears to play an important role in fine tuning the gating kinetics of cardiac calcium channels and likely plays an important role in shaping the cardiac action potential and regulating Ca2+ dynamics in the heart.

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