In this paper, we investigate the boundedness character, the global attractivity and the periodic nature of the system of rational difference equations: xn+1 = p+yn-k/xn, yn+1 = q+xn-k/yn, n=0,1,2⋯, where p>0, q>0, k∈ {1,2,⋯} and the initial values xi, yi∈(0, ∞), i=-k, -k+1, ⋯,0. Some new results are obtained.

In this paper, we investigate the boundedness character, the global attractivity and the periodic nature of the system of rational difference equations: xn+1 = p+yn-k/xn, yn+1 = q+xn-k/yn, n=0,1,2⋯, where p>0, q>0, k∈ {1,2,⋯} and the initial values xi, yi∈(0, ∞), i=-k, -k+1, ⋯,0. Some new results are obtained.

Objective: To investigate the interaction between tanshinone IIA (TS IIA) and cholesteryl ester transfer protein (CETP), and to explore the ways of impact on CETP. Methods: The various structures of TS IIA and CETP were built based on the crystal structure and then performed molecular dynamics (MD). The simulation software is Gromacs 4.0 with force field of Gromos 96 53a6. The temperature is 300 K and the simulation time is 20 ns. All trajectories were recorded to analyze the changes of overall shape and local structures of CETP, and the interaction energy between TS IIA and CETP. Results: When the phosphatidyl choline zones of CETP were full, the structure was rigid. When only the cavity was loaded, CETP was easy to change. The out area of two side, phosphatidyl choline area and cavity change greatly corresponded to the frame changes of CETP. Stronger interaction between TS IIA and CETP occured in the two phosphatidyl choline area and the left side of cavity. Conclusion: CETP is a carrier protein with easily changed structure which changes according to the differences in the number and structures of loading ligands. TS IIA might affect the morphology of the CETP and then inhibit its transportation ability under the help of phosphatidyl choline or cholesterol ester.

Aim To explore the protective mechanisms of Chaiqinchengqi decoction (CQCQD) on liver injury during severe acute pancreatitis ( SAP) based on TLR4/NF-kB p65 pathway. Methods Thirty-six KM mice were randomly divided into control group (Control) , SAP and SAP + CQCQD (treatment group) (n = 12). The mice in SAP group were injected with 20% L-arginine intraperitoneal^ (3.3 g • kg"1, 2 times, 1 h interval). The mice in SAP + CQCQD group were intragastrically administered with Chaiqinchengqi decoction (19 g • kg-1 • d"1) following induction of SAP. Histopathologic^ changes of pancreas and liver were observed 72 hours after model establishment. The endotoxin in serum was tested, and the TLR4 and p-NF-kb p65 expression, as well as some inflammatory cytokines in liver was detected. Re-suits Compared to control group, the pathological damages of the pancreas and liver in SAP group were aggravated, serum endotoxin increased, the expression of TLR4 and p-NF-kB p65 in liver increased, and IL-6, TNF-a and MIP-1 a mRNA in liver were significantly elevated. Compared to SAP group, the intervention of CQCQD partially relieved the pathological damages of the pancreas and liver, reduced the endotoxin in serum , and decreased the expression of TLR4 and p-NF-kB p65, as well as IL-6, TNF-a and MIP-1 a mRNA in the liver. Conclusion CQCQD appears to protect liver injury during SAP via inhibiting TLR4/NF-kB p65 activation, then decreasing cytokines and chemo-kines.

Personalized targeted therapy in addition to standard chemotherapy has become a hot topic in the treatment of metastatic colorectal cancer (mCRC). KRAS gene mutation has been considered as a predictor for poor response to anti-epidermal growth factor receptor monoclonal antibody (anti-EGFR) therapy in patients with mCRC. The percentage of KRAS mutation is 35%-45% in patients with mCRC, and these patients have poor response to anti-EGFR; while only 50% of patients with wild-type KRAS respond to anti-EGFR, which suggests that the activation and variation of other molecules in the downstream of EGFR signaling pathway can influence the therapeutic effects. The two major EGFR-dependent signaling pathways - RAS-RAF-MAPK and PI3K-PTEN-AKT may be involved in poor response to anti-EGFR in the treatment of mCRC. In addition, the increased EGFR gene copy number (GCN) is associated with the efficacy of anti-EGFR therapy, but not associated with the expression level of EGFR protein which has no correlation with the efficacy of anti-EGFR therapy. Additional detection of mutations in BRAF and PIK3CA genes as well as deletion of PTEN gene in wild-type KRAS patients with mCRC may be helpful in further selection of patients with anti-EGFR resistance. This paper reviews recent progress on molecular markers associated with treatment outcome and prognosis predictions in the treatment of mCRC, in order to guide individualized molecular targeted therapy for mCRC. Copyright© 2011 by TUMOR.

Objective To investigate the changes of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) and angiotensin converting enzyme (ACE)/angiotensin II(Ang II)/angiotensin II type 1 receptor (AT1R) axis and their impact on the development and progression of silicotic fibrosis. MethodsSixty male Wistar rats were randomly divided into 6 groups (n=10). The rats inhaled dust for 0, 2, 4, 8, 12, and 16 weeks (w) respectively to reproduce silicosis model. HE staining was performed to observe the pathological changes of the lung tissue. The expression of α smooth muscle actin (α-SMA), collagen I (Col I), fibronectin (Fn), ACE and AT1R were measured by Western blotting. The levels of Ac-SDKP and Ang II in lung tissue were detected by ELISA. ResultsMacrophage infiltration and widened alveolar wall were observed by HE staining in the silicosis 2-w group. Isolated cell lesions which composed of macrophages were seen in silicosis 4-w group. The alveolar wall widened obviously and the number of silicotic nodules increased at 8w and 12w. The fusion of silicotic lesions, interstitial fibrosis and fibrous lesions were observed at 16w. Compared with control group, the expressions of α-SMA, Col I and Fn protein in silicosis 4-, 8-, 12-, and 16-w group increased gradually. In silicosis 2-, 4-, 8-, 12-, 16-w group, the expressions of ACE, Ang II and AT1R gradually increased compared to the control. The level of Ac-SDKP in the lung tissue of silicosis 2-w group was significantly higher than that in control group, and then decreased gradually, and significantly lower in the silicosis 12- and 16-w group than the control (P<0.05). ConclusionAlong with the development and progression of silicosis, ACE, Ang II, and AT1R expressions gradually increase in local lung tissue, while the expression of Ac-SDKP gradually decreases. Ac-SDKP and Ang II signal would participate the silicotic fibrosis process in rats.

