Objective To investigate the effects of ulinastatin combined with octreotide in patients with severe acute pancreatitis TAP, SAA and serum inflammatory factors. Methods From February 2011 to September 2016,one hundred and seventy-eight patients with severe acute pancreatitis treated in the Second Affiliated Hospital of Hainan Medical University were enrolled in the study and were divided into the control group(81 cases) and observation group (97 cases). On the basis of routine treatment,the control group was treated with 0. 50 mg octreotide +0. 9% sodium chloride injection,continuous intravenous infusion at 20 mg/h, and 1 time /d,with a total of 3 d. On the basis of the control group,the observation group was given ulinastatin 100 thousand U+250 ml 0. 9% sodium chloride solution intravenous drip,2 times /d,with a total of 3 d. Before and after treatment,TAP,SAA and serum inflammatory factors in two groups were detected and analyzed. Results The levels of TAP,SAA,lipase and amylase in the observation group were (45. 21±9. 64) nmol/L,(458. 62 ±75. 41) mg/L, ( 14731. 7 ± 812. 5) U/L and ( 9341. 3 ± 831. 3) U/L respectively, compared with ( 26. 38 ±7. 13) nmol/L, ( 201. 23 ± 64. 31 ) mg/L, ( 10 321. 4 ± 762. 8) U/L and ( 5 416. 7 ± 306. 8) U/L after treatment. Before treatment,the control group were (43. 14±8. 53) nmol/L,(463. 71±62. 83) mg/L,(13826. 2 ±731.3) U/L and (9126.4±835.1) U/L,and the control group were (37.41±8.32) nmol/L,(316.42 ±68. 71) mg/L,(12 318. 5±797. 3) U/L and (7 423. 1±752. 3) U/L. After treatment,the two groups were lower than those before treatment (P＜0. 05),and the decrease was more obvious in the observation group after treatment. Compared with the control group,the difference was statistically significant ( P＜0. 05) . The level of calcitonin,C reactive protein and triglyceride in the observation group were ( 6. 04 ± 1. 25) ng/mL, ( 237. 3 ±13. 2) mg/L and ( 32. 18 ± 1. 32) mmol/L respectively before treatment. After treatment, they were ( 2. 37 ±0. 96) ng/mL,(48. 9±11. 2) mg/L and (12. 73±3. 61) mmol/L. Before treatment,the control group was (5. 72 ± 1. 43 ) ng/mL, ( 213. 1 ± 16. 2 ) mg/L, ( 30. 76 ± 1. 94 ) mmol/L and ( 5. 32 ± 1. 21 ) mmol/L, respectively. After treatment,they were (4. 21±1. 32) ng/mL,(156. 2±14. 7) mg/L and (24. 69±1. 26) mmol/L respectively. The levels of calcitonin,C reactive protein and triglyceride in the two groups were lower than those before treatment (P＜0. 05),and the decrease was more obvious in the observation group after treatment,and the difference was statistically significant compared with the control group. (P＜0. 05); tn the observation group,the levels of interleukin 6,interleukin 8,TNF - alpha,thromboxane and prostacyclin were (292. 48±19. 57) ng/L, (105. 52 ± 11. 41 ) ng/L, ( 4. 31 ± 0. 58 ) ng/L, ( 442. 16 ± 40. 23 ) ng/L and ( 167. 42 ± 12. 29 ) ng/L respectively.After treatment,they were (67.43±9.21) ng/L,(23.19±3.26) ng/L,(1.27±0.32) ng/L, (192. 20± 16. 89) ng/L and ( 364. 57 ± 27. 02) ng/L respectively. Before treatment, the control group was (278. 31±22. 49) ng/L,(113. 21±11. 45) ng/L,(4. 32±0. 48) ng/L,(428. 32±36. 54) ng/L and (159. 31 ±13. 42) ng/L,compared with (125. 74±16. 52) ng/L,(67. 21±7. 65) ng/L,(3. 16±0. 29) ng/L,(321. 46 ±25. 51) ng/L,(246. 73±20. 52) ng/L after treatment. After treatment,the levels of IL-6,IL-8,TNF-alpha and thromboxane in the two groups were all lower than those before the treatment ( P＜0. 05 ) . The levels of prostacyclin in the two groups were all higher than those before treatment ( P＜0. 05) . Conclusion Ulinastatin combined with octreotide in the treatment of severe acute pancreatitis can reduce the level of blood lipid,reduce inflammatory factors,reduce systemic inflammatory response, improve the patient's inhibition of inflammatory response and promote the balance of inflammatory reaction, and test the patient's TAP, SAA and serum inflammatory response factors to the diagnosis of SAP and the judgment of the disease,and have certain clinical guidance.

OBJECTIVE To investigate the mechanism of Yifei xuanfei jiangzhuo formula （YFXF） against vascular dementia （VD）. METHODS The differentially expressed genes of YFXF （YDEGs） were obtained by network pharmacology. High-risk genes were screened from YDEGs by using the nomogram model. The optimal machine learning models in generalized linear， support vector machine， extreme gradient boosting and random forest models were screened based on high-risk genes. VD model rats were established by bilateral common carotid artery occlusion， and were randomly divided into model group and YFXF group （12.18 g/kg， by the total amount of crude drugs）， and sham operation group was established additionally， with 6 rats in each group. The effects of YFXF on behavior （using escape latency and times of crossing platform as indexes）， histopathologic changes of cerebral cortex， and the expression of proteins related to the secreted phosphoprotein 1 （SPP1）/phosphoinositide 3-kinase （PI3K）/protein kinase B （aka Akt） signaling pathway and the mRNA expression of SPP1 in cerebral cortex of VD rats were evaluated. RESULTS A total of 6 YDEGs were obtained， among which SPP1， CCL2， HMOX1 and HSPB1 may be high-risk genes of VD. The generalized linear model based on high-risk genes had the highest prediction accuracy （area under the curve of 0.954）. Compared with the model group， YFXF could significantly shorten the escape latency of VD rats， significantly increase the times of crossing platform （P＜0.05）； improve the pathological damage of cerebral cortex， such as neuronal shrinkage and neuronal necrosis； significantly reduce the expressions of SPP1 protein and mRNA （P＜0.05）， while significantly increase the phosphorylation levels of PI3K and Akt （P＜0.05）. CONCLUSIONS VD high-risk genes SPP1， CCL2， HMOX1 and HSPB1 may be the important targets of YFXF. YFXF may play an anti-VD role by down-regulating the protein and mRNA expressions of SPP1 and activating PI3K/Akt signaling pathway.