Objective To retrospectively investigate the cause of spontaneous rupture of the large intestine,pathology, diagnosis, treatment and prognosis of the relevant factors. Methods The collection of domestic medical records of 155 cases of spontaneous rupture of the large intestine in last decades,combined with 5 cases collected in our hospital since 2002. All the cases underwent emergency surgery confirmed the preoperative diagnosis of straight,colon rupture in 25 cases. Surgical repair for rupture in 5 cases,rupture of an external repair in 5 cases,rupture of the proximal colostomy repair combined with single or dual-chamber in 43 cases of ruptured bowel resection and anastomosis of the proximal intestine fistula combined with single or dual-chamber in 61 cases ruptured bowel resection stump of dual-chamber fistula in 6 cases, rupture of bowel resection and anastomosis in 5 cases, rupture of intestine directly fistula 9 cases. Surgical presentation in the remained cases were unknown. Results One hundred and seventeen patients cured, 43 cases died. Conclusions Most spontaneous colon rupture occurred in elderly patients,and is rare disease. The diagnosis rate is low and easy to delay in the treatment. Moreover, the intraabdominal infections caused by pollution would leed to a direct life-threatening toxic shock. Therefore, prompt diagnosis and timely surgery is important to improve the cure rate.

Objective Identify the arsenic and fluorin contents in coal from major producing coal mines in south of Shaanxi,providing a scientific foundation for the formulation of the prevention strategy.Methods In the 6 major coal mine areas governed by Ankang and Hanzhong city,the 62 mines with comparatively large production scales and sales locally,which may have some effective forces on the causing of the local arsenic and fluorin poisoning,were inveatigated,on-the-spot sampling are carried out,the fluorine in coal was determined by the combustion-hydrolysis/fluoride-ion selective electrode method and the arsenic in coal was determined by the atomic fluorescence.Results The maximum of the fluoride content in coal from the 62 investigated coal mines was 3 053.04 mg/kg,and the minimum was 6.58 mg/kg;the arithmetic mean was 1 034.30 mg/kg;the geometric mean was 656.85 mg/kg;The maximum of arsenic content in coal was 484.71mg/kg,and the minimum was 29.64 mg/kg;the arithmetic mean was 197.64 mg/kg,the geometric mean was 174.29 mg/kg.Conclusion The contents of fluoride and arsenic are seriously exceeded the standard limits in the 62 investigated coal mines,especially in stone coal mines.

Nowadays, tumor is one of the most challenging human health diseases, which oblige human tirelessly to studied for the tumor.Gene therapy is a promising treatment in oncotherapies. Suicide gene therapy is the most widely researched among gene therapies. At the same time, bystander effect take important role in the mechanism of suicide gene therapy. Therefore, more researchers devote themselves to studyinghow enhance the bystander effect in order to improve the effect of suicide gene therapy. This article reviewed in short how to augment bystander effect of suicide gene therapy against cancer.

Objective:To explore the cause and treatment of hemorrhage in laparoscopic cholecystectomy(LC).Methods:The clinical data of 112 cases of LC were analyzed to summarize the causes and treatment of hemorrhage.Results:The causes of hemorrhage in LC included subjective and objective elements.All of them were successfully hemostatic in different ways including reclamping,coagulation,suturing,packing hemostasis and suspension of falciform ligament of liver.Conclusion:Hemorrhage is the serious and most common complication in LC,but it can be avoided through an immediate and effective process.

Objective To assess the value of real-time myocardial contrast echocardiography (RTMCE) and intermittent triggered myocardial contrast echocardiography (ITMCE) in the detection of myocardial no-reflow phenomenon after reperfusion in acute myocardial infarction on mini-swine models. Methods Thirty close-chest mini-swines were used to create acute myocardial infarction and reperfusion model through interventional method. RTMCE and ITMCE were performed at baseline, 2 h after occlusion of left anterior descending coronary artery and 3 h after reperfusion. The myocardial perfusion defects after occlusion was measured as risk area (RA) and that after reperfusion was measured as no-reflow area (NRA). NRA/RA was calculated and compared with pathological findings. Results The whole study protocol was successfully performed in 27 mini-swines. NRA/RA obtained from RTMCE, ITMCE and pathological staining was (47.94±21.29)%, (38.20±21.04)% and (30.07±14.62)% , respectively. NRA/RA had no significant difference by ITMCE and pathological staining (P=0.124), RTMCE and ITMCE (P=0.071). The correlation coefficient of RTMCE and staining was 0.700 (P<0.001), ITMCE and staining was 0.765 (P<0.001), RTMCE and ITMCE was 0.897 (P<0.001). The sensitivity, specificity and accuracy in the detection of myocardial no-reflow was 100%, 58.33% and 79.17% for RTMCE, 91.67%, 73.33% and 81.48% for ITMCE. Conclusion Both RTMCE and ITMCE could be used as noninvasive methods to reveal the myocardial perfusion and quantitatively detect myocardial no-reflow after reperfusion therapy.

Objective To analyze the common reasons for misdiagnosis of atypical pulmonary embolism (APE) ,and to im‐prove the identification of APE .Methods The risk factors ,clinical manifestations ,laboratory examinations and radiographic data of 120 cases of APE diagnosed from January 2006 to December 2013 in the department of cardiovascular medicine and respiratory medicine of Xinqiao Hospital and the Affiliated Hospital of Luzhou Medical College were studied retrospectively .Results Among those 120 cases of APE ,39 cases were misdiagnosed on admission (32 .5% ) .8 cases were misdiagnosed as acute coronary syn‐drome ,7 cases as stable angina pectoris ,7 cases as chronic cor pulmonale ,5 cases as pneumonia ,3 cases as pleural effusion ,3 cases as tuberculosis ,3 cases as asthma ,1 case as atrial septal defect ,1 case as acute heart failure ,and 1 case as cardiogenic syncope .Con‐clusion APE is easy to be misdiagnosed for its non‐specific clinical manifestation .Pulmonary enhanced CT or CTPA should be car‐ried out in time for those highly suspected patients ,in order to reduce the misdiagnosis of APE .

Objective To observe the change of the protein and gene expression of hypoxia inducing factor-1α(HIF-1a) and vascular endothelial growth factor (VEGF) in the nude mouse tumor,which has been treated by HIFU combined with nanoscale ultrasound molecular probes with HSV1-TK gene microvascular density.Methods Sixty nude mice were implanted with HepG2 Cells to establish subcutaneous transplanted tumor.Divided this mice into six groups at random after treated by HIFU:MB+ HSV-TK+ GPC3 (group A),MB + HSV-TK (group B),HSV-TK +GPC3 (group C),HSV-TK (group D),MB + GPC3 (group E),PBS (group F).They were injected into the tail vein every after 3 days.Mice in group A,B,D and E were exposed to ultrasound by 2 W/cm2,1 MHz,5 mintues and 0.2 mL ganciclovi(GCV) was intraperitoneally injected at the first 48 hours after injection.After the treatment,immunohistoche were used to detect the microvascular density(MVD),Western blot and immunohistoche was employed to test the protein change of the VEGF and HIF-1α,Q-PCR was used to test the mRNA gene transcription of VEGF and HIF-1α in the tumor tissues.Results After 14 days,the protein expression of HIF-1α and VEGF in group A was significantly lower than that in group B,C,D,E and F (P＜0.05),the MVD level in the tumor is also like this,and the difference is statistically significant.Conclusion Anoscale ultrasound molecular probes with HSV1-TK can reduce the the level of VEGF,MVD and HIF-1α in the tumor which has been treated by HIFU,so it can inhibit tumor growth and improve the therapeutic efficacy after HIFU treatment.

AIM: To construct a recombinant adenovirus vector carrying AFP promoter to specifically express a targeting gene in hepatocellular carcinoma HepG2 cells. METHODS: Based on the Adeno-X~TM Expression system, the CMV promoter was replaced by a 300 bp a-fetoprotein promoter. The EGFP(enhanced green fluorescent protein) gene as a report gene was inserted to the multiple-cloning site(MCS). The normal liver LO2 cells, hepatocellular carcinoma HepG2 cells and HeLa cells were infected by the recombinant adenovirus, respectively. Northern blotting and fluorescence microscope were used to detect the transcription level of EGFP gene and its protein expression, respectively. RESULTS: Northern blotting showed that the target gene was markedly transcribed in HepG2 cells, but slightly in LO2 and HeLa cells. Under the fluorescence microscope, strong EGFP expression was seen in HepG2 cells but very weakly in HeLa and LO2 cells. CONCLUSION: Under the control of the 300 bp human AFP promoter, the target gene carried by the recombinant adenovirus was expressed in the AFP-producing HepG2 cells at a very high level, but not or very weakly in AFP negative cells. This adenovirus system can be used as a new, potent and specific approach for the gene-targeting therapy for the AFP producing primary hepatoma. [

AIM: To observe the changes of interleukin1 receptor associated kinase-4(IRAK-4) in ischemia/reperfusion(I/R) liver pretreated with lipopolysaccharide(LPS) and to explore the protective mechanisms of LPS pretreatment against hepatic I/R injury.METHODS: Male Sprague-Dawley rats,weighing 240-280 g,were divided into three groups: control,ischemia/reperfusion group(I/R group) and LPS-pretreated group(LPS group).On the first day,LPS group received 0.1 mg/kg LPS via the tail vein,followed by 0.5 mg/kg on the 2nd,3rd,4th and 5th day.I/R group received the equivalent volumes(0.5 mL) of sterile PBS.Experiments of I/R injury was induced by temporary ischemia of the left lateral liver lobe for 90 min followed by 3 h reperfusion on 2 days after the last LPS treatment.At 0 min,60 min and 180 min after reperfusion,the expression of IRAK-4 gene and protein level were determined by RT-PCR and Western blotting.The activity of NF-?B and the serum TNF-? level were also detected by ELISA.RESULTS: Although the level of IRAK-4 gene and protein were higher in the LPS group than that in I/R group and control group(P0.05) at 0 min after reperfusion.However,all those indexes were evidently lower in the LPS group than those in I/R group(P

Objective To explore the regulation mechanism of X box binding protein 1 (XBP1)signal transduction pathway for TNF-α and effective approach in ischemia/reperfusion (I/R) injury of liver transplantation for short hairpin RNA (shRNA) interference used to gene therapy in liver graft.Methods Male Sprague-Dawley rats were divided into three groups: the cold ischemia transfection group (CIT), the in vivo transfection group (IVT) and the control group. Experiments of orthotopic liver transplantation were performed by two cuff method. The rats in CIT were perfused with XBP1-shRNA plasmid (pSIXBP1) during cold ischemia phase, those in IVT received the equivalent volume (2 ml) of pSIIRAK 4 after portal vein inoculation, and those in the control group were not subjected to any treatment. Rats were killed at 60 or 180 min after restoring reperfusion of hepatic portal vein.Histopathological damage degree of graft liver was observed by light microscope. The expression levels of XBP1 gene and protein were detected by RT-PCR and Western blotting. The activities of NF-κB and the serum TNF-α level were detected by ELISA. Results All the indexes including the degree of histopathological damage, the expression levels of XBP1 mRNA and protein and the TNF-α level were significantly decreased in CIT as compared with IVT and control group (P＜0. 05). However,there was no significant difference in NF-κB activity among the three groups (P＞0. 05). Conclusion The role of XBP1 pathway in TNF-α gene regulation and that of NF-κB pathway in rat liver I/R injury are two relatively independent aspects, and the depression of XBP1 expression with XBP1 shRNA through portal vein perfusion during cold ischemia phase could effectively alleviate graft hepatic I/R