Along with the increase of the population having malignant tumors with time,the effective treatment strategy is far behind the clinical needs. There are significant individual variation in terms of treatment response and toxic profile with the same chemotherapy regimen. Therefore,the research about the occurrence and the individualized treatment of malignant tumor is one of the current hot topics. cytochrome P450(CYPs) is part of I metabolism enzymatic system,and also is the most rich in content,the most widespread in distribution and has the broadest substrate spectrum in nature. This article reviews the relationship between cytochrome P450 and the occurrence and treatment of malignant tumors.

Objective To explore the effects of fasudil on inhibiting vascular smooth muscle cells (VSMCs) proliferation in vitro,increasing cell apoptosis,and inhibiting the Ras-MEK 1/2-ERK 1/2 pathway.Methods Healthy male SD rats (80～100 g) were selected.VSMCs were separated by the thoracoabdominal aortic vascular membrane dissection.Cultured VSMCs were randomly divided into 5 groups:serum-free group; serum group; serum + 1 μmol/L fasudil intervention group; serum + 10 μmol/L fasudil intervention group; serum + 100 μmol/L fasudil intervention group.The proliferation and migration of VSMCs were detected by MTT method and wound healing assay.Cell cycle and apoptosis of VSMCs were examined by flow cytometric analysis.The mRNA expressions of pro-apoptotic protein (Bax) and anti-apoptotic protein(Bcl-2) were determined by RT-PCR method,and the ratio of Bax/Bcl 2 was calculated.Western blot were performed to detect the protein expressions of Ras,MEK1/2,ERK1/2 and Akt in VSMCs.Results Fasudil inhibited rat VSMCs proliferation and migration,and blocked FBS-induced progression from the G0/G1 phase to S phase in a dose-dependent manner.Fasudil inhibited the early and late apoptosis in VSMCs,increased Bax mRNA expression and inhibited Bcl 2 mRNA expression.Fasudil significantly inhibited the protein expressions of FBS-stimulated intracellular Ras,phosphorylated MEK1/2,ERK1/2 in a dosedependent manner,but did not affect the protein expression of phosphorylated Akt.Conclusions Fasudil can attenuate VMSCs proliferation by blocking Ras-MEK1/2-ERK1/2 pathway and increasing cell apoptosis.

Neonatal inherited metabolic diseases are a group of metabolic disorders caused by singe gene defect to cause a series of clinical symptoms.Neonatal dried blood spots have the advantages of simple preparation,safety,good stability,and show strong practicability in different screening methods for inherited metabolic diseases.With the development of screening methods,more and more diseases could be diagnosed by screening.The emergence of tandem mass spectrometry and molecular biological techniques promote the newborn screening and automation for inherited metabolic disease effectively.Inherited metabolic diseases induce great harm to the newborn,which could cause not only system organs damage,but also lead to death.Therefore,early screening is important for patients' prognosis.

Objective To analyze the differences in protein pro fi le between laterally spreading tumor (LST) cell line and SW480 cell line using t wo-dimensional electrophoresis (2-DE). Methods 2-DE was empl oyed to isolate the total proteins of the two cell lines.The gels were stained with silver, and the differential protein expressions were analyzed with Melanin e 3 software. Results The protein spots of the two cell lines w ere 1285?51(LST) and 1184?47(SW480) respectively,containing 96?7 differential protein spots with 50?6 expressed or obviously increased only in LST cell line and 47?5 in SW480 cell line. Conclusion The protein profiles between LST and SW480 cell lins are different and further analysis on the differ ent interested spots is required to acquire the biology-associated proteins spe cific LST.

Objective To observe the influence on adhesion between LST-R1 cell and collagen Ⅰ mediated by galectin-1 antibody inhibition. Methods Laser confocal scanning microscopy was employed to detect the expression of galectin-1 on LST-R1 cell membrane.LST-R1 cells inhibited by galectin-1 antibody or not were seeded in the 48-well plate coated with collagen Ⅰ (20?g/well), and the morphology of the adhesive LST-R1 cells was observed and the adhesive cells were counted. Results Laser confocal scanning microscopy showed the expression of galectin-1 on the membrane of LST-R1 cells.The binding rate between galectin-1 and its antibody was 38.2%?0.92%. In the galectin-1 antibody inhibiting group,more and more irregular angular adhesive cells appeared, and most of the adhesive cells were growing in singles, while the adhesive cells,mainly clustered, in the control group were round or roudish. The numbers of adhesive LST-R1 cells in the antibody inhibiting group and the control group were 40 4 and 30 4 respectively (P

