LI-cadherins are a new member of cadherin superfamily,which transmembrane glycoproteins mediate Ca2 + dependent cell-cell adhesion independent of cytoplasmic interactions.They play an pivotal role during tissue development and are critical for the maintenance of junctional complexes between cells and tissues,LI-cadherin high expression in hepatocellular carcinoma results in the decrease of intercellular adhesion effect,cause hepatocellular carcinoma metastasis.

Objective To detect the sequence of SLC29A1 gene rs1288 single nucleotide polymorphism (SNP) in advanced pancreatic cancer patients,and to explore its correlation with gemcitabine toxicity and prognosis.Methods Peripheral blood samples were collected and DNA was extracted.The segment containing SLC29A1 gene SNP (rs1288) was amplified by PCR,and then DNA sequencing was conducted to identify SLC29A1 gene SNP (rs1288).According to the sequencing results,the patients were divided into SLC29A1 gene rs1288 T→A mutation type group and wild type group.Clinical data,toxicity of gemcitabine chemotherapy,progression free survival (PFS) and overall survival (OS) between two groups were compared.Results A total of 83 pancreatic cancer patients were enrolled.Sequencing results showed that SLC29 A1 gene 1288 T→A mutation type was present in 52 patients and wide type was observed in 31 patients,so mutation rate was 62.7％.All the patients in both two groups could tolerate the gemcitabine toxicity,and no chemotherapy related death occurred.There were no statistical differences on the gender,age,CA19-9,tumor site,size and TNM stage between the two groups.There were statistically higher iucidences of leukopenia and thrombocytopenia in the SLC29A1 gene rs1288 T →A mutation type group compared to the wild type group (55.8％ vs 32.3％,P＜0.05;40.4％ vs 19.4％,both P＜0.05).Median OS and PFS in mutation type group were shorter than those in wide type group (11 months vs 14 months,P ＜ 0.05;9 months vs 12 months,P ＜ 0.05).Conclusions Advanced pancreatic cancer patients with the SLC29A1 gene rs1288 T→A mutation type had a higher incidence of adverse reaction in gemcitabine chemotherapy and a worse therapeutic effect,and thus detecting the mutation of SLC29A1 gene rs1288 point mutation may serve as a marker for evaluating the toxicity and prognosis of gemcitabine chemotherapy in patients with pancreatic cancer.

