ObjectiveTo investigate the effect of early fluid resuscitation on the prognosis of SAP patients.MethodsPatients who were admitted to our hospital within 72 h after the onset of the SAP were enrolled.The parameters for the fluid resuscitation were as follow: heart rate ＜120 beat/h,urine output ≥ 1 ml ·h-1 · kg-1,hematocrit ≤35％ and mean arterial pressure 65 ～ 85 mmHg ( 1 mmHg =0.133 kPa).The effects of different time of reaching fluid resuscitation ( ＜48 h,48 -72 h,＞72 h) and parameters achieved (0 ～ 1parameter,2 parameters,3 parameters,4 parameters) on the prognosis were analyzed.ResultsThere were 70 patient enrolled in this study and 41 ( 58.6％ ) developed complications,20 ( 28.6％ ) were referred to surgical operation and 10( 14.3％ ) died.The median hospital stay was 23.5 d,and the median medical cost was 71.9(5.7～567.4 thousands RMB).The rates of surgical intervention in ＜48 h,48 ～72 h,＞72 h groups were 20.0％,33.3％,75.0％,and the rates of acute kidney injury were 20.0％,25.0％,75.0％,while the rates of complications were 50.0％,83.3％,100％,and the difference among the 3 groups was statistically significant (P ＜ 0.05 ).The rates of surgical intervention in patients achieving 0 ～ 1,2,3,4parameters within 48h of SAP onset were 50.0％,26.3％,13.0％,25.0％,and the rates of acute kidney injury were 45.0％,31.6％,17.4％,0,while the rates of ARDS were 35.0％,31.6％,13.0％,0,which showing a significant decreasing trend.ConclusionsAn appropriate fluid resuscitation in the first 48 h after the onset of SAP was benefit for improving the treatment effects and patients' outcome.

Severe acute pancreatitis (SAP) is a critical disease which has a high mortality. In order to make the diagnosis and treatment much more promptly, rationally and effectively, this article briefly introduces some methods for assessment of the severity and risk of SAP by clinical manifestation, risk factors,scoring systems, radiology and laboratory examinations.

Oxidative stress induced injury mediated by active oxygen radicals(AOR) is one of important pathophysiologic characteristics in critical illness such as severe trauma,shock,sepsis and pancreatitis.Large amounts of AOR can be generated and the function of antioxidant system will be severely compromised with the result of an imbalance between oxidative and anti oxidative.Supplementation with anti oxidant via nutrition supports may be an important way to reduce oxidative stress induced injury in critical care.But there are some problems such as the timing,methods,dosage,safety and effectiveness of this regime.

Objective: To evaluate the therapeutic effects of early enteral nutrition in the treatment of severe acute pancreatitis by nasojejunal tube.Methods: Forty-one cases of SAP were retrospectively analyzed and divided into 2 groups.There were 20 cases in conventional therapy group and 21 cases in enteral nutrition group.Major causes,treatments and clinical results were analyzed and APACHEⅡ score,CT score,serum albumin and prealbumin were compared between two groups.Results: Fortyone cases were cured and no one needed surgical intervention except six pateints with pseudocysts.EN cases were fed via a nasojejunal tube placed at the seventh day after admission.EN was well tolerated throughout the course of disease.The improvement of APACHEⅡ score of the EN group was significantly higher than that of conventional therapy group(P

The medical records of 197 patients on linezolid therapy were collected retrospectively.The prevalence and risk factors for linezolid-induced reduction of hemoglobin were identified.The incidence of linezolid-induced reduction of hemoglobin was 31.98％.The patients with reduction of hemoglobin had older age [(68 ± 14) vs.(59 ± 18) years,P =0.000] and lower creatinine clearance (CCr) [(72 ±42)vs.(98 ± 52) ml/min,P =0.000].Multivariate logistic regression analysis showed that age ≥65 years,treatment duration ≥ 15 days,CCr ＜ 65 ml/min and pre-treatment hemoglobin value ＜ 95 g/L were significant risk factors for linezolid-induced reduction of hemoglobin.

