Objective To improve the understanding of acute typhlitis.Methods all 5 cases of acute typhlitis from February 1999 to August 2001 were reviewed,5 cases were preoperatively misdiagnosed as acute appendicitis and subsequently performed emergency operations.Moreover,misdiagnosis was made intraoperatively as tumor in 2 cases,Crohn disease in 2 cases and diverticulitis in 1 case.Right hemicolectomy was performed in 4 cases;resection of necrotic mass and ileostomy was performed in 1 case.Results The pathologic change was acute non-specific inflammation of cecum in 5 cases.All cases recovered uneventfully.They are in good condition during the follow-up range 4 to 30 months.Conclusions The clinical manifestation of typhlitis was nonspecific.It was extremely difficult to diagnose preoperatively.Inflammatory mass of external lateral wall of cecum was characteristic finding of typhlitis during laparatomy.It is difficult to differentiate from tumor or Crohn disease at intraoperation.Right hemicolectomy was satisfactorily recommended.

Objective To summarize the experience in the diagnosis and treatment of traumatic spleen rupture.MethodsThe diagnosis and treatment of consecutive 293 patients with traumatic spleen rupture from January 1992 to October 2000 were reviewed.ResultsThe diagnosis was established by the history of injury, clinical presentations, diagnostic peritoneal punctures, abdominal ultrasonography and/or CT. The accuracy rate of diagnosis was 96 3% (282/293). Thirty one patients were treated nonoperatively and cured. Two hundred and fifty of 259 patients treated operatively were cured.Seven had postoperative complications with effusion in the splenic fossa.The total cure rate was 95 9%(281/293).Twelve patients died of uncontrolable hemorrhage or severe multiple injuries.ConclusionsSplenectomy for the treatment of traumatic spleen rupture is satisfactory.The morbidity and mortality of splenectomy are low.

Hyperlipidemia aggravates the pancreatitic injury in the course of severe acute pancreatitis.At present,the research on the pathogenesis has attracted wide attention though it has still not been fully clarified.In many theories of pathogenesis which explained the hyperlipidemic severe acute pancreatitis,the toxic effect of free fatty acids,the theory of accelerated activation of trypsinogen and the theory of pancreatic microcirculation disturbance were the dominant hypothesis.In recent years,concerns have also been raised over the theory of intestinal bacterial.translocation and the theory of calcium overload of pancreatic acinar cells.In this article,the author will review the recent advances in the pathogenesis of hyperlipidemic severe acute pancreatitis.

Objective To detect plasma K-ras gene mutation by using CED-RFLP/PCR to diagnose pancreatic cancer. Methods CED-RFLP/PCR technique was used to detect K-ras gene mutation in the plasma specimens of pancreatic cancer patients, patients with benign pancreatic diseases and healthy subjects. Results In pancreatic cancer patients the positive rate of plasma K-ras gene mutation was 73%, without false positivity, and higher than that in the pancreatic juice and duodenal juice, but lower than that in the fine-needle aspirates. Plasma K-ras gene mutation was not found in patients with benign pancreatic disease and healthy subjects. Conclusion The detection of plasma K-ras gene mutation by CED-RFLP/PCR is simple and effective, and could avoid the faults of other detection methods. It is helpful for the diagnosis and identification of pancreatic cancer.

Objective To investigate the relationship between continuous hyperglycemia and the progression of early acute pancreatitis (AP) Methods Five hundred and twelve AP patients were included in this study, in which 418 patients were mild acute pancreatitis (MAP) and 94 were severe acute pancretitis (SAP) Fasting blood sugar was determined and APACHE Ⅱ score was calculated on admission, 2nd and 3rd day of hospitalization respectively Serum tumor necrosis factor (TNF?) and C reaction protein (CRP) levels were determined on the 2nd day of hospitalization Results The incidence of hyperglycemia was higher in SAP patients than that in MAP patients (74 5% vs 25 8%, P =0 001) In SAP, APACHE Ⅱ score in continuous hyperglycemia group (CHG) was significantly higher than that of non continuous hyperglycemia group (NCHG) on admission, 2nd and 3rd day of hospitalization respectively (13?4 vs 11?3, P =0 017; 13?4 vs 11?3, P =0 010; 14?4 vs 10?4, P =0 010, respectively) Continuous hyperglycemia was related to the severity of SAP ( ? 2=7 77, P =0 005) Moreover, serum TNF? and CRP levels of the CHG were also markedly higher than that of NCHG (20?14 vs 14?11, P =0 019; 123?81 vs 93?55, P =0 036, respectively) Conclusion Continuous hyperglycemia might be a risk factor for the aggravation of early acute pancreatitis

Objective To study the effect of aquaporin 1 on intestinal capillary endothelial barrier in rats with experimental acute necrotizing pancreatitis (ANP).Methods In this study,160 male Sprague-Dawley rats were randomly divided into five groups:Control group ( n =32),ANP group (n =32),NS group,Dexamethasone group,and Acetazolamide group.Eight rats in each group were sacrificed at 3,6,12 and 18 h after induction of experimental models.Volume of ascites and levels of serum amylases were deternined at each time point.Pathological changes in intestine tissues were observed under electron microscope after HE staining.Capillary permeeabilities in intestine tissues were detected by Evans blue (EB) extravasation experiment.The mRNA and protein expressions of AQP1 in intestine tissue were determined by real-time PCR and Western blotting,respectively.Results Serum amylase level in ANP group was significantly higher than that in control group.Amylase level in dexamethasone group was lower than that in ANP group,and amylase level in acetazolamide group was higher than that in ANP group at 12 h (P ＜0.05 ) ; The concentration of EB in intestine tissues at each time point in ANP group was significantly higher than those in control group,and EB in dexamethasone group was lower than those in ANP group at 6,12 and 18 h.EB in acetazolamide group was higher than that in ANP group at 3 h ( P ＜ 0.05 ) ; The mRNA expression of AQPI in ANP group was significantly lower than that in control group.The expression of AQP1 in dexamethasone group was higher than those in ANP group at 6,12 and 18 h,and the expression of AQP1 in acetazolamide group was lower than that in ANP group at 3,6,12 h in intestine tissue ( P ＜ 0.05 ).Protein expression of AQPI in tissues in ANP group was significantly lower than that in control group.The expression of AQP1 in dexamethasone group increased more than that in ANP group at 3,6,12 h,and the expression of AQP1 in acetazolamide group was lower than that in ANP group at 3 h,6 h ( P ＜ 0.05 ).Conclusions The expression of AQP1 is down-regulated in intestine tissue in rats with acute necrotizing pancreatitis,and AQP1 could play an important role in the pathogenesis of capillary endothelial barrier dysfunction.

Objective To detect the expression of aquaporin 1 in pancreas of rats with acute necrotizing pancreatitis (ANP) and to study the effect of Dachengqi decoction on it.MethodsOne hundred and sixty male SD rats were randomly divided into control group ( C group,n =32 ),ANP group ( n =32),Dexamethasone group (De group,n =32),Acetazolamide group (A group,n =32) and Dachengqi decoction group (DD group,n =32).ANP model was induced by retrograde injection of 5％ sodium taurocholate into the biliary and pancreatic duct.Rats in De group received dexamethasone (4 mg/kg) intravenously after ANP induction; while rats in A group received 1 ml acetazolamide via gastric lavage 2 h before ANP induction; rats in DD group received 2 ml Dachengqi decoction via gastric lavage 48,24,2h before ANP induction; rats in C group received laparotomy.Eight rats in each group were sacrificed at 3 h,6 h,12 h and 18h after induction of ANP models.Quantity of ascites and levels of serum amylases were measured.Pathological changes in pancreas tissue were detected by HE and electron microscope.Capillary permeability in pancreas tissue was detected by Evans Blue (EB) extravasations method.AQP1 expression in pancreas tissue was detected by real-time PCR and Western blotting.ResultsLevels of serum amylase in ANP group was significantly higher,and the pancreatic injuries were obvious ; the levels of serum amylase in De group and DD group was lower than that in ANP group,and the pancreatic injuries were attenuated.The levels of serum amylase in A group were higher than that in ANP group,and the pancreatic.injuries were more severe than that in ANP group.Six hours after ANP induction,the levels of EB in pancreas were (13.44 ±2.56),(126.35 ± 14.80),(86.31 ± 14.46),( 108.99 ± 15.07 ),(78.29 ± 16.85 ) mg/L In C group,ANP group,De group,A group and DD group,and the expression of AQP1 mRNA in pancreatic tissue was ( 170.07 ± 22.48 ) ％,( 83.93 ± 8.98 ) ％,( 117.09 ±10.70 ) ％,( 69.00 ± 8.98 ) ％,( 112.82 ± 11.79 ) ％ ; and the expression of AQP1 protein was 0.23 ± 0.06,0.10 ±0.02,0.32 ±0.03,0.13 ±0.02,0.45 ±0.04.The content of EB in ANP group was higher than that in C group,while the expression of AQP1 mRNA and protein in ANP group was significantly lower than that in C group (P ＜ 0.05 ).The content of EB in De group and DD group was significantly lower than that in ANP group,while the expression of AQP1 mRNA and protein was significantly higher than that in ANP group (P ＜ 0.05).ConclusionsAQP1 plays an important role in the pathogenesis of capillary endothelial barrier dysfunction in rats with ANP.Dachengqi Decoction can attenuate pancreatic injuries of rats by regulating the expression of AQP1.

BACKGROUND:Shengjiyuhong ointment has been reported to inhibit hypertrophic scarring. OBJECTIVE:To verify the effects of Shengjiyuhong ointment on hypertrophic scarring of in a rabbit ear model. METHODS:Each ear of thirty-six Japanese rabbits was used to make four 1-cm-diameter circular ful-thickness skin wounds with the entire perichondrium removed. Final y, 288 wounds were made and randomly divided into 6 groups:model, negative control (no drugs were administered), low-, moderate-, high-crude herbal dose drugs (Shengjiyuhong ointment was administered topical y at concentrations of 8.39%, 25.18%, and 75.54%), and positive control (recombinant bovine basic fibroblast growth factor was administered topical y). Shengjiyuhong ointment was administered twice daily til wound healing. The wounds were evaluated by the Vancouver scar scale (VSS). Scar elevation index (SEI) of scar specimens was calculated under a microscope at 40× magnification. mRNA expression levels of type I and III col agen, connective tissue growth factor, fibronectin, andα-smooth muscle actin (α-SMA) were determined by fluorescent quantitative PCR. Protein expression levels of type I and III col agen andα-SMA were detected by western blot assay.α-SMA immunoreactivity was determined by immunofluorescent staining. RESULTS AND CONCLUSION:VSS scores and SEI were significantly increased in each group at 30 days (P<0.05). VSS scores and SEI were significantly decreased in the moderate-and high-crude herbal dose drug groups and positive control groups compared with the model, negative control, and low-crude herbal dose drug groups (P<0.05 or P<0.01). mRNA expression levels of type I and III col agen, connective tissue growth factor and fibronectin, and protein expression levels of type I and III col agen andα-SMA were significantly inhibited after moderate-crude herbal dose Shengjiyuhong ointment and positive drug treatment (P<0.01). These findings suggest that Shengjiyuhong ointment can reduce hypertrophic scars by inhibiting fibroblast proliferation and col agen deposition.

Objective: to observe the effects of Huanglian ointment promote wound healing and angiogenesis by the AKT/VEGF/eNos pathway in full-thickness skin defect mice. Methods: 7.5 mm diameter full-thickness skin excision modelwas made in the back of the 45 male C57 BL/6 J mice respectively. That were subsequently randomly placed into 3 groupswith Random number table method; i.e., vehicle, Huanglian ointment groups and the control group. In the Huanglianointment group, topical Huanglian ointment was applied to the wound, in the vehicle group were treated with vehicleointment, and in the control group were treated with nothing. Changes in the size of their wounds was monitored by takingpictures with a digital camera on days 0, 3, 7, 10, and 14 after wound creation. The mice were sacrificed on the 3, 7, and14 days after wound creation, and the tissue samples of the wounds were obtained for m RNA level of b FGF and PDGF、CD-31 cells and expression of AKT、VEGF-A、eNos were measured too. Results: Comparison of the sizes of the woundsamong the groups showed that there was no significant difference on the 0, 3 and 7 days, the most significant decreaseswere found in experimental Huanglian ointment group on the day10 (Huanglian ointment versus vehicle: (76±7) ％ VS (48±9) ％, huanglian ointment versus control: (76±7) ％ VS (46±7) ％, P＜0.01), and day14: (Huanglian ointment versus vehicle: (93±5) ％ VS (68 ±11) ％, huanglian ointment versus control: (93 ±5) ％ VS (64±9) ％, P＜0.01) . The percentage of CD-31 cells on the Huanglian ointment group were significantly higher than that of the vehicle and control groups on the 3、7 days, (Huanglian ointment versus vehicle: day3: (16.3±3.2) ％ VS (12.5±4.6) ％, P＜0.05;day7: (33.6±5.0) ％ VS (19.2±4.0) ％, P＜0.01; (Huanglian ointment versus control: day3: (16.3±3.2) ％ VS (8.4±2.4) ％, P＜0.05;day7: (33.6±5.0) ％ VS (17.8±6.0) ％, P＜ 0.01. The m RAN of b FGF on the Huanglian ointment group were significantly higher than the vehicleand control groups on the 3 and 7 days, (day3: Huanglian ointment versus vehicle: (1.75±0.22) VS (0.96±0.13), day7: (2.98±0.35) VS (1.53±0.24), P＜0.01) ); (day3: Huanglian ointment versus control (1.75±0.22) VS (0.78±0.24), and day7: (2.98 ± 0.35) VS (1.64 ± 0.31), P＜0.01) . But on 14 day, the vehicle and control groups were significantly higher thanHuanglian ointment group, Huanglian ointment versus vehicle (1.43±0.42) VS (1.88±0.38), Huanglian ointment versuscontrol (1.43±0.42) VS (2.03±0.21), P＜ 0.05. The m RAN of PDGF on the Huanglian ointment group were significantlyhigher than the vehicle and control groups on the 3、7 days, (day3: Huanglian ointment versus vehicle (1.04±0.28) VS (0.56±0.15), Huanglian ointment versus control (1.04±0.28) VS (0.67±0.20) (P＜0.01); day7: Huanglian ointment versusvehicle (1.82±0.25) VS (1.38±0.21), Huanglian ointment versus control (1.82±0.25) VS (1.45±0.26) (P＜0.05) . On the 7 day, the protein of P-AKTS308 and P-AKTS437 in wound tissue on the Huanglian ointment group were significantlyhigher than the vehicle and control groups, (P-AKTS308: Huanglian ointment versus vehicle: (0.45±0.04) VS (0.23±0.06), Huanglian ointment versus control: (0.45 ± 0.04) VS (0.19 ± 0.08), (P＜0.05); (P-AKTS437: Huanglian ointmentversus vehicle: (0.27±0.03) VS (0.16±0.04); Huanglian ointment versus control: (0.27±0.03) VS (0.20±0.05), (P＜0.01) .the protein of VEGF-A and e NOS on the Huanglian ointment group were significantly higher than the vehicle and controlgroups too, Huanglian ointment versus vehicle: (VEGF-A: (0.18±0.02) VS (0.26±0.04), P＜0.01, e NOS: (0.12±0.05) VS (0.14±0.07, P＜0.01) ); Huanglian ointment versus control: (VEGF-A: (0.18±0.02) VS (0.13±0.06), P＜0.01, e NOS: (0.12±0.05) VS ((0.17±0.03), (P＜0.01) ) . Conclusions: Huanglian ointment promotes wound healing and enhance b FGF, PDGFand VEGF-A content by increasing the angiogenesis with the AKT/VEGF/eNos pathway.

Objective: To investigate the role and molecular mechanism of miR-520d in reversing the chemoresistance of triple negative breast cancer (TNBC) by regulating autophagy. Methods: Docetaxel (Doc) resistant cell lines MDA-MB-231/Doc and MDA-MB468/Doc were constructed by using human TNBC cell lines MDA-MB-231 and MDA-MB-468 as parental cells, and the cells were divided into blank group (parental cells), control group (drug-resistant group), and miR-520d over-expression group. The expression levels of miR-520d in cells of the blank and drug-resistant groups were detected by qPCR. The Doc-sensitivity of resistant cells over-expressing miR-520d was detected by MTT assay.After MDC staining, the generation of autophagosome in cells was observed under fluorescence microscopy; the number of miR-520d over-expressed resistant cells with positive LC3 expression was observed under confocal microscopy. The luciferase reporter gene assay was used to verify the targeting relationship between miR-520d and Beclin1. The effect of miR-520d mimics on the expression of autophagy-associated protein Beclin1, and LC3Ⅰ, LC3Ⅱ in cells was detected by WB assay. Results: The results of qPCR showed that the expression of miR-520d in the drug-resistant TNBC cells was significantly lower than that of normal cells (P<0.01). In drug-resistant cells over-expressing miR-520d, the Doc-sensitivity was significantly improved, while the autophagy activity was significantly reduced (all P<0.01).At the same time, luciferase experiments demonstrated that Beclin1 was a possible target molecule of miR-520d (P<0.05). WB results showed that the combination of docetaxel and miR-520d mimics reduced the LC3-II/I ratio and the expression of autophagy protein Beclin1 in drug-resistant TNBC cells (all P<0.05). Conclusion: The regulation of miR-520d levels may alter the expression of autophagy protein Beclin1, thereby reversing Doc chemotherapy resistance in TNBC cells.