Pancreatic acinar cell death modality is a significant factor which determines the course and prognosis of acute pancreatitis (AP).The severity of AP is positively correlated with acinar necrosis,while negatively correlated with acinar apoptosis.Adenosine triphosphate (ATP) level is the key to control the manner of death,and acts as a switch during the conversion of necrosis and apoptosis in a variety of pathophysiological settings:low levels of ATP can accelerate cell necrosis and high levels of ATP might promote apoptosis.Hypoxia inducible factor 1 (HIF-1) is a highly expressed transcription factor in anoxic conditions which can effectively regulate cell energy metabolism and play an important role in regulating cell death and inflammatory injury.Therefore,this review aimed to provide a reference about better understanding of the pathogenesis and new therapeutic targets of HIF-1 in AP.

The onset of acute pancreatitis (AP) is a complex pathophysiological process mediated by multifactors which are not only interdependent but also influencing each other.So far,the specific molecular mechanism remains uncertain.Autophagy widely exists in a variety of vital phenomena in eukaryotes including the growth,development and pathophysiological progression of normal cells.Autophagy plays an important role in the early damage of acinar cells as well as the development of AP.However,the mechanism is still in doubt.Thus,we overviewed the role of autophagy in the occurrence and progression of AP in order to further enrich the understanding on the pathogenesis.

Borderline resectable pancreatic cancer (BRPC),characterized by low resectability rate and high postoperative recurrence rate,is a special kind of pancreatic cancer between resectable type and nonresectable one.Currently,the efficacy of neoadjuvant therapy for BRPC has become a hot topic in the field of pancreatic cancer.Although neoadjuvant therapy plays a critical role in obviously improving the R0 resectability rate and survival status of BRPC patients,the normalized therapeutic regimen has not been established.In this article,we overviewed the recent progress on the neoadjuvant therapy in treating BRPC.

Obesity is an independent risk factor for acute pancreatitis (AP),and the morbidity risk and severity of AP in obese patients were significantly increased than those in non-obese patients.However,the exact mechanism has not been fully elucidated.In recent years,the researches on the role of adipose tissue (AT) in AP have gradually attracted wide attention of scholars both at home and abroad.To better understand the pathogenesis and new therapeutic targets of AP,in this paper,we overviewed the recent research progress on the role of AT in AP.

Recurrent pancreatitis ( RP) can be further divided into two items , including recurrent acute pancreatitis ( RAP ) and recurrent chronic pancreatitis ( RCP ) .In recent years, with the rising incidence of pancreatitis , the incidence of RP has also been increased .During the development of pancre-atic diseases, RP may serve as a transitional disease .Thus, this article reviewed the latest research progress on RP in order to discuss its role in the development of the related pancreatic di-seases and the effects on clinical prognosis , and provide a refe-rence for preventing and treating RP and even cancer .

Objective To investigate the effects of biatrial infusion on pulmonary artery pressure (PAP)after cardiopulmonary bypass (CPB) in patients undergoing mitral valve replacement.Methods Twenty NYHA Ⅱ or Ⅲ patients aged 22-53 yr weighing 34-57 kg undergoing mitral valve replacement complicated by pulmonary hypertension (mean pulmonary artery pressure (MPAP) ＞ 50 mm Hg) were randomly divided into 2 groups ( n = 10 each): infusion via right atrium group (group R) and infusion via both atria group (group B). After induction of anesthesia, a three cavity floating Swan-Ganz catheter was placed via right internal jugular vein to monitor CVP,PAP, pulmonary capillary wedge pressure (PCWP) and CO. The patients received infusion of prostaglandin E1 30-150 ng· kg- 1 · min - 1 and phenylephrine 0.2-0.6 μg· kg- 1 · min- 1 via central veins in group R and infusion of prostaglandin E1 30-150 ng·kg-1 ·min-1 via central veins and phenylephrine 0.2-0.6 μg·kg-1 ·min-1 via left atrium in group B. MAP, HR, MPAP, PCWP, CVP and CO were recorded 5 min before administration (T0), and 5,10, 30 and 60 min after administration (T1-4). Pulmonary vascular resistance index (PVRI), systemic vascular resistance index (SVRI) and CI were also calculated. Results D:\1111111111\MDB\zhmzxzz98201008.mdbCompared with the value at T0, MAP, MPAP, PCWP and PVRI were significantly decreased, while CI was increased at T1-4 in group R, and MAP, CI and SVRI were significantly increased, while HR, MPAP, PCWP, CVP and PVRI decreased at T1-4 in group B ( P ＜ 0.05).MAP, CI and SVRI were significantly higher, while HR, MPAP, PCWP, PVRI and CVP lower in group B than in group R ( P ＜ 0.05). Conclusion Biatrial infusion can effectively reduce PAP and pulmonary vascular resistance after CPB in patients undergoing mitral valve replacement.

