In recent years,the"release control service"policy of scientific research funds focused on expanding the self-management right and optimizing the scientific research funds management.Public hospitals,as public welfare institutions undertaking the task of"medical education,research and prevention",have their own particularities in the management of scientific research funds.It analyzes the types and characteristics of control traces in public hospitals from the perspective of internal control traces of scientific research funds.It is concluded that there are some problems in the control trace management of scientific research funds in public hospitals,such as lack of targeted policies,lack of result-oriented control traces,and blurred boundaries of project management rights and responsibilities.Suggestions for improvement are put forward from the perspectives of exploring targeted policies,establishing result-oriented trace list,establishing differentiated management functions,and improving the authority and responsibility arrangement of indirect funds and reward system.

Objective:To investigate the effect of ginsenoside octanoate(Rh2-O)on inducing immunogenic cell death in hepa-tocellular carcinoma cells and its molecular mechanism.Methods:Effects of ginsenoside caprylate(Rh2-O)and autophagy inhibitor 3-MA on the activity of hepatocellular carcinoma cells were detected by CCK-8 assay.The effect of Rh2-O on CRT membrane eversion in Hepa1-6 cells were detected by immunofluorescence assay.Rh2-O treated mouse hepatocellular carcinoma cells were used to pre-pare a tumor vaccine for in vivo vaccination experiments in mice.Extracellular ATP levels were detected in real-time.The expression of autophagy-related genes and proteins were measured by real-time fluorescence PCR and Western blot,and the mitochondrial morphol-ogy and co-localization with autophagy proteins were observed by laser confocal microscopy.Results:Rh2-O showed strong cytotoxicity to Hepa1-6 cells[cell viability:(58.54±3.56)%]at a concentration of 150 μmol/L,and a large amount of CRT was observed on the surface of the cell membrane.The tumor emergence rate was 36.36%in the vaccinated group and 100%in the control group.The tumor vaccine prepared by Rh2-O effectively protected mice from the same type of tumor attack;Rh2-O induced an increase in the level of cellular secreted ATP(P<0.05),the mRNA of autophagy-related genes ATG3,p62,LC3 expression levels and autophagy-associated proteins LC3A and LC3B expression levels were increased(P<0.05),and co-localization of mitochondria with autophagy proteins was significantly increased(P<0.05).In addition,Rh2-O action on 3-MA pretreated hepatocellular carcinoma cells resulted in a signifi-cant decrease in extracellular ATP levels(P<0.001).Conclusion:Rh2-O may induce immunogenic cell death by inducing autophagy in hepatocellular carcinoma cells.

In recent years,the"release control service"policy of scientific research funds focused on expanding the self-management right and optimizing the scientific research funds management.Public hospitals,as public welfare institutions undertaking the task of"medical education,research and prevention",have their own particularities in the management of scientific research funds.It analyzes the types and characteristics of control traces in public hospitals from the perspective of internal control traces of scientific research funds.It is concluded that there are some problems in the control trace management of scientific research funds in public hospitals,such as lack of targeted policies,lack of result-oriented control traces,and blurred boundaries of project management rights and responsibilities.Suggestions for improvement are put forward from the perspectives of exploring targeted policies,establishing result-oriented trace list,establishing differentiated management functions,and improving the authority and responsibility arrangement of indirect funds and reward system.

Objective:To investigate the effect of ginsenoside octanoate(Rh2-O)on inducing immunogenic cell death in hepa-tocellular carcinoma cells and its molecular mechanism.Methods:Effects of ginsenoside caprylate(Rh2-O)and autophagy inhibitor 3-MA on the activity of hepatocellular carcinoma cells were detected by CCK-8 assay.The effect of Rh2-O on CRT membrane eversion in Hepa1-6 cells were detected by immunofluorescence assay.Rh2-O treated mouse hepatocellular carcinoma cells were used to pre-pare a tumor vaccine for in vivo vaccination experiments in mice.Extracellular ATP levels were detected in real-time.The expression of autophagy-related genes and proteins were measured by real-time fluorescence PCR and Western blot,and the mitochondrial morphol-ogy and co-localization with autophagy proteins were observed by laser confocal microscopy.Results:Rh2-O showed strong cytotoxicity to Hepa1-6 cells[cell viability:(58.54±3.56)%]at a concentration of 150 μmol/L,and a large amount of CRT was observed on the surface of the cell membrane.The tumor emergence rate was 36.36%in the vaccinated group and 100%in the control group.The tumor vaccine prepared by Rh2-O effectively protected mice from the same type of tumor attack;Rh2-O induced an increase in the level of cellular secreted ATP(P<0.05),the mRNA of autophagy-related genes ATG3,p62,LC3 expression levels and autophagy-associated proteins LC3A and LC3B expression levels were increased(P<0.05),and co-localization of mitochondria with autophagy proteins was significantly increased(P<0.05).In addition,Rh2-O action on 3-MA pretreated hepatocellular carcinoma cells resulted in a signifi-cant decrease in extracellular ATP levels(P<0.001).Conclusion:Rh2-O may induce immunogenic cell death by inducing autophagy in hepatocellular carcinoma cells.