Objectives: To investigate the effect of butyrate, the by-products of diet fiber fermented in colon, on the apoptosis of human colon cancer cell and its mechanism for colon cancer prevention. Methods: The subculture of human colon cancer cell line SW1116 was cultured in medium without or with different concentration of butyrate(2、3、4、7 and 10 mmol/L). The cell proliferation rate and apoptosis were measured by MTT and flow cytometer or electro-microscopy respectively after 6、24、48 and 72 cultivation. Results: By the increasing of butyrate concentration and cell culture time, the proliferation of SW1116 cell was inhibited gradually with a highest rate of 59.19% during the study period. The percent of G 1 cell was increased gradually whereas the percent of S cell was decreased. The apoptosis rate of SW1116 was increased gradually with a highest rate of 30.62% at the same time. The ultrastructure of SW1116 cell was changed after butyrate was added to culture medium. Conclusions: Butyrate could not only inhibit the proliferation of colon cancer cell line but also induce it apoptosis.

Objective: To investigate the mechanism of butyrate,which is the by-products of diet fiber fermented in colon and induce the apoptosis of human colon cancer cell. Methods: The subculture of human colon cancer cell line SW1116 was cultured in medium with different concentration of butyrate(0、2 、3 、4、7 and 10 mmol/L).The mRNA and proteins of bcl-2 or bax in cell lines were detected respectively by RT-PCR and Western Blotting while the concentration of p53 protein and the activity of caspase-3 was detected by flow cytometer and fluorescent quantitative assay respectively after 6、24、48 and 72h cultivation.Results: There was no expression of bcl-2 mRNA and its protein in SW1116 cell during the study periods but the expression of bax mRNA and its protein,the p53 protein concentration and the caspase-3 activity increased gradually when the butyrate concentration was increased and the cultivation time was prolonged. Conclusion: By up-regulating the expression of bax mRNA and its protein,butyrate induce the apoptosis of colon cancer cell on a p53 dependent way.

Objective To detect genetic causes of idiopathic mental retardation/developmental delay in 20 male patients with epilepsy and to analyze their clinical characteristics of positive mutation carriers.Methods The families,consisted of the patient and his parents were recruited.Genomic DNA was extracted from peripheral blood,and candidate gene mutation screening was carried out by next-generation sequencing technology.Mutations in positive gene were verified by polymerase chain reaction(PCR) and direct sequencing.Results Three missense mutations were identified among 3 patients out of 20 cases,with a detection rate of 15％.They were:OPHN1 gene c.1996 C ＞ G,RAB39B gene c.542 C ＞ T and AFF2 gene c.427 A ＞ T,none of which had been reported before.All of these mutations were likely to be pathogenic based on gene function,evolutionary conservation,variant frequency in normal population (NHLBI Exome Sequencing Project and 1 000 Genomes),bioinformatics prediction and inheritance patterns.In addition,all 3 genes disrupted were residing on the X chromosome previously demonstrated to be associated with X-linked mental retardation(XLMR),indicating that they were probably pathogenic or might serve as one of the risk factors.Conclusions Abnormal function of genes on the X chromosomal is one of the most impotent causes of XLMR.X chromosomal gene mutation screening would be recommended for male children suffering from idiopathic mental retardation with epilepsy.

Aim To investigate the effect of urotensin Ⅱ on vascular calcification.Methods Calcified VSMCs of rat in vitro were induced by ?-glycerophosphate.Cellular calcium content,ALP activities,45Ca accumulation and osteocalcin content were measured.Results Compared with those of control group,calcium content,ALP activities,45Ca uptake and osteocalcin in calcified VSMCs increased greatly(P

Aim To investigate the effect of urotensin Ⅱ on vascular calcification.Methods Calcified VSMCs of rat in vitro were induced by β-glycerophosphate.Cellular calcium content,ALP activities,~(45)Ca accumulation and osteocalcin content were measured.Results Compared with those of control group,calcium content,ALP activities,~(45)Ca uptake and osteocalcin in calcified VSMCs increased greatly(P<0.01).Calcium content,ALP activities,~(45)Ca uptake and osteocalcin of calcified VSMCs stimulated by urotensin Ⅱ (10~(-10)、10~(-9) and 10~(-8) mol·L~(-1))were greatly increased in a concentration-dependent manner as compared with those of calcified group(P<0.01).Conclusion UrotensinⅡ aggravates the calcification of VSMCs induced by β-glycerophosphate.