Responses of photosynthetic characteristics of Phragmites australis to simulated warming in salt marshes of the Yellow Sea and Bohai Sea, China.

Coastal wetlands are highly efficient in blue carbon sequestration. The impacts of climate warming on photosynthetic rates and light response characteristics of wetland plants would change the magnitude of carbon sequestration in coastal wetlands. We constructed warming observation stations in Phragmites australis (Phragmites) wetlands located in the Yellow River Delta in Dongying with dry climate, and in Yancheng by the Yellow Sea with wet climate. By using a Li-6800 photosynthesis system, we investigated the responses of simulated warming on photosynthetic characteristics of Phragmites in both wetlands, and compared the difference between months (June and August) in Dongying wetland. The results showed the photosynthetic rates of Phragmites were higher in June than in August. Warming increased net photosynthetic rate (Pn), transpiration rate (Tr), stomatal conductance (gs) and intercellular carbon dioxide concentration (Ci) in the two months, but the variability of Pn to warming was lower in August. The Pn and water use efficiency (WUE) of Phragmites in the Yancheng wetland were higher than Dongying wetland, and the maximum net photosynthetic rate (Pn max), light saturation point (LSP), apparent quantum efficiency (AQY), and dark respiration rate (Rd) of the former responded more positively to warming. The values of AQY, LSP and Pn max of Phragmites in the Yancheng wetlands were increased by 16.7%, 53.6% and 30.3%, respectively, in the warming plots. Our results suggested that warming could improve the utilization efficiency of weak light, the adaptability to strong light and photosynthetic potential of Phragmites under rainy and humid conditions. This study is of importance for accurately quantifying carbon sequestration of coastal wetlands at the regional and seasonal scales in the context of climate warming.

[Effect on dose owing to source displacement in coronary endovascular brachytherapy].

OBJECTIVE: To investigate the effect on the dose distribution of source position displacement with the target region margin in catheter-based 192Ir line source endovascular brachytherapy. METHOD: Dose rate distribution along longitudinal axes was estimated by the formula recommended by AAPM No.60 and No. 43. RESULTS: In the two cases of source displacement (1.1 and 5 mm) doses of target region margin was decreased dramatically (at most 53.9% and 565.8% respectively) were compared to that of no source displacement, and the affected range was 6 mm and 9 mm respectively. CONCLUSION: Source displacement will lead to the decrease of dose in target region margin.

Study on the mechanism of epidermal growth factor-induced proliferation of hepatoma cells.

AIM: Many growth factors, such as epidermal growth factor (EGF), are associated with the carcinogenesis. EGF plays its role in the proliferation of hepatoma cells through binding with EGF receptor (EGFR) and a series of signal transduction. But the postreceptor pathway is still not clear. In the present experiment, we studied the effect of tyrosine kinase, protein kinase C, Na(+)/H(+) exchange, calmodulin and voltage-dependent Ca(2+) channel on EGF-induced hepatoma cell proliferation. METHODS: Hepatoma cell line SMMC7721 was cultured in RPMI1640 serum-free medium. In order to study the effect of thyrosine kinase, protein kinase C, Na(+)/H(+) exchange, calmodulin and voltage-dependent Ca(2+) channel on human heptoma cell proliferation induced by epidermal growth factor (EGF), DNA synthesis rate of hepatoma cells was measured by the method of (3)H-TdR incorporation. RESULTS: EGF (10(-9) M) stimulated the proliferation of heptoma cells significantly ((3)H-TdR incorporation was 1 880+/-281 cpm/well, P<0.05), and this effect was significantly inhibited by tyrosine kinase inhibitor genistein ((3)H-TdR incorporation was 808+/-209 cpm/well, P<0.001). Calmodulin inhibitor W-7, protein kinase C inhibitor H-7 and Na(+)/H(+) exchange inhibitor amiloride individually had significant inhibiting effect on EGF-induced proliferation of hepatoma cells ((3)H-TdR incorporation was 978+/-87.3 cpm/well, 1 241+/-147 cpm/well, 1 380+/-189 cpm/well, respectively, P<0.001, P<0.01, P<0.05), but they all had no effect on the basal level proliferation of cultured hepatoma cells ((3)H-TdR incorporation was 1 284+/-260 cpm/well, 1 179+/-150 cpm/well, 1 392+/-152 cpm/well, respectively, (3)H-TdR incorporation of the control was 1 353+/-175 cpm/well, P>0.05). Voltage-dependent Ca(2+) channel inhibitor verapamil had no inhibition on EGF-induced proliferation of hepatoma cells ((3)H-TdR incorporation was 1 637+/-133 cpm/well, P>0.05), it also had no effect on the basal level proliferation of cultured hepatoma cells ((3)H-TdR incorporation was 1 196+/-112 cpm/well, P>0.05). CONCLUSION: Our data suggest that tyrosine kinase, Ca(2+)-calmodulin-dependent pathway, protein kinase C and Na(+)/H(+) exchange play a critical role in EGF-induced proliferation of hepatoma cells and that the effect of EGF is independent of voltage-dependent Ca(2+) channel.