Objective To investigate the changes in the abilities of invasion and metastasis in surviving human lung adenocarcinoma (A549) cells after X-ray irradiation and the related mechanism.Methods The change in radiosensitivity after X-ray irradiation was determined by colony formation assay.The abilities of invasion and metastasis were evaluated by MTF adhesion assay and Transwell invasion and migration assay in vitro.The mRNA and protein expression of E-cadherin,vimentin,tumor growth factor (TGF)-β1,matrix metalloproteinase (MMP)-2,and MMP-9 was measured by real-time RT-PCR using SYBR Green fluorescence and Western blot.Results The colony formation assay showed that the surviving A549 cells after X-ray irradiation were more resistant to irradiation (ratio of D0 values =0.94).Their abilities of adhesion,invasion,and migration were significantly increased by 1.46 times,1.40 times,and 1.45 times,respectively.In addition,the surviving cells showed enlarged intercellular spaces and had many long pseudopodi.Compared with those in the control group,the mRNA expression levels of vimentin,TGF-β1,MMP-2,and MMP-9 of surviving cells were increased by 1.37 times,2.37 times,1.80 times,and 1.50 times,respectively,the protein expression levels of the above substances were increased by 1.60 times,1.80 times,1.10 times,and 1.20 times,respectively,and the mRNA and protein expression levels of E-cadherin were decreased by 59.4％ and 74.6％.Conclusions The surviving A549 cells after X-ray irradiation have significantly increased abilities of invasion and metastasis.This may be due to radiationinduced TGF-β1 expression increase that in turn promotes epithelial-mesenchymal transition and also due to radiation-induced MMP-2 and MMP-9 expression increase.

OBJECTIVETo determine the mid-term effects of cutting balloon angioplasty (CBA) on in-stent restenosis.

METHODSA total of 69 patients with in-stent restenosis were divided into 2 groups randomly: cutting balloon angioplasty and plain old balloon angioplasty. The mechanisms of restenosis and dilation results were determined by quantitative coronary angiography and intravascular ultrasound. Follow-up was performed.

RESULTSThe procedural success rate was 100% without death and acute closure. One patient experienced dissection at the distal end of the stent and needed another stent. The mean follow-up period was 6.7 +/- 2.3 months. The final re-restenosis rate was 15% and 18% at 3 months and 6 months respectively, markedly lower than after plain old balloon angioplasty (38% and 43%). Acute gain by intravascular ultrasound (IVUS) was 1.72 +/- 0.52 mm after cutting balloon angioplasty, higher than 1.15 +/- 0.54 mm after plain old balloon angioplasty. The lumen diameter late loss in the cutting balloon group was 0.26 +/- 0.05 mm and 0.38 +/- 0.06 mm at 3 months and 6 months respectively, significantly lower than for those in conventional balloon group (0.78 +/- 0.19 mm and 0.89 +/- 0.16 mm, respectively, P < 0.001). As shown by IVUS, the main mechanism of cutting balloon angioplasty was marked reduction of plaque area without significant increase of vessel area (less vessel trauma).

CONCLUSIONCutting balloon angioplasty is feasible and effective for the treatment of in-stent restenosis with less vessel trauma.

Aged ; Angioplasty, Balloon ; methods ; Coronary Angiography ; Coronary Restenosis ; therapy ; Coronary Vessels ; pathology ; physiopathology ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Stents ; Time Factors ; Treatment Outcome