1.Situation and thought on constructing confidence ethics in hospitals
Shouping GONG ; Junrong WEI ; Bianling DANG ; We CHAI
Chinese Medical Ethics 1995;0(04):-
This article analyzed the ethical situation in hospitals. The author pointed out the defect of confidence between doctor and patient is the primary cause that leaded to the deterioration of doctor-patient relation, and the retardation of medical service management is the important factor that affected the confidence construction. According to all this above, the author proposed the suggestion of strengthening the understanding and communication between doctor and patient, transforming the medical service concept, enhancing the medical service quality, completing the supervising system, increasing the hospital ability of realizing medical service defect and improving the five thoughts of follow up confidence system to direct the hospital confidence ethical construction.
2.Circ_0068655 Promotes Cardiomyocyte Apoptosis via miR-498/ PAWR Axis
Qiaoying CHAI ; Mingqi ZHENG ; Zheng WANG ; Mei WE ; Yajuan YIN ; Fangfang MA ; Xinping LI ; Haijun ZHANG ; Gang LIU
Tissue Engineering and Regenerative Medicine 2020;17(5):659-670
BACKGROUND:
The cardiomyocyte apoptosis is considered as one of major contributions to cardiac remodeling after myocardial infarction (MI). Numerous studies find that circular RNAs (circRNAs) play pivotal roles in a variety of biological functions. However, the role of circ_0068655 in MI and human induced pluripotent stem-derived cardiomyocytes (HCMs) remains unknown.
METHODS:
The expression of circ_0068655, miR-498, and PRKC apoptosis WT1 regulator (PAWR) in human MI heart tissues and hypoxia subjected HCMs was evaluated with qRT-PCR and Western blot. The effects of circ_0068655 on hypoxia-induced apoptotic death and cell migration in HCMs were evaluated with qRT-PCR, cell viability, cell death ELISA (POD), and Caspase-3 activity assay, and Trans-well assay, respectively. Furthermore, luciferase assay, qRT-PCR, biotin-labeled miRNA pulldown assay, and Western blot were employed in the functional studies.
RESULTS:
We found that the expression of circ_0068655 and PAWR was enhanced in MI patients and hypoxia subjected HCMs; by contrast, the expression of miR-498 decreased. Inhibited expression of circ_0068655 in HMCs counteracted hypoxia-induced apoptotic death and impaired cell migration, in sharp contrast to circ_0068655 knockdown. We identified that circ_0068655 sponged an endogenous miR-498 to sequester and inhibit its activity, leading to the increased PAWR expression.
CONCLUSIONS
Our findings reveal that the expression of circ_0068655 can promote cardiomyocyte apoptosis through the modulation of miR-498-PAWR axis in vitro, which highlights the diagnostic and therapeutic value of circ_0068655 in patients with MI.
3.Circ_0068655 Promotes Cardiomyocyte Apoptosis via miR-498/ PAWR Axis
Qiaoying CHAI ; Mingqi ZHENG ; Zheng WANG ; Mei WE ; Yajuan YIN ; Fangfang MA ; Xinping LI ; Haijun ZHANG ; Gang LIU
Tissue Engineering and Regenerative Medicine 2020;17(5):659-670
BACKGROUND:
The cardiomyocyte apoptosis is considered as one of major contributions to cardiac remodeling after myocardial infarction (MI). Numerous studies find that circular RNAs (circRNAs) play pivotal roles in a variety of biological functions. However, the role of circ_0068655 in MI and human induced pluripotent stem-derived cardiomyocytes (HCMs) remains unknown.
METHODS:
The expression of circ_0068655, miR-498, and PRKC apoptosis WT1 regulator (PAWR) in human MI heart tissues and hypoxia subjected HCMs was evaluated with qRT-PCR and Western blot. The effects of circ_0068655 on hypoxia-induced apoptotic death and cell migration in HCMs were evaluated with qRT-PCR, cell viability, cell death ELISA (POD), and Caspase-3 activity assay, and Trans-well assay, respectively. Furthermore, luciferase assay, qRT-PCR, biotin-labeled miRNA pulldown assay, and Western blot were employed in the functional studies.
RESULTS:
We found that the expression of circ_0068655 and PAWR was enhanced in MI patients and hypoxia subjected HCMs; by contrast, the expression of miR-498 decreased. Inhibited expression of circ_0068655 in HMCs counteracted hypoxia-induced apoptotic death and impaired cell migration, in sharp contrast to circ_0068655 knockdown. We identified that circ_0068655 sponged an endogenous miR-498 to sequester and inhibit its activity, leading to the increased PAWR expression.
CONCLUSIONS
Our findings reveal that the expression of circ_0068655 can promote cardiomyocyte apoptosis through the modulation of miR-498-PAWR axis in vitro, which highlights the diagnostic and therapeutic value of circ_0068655 in patients with MI.