Objective A prospective study was performed to determine the effects of angiostatic agents on endometriosis. Methods Eutopic endometrium from endometriosis was transplanted to a non-vascular region of a chick embryo chorioallantocic membrane (CAM), and angiostatic compounds including recombinant human endostatin, thalidomide, monoclonal antibody of integrin ?v?3 and VEGF were given, their effects on the angiogenesis and on endometriosis-like lesion formation in CAM model were examined. Results Transplantation of endometrium onto the CAM led to a strong angiogenic response in the chick embryonic tissue; a number of newly formed vessels were significantly decreased in the groups using angiostatic agents compared with the control group. Endometriosis-like lesion formation was significantly impaired after treatment with angiostatic agents, and it was associated with decreased vessel density in the surrounding chorioallantoic membrane, accomponied by various degree of necrosis in the endometriosis-like lesions under microscopic observation. Conclusion Endometrium induced angiogenic response in the ectopic environment is critical for implantation and subsequent survival of the tissue. Angiostatic agents can inhibit the angiogenesis induced by eutopic endometrium and has a remarkable anti-endometriosis effect.

0.05),and significantly higher than that of volunteers after trials(P

Objective To compare the potential cytotoxicity induced by Veratrum nigrum coadministered with Panax ginseng, and to provide experimental evidence on the mode of herb-herb interaction based on human liver drug metabolizing enzymes.Methods The effect of V.nigrum and coadministration on cultured human hepatoma (HepG2) cells was investi-gated by detecting morphological changes , cell viability , cytomembrane integrity and apoptosis after the cells were treated for 24 h.The mRNA expression levels of drug metabolizing enzymes influenced by P.ginseng were determined by real-time quantitative reverse-transcriptase polymerase chain reaction .Results V.nigrum coadministered with P.ginseng had a better inhibitive effect on the growth of HepG2 cells at the IC50value of (15.18 ±1.03) mg/ml than at the value of IC50 (21.46 ±1.10) mg/ml of V.nigrum.Coadministration more significantly raised the LDH level in cell culture medium than at the same dose of V.nigrum.Moreover, in coadministration group, compared with the same dose of V.nigrum,the total apoptosis and necrosis of HepG2 cells were significantly increased .P.ginseng had effect on the expression of CYP3A4, CYP1A1, CYP1A2, CYP2B6 and CYP2E1 mRNA.Conclution Compatibility of medicines in a prescription also has herb-herb interactions based on drug metabolizing enzymes .The interaction mode is that the P.ginseng inhibits and induces CYPs and the modulated CYP isozymes ,inturn,have an impact on the metabolism of constituens in coadministered herbs causing herb-herb interaction .

Objective To investigate the outcome of damage control sugery in patients with acute superior mesenteric occlusion (ASMO).Methods Seventeen patients with acute superior mesenteric occlusion from June 2008 to May 2012 were reviewed retrospectively.Diagnosis was confirmed by CT and/or DSA.Patients were divided into two groups:seven patients in damage control group (shortening surgical time,bowel exteriorization,temporary abdominal closure) ; ten patients in conventional surgical treatment group.The treatment outcomes of the two groups were compared.The survival of all patients was followed up for 6 months to 5 years at outpatient clinic.Results The overall mortality rate was (5/17) and surgical complications rate was (8/17).Operation time was (97 ±42) min and (236 ± 137) min(t =-4.72,P ＜0.01,P ＜ 0.05) respectively in damage control group and conventional surgical treatment group.Intestine resection length was (114 ± 94) cm and (229 ± 93) cm (t =-2.49,P =0.03,P ＜ 0.05) respectively.Complications rate was (1/7) and (7/10) (Fisher's dxact test P =0.05,P ≤0.05) respectively; mortality was (1/7) and (4/10) (Fisher's dxact test P =0.34,P ＞ 0.05) respectively.Conclusions Although damage control does not significantly reduce mortality,but the rational use of damage control can effectively reduce operation time,shorten intestine resection length and decrease surgical complications.

Objective To evaluate the relationship between aberrant crypt foci(ACF) and colon cancer by observing the sequential development of ACF in cancer models of rats. Methods The colon cancer models in 60 Wistar rats were established by subcutaneously injection of dimethylhydrasine (DMH) once a week for 18 weeks. The rats were sacrificed and the colon tissues stained by methylene blue were observed with a stereomicroscope. Results There were two types of ACF, named cACF and dACF. The microscopic findings in dACF were similar with that in early colon cancer, while those in cACF were not. The expression of β-catenin in cACF and dACF were 4. 84% and 100% (P =0. 000) , respectively, and the expression of MMP-7 were 7. 87% and 81.82% (P =0. 000), respectively. There was no significant difference in expression of β-catenin and MMP-7 between dACF and colon cancer ( P ＞ 0. 05 ). Conclusion The microscopic and molecular changes in dACF is similar with that in colon cancer, and dACF may progress to cancer through Wnt pathway.