Objecltive To intensify the coordination and nursing in the operation room in order to prevent surgical site infection after gastrointestinal operation. Methods 337 medical history of patients received gastrointestinal operation and third rate healing from 1999 to 2006 were collected. A series of intensified measures were applied to surgical site infection from 2003 gradually, including invocation of new surgical handwashing method, modified skin disinfection manner, adoption of degreasing with ethanol first before disinfection with iodophor, placement of incision protector and clean bag for incision protection after entering abdomen, changing to use new gastrointestinal anastomofic thimerosal,standardization of operation order and clean manage-ment in operation room. The incidence rate of surgical site infection after gastrointestinal operation of patients from 1999 to 2002 and from 2003 to 2006 underwent χ2 test. Results The incidence rate of surgical site in-fection after gastrointestinal operation greatly decreased after adoption of intensified nursing intervention, Signifi-cant difference existed in rate of patients with third rate healing between the year 1999 to 2002 and 2003 to 2006. Conclusions Modified nursing intervention for surgical incision after gastrointestinal operation can de-crease incision infection rate evidently.

Objective To evaluate the changes of splanchnic hemodynamics after selective decongestive devascularization shunt of gustrosplenic region (SDDS-GSR) in the treatment of patients with portal hypertension. Methods All these 41 portal hypertensive patients underwent a combination surgery including partially occlusion of the splenic artery, Warren distal splenorenal shunt and devascularization. Postoperative patients were followed-up by ultrasonography for changes of splanchnic hemodynamics. Results were compared with that of 21 healthy volunteers. Results The thickness of spleen 2 weeks and 1 year after surgery (47±8) mm, (46±8) nun decreased from preoperative (60±9) mm (P<0.01). The diameter of portal vein (1.13±0.19) cm and splenic artery (0.49±0.08) cm 2 weeks after surgery decreased (P<0.05) and that of hepatic artery (0.40±0.07) cm increased (P<0.05). Patients' preoperative portal vein blood flow volume (1716±1262) ml/min and splenic artery (1269±570) ml/min were larger than that of normal group (P<0.05), while that of hepatic artery (321±126) ml/min was significantly less than that of normal group (P<0.05). The portal blood flow (649±294) ml/min and that of splenic artery (446±254) ml/min 2 weeks after surgery decreased significantly (P<0.01). The hepatic artery blood flow (612±295) ml/min increased significantly (P<0.01). When reevaluated at 1 year the hepatic artery blood flow (401±152) ml/min was not significantly different compared with that before surgery and that in normal group (P>0.05). Conclusions There are significant alterations in hepatic and splenic hemodynamics in patients with portal hypertension, and that SDDS-GSR can partially reverse the chaos of the hepatic and splenic hemodynamics in cirrhotic portal hypertensive patients.

This article analyzed, organizde, and summarized the specific meaning of yin and yang in Shang Han Lun, holding the idea that Zhongyang in Shang Han Lun contains fluid. YE Tian-shi's Tong Yang Bu Zai Wen Er Zai Li Xiao Bian is derived from Zhong jing method, and is more suitable to be used in damp-heat syndromes, reflecting that YE Tian-shi is not confined to traditional methods, but follows traditional prescriptions and flexible thoughts, which provides references for learning and flexibly applying prescription ideas.

A stable and reliable infected necrotizing pancreatitis (INP) model in rats was established in order to study the pathophysiological mechanism and pathological development rule of INP and explore the new therapeutic methods for the diseases. Forty-six SD rats were randomly divided into 5 groups. The animals in group A received the injection of 5% sodium taurocholate into the pancreatic duct and those in group B underwent that of E. coli into the pancreatic duct. The rats in groups C, D and E were subjected to the injection of 5% sodium taurocholate in combination with different concentrations of E. coli (10(3), 10(4), 10(5)/mL, respectively) into the pancreatic duct. The dose of injection was 0.1 mL/100 g and the velocity of injection was 0.2 mL/min in all the 5 groups. Eight h after the injection, the survival rate of animals was recorded and the surviving rats were killed to determine the serum content of amylase and perform pathological examination and germ cultivation of the pancreatic tissue. The results showed that acute necrotizing pancreatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct. The positive rate of germ cultivation in group A was 12.5%. The acute necrotizing pancreatitis model was not induced by injection of E. coli into the pancreatic duct and the positive rate of germ cultivation in group B was 0. The INP model was established in groups C to E. The positive rate of germ cultivation was 60%, 100% and 100% and 8-h survival rate 100%, 100% and 70% in groups C, D and E, respectively. It was concluded that a stable and reliable model of INP was established by injection of 5% sodium taurocholate in combination with 10(4)/mL E. coli into the pancreatic duct with a dose of 0.1 mL/100 g and a velocity of 0.2 mL/min. The pathogenesis of INP might be that the hemorrhage and necrosis of pancreatic tissue induced by sodium taurocholate results in weakness of pancreatic tissue in fighting against the germs. Meanwhile, the necrotic pancreatic tissue provides a good proliferative environment for the germs.
Cholagogues and Choleretics/*pharmacology ; Disease Models, Animal ; Escherichia coli/*metabolism ; Injections, Intraperitoneal ; Pancreas/enzymology ; Pancreas/microbiology ; Pancreatic Ducts/enzymology ; Pancreatic Ducts/microbiology ; Pancreatitis, Acute Necrotizing/*chemically induced ; Pancreatitis, Acute Necrotizing/*microbiology ; Rats, Sprague-Dawley ; Taurocholic Acid/*pharmacology ; Time Factors

A stable and reliable infected necrotizing pancreatitis (INP) model in rats was established in order to study the pathophysiological mechanism and pathological development rule of INP and explore the new therapeutic methods for the diseases. Forty-six SD rats were randomly divided into 5 groups. The animals in group A received the injection of 5% sodium taurocholate into the pancreatic duct and those in group B underwent that of E. Coli into the pancreatic duct. The rats in groups C, D and E were subjected to the injection of 5% sodium tanrocholate in combination with different con-centrations of E. Coli (103, 104, 105/mL, respectively) into the pancreatic duct. The dose of injection was 0.1 mL/100 g and the velocity of injection was 0.2 mL/min in all the 5 groups. Eight h after the injection, the survival rate of animals was recorded and the surviving rats were killed to determine the serum content of amylase and perform pathological examination and germ cultivation of the pancre-atic tissue. The results showed that acute necrotizing panereatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct. The positive rate of germ cultivation in group A was 12.5%. The acute necrotizing pancreatitis model was not induced by injection of E. Coli into the pan-creatic duct and the positive rate of germ cultivation in group B was 0. The INP model was estab-lished in groups C to E. The positive rate of germ cultivation was 60%, 100% and 100% and 8-h sur-vival rate 100%, 100% and 70% in groups C, D and E, respectively. It was concluded that a stable and reliable model of INP was established by injection of 5% sodium taurocholate in combination with 104/mL E. Coli into the pancreatic duct with a dose of 0.1 mL/100 g and a velocity of 0.2 mL/min. The pathogenesis of INP might he that the hemorrhage and necrosis of pancreatic tissue in-duced by sodium taurocholate results in weakness of pancreatic tissue in fighting against the germs.Meanwhile, the necrotic pancreatic tissue provides a good proliferative environment for the germs.

Objective:To analyze 12 antithrombins (AT) gene mutations that cause AT deficiency and discuss the relationship between the SERPINC1 gene. mutations and venous thrombotic events.Methods:This study belongs to case series of observational studies. Collected the clinical data of 12 AT deficiency cases in the First Affiliated Hospital of Wenzhou Medical University from April 2014 to April 2021 and collected the blood samples before treatment. The AT activity (AT: A) and AT antigen (AT: Ag) was detected by chromogenic substrate and immunoturbidimetry, respectively. The 7 exons and flanking sequences of the SERPINC1 gene were sequenced directly by PCR, the suspected mutations were validated by reverse sequencing. Analyzed the correlation between the SERPINC1 gene. mutations and venous thrombotic events and figured out the proportion.Results:The AT: A of the 12 patients all decreased significantly, ranging from 30% to 66%, and the AT: Ag of the 7 patients decreased accordingly, showing type Ⅰ AT deficiency, and the AT: Ag of the other 5 patients were normal, presented type Ⅱ AT deficiency. 12 mutations were found including 6 heterozygous mutations which were discovered for the first time: c.456_458delCTT(p.phe121del), c.318_319insT(p.Asn75stop), c.922G>T(p.Gly276Cys), c.938T>C (p.Met281Thr), c.1346T>A(p.Leu417Gln)and c.851T>C(p.Met252Thr). All 12 patients had venous thrombosis, and 3 cases including 2 compound heterozygotes and 1 single heterozygote all suffered from deep venous thrombosis (DVT) when they were younger without obvious triggers. The other 9 patients all combined with the other thrombotic factors including old age, hypertensive, smoking, pregnancy, and prolonged immobilization.Conclusion:Patients with AT deficiency caused by SERPINC1 gene defects are prone to venous thrombosis, especially combined with other thrombotic factors.