OBJECTIVE: To investigate the protective effect of fenofibrate (Fen) on acute focal cerebral ischemia reperfusion injury in mice and its mechanisms. METHODS: Cerebral ischemia was induced by middle cerebral artery occlusion in mice for 90min and then reperfusion. Fen (10, 80 mg · kg-1) was intragastrically administered at the same time of reperfusion and 2 h after reperfusion respectively. The neurological deficit score, infarct volume and brain edema degree were determined 24 h after reperfusion. At the same time the expression of PPARα mRNA in brain tissue was measured by real-time RT-PCR. The contents of maiondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the brain tissue were measured by biochemical assay. The disruption of blood-brain barrier(BBB) was evaluated by the extravasations of Evans Blue (EB). MK886, an antagonist of PPARα receptor, was used to investigate the involvement of PPARα in the protective effect of Fen. RESULETS: Fen (80 mg · kg-1) ameliorated neurological function, reduced infarct volume, attenuated brain edema degree, decreased the extravasations of EB, increased the expression of PPARα mRNA, and attenuated the lipid peroxidation in brain tissues. MK886 abolished the protective effect of Fen. CONCLUSION: Fen has protective effect against acute focal cerebral ischemia reperfusion injury in mice by increasing the expression of PPARα mRNA and reducing lipid peroxidation in brain tissue.

Objective: To analyze the genetic relationship among the medicinal plants of Potentilla L. Methods: Six species of germplasm resources in Potentilla L. were analyzed by ISSR molecular markers. To make up the systematic diagram of genetic relationship by Popgene 1.32 software, cluster by UPGMA method, and establish the dendrogram. Results: A total of 105 ISSR bands were scored for 11 primers, among which 89 were polymorphic bands. The average percentage of polymorphic bands was 84.76%. Genetic similarity coefficient changed from 0.4476 to 0.7905. Conclusion: By cluster analysis, it shows that some of the medicinal plants in Potentilla L. from the same region are in the same group and demonstrates the rule of geographical distribution in the tested materials. This study will provide the foundation for identification and development of medicinal plants in Potentilla L., and guide collection and evaluation of germplasm resources.

Objective: To isolate the chemical constituents newly produced in processing of Polygonati Rhizoma and to analyze the content changes during its processing. Methods: Two new chemical constituents were isolated from the processed Polygonati Rhizoma by using chemical extraction and identified by LC-MS. Then HPLC analysis was performed to analyze the content changes of the two newly produced constituents in three species of wine-processed Polygonati Rhizoma during different processing periods. The contents of the two compounds in 15 batches of commercially available wine-processed Polygonati Rhizoma were determined. The HPLC was performed on a Zorbax SB-C18 column (250 mm × 4.6 mm, 5 μm) with methanol-water (8:92) as the mobile phase at 1.0 mL/min, detection wavelength was 280 nm, and column temperature at 45°C. Results: The newly produced chemical constituents were 2, 3-dihydro-3, 5-dihydroxy-6-methyl-4H-pyran-4-one (DDMP) and 5-hydryoxymethyl-furfural (5-HMF). The content of DDMP in Polygonatum cyrtonema increased to the top when processed to 24 h and then decreased. The content of 5-HMF was increased gradually throughout the processing. The two chemical constituents were found in the three kinds of wine-processed Polygonati Rhizoma. In the 15 batches of commercially available Polygonati Rhizoma, the range of DDMP in 13 batches was from 1.395% to 5.265%, and the range of 5-HMF in 14 batches was from 0.079% to 0.708%. Moreover, the contents of the two constituents in the three kinds of wine-processed Polygonati Rhizoma (16 h) were within the above ranges. Conclusion: The contents of the two chemical constituents in Polygonati Rhizoma change with the processing time. Therefore, these results could provide the basis for making the quality standard and defining the processing time endpoint of Polygonati Rhizoma.

Objective: To clone and analyze the full-length cDNA of chalcone isomerase (CHI) gene from Fagopyrum dibotrys (FdCHI). To analyze the expression of CHI and the total flavonoids content during florescence of F. dibotrys. Methods: The cDNA sequence of CHI was cloned by homology cloning from F. dibotrys. The expression of CHI was analyzed in the different tissues during florescence by semi-quantitative RT-PCR. The content of total flavonoids was measured by AlCl3 method. Results: The open reading frame (ORF) of FdCHI was 750 bp and encoded a protein with 249 amino acids. Bioinforamtion analysis suggested that the amino acid sequence of FdCHI had the high homology with those in other plants. Gene expression analysis showed that FdCHI was highly expressed in the flowers, followed by the roots and leaves, while lower in the stems. The content of total flavonoids was the highest in the flowers then the leaves and stems, and the lowest was in the roots. Conclusion: The cDNA sequence of FdCHI is firstly obtained from F. dibotrys and its coding protein has the typical characteristic of CHI homologous protein. The gene expression of FdCHI shows the same to the total flavonoids content in the stems, leaves, and flowers, but different in the roots of F. dibotrys.