OBJECTIVE: To study on the expression and significance of MMP-2 and MMP-9 in the nasus epithelial carcinoma and their signification. METHOD: Fifty cases of epithelial carcinoma tissue and 50 cases of normal nasus tissue were detected for MMP-2 and 9 by immunohistochemistry technique (SP), and analysed their relationships between expression of MMP-and some clinical symptoms. RESULT: The positive ratio of expression of MMP-2 in 50 cases of epithelial carcinoma was 52.0% (26/50), which was significantly higher than those in the normal nasus tissue 28.0% (14/50), P < 0.05. The positive ratio of expression of MMP-9 in 50 cases of epithelial carcinoma was 58.0% (29/50), which was significantly higher than those in the normal nasus tissue 10.0% (5/50), P < 0.05. CONCLUSION It was suggested that there was a close relationship between pathogenesis and development of nasus epithelial carcinoma and the expression of MMP-2, MMP-9 in the epithelial carcinoma tissues. The positive results of MMP-2, MMP-9 is partly valid for diagnosis of prognosis rate of MMP-2 and MMP-9 expression was high in nasus epithelial carcinoma tissues, MMP-2 and MMP-9 expression levels might be able to provide prognostic information.
Carcinoma, Squamous Cell ; diagnosis ; metabolism ; pathology ; Female ; Humans ; Lymphatic Metastasis ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Prognosis ; Uterine Neoplasms ; diagnosis ; metabolism ; pathology

Objective To investigate the inhibitory effect and molecular mechanism of Huaier granule on the growth of sorafenib resistant hepatocellular carcinoma(HCC)cells.Methods The gradient concentration of Huaier granule was used to treat HCC cells,and the effect of Huaier granule on the proliferation,migration and invasion of sorafenib resistant HCC cells was analyzed.Bioinformat-ics methods were used to analyze the possible interaction between microRNA-31-5p(miR-31-5p)and sprouty-related proteins with an EVH1 domain 1(SPRED1).The expression levels of miR-31-5p and SPRED1 in HCC cells were detected by real time fluorescence quantitative polymerase chain reaction(qRT-PCR);cell viability,proliferation,migration,invasion and apoptosis were detected by CCK-8,colony formation,scratch healing,Transwell and flow cytometry;RNA immunoprecipitation(RIP)as-say and dual luciferase assay were used to verify the binding relationship between miR-31-5p and SPRED1.Results Huaier granule could significantly inhibit the proliferation,migration and invasion of sorafenib resistant HCC cells,and induce apoptosis.Bioinformatics analysis showed that miR-31-5p was highly expressed in HCC,and Huaier granule was able to down-regulate the expression of miR-31-5p,inhibit the proliferation and metastasis of sorafenib resistant HCC cells,and induce apoptosis;miR-31-5p showed a targeted inhibition effect on the expression of SPRED1.SPRED1 was down-regulated in HCC,and overexpression of SPRED1 was able to reverse the promoting effect of overexpression of miR-31-5p on proliferation and metastasis of sorafenib resistant HCC.Conclusion Huaier granule can inhibit sorafenib resistant HCC metastasis through the miR-31-5p/SPRED1 axis,indicating that Huaier granule has the potential to be used as a novel drug for HCC treatment.

Objective To investigate the inhibitory effect and molecular mechanism of Huaier granule on the growth of sorafenib resistant hepatocellular carcinoma(HCC)cells.Methods The gradient concentration of Huaier granule was used to treat HCC cells,and the effect of Huaier granule on the proliferation,migration and invasion of sorafenib resistant HCC cells was analyzed.Bioinformat-ics methods were used to analyze the possible interaction between microRNA-31-5p(miR-31-5p)and sprouty-related proteins with an EVH1 domain 1(SPRED1).The expression levels of miR-31-5p and SPRED1 in HCC cells were detected by real time fluorescence quantitative polymerase chain reaction(qRT-PCR);cell viability,proliferation,migration,invasion and apoptosis were detected by CCK-8,colony formation,scratch healing,Transwell and flow cytometry;RNA immunoprecipitation(RIP)as-say and dual luciferase assay were used to verify the binding relationship between miR-31-5p and SPRED1.Results Huaier granule could significantly inhibit the proliferation,migration and invasion of sorafenib resistant HCC cells,and induce apoptosis.Bioinformatics analysis showed that miR-31-5p was highly expressed in HCC,and Huaier granule was able to down-regulate the expression of miR-31-5p,inhibit the proliferation and metastasis of sorafenib resistant HCC cells,and induce apoptosis;miR-31-5p showed a targeted inhibition effect on the expression of SPRED1.SPRED1 was down-regulated in HCC,and overexpression of SPRED1 was able to reverse the promoting effect of overexpression of miR-31-5p on proliferation and metastasis of sorafenib resistant HCC.Conclusion Huaier granule can inhibit sorafenib resistant HCC metastasis through the miR-31-5p/SPRED1 axis,indicating that Huaier granule has the potential to be used as a novel drug for HCC treatment.