Purpose: To study the treatment of metastasis of late digestive tract cancer?Methods:58 patients with late digestive tract cancer were divided into two groups. One group (reference group) of patients 28 cases were underwent chemotherapeutic treatment while another (treatment group) 30 cases were treated with DDP by CHPP. Results:Through DDP by CHPP (treatment group) the treatment show effectiveness as much 63.3% higher than that of reference group as 39.3%. This indicates the fact that there were significant differences between the groups ( P 0.05)Conclusions: DDP with Cisplatin by CHPP on patients with late digestive tract cancer, especially those patients followed by ascites, can evidently enhance the effectiveness of the treatment.

Objective To compare the effects of ticagrelor and clopidogrel on patients undergoing percutane-ous coronary intervention(PCI)with acute ST elevated myocardial infarction (STEMI).Methods 120 patients with STEMI received PCI within 12h of symptom onset in our hospital were randomly divided into clopidogrel treated group (n=60)and ticagrelor treated group (n=60).Serum was collected before surgery and 36 hours after PCI for ALT, Cr,CK-MB,and MA.Cardiac ultrasound was examined,too.All patients were followed 6 months post-PCI for main adverse cardiovascular and cerebrovascular events (MACCE)and medicine side effect.Results No significantly difference was noted in baseline between the two groups.The level of CK-MB and MA in the ticagrelor treated group [CK-MB(56.5 ±8.3)U/L,MA (45.9 ±6.4)mm[and clopidogrel treated group[CK-MB(74.3 ±9.6)U/L,MA (35.6 ±7.3)mm]were significant difference (CK-MB,P=0.043;MA,P=0.038).The MACCE of patients in ticagrelor treated group were significantly lower than patients in clopidogrel treated group during post-PCI 6 months follow-up(The ratio of angina in ticagrelor group was 1.7%,while in clopidogrel group was 6.7%,P=0.042). Conclusion Ticagrelor is more effective in suppress the function of platelet,decrease MACCE in patients with STE-MI undergoing PCI.

OBJECTIVE:To observe therapeutic efficacy and safety of amlodipine besylate combined with valsartan in the treatment of hypertension. METHODS:158 patients with hypertension were randomly divided into control group (n=78) and treatment group (n=80). Control group was treated with amlodipine besylate,2.5 mg/time,3 times/d;treatment group was addi-tionally treated with valsartan,80 mg/time,once a day. A treatment course lasted for 4 weeks,and both received 5 courses. Clini-cal efficacy,blood pressure,plasma concentrations of ET-1,NT-proBNP and Ang Ⅱ were compared between 2 groups. RE-SULTS:The compliance rates of treatment group after 4,8,12,16,20 weeks were higher than that of the control group(P<0.05). Compared with control group,SBP and DBP of treatment group were decreased significantly after 4,8,12 and 20 weeks,with sta-tistical significance(P<0.05). After 20 weeks,the serum levels of ET-1,NT-proBNP and Ang Ⅱwere decreased significantly,es-pecially treatment group,with statistical significance (P<0.05). There was no statistical significance in the incidence of ADR be-tween 2 groups (P>0.05). CONCLUSIONS:Amlodipine besylate combined with valsartan can effectively control the blood pres-sure in patients with hypertension,which may be related to the inhibition of ET-1,NT-proBNP and AngⅡ.

Objective:To explore bromodomain and extra-terminal (BET) inhibition in the regulation of vascular endothelial cells activation and early atherosclerosis formation and its potential molecular mechanisms.Methods:1.Human umbilical vein endothelial cells (HUVEC) and mouse heart endothelial cells (MHEC) were isolated,and tumor necrosis factor α (TNFα) was used to activate in flammatory genes transcription in the presence or absence of JQ1,a specific BET inhibitor.The groups are as follows:(1)Normal control group;(2) TNFα(25 ng/mL)group;(3) TNFα+JQ 1 group.The gene mRNA and protein expression of inflammatory cytokines were measured by both real-time PCR and flow cytometry (FCM).2.LDL receptor-deficient (LDLR-/-) mice were randomly divided into 2 groups:JQ1 group (n=8,JQlintraperitoneal,50 mg/kg,daily) and control group (n=8,DMSO,daily).After 8 weeks feeding with high cholesterol diet,vascular cell adhesion molecule-1 (VCAM-1) expression in aortic arch was measured by immunohistochemistry.The activity of nuclear factor kappa B (NF-κB) signaling was monitored by 5XκB luciferase reporter assay in HEK293.Results:TNFα dramatically induced the mRNA and protein expression of inflammatory genes and JQ 1 significantly downregulated the induction of them (E-selectin,P-selectin,VCAM-1,IL-8)(P＜0.01).Immunohistochemistry detection indicated that JQ1 significantly downregulated the expression of VCAM-1 in aortic arch induced by 8 weeks high cholesterol diet feeding comparing to control group.In addition,BET bromodomain inhibition downregulated TNFα upregulated NF-κB transcriptional activity (P＜0.01).Conclusions:Our study demonstrated that BET bromodomain was involved in NF-κB mediated inflammatory genes expression;inhibition of BET bromodomain suppressed vascular endothelial activation in vitro,and attenuated early atherogenesis in vivo.

