This study explores the construction and application of online platform for medical continuing education based on libraries and academic conferences. With the consent of the experts participating in the conference, the contents of the conferences are recorded and made into learning videos for continuing education. By constructing network servers, cloud services, and other platforms, the online continuing education can be realized, and such procedures as giving credits also can be completed. And combined with other professional continuing education platforms, a complete continuing education system can be constructed. We have initially designed out the construction mode of medical continuing education platform. The construction of medical continuing education platform has enhanced the class or position of the symposium organization institutions, facilitated the continuing education of professionals and technical personnel, with good social and economic effects, which is worthy of promotion.

Amino Acid Sequence ; Autophagy ; Binding Sites ; Genomics ; Molecular Sequence Data ; Phosphorylation ; Saccharomyces cerevisