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The statistical model (log-normal model), niche models (Zipf model, broken stick mo-del, niche preemption model), and neutral model were used to fit the species-abundance distribution patterns based on the measurements of environmental factors and inventory data of trees with DBH≥1 cm in a 1.5 hm 2 plot in the primary forest (PF) and a 1.5 hm 2 plot in the secondary forest (SF). The results showed that species-abundance distribution was affected by habitat heterogeneity in Q. aliena var . acutiserrata forest. Topography had a predominant impact on the species-abundance distribution in PF. Species distribution was affected by both neutral and niche processes, with neutral process having a less prominent effect in large convexity habitats. While the neutral model was rejected by the K-S and Chi-square test in low convexity habitats, the species-abundance distribution satisfied the assumption of niche theory. Niche process and neutral process were equally important in the community in areas with steep slopes, while niche differentiation was the dominant in flat areas. In SF, the main factors affecting species distribution were soil nutrients. The niche process was the mainly ecological process affected species-abundance distribution in habitats with high soil available phosphorus, while the niche and neutral processes existed simultaneously in habitats with low soil phosphorus availability. There was a significant scale effect on the species-abundance distribution pattern of Q. aliena var . acutiserrata forests in Taibai Mountain. The niche and neutral processes could protect the species-abundance distribution at the 20 m×20 m scale in PF, while the niche process could explain the species-abundance distribution at the 40 m×40 m and 70 m×70 m scales. The niche and neutral processes combined acted on the species abundance distribution at the 20 m×20 m, 40 m×40 m and 70 m×70 m scales in SF, with niche process being more important than neutral process. Moreover, besides the scale and habitat heterogeneity, the species-abundance distribution patterns of Q. aliena var. acutiserrata forests differed significantly between primary forest and secondary forest under anthropogenic disturbance.

Objective: CD133(+) tumor cells are regarded as cancer stem cells (CSCs), responsible for tumor initiation, development, and relevant with chemo- and radio-resistance of tumors. However, how the destiny of CD133(+) cells is regulated by their niche remains largely unknown. In this study the interpretation of the relationship between CD133(+) cells and their niche were performed through investigating the distribution characteristics of CD133(+) cells in transplanted human glioma xenograft., Methods: CD133(+) tumor cell spheres or tumor cells transfected with red fluorescent protein (RFP) gene were implanted in situ, subcutaneously or intraperitonealy in nude mice, then the xenografts were dissected and embedded in paraffin, stained with hematoxylin-eosin (HE), tumor tissues were further stained against CD133 with immunohistochemical and immunofluorescent techniques. The pathological structures of tumors and distribution characteristics of CD133(+) tumor cells were observed under microscope and confocal fluorescence microscope., Results: Under microscope, distribution of CD133(+) glioma cells showed certain regularity and can be classified morphologically into three types: cell clusters, in pairs and single cells. Distribution of CD133(+) cells can also be classified according to their distribution location: accumulating around tumor vasculature areas, among the vascular endothelial cells, or in the normal brain tissue and ventricles. Under fluorescence microscope and laser confocal microscope, some of vascular endothelial cells inside the tumor region and some cells around tumor vessels co-express CD133 and RFP., Conclusion: CD133(+) tumor cell clusters in nude mice are actually similar to those in CSCs spheres cultured in vitro. The single CD133(+) cells and CD133(+) cells in pairs represent asymmetric and symmetric division of CSCs within the CSCs niche, respectively. CD133(+) cells residing along tumor vessels are CSCs depending on CSC niche, and those locating far away from tumor blood vessels or tumor tissues, residing in normal brain tissues are the disseminated CSCs or neural stem cells which are not controlled or regulated by CSCs niche.

Through laboratory lysimeter experiments and artificial rainfall experiments, characteristics of P and La transportation from both vertical and horizontal directions are investigated. The association between La and P loss from soil is preliminarily discussed. Results of lysimeter experiment show that both La and P are difficult to transport vertically. Downward depths are no deeper than 6-8 cm for all forms of La and P. With the increasement of exogenous La amount, the amount of Water soluble P, NaHCO3-extractable P and NaOH-extractable P decrease, while HCl-extractable P and residual form of P increase. Results of artificial rainfall experiment show that majority of La and P transport with fine soil particles in runoff, which is more than 95%. Loss of total P and La in runoff from the manure-applied soil are correlated significantly, both in loss rate and loss amount.

384 surface sediment samples were collected from mud flat, silt flat and mud-silt flat of Bohai Bay by 1 m and 10 m interval using grid sampling method. Concentrations of Al, Fe, Ti, Mn, Ba, Sr, Zn, Cr, Ni and Cu in each sample were measured by ICP-AES. To figure out the random distribution and concentration characteristics of these heavy metals, concentration of them were compared between districts with different grain size. The results show that varieties of grain size cause the remarkable difference in the concentration of heavy metals. Total concentration of heavy metals are 147.37 g x kg(-1), 98.68 g x kg(-1) and 94.27 g x kg(-1) in mud flat, mud-silt flat and silt flat respectively. Majority of heavy metals inclines to concentrate in fine grained mud, while Ba and Sr have a tendency to concentrate in coast grained silt which contains more K2O * Al2O3 * 6SiO2. Concentration of Sr is affected significantly by the grain size, while concentration of Cr and Ti are affected a little by the grain size.

Objective: To explore the molecular mechanism of increasing the invasion of colon cancer cells by gastrin 17., Methods: The plasmid pCR 3.1/GR expressing the gastrin receptor cholecystokinin-2 receptor (CCK-2R) was transfected into colonic carcinoma cells of the line Colo320 by Lipofectamine 2000. The clones expressing stably CCK-2R were screened by G418 and named as Colo320WT cells. The expression levels of gastrin receptor of the Colo320 and Colo320WT cells were assayed by RT-PCR and Western blotting. The Colo320WT cells were treated by gastrin-17, and the expression levels of phosphorylated FAKTyr397 and total focal adhesion kinase (FAK) in the Colo320WT cells at the time points 0, 1, 6, 12, 24, and 48 h were detected by Western blotting. Another Colo320WT cells were treated by L365, 260, gastrin17 receptor blocker, for 30 minutes firstly and then treated by gastrin17 again for 12 hours, and then Western blotting was used to detect the expression levels of phosphorylated FAKTyr397 and total focal adhesion kinase (FAK) at the time points 0, 1, 6, 12, 24, and 48 h. Confocal microscopy was used to observe the phosphorylated FAKTyr397 localizing in the lamellipodia. The information of FAK-Src-p130(Cas)-Dock180 signaling complex was assayed by coimmuniprecipation and immunity blotting. The level of Rac-GTPase was tested by pull down assay., Results: The level of phosphorylated FAKTyr397 expression in the Colo320WT cells after the gastrin17 intervention increased time-dependently and peaked at the time point of 12 h, and the phosphorylated FAKTyr397 expression in the Colo320WT cells treated by L365, 260 decreased remarkably, but the level of total FAK remained unchanged. The phosphorylated FAKTyr397/FAK levels were 2.82%, 9.28%, 22.62%, 38.59%, 28.41%, and 14.94%, 0, 1, 6, 12, 24, and 48 h after the gastrin17 treatment respectively, and the level was 7.21% after L365, 260 treatment. The amount of phosphorylated FAKTyr397 localizing in the lamellipodia of the Colo320WT cells that were treated by gastrin17 increased time-dependently and peaked at the time-point 12 h. FAK-Src-p130(Cas)-Dock180 signaling complex was formed in the Colo320WT cells stimulated with gastrin17. Gastrin17 activated Rac, but did not affect the total Rac expression., Conclusion: The mechanism of increasing the colon cancer cells' invasion by gastrin17 is probably that gastrin17 makes FAK-Tyr397 phosphorylated and be localized to lamellipodia, causes the forming of FAK-Src-p130(Cas)-Dock180 signaling complex when it is bound to its receptor CCK-2, and activation of Rac.

Objective: To study the effect of gastrin on the mRNA and protein expression of urokinase-type plasminogen activator (u-PA) in human colon cancer cells and detect the role of p38 MAPK in this process., Methods: Lipofectin method was used to transfect pCR3. 1/CCK2R vector expressing gastrin receptor into a colon cancer cell line colo320. Gastrin and gastrin antagonist were used to up-regulate and down-regulate the signaling pathway, respectively. Human colon cancer colo320 cells and colo320/ CCK2,R cells were cultured and then stimulated with gastrin for different time; SB203580 was added into culture medium to prevent p38 kinase pathway before incubating with gastrin; Western blot and RT-PCR were used to examine the u-PA expression. Western blot was employed to detect p38 kinase phosphorylation., Results: Gastrin increased evidently the mRNA and protein expressions of u-PA and induced p38 kinase phosphorylation in colo320/CCK,R cells time-dependently. However, the extent of enhancement of u-PA and p38 MAPK expression in colo320 cells was much less than that in colo320/CCK2R cells. The gastrin antagonist L-365, 260 showed an effect of competitive inhibition on gastrin-induced u-PA expression and p38 kinase phosphorylation. The inhibitor SB203580 could sufficiently suppress gastrin-induced p38 kinase phosphorylation and significantly attenuate gastrin-induced u-PA mRNA and protein expressions in colo320/ CCK2 R cells in a dose-dependent manner., Conclusion: Gastrin-gastrin receptor signal transduction pathway can obviously induce u-PA expression in human colon cancer cells via activating the phosphorylation of p38 kinase.

Objective: To determine the effect of uvulopalatopharyngoplasty (UPPP) therapy on post-surgery continuous positive airway pressure (CPAP) treatment during non-rapid eye movement (NREM) and rapid eye movement (REM) sleep in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), and to evaluate the use of Bi-level positive airway pressure (BiPAP) in whom CPAP therapy failed., Methods: Thirty-four OSAHS patients after UPPP surgery were tested more than 3 months after the procedure. Among them 25 patients were treated with classical UPPP (cUPPP), in which all of the uvula and part of the soft palate were removed. Nine underwent modified UPPP (mUPPP), keeping part of the uvula. The control group consisted of 34 age, body mass index (BMI) and apnea hypopnea index (AHI) matched, newly diagnosed OSAHS patients without prior treatment. Four patients receiving both pre- and post-surgery tests were included in both groups. A manual titration of CPAP to determine the optimal CPAP pressure (oCPAP) and the highest CPAP pressure (hCPAP) the patient can tolerate was performed during both NREM and REM sleep in all 68 patients., Results: 72% of the UPPP patients had less than 50% decrease in AHI, and 82% of the 34 patients still had AHI > 15 during post-operation PSG test. Hence, most of them needed further therapy. All of the untreated OSAHS patients could tolerate 17-20 cm H2O of CPAP during NREM and REM sleep. None had severe mouth air leak before an oCPAP was reached. In contrast, five in the surgery group failed to respond to CPAP treatment during both NREM and REM sleep, and one more during REM sleep. All of the nine patients who had a mUPPP could tolerate CPAP. One of the four tested both before and after surgery failed to respond to CPAP treatment after surgery during REM sleep and one during both NREM and REM sleep. However, the six patients failed to respond to CPAP treatment tolerated BiPAP therapy well., Conclusions: In a considerable number of patients with OSAHS, UPPP may compromise the applicability of nasal CPAP as a subsequent therapy, and BiPAP might be a treatment option for patients who could not tolerate CPAP treatment.

Objective: To investigate the effect of uvulopalatopharyngoplasty (UPPP) on postoperation continuous positive airway pressure (CPAP) treatment in patients with obstructive sleep apnea hypopnea syndrome (OSAHS)., Methods: 66 OSAHS patients underwent UPPP were recruited and all were followed up for more than 12 months. Among them 24 patients were treated with classical UPPP, 42 had modified UPPP treatment. The efficacy of surgery was compared between the two groups. The post-operation tolerance to CPAP pressure was tested during sleep CPAP titration in 24 classical UPPP patients and in 15 modified UPPP patients., Results: The validity ratio is 58.3% and 61.9% 12 months after operation. There was no significant difference between classical UPPP and modified UPPP in regard to surgery efficacy, and most of them need further CPAP therapy. During CPAP treatment, compared with untreated OSAHS patients, the highest CPAP pressure classical UPPP group could tolerant decreased significantly, however, classical UPPP group did not. 16.7% of classical UPPP patients had severe mouth air leak before optimal CPAP pressure was titrated, but none of the 15 post modified UPPP failed to sequential CPAP therapy., Conclusion: The efficacy was similar between modified UPPP and classical UPPP treatment, post modified UPPP patients had better tolerance to sequential CPAP treatment. It may be better to treat OSAHS patients with modified UPPP instead of classical UPPP.