Decreased and dysfunctional circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>It has been widely demonstrated that endothelial progenitor cells are involved in several diseases and that they have therapeutic implications. In order to define the altered pulmonary vascular homeostasis in chronic obstructive pulmonary disease, we sought to observe the level and functions of circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease.</p><p><b>METHODS</b>The total study population included 20 patients with chronic obstructive pulmonary disease and 20 control subjects. The number of circulating endothelial progenitor cells (CD34(+)/CD133(+)/VEGFR-2(+) cells) was counted by flow cytometry. Circulating endothelial progenitor cells were also cultured in vitro and characterized by uptake of DiIacLDL, combining with UEA-I, and expression of von Willebrand factor and endothelial nitric oxide synthase. Adhesion, proliferation, production of nitric oxide, and expression of endothelial nitric oxide synthase and phosphorylated-endothelial nitric oxide synthase were detected to determine functions of circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease.</p><p><b>RESULTS</b>The number of circulating endothelial progenitor cells in the chronic obstructive pulmonary disease group was lower than in the control group: (0.54 ± 0.16)% vs. (1.15 ± 0.57)%, P < 0.05. About 80% of adherent peripheral blood mononuclear cells cultured in vitro were double labeled with Dil-acLDL and UEA-1. The 92% and 91% of them were positive for von Willebrand factor and endothelial nitric oxide synthase, respectively. Compared with the control, there were significantly fewer adhering endothelial progenitor cells in chronic obstructive pulmonary disease patients: 18.7 ± 4.8/field vs. 45.0 ± 5.9/field, P < 0.05. The proliferation assay showed that the proliferative capacity of circulating endothelial progenitor cells from chronic obstructive pulmonary disease patients was significantly impaired: 0.135 ± 0.038 vs. 0.224 ± 0.042, P < 0.05. Furthermore, nitric oxide synthase (112.06 ± 10.00 vs. 135.41 ± 5.38, P < 0.05), phosphorylated endothelial nitric oxide synthase protein expression (88.89 ± 4.98 vs. 117.98 ± 16.49, P < 0.05) and nitric oxide production ((25.11 ± 5.27) µmol/L vs. (37.72 ± 7.10) µmol/L, P < 0.05) were remarkably lower in endothelial cells from the chronic obstructive pulmonary disease group than the control.</p><p><b>CONCLUSION</b>Circulating endothelial progenitor cells were decreased and functionally impaired in patients with chronic obstructive pulmonary disease.</p>

Study on the spatiotemporal trend of Japanese encephalitis in Guangxi,based on geographic information system and space-time permutation scan statistic / 中华流行病学杂志

Objective To study the spatiotemporal trend of Japanese encephalitis in Guangxi Zhuang Autonomous Region between 1989 and 2006.Methods Retrospective space-time permutation scan statistic and inverse distance weighted (IDW) interpolation were employed to detect the spatiotemporal trend of Japanese encephalitis in Guangxi,from the year 1989 to 2006.Results The spatiotemporal pattern of Japanese encephalitis was divided into four phases by IDW interpolation maps,from 1989 to 2006.The first phase was spatiotemporal cluster located in southeast region,from 1989 to 1996.The second phase showed discrete distribution from 1997 to 1998.The third phase of spatiotemporal cluster located in Lingshan county,Pubei county and Bobai county,in 1999.And the last phase was spatiotemporal cluster located in northwest region from 2000 to 2006.Three statistically significant spatiotemporal clusters were detected by retrospective space-time permutation scan statistic.The primary cluster appeared in 1999 (LLR=253.25,P=0.001,RR=4.62),with 109°54′ E,22°28′ N (located in Pubei county) as its center and radiated 45.24 km.From 2000 to 2006,the secondary cluster showed in northwest (LLR=75.91,P=0.001,RR = 1.88),with center located at 105°23′ E,24°68′ N (Longlin county),and radiated 199.85 kn.From 1989 to 1996,the other secondary cluster appeared in the southeast area(LLR=46.29,P=0.001,RR= 1.16),with center located at 110°94′ E,24°03′N(Zhaoping county) and radiated 229.12 km.Conclusion Space-time permutation scan statistic and geographical information system could be applied to quantitatively detect the potentially spatiotemporal trend of the disease.The spatiotemporal cluster shifted from southeast to northwest,from 1989 to 2006.

Effect of atorvastatin on lipopolysaccharide-induced expression of C-reactive protein in human pulmonary epithelial cells / 中南大学学报(医学版)

OBJECTIVE@#To determine the effect of atorvastatin on lipopolysaccharide-induced expression of C-reactive protein in cultured A549 cells.@*METHODS@#A549 cells were incubated in DMEM medium containing lipopolysaccharide in the absence or presence of various concentrations of atorvastatin. After the incubation, the medium was collected and the level of C-reactive protein was measured by enzyme-linked immunosorbent assay. The cells were harvested and C-reactive protein mRNA was analyzed by reverse transcription polymerase chain reaction.@*RESULTS@#Incubation with lipopolysaccharide significantly induced a time and dose dependent increase in the mRNA expression and the production of C-reactive protein in A549 cells (P<0.05). Atorvastatin significantly decreased the lipopolysaccharide induced the mRNA expression and the production of C-reactive protein in a dose dependent manner in A549 cells (P<0.05).@*CONCLUSION@#Atorvastatin downregulates lipopolysaccharide-induced expression of C-reactive protein in cultured A549 cells, which may be its mechanism of anti-inflammation.