OBJECTIVETo study the relationship between sensitivity to 5-FU and the status of a panel of microsatellite loci in three human colon cancer cell lines.

METHODSCell viability in several concentrations of 5-FU was assessed by the MTT test. Expression of hMSH2 and hMLH1 in LoVo, SW480 and SW1116 cells were analyzed by immunocytochemical staining.Ten mononucleotide and dinucleotide microsatellite loci were analyzed by the PCR-SSLP-silver staining method.

RESULTSBy MTT assay, it showed that LoVo cells were more sensitive than SW480 and SW1116 cells (0.8 micromol/L,2.2 micromol/L and 1.9 micromol/L, respectively, P < 0.05). By immunocytochemical staining, hMSH2 was expressed in SW480 and SW1116 cells but not in LoVo cells, while hMLH1 was positive in all three cell lines. The PCR-SSLP-silver staining of 10 microsatellite loci revealed that LoVo cells had a different pattern of electrophoretic bands compared with SW480 and SW1116 cells, manifesting both additions and band-shifts.

CONCLUSIONTogether with hMSH2 and hMLH1, the status of a panel of microsatellite loci may be used as convenient predictors for drug-optimization or prognosis-assessment in colorectal cancer patients before chemotherapy.

Adaptor Proteins, Signal Transducing ; Antimetabolites, Antineoplastic ; pharmacology ; Base Pair Mismatch ; Carrier Proteins ; Colorectal Neoplasms ; drug therapy ; genetics ; pathology ; DNA Repair ; DNA-Binding Proteins ; Fluorouracil ; pharmacology ; Humans ; Immunohistochemistry ; Microsatellite Repeats ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; Neoplasm Proteins ; genetics ; Nuclear Proteins ; Polymerase Chain Reaction ; Proto-Oncogene Proteins ; genetics ; Tumor Cells, Cultured

Adult ; Chondrosarcoma ; metabolism ; pathology ; Collagen Type II ; metabolism ; Diagnosis, Differential ; Femoral Neoplasms ; metabolism ; pathology ; Giant Cells ; pathology ; Humans ; Male ; Osteoclasts ; pathology ; Osteosarcoma ; metabolism ; pathology ; S100 Proteins ; metabolism ; Vimentin ; metabolism

Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Dendritic Cell Sarcoma, Follicular ; metabolism ; pathology ; Dendritic Cell Sarcoma, Interdigitating ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Granuloma ; metabolism ; pathology ; surgery ; Head and Neck Neoplasms ; metabolism ; pathology ; surgery ; Humans ; Leukocyte Common Antigens ; metabolism ; Lymph Nodes ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Lymphoma, T-Cell ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasms, Multiple Primary ; metabolism ; pathology ; surgery ; Receptors, Cell Surface ; metabolism ; S100 Proteins ; metabolism ; Tonsillar Neoplasms ; metabolism ; pathology ; secondary

Calcium-Binding Proteins ; metabolism ; Diagnosis, Differential ; Female ; Fibroma ; metabolism ; pathology ; surgery ; Humans ; Inclusion Bodies ; pathology ; Infant ; Microfilament Proteins ; metabolism ; Skin Neoplasms ; metabolism ; pathology ; surgery ; Soft Tissue Neoplasms ; pathology ; Tendons ; pathology ; Toes ; Vimentin ; metabolism

Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Diagnosis, Differential ; Histiocytoma, Benign Fibrous ; metabolism ; pathology ; surgery ; Humans ; Male ; Middle Aged ; Neprilysin ; metabolism ; Receptors, Cell Surface ; metabolism ; Skin Neoplasms ; metabolism ; pathology ; surgery ; Thigh ; Vimentin ; metabolism

Objective To investigate the clinical efficacy and safety of the cytokine-induced killer cells (CIK) treated in patients with advanced pancreatic cancer. Methods 74 cases (hospitalized from January 2012 to December 2013) with advanced pancreatic cancer (Ⅲ ~ Ⅳ stage) were selected. The patients were randomly divided into two groups: CIK cells treated group (38 patients) and chemotherapy group (36 cases). Patients in CIK cells group received CIK cell infusion therapy , and patients in chemotherapy group received only gemcitabine. The efficacy and safety of all patients were observed. Results The efficacy rate of CIK cells group was 29.0%, with no statistical significance compared to chemotherapy alone group (16.7%). Disease control rate was 63.2%, with statistical significance compared to the chemotherapy group (38.9%). The PFS was 3 months (95%CI:2.5 ~ 3.5), OS 6.8 months (95%CI:6.1 ~ 7.5). 6-month survival rate 41.7%, with statistically significance compared to chemotherapy group. Conclusion CIK cells treated in patients with advanced pancreatic cancer is feasible and safe , and can improve disease control rate , improve immunity and produce clinical benefit in patients.