Objective To compare the effects of limited fluid resuscitation and aggressive fluid resuscitation in treatment of uncontrolled hemorrhagic traumatic shock,and to improve the cure rate.Methods One hundred and twenty patients with hemorrhagic traumatic shock on the basis of outpatient registration number of single and double were divided into limited fluid resuscitation group(limited group,56 cases) and aggressive fluid resuscitation group (positive group,64 cases),respectively.The preoperative blood lactic acid,base excess,prothrombin time,hemoglobin was compared and the preoperative infusion and the number of patients with death was recorded.Results The preoperative infusion in limited group was significantly less than that in positive group [(1 050 ± 212) ml vs.(2 120 ± 186) ml],the difference was statistically significant (P ＜ 0.01).The mortality rate in limited group was significantly lower than that in positive group [12.50％(7/56) vs.28.12％(18/64)],the difference was statistically significant (P＜ 0.05).The preoperative blood lactic acid,base excess,prothrombin time in limited group were significantly lower than those in positive group [(3.31 ± 0.29) mmol/L vs.(5.78 ± 0.15) mmol/L,(5.42 ± 1.13) mmol/L vs.(9.86 ± 1.21) mmol/L,(11.7 ± 1.9) s vs.(18.1 ± 1.7) s],and the hemoglobin in limited group was significantly higher than that in positive group [(96 ± 18) g/L vs.(83 ± 20) g/L],the differences were statistically significant (P ＜0.01).Conclusions If hemorrhage is not controlled,early limited fluid resuscitation can maintain blood perfusion of vital organs,alleviate acidosis,reduce mortality and creat good conditions for advanced treatment.Limited fluid resuscitation is superior to aggressive fluid resuscitation in operative intervention for patients with uncomtrolled hemorrhagic traumatic shock.

Objective To observe the effect of a specific T-cell induced by lysate-pulsed human dendrtic cells against pancreatic cancer(PC) cells . Methods Dendritic cells were amplified and purified from peripheral blood of PC patient and were pulsed with tumor cells.Then they were co-cultured with autologus T-cell in vitro and divided into lysate-pulsed DCs group, unplused DCs group, lysates group,and control group. The supernatants of every co-culture group were collected and the concentration of IL-12 and IFN-? were measured by ELISA. The capacity of DC induced proliferation of T-cells was tested.The specific cytolytic activity of CTL was assessed in a 4-hr 51 Cr-release assay. Results Difference in the concentration of IL-12 and IFN-? was statistically significant in lysate-pulsed DCs group(1161?239 pg/ml and 1044?312 pg/ml)than these in unplused DCs group and lysates group (P

In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6 weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of I(CaL) decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alpha1c, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant. It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes, which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.

According to the unique geographical conditions,climatic factors,human constitution,dietary custom,social environment and so on,the main etiology of exogenous cough in Lingnan areas is pathogenic dampness;and the main pathogenesis is phlegm-dampness internal retention and impaired and descending of lung.The syndrome of phlegm-dampness and syndrome of phlegm-heat are more common clinical types.We propose eliminating dampness and resolving phlegm,dispersing and descending lung qi as its main therapeutic methods.For chronic cough,it often have to take the therapeutic methods of strengthening spleen and nourishing lung.

Objective To investigate the effect and mechanism of decitabine (DAC) on the proliferation of human cholangiocarcinoma CCLP1 cells in vitro and in vivo.Methods After treated with various concentrations of DAC,cell growth inhibition rates were determined by CCK-8 assay.Cell cycle and cell apoptosis were analyzed by flow cytometry.Cell autophagy was observed under fluorescence microscope.The effect of DAC on the growth of cholangiocarcinoma in vivo was determined in a CCLP1 mice xenograft model.Results The proliferation rate of CCLP1 cells in the DAC-treated group decreased in a time-concentrated dependent manner.After treatment with DAC,the cell cycle of CCLP1 cells was arrested at the G2/M phase.The apoptosis rate was significantly higher in the treatment group over the control group.Cell autophagy was observed after treatment with DAC in CCLP1 cells.The tumor growth of implanted CCLP1 cells significantly slowed down after the mice were treated with 0.8 mg/kg DAC,6 times weekly for 2 weeks.Conclusion DAC can inhibit the proliferation of cholangiocarcinoma in vitro and in vivo.

Objective To study the role of protective antigen(PA)and N-terminal segment of lethal factor (LFn)in the entrance of EGFP(enhanced green fluorescent protein)into HeLa cells. Methods The DNA fragments encoding LFn and EGFP were amplified,respectively,and cloned into the plasmid pET-21 a(+)one after another to construct a recombinant plasmid pET-LFn-EGFP. The plasmid was txansformed into BL21 cells to express LFn-EGFP protein under the induction of IPTG. The protein was purified by Ni chelating chromatography. After incubation with LFn-EGFP in the presence of PA or not, the HeLa cells were analyzed by flow cytometry or laser confocal microscopy. Results The fusion protein LFn-EGFP was purified by over 90% homogeneity and retained the ability of LF to bind with PA when incubated with J774A.1 macrophage cells,and could get into HeLa cells. Conclusion The LFn-EGFP could enter the HeLa cells in a PA independent pathway. But PA could help more LFn-EGFP molecules enter into HeLa cells.

AIM: To study the preventive effects of Keningfang decoction on the experimental influenza virus pneumonia in mice and its mechanism. METHODS: Fifty NIH mice were divided into five groups randomly (ten mice in each group), normal control group, model group, virazole treatment group, Keningfang I treatment group, Keningfang II treatment group. The FM 1 virus strain that kept in frozen condition were revived and cultured in chick embryo. The mice in every group that were lightly anesthetized by aether, and infected by dropping FM 1 15 LD 50 into the nose, except for the normal control group, by equal volume distilled water. Mice were treated with drugs or distilled water two days before the model was made (0 3 mL, 2 times a day). The mice were treated with drug for six days, then was killed, the lungs were collected, and kept in -70 ℃. HSP70 was measured in the lung tissue by Western blot. Pathologic changes of the mice lungs were observed under microscope. RESULTS: Compared with the normal control group, HSP70 in the other groups were increased significantly (P

Objective:To compare the clinical efficacy of drug coated balloon (DCB) vs. plain old balloon (POB) on in-stent restenosis (ISR) of femoropopliteal artery occlusive disease of the lower limb. Methods:The clinical data of 91 ISR patients admitted at Shanxi Bethune Hospital from Jul 2016 to Dec 2017 were retrospectively analyzed. The primary patency rates were compared.Results:There were 43 patients treated with drug coated balloons and 48 patients treated with plain old balloons. The surgical procedure was successful in all cases, and the symptoms of lower limb ischemia were significantly improved after surgical procedure. The primary patency rate of patients who were treated by drug coated balloons was significantly higher than by plain old balloons at 12 months after surgery (83.7% vs. 62.5%, P<0.05). Conclusion:The use of drug coated balloons could acquire more satisfactory short-term clinical efficacy for ISR patients of femoropopliteal artery occlusive disease.

OBJECTIVETo clarify the relationship between the loss of expression of the deleted in pancreatic carcinoma locus 4 (DPC4) proteins and the pathogenesis of biliary tract carcinoma.

METHODS71 primary biliary tract carcinoma (BTCa), including 38 common bile duct (CBD) carcinomas, 18 gallbladder carcinomas, 15 hilar bile ducts (HBD) carcinomas were examined by immunohistochemical staining. In addition, the CBD carcinomas were divided into two groups: tumors with metastasis (M(+) group, 27 cases) and tumors without metastasis (M(-) group, 11 cases).

RESULTSThe frequency of loss of the expression of DPC4 protein was 32.8% in BTCa, 47.3% in CBD carcinoma, 11% in gallbladder carcinoma, 13% in HBD carcinoma. Comparison of the frequency of loss expression of DPC4 was significant statistical difference in CBD carcinoma versus gallbladder carcinoma and HBD carcinoma (P < 0.01). The frequency of loss expression of DPC4 was 48.1% in the M(+) group and 45.4% in the M(-) group.

CONCLUSIONThere are a close relationship between pathogenesis of BTCa and inactivation of DPC4 and different frequencies of DPC4 gene alternation in various locations of the biliary tract, which are not significantly increased with tumor metastasis in BTCa.

Myocardial fibrosis is a key link in the occurrence and development of diabetic cardiomyopathy. Its etiology is complex, and the effect of drugs is not good.Cardiomyocyte apoptosis is an important cause of myocardial fibrosis. The purpose of this study was to investigate the effect of gaseous signal molecule sulfur dioxide (SO2 ) on diabetic myocardial fibrosis and its internal regulatory mechanism. Masson and TUNEL staining, Western-blot, transmission electron microscopy, RT-qPCR, immunofluorescence staining, and flow cytometry were used in the study, and the interstitial collagen deposition, autophagy, apoptosis, and changes in phosphatidylinositol 3-kinase (PI3K)/AKT pathways were evaluated from in vivo and in vitro experiments. The results showed that diabetic myocardial fibrosis was accompanied by cardiomyocyte apoptosis and down-regulation of endogenous SO2 -producing enzyme aspartate aminotransferase (AAT)1/2 . However, exogenous SO2 donors could up-regulate AAT1/2 , reduce apoptosis of cardiomyocytes induced by diabetic rats or high glucose, inhibit phosphorylation of PI3K/AKT protein, up-regulate autophagy, and reduce interstitial collagen deposition. In conclusion, the results of this study suggest that the gaseous signal molecule SO2 can inhibit the PI3K/AKT pathway to promote cytoprotective autophagy and inhibit cardiomyocyte apoptosis to improve myocardial fibrosis in diabetic rats. The results of this study are expected to provide new targets and intervention strategies for the prevention and treatment of diabetic cardiomyopathy.