Objective To observe the inhibition of amikacin in vitro on platelet aggregation and blood coagulation tests, and to study its effects on hemostasis and the related mechanisms.Methods Plateletrich plasma and platelet-poor plasma from donors were mixed with different concentration of amikacin, which was divided into four groups:0 mg/L, 30 mg/L, 91 mg/L and 910 mg/L group.The maximial ratio of platelet aggregation induced by ADP were measured with Platelet Aggregation Analyzer.The expression levels of P-selectin, GP Ⅱ b/Ⅲ a and Fg-R were determined with Flow Cytometer.The PT, APTT, TT and Fg of platelet-poor plasma were detected with Blood Coagulation Analyzer. The four concentration of amikacin mentioned above and two anticoagulants (62.5 U/ml of sodium heparin and 109 mmol/L of sodium citrate)were interacted with fresh whole blood, in which the blood CT and plasma Ca2+ were detected. Blood samples were collected from 10 patients with acute lower respiratory tract infection before and 30 minutes after routine amikcin treatment respectively.The maximial ratio of platelet aggregation, the expression levels of P-selectin, GPⅡ b/Ⅲa and Fg-R induced by ADP were measured; while PT, APTT, CT and plasma Ca2+ were determined.Results At 30 mg/L of amikacin group, the maximal ratios of platelet aggregation (65.8±3.9)%, the expression levels of P-selectin (9.2 ± 1.0)% and Fg-R (12.6 ± 1.7)% were statistically lower than those [(88.0 ±4.6%, (16.1 ± 1.3)% and (31.0 ±2.5)%]at 0 mg/L of amikacin group ( t = 9.442,8.432,9.993,P ＜ 0.01 ).At 30 mg/L of amikacin group, the APTT (80.5 ±6.8) s and CT ( 857 ± 66) s were significantly higher than those [(33.0 ± 3.6) s and (447 ± 35 ) s] at 0 mg/L of amikacin group ( t = 11.312, 13.211, P ＜ 0.01 ). There was a negative correlation between amikacin concentration and maximial ratio of platelet aggregation ( r = - 0.832, P ＜ 0.05 ), but a positive correlation between amikacin concentration and inhibitory rates of platelet aggregation ( r = 0.939, P ＜0.05) was observed, as well as APTT (r ＞0.870, P＜0.05).At 30 mg/L, 91 mg/L, and 910 mg/L of amikacin groups, the P-selectin and Fg-R expression were remarkably inhibited with a dose-dependent manner, the CT was notably enhanced [Fwithin subjects =21.44, 26.24, ( ＞29.81 ), P ＜0.01].At 0 mg/L,30 mg/L, 91 mg/L and 910 mg/L of amikacin groups, the PT values were ( 14.7 ± 1.9) s, ( 15.2 ± 1.7) s,(15.6±1.5) s and (22.1 ±2.1) s, respectively (F=8.21,P＜0.05), but there was no markeddifference for the levels of GP Ⅱ b/Ⅲ a, TT, Fg and plasma Ca2+ among the four groups ( P ＞ 0.05 ).After 30 minutes of amikacin treatment, the maximial ratio of platelet aggregation (51.6 ± 10.1)%, the expression levels of P-selectin (6.8 ± 1.8) % and Fg-R ( 20.1 ± 5.8 ) % were significantly lower than those [(66.8 ± 11.4)%, ( 10.9 ±3.1 )% and (28.5 ±7.4)%] before amikacin treatment, but APTT (49.8 ±5.9) s and CT (660 ±59) s were remarkably higher than those [(26.9 ±3.8) s and (410 ±45) s] before amikacin treatment, respectively ( t = 5.456,8.875,7.423,10.012,11.322, P ＜ 0.01 ), while the GP Ⅱ b/Ⅲ a expression, PT and Ca2+ concentration had no significant changes ( P ＞ 0.05).Conclusions There are inhibitory effects of amikacin on platelet aggregation mainly through the inhibition of both fibrinogen receptor activation and secretion reaction of activated platelet. Amikacin may also inhibit pathway of coagulation system factor to prevent blood coagulation.Therefore, risk of hemorrhage may be investigated in the patients with amikacin for anti-infection treatment.

Objective To investigate the energy expenditure of mechanically ventilated patients,compare the measured energy expenditure (MREE) with the energy expenditure expected from the Harris-Benedict equation adjusted with correction factors (PREE). Methods Twenty-four critically ill adult patients who were mechanically ventilated in the intensive care unit were enrolled in this study. Data during the 72 hours of mechanical ventilation were collected for computation of severity of illness. Resting energy expenditures were derived at 72hours after mechanical ventilation by indirect calorimetry. Predicted basal energy expenditure was obtained at the same time using the Harris-Benedict equation and predicted resting energy expenditure was calculated using the Harris-Benedict value adjusted with correction factors for illness. Results The Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ)scores and Marshall scores were 14 ± 5 and 6 ± 3, respectively. MREE and PREE were (6 793.64 ± 1 197.15) and (8 041.02 ± 1 971.54) kJ/day, respectively. There was no correlation between MREE and PREE (r2 = 0. 28, P = 0. 07), and the difference between MREE and PREE was statistically significant (t = 7.62, P = 0.04). No statistically significant correlations were observed between both MREE or PREE and APACHE Ⅱ score or Marshall score (r2 = 0. 14, P = 0. 08; r2= 0. 08, P = 0. 63; r2 = 0. 05, P =0. 65; r2 = 0.03, P = 0. 87, respectively). Conclusions In mechanically ventilated patients, the energy expenditure is not correlated with the severity of illness. The Harris-Benedict prediction modified with correction factors for severity of illness systematically overestimates the total energy expenditure.

event and treat circular,respiratory and renal insufficiency.

Objective To investigate the relative factors of insulin resistance(IR)during elective abdominal surgery and the mechanism of IR induced by surgery.Methods Fourteen patients underging elective abdominal surgery were studied.Fasting blood glucose(FBG),fasting plasma insulin(FPI),plasma TNF-α,IL-6 and CRP were tested for elective surgery patients on the day before,during operation and on one day after surgery.Insulin resistance index(HOMA-IR)and the index of insulin secretion(HOMA-β)were ealculated with homeostasis model assessment(HOMA).Insulin receptor and GLUT4 mRNA expression in skeletal muscle were assessed before operation and at the end of operation by use of RT-PCR.Results Significant differences were found in fasting blood glucose (5.95±1.08)mmol/L vs(8.92±2.41)mmol/L,fasting plasma insulin(19.95±3.33)mU/L vs(25.44±5.36)mU/L,IL-6(33.98±5.01)ng/L vs(45.29±7.81)ng/L and plasma TNF-α(86.70±9.27)ng/L vs(114.46±15.33)ng/L during and after operation(P＜0.01).A significant elevation of HOMA-IR levels was found after operation compared with that before operation[(9.59±2.89)vs(4.111.86)](P＜0.001).However there wag no significant difference in HOMA-β among three points(groups)of time(P=0.103).The result of RT-PCR showed that the expression of GLUT4 in muscle of patients at the end of operation reduced significantly compared with preoperation(t=12.488,P＜0.001)but there was no significance in INSR mRNA expression(P=0.165).ISI showed negative correlation with opermive time(r=-0.736、P＜0.001),blooding during operating (r=-0.594、P=0.032)and post-operative TNF-α(r=-0.641、P=0.018).Conclusion Insulin resistance occurs in elective abdominal surgery patients.The defective site is at postreceptor.To shorten the operation time,control the intensity of surgery and reduce the bleeding is helpful for decreasing IR.

Objective To summarize clinical characteristics and experiences in treatment of severe hyperlipidemic pancreatitis (SHLP). Methods A retrospective analysis for 22 cases of SHLP and 91 cases of severe acute biliary pancreatitis (SABP) hospitalized during January 1, 2000 to December 31, 2006 was carried out to compare their clinical characteristics and treatment outcomes. Results Activities of serum and urine amylase in SHLP patients at admission were (715 ± 99) and (382 ± 56) U/L, respectively, significantly lower than those in SABP patients (1551 ± 107) and (773 ± 66) U/L, respectively (P < 0.01). About 55% (12/22) of SHLP patients had pulmonary infection, 36% (8/22) with circulatory failure, 41% (9/22) with respiratory failure and 23 % (5/22) with renal failure, all significantly higher than those in SABP patients SABP [32% (29/91), 14% (13/91), 7% (6/91) and 5% (5/91), respectively, P < 0.01]. Two died of SHLP and 11 of SABP, respectively. Conclusions In diagnosis of SHLP, it should be noticed that no remarkable elevation of activities in serum and urine amylase usually, so during the course of treatment for SHLP, it is important to prevent and treat multi-organ failure, respiratory failure and renal failure in an active way.

Objective To compare the clinical characteristics and the outcomes of severe hyperlipidemic pancreatitis (SHLP) and severe acute gallstone pancreatitis (SAGP).Methods The clinical data of 22 patients with SHLP and 91 patients with SAGP admitted from January 2009 to December 2015 were retrospectively reviewed.The clinical manifestations,laboratory tests,organ dysfunction,medical treatment,complications and outcomes in 30 d after admission were analyzed and compared between two groups of patients.Results There were 16 males and 6 females with a mean age of (60.5 ± 9.1) years in SHLP group;while 32 males and 59 females with a mean age of (54.3 ± 5.4) years in SAGP group.The blood and urine amylase levels in SHLP group were significantly lower than those in SAGP group [(715 ±99) U/L vs.(1 551 ± 107) U/L,t =4.65,P =0.00;(382 ±56) U/L vs.(773 ± 66) U/L,t =4.52,P =0.00,respectively].The incidence of circulation insufficiency,respiratory insufficiency,renal dysfunction,and long-term puhnonary infection in SHAP patients was significantly higher than that in SAGP patients [36 ％ (8/22) vs.14 ％ (13/91),x2 =5.22,P =0.01;41％ (9/22) vs.7 ％ (6/91),x2 =9.46,P =0.01;23％(51/22) vs.5％ (5/91),x2 =4.20,P=0.03;55％(12/22) vs.32％ (29/91),x2 =7.02,P =0.01].Two cases died in the SHLP group and 9 cases died in SAGP group due to critical infection,cardiac events and bleeding.Conclusion Compared to SAGP patients,the blood and urine amylase levels are usually not remarkably high in SHLP patients,and the prevention and management of multi-organ failure and lung infection are more important for SHLP patients.

Objective To observe the in vitro inhibitory effects of brucea javanica oil on human washed platelet and explore the possible mechanism.Methods Human washed platelets were mixed withdifferent concentration of brucea javanica oil which were divided into four groups[untreated control group,negative control group,9.0% of brucea javanica oil group,and 22.5%of brueea javanica oil group].The maximal ratio of platelet aggregation induced by adenosine liphosphate(ADP),arachidonic acid(AA),collagen,and thrombin,respectively,was measured with platelet aggregation analyzer.The expressions of fibrinogen receptor(FIB-R)and P-selectin(CD_(62p))on external membrane of activated platelet were determinated with flow cytometry.The F-actin of cytoskeletal structure in activated platelet was detected by SDS-PAGE.Results At 9.0% of brucea javanica oil,the maximal ratio of platelet aggregation[(57.7±4.0)%,(62.2±3.9)%,(66.9±5.0)%and(71.8±5.1)%]induced by ADP,AA,collagen,and thrombin,was significantly lower than that[(75.3±4.1)%,(79.3±4.8)%,(80.6±5.4)%,(84.1±6.2)%]at negative control(0% of brucea javanica oil)(P<0.01),but makedly higher than that[(39.2±3.5)%,(45.8±3.4)%,(51.2±3.9)%and(56.7±4.8%)]at 22.5%,respectively(P<0.01).The inhibitory rate of platelet aggregation(47.9%,42.2%,36.5%and 32.6%)at 22.5%of brucea javanica oil was notably higher than that(23.4%,21.6%,17.0%and 14.6%)at 9.0%,respectively(P<0.001).There was a negative correlation between brucea javanica oil concentration and the aggregation ratio of platelet stimulated by the four agonists,respectively(r=-0.952,-0.961,-0.970,-0.975,P<0.001).At 9.0% of brucea javanica oil,the expression levels of FIB-R[(64.7±4.0)%]and CD_(62p) [(3.91±0.21)%] of platelet activated by ADP were significantly lower than that[(85.5±4.6)%and (5.05±0.27)%]at negative control,but remarkably higher than that[(36.2±3.9)%and(2.34±0.15)%]at 22.5%,respectively(P<0.01).There was a much higher inhibitory rate of platelet aggregation(57.7%)at 22.5%than that(24.3%)at 9.0%(P<0.01).The ratios(1.68±0.10 and 1.77±0.12)of F-actin photodensity at 22.5%and 9.0%to that in blank control were significantly lower than that(2.22±0.15)at negative control(P<0.01)but there was no statistical difference between the ratios in the group of 9.0%and 22.5%brucea javanica(P>0.05).Conclusions brucea javanica oil has special inhibitory effect on activated platelet and thrombosis in a dose-dependent manner.The mechanism is to inhibit the expression of fibrinogen receptor on external membrane of activated platelet,which is also related to the inhibition of F-actin and secretion of platelet.

Objective To study the role of low-dose glucocorticoids in improving prognosis and adjusting septic shock. Methods A total of 46 patients with a confirmed diagnosis of septic shock were retrospaetivley analyzed. 24 patients without glucocorticoids treatment were taken as control group; 22 patients with glucocorticoids as therapy group (n = 22). The two group received standard treatment for septic shock. Results The percentage of shock reversal on day 7 was higher in therapy group than that in control group (P <0.05). However,there were notstatistical significances in the duration of mechanical ventilation, the length of ICU stay, the incidence of multiple or-gan dysfunction syndrome (MODS) and mortality between the two groups (P > 0.05). Conclusion Low-dose glucocorticoids can effectively accelerate refractory septic shock reversal and vasopreasor withdrawal. This seems to be related to the reduced production of CRP but the beneficial effects of low-dose steroids regimens on long-term outcome have not yet be determined.