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Globally, the incidence of pancreatic cancer is on a rise. Pancreatic cancer is characterized by difficulty in early diagnosis, frequent distant metastasis, low surgical resection rate, and high risk of postoperative recurrence. Better treatments need to be developed to prolong the prognosis. Studies have confirmed that inflammation is closely correlated with tumorigenesis, and inflammatory mediators play important roles on tumor microenvironment of pancreatic cancer and lead to poor prognosis. This article reviewed the progress on the correlation between peripheral blood inflammatory index and the prognosis of pancreatic cancer.
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Objective:To investigate the safety and efficacy of early oral feeding in the treatment of mild acute pancreatitis (MAP).Methods:Data of 100 MAP patients from April 2015 to June 2018 admitted in Department of General Surgery in Shanxi Bethune Hospital were collected. According to the time of food intake through the mouth, the patients were divided into early oral feeding group (food intake started when the symptoms of abdominal pain and abdominal distension were alleviated with gastrointestinal functional recovery, but serum amylase and lipase did not decrease to a level below 2 times of normal upper limits) and traditional oral feeding group (food intake started when the symptoms of abdominal pain and abdominal distension were alleviated with gastrointestinal functional recovery, but serum amylase and lipase decreased to a level below 2 times of normal upper limits), with 50 cases in each group. The incidence of abdominal pain or bloating, serum amylase, CRP, organ dysfunction, morbidity and mortality, and median length of hospital stay after eating were compared between the two groups.Results:There were no statistically significant differences on gender, age, etiology, abdominal pain and distension, increased serum amylase, increased blood CRP, and number of organ dysfunction cases between two groups, and there were no deaths in either group. However, the feeding time and length of hospital stay in the early oral feeding group were significantly shorter than those in the traditional oral feeding group, and the differences were statistically significant [(3.00±0.18)d versus (4.84±0.27)d, (8.24±0.33) D versus (9.00±0.26)d, both P<0.05]. Conclusions:Early oral feeding in MAP patients did not aggravate the disease, but helps to correct the nutritional status of the patients, with higher safety and effectiveness.
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Objective To investigate whether astragaloside Ⅳ can regulate the multidrug resistance of HepG2/GCS-resistant cell lines,restore the sensitivity of drag-resistant cell lines to adriamycin (ADM) and its mechanism.Methods We used recombinant GCS (shRNAS) and control recombinant plasmids and did the transfection with HepG2 cells.RT-PCR and Western blot were used to analyze the expression of GCS.Astragaloside Ⅳ cytotoxicity experiments and ADM were performed in experimental and control groups.Hoechst 33258 was detected in two groups,apoptosis was detected by flow cytometry,and protein expression of caspase 9,3,Bax,and bcl-2 were detected by Western blot.Results RT-PCR and fluorescence observation showed that GCS was highly expressed after the transfection.Western blot showed that compared with control group,and HepG2GCS group,GCS and MDR1 expression were higher than;Astragaloside Ⅳ cytotoxicity experiment showed tumor proliferation was not regulated by GCS(FHepG2GCS=0.308,FHepG2EV =0.216,FHepG2 =0.153,P＞ 0.05),ADM in vitro tumor cell inhibition experiments showed that HepG2GCS cells were resistant to ADM (50％ cell transplantation concentration were 7.5,7.5,15 μg/ml);Hoechst 33258 and flow cytometry showed that Astragaloside Ⅳ can restore ADM tumor inhibition;Western blot showed that compared to untreated HepG2EV and HepG2GCS cells,protein level of caspase 9,caspase 3 were increased in Ast+HepG2EV and Ast+HepG2GCS groups (t=7.17,P＜0.05).At the same time,Bax and Bcl-2 were significantly different in each group (P＜ 0.05).Conclusions Astragaloside Ⅳ reverses multidrug resistance in HepG2/GCS cell lines,restores its sensitivity to ADM,promotes apoptosis in tumor cells through the caspase pathway and Bax pathway,and thus plays an important role in cancer chemotherapy.
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Objective To investigate the expression of scaffold protein palladin in pancreatic ductal adenocarcinoma (PDAC) tissues and to discuss its clinicopathological significance.Methods 56 samples of PDAC and corresponding adjacent normal pancreas (NP) tissues were collected.Another 10 samples of chronic pancreatitis (CP) tissues were collected.Western blot analysis and immunohistochemistry assay were performed to detect the expression of protein palladin.The correlation of palladin expression with clinicopathological factors of PDAC was analyzed.Results Western blot analysis revealed that the expression of palladin in PDAC,CP and NP tissues were respectively 0.93±0.07,0.41±0.07 and 0.20±0.06,and the expression of palladin was significantly increased in PDAC tissues compared with NP and CP tissues (P ＜ 0.05),and its expression was significantly increased in CP tissues compared with NP tissues (P ＜ 0.05).Immunohistochemical staining showed that palladin was mainly expressed in activated myofibroblasts in PDAC tissues.The rate of palladin expression was 79 ％ (44/56),which was higher than that in NP tissues (2/10) and CP tissues (4/10),and its expression was found to be correlated with the degree of tumor differentiation,lymph node metastasis and clinical TNM classification (P ＜ 0.05),and it had no correlation with patient' s sex,age,tumor location and distant metastasis (P ＞ 0.05).Conclusions Scaffold protein palladin is highly expressed in PDAC tissues,and it is expressed in the activated myofibroblasts within tumor microenvironment.Scaffold protein palladin may be involved in the invasion and metastasis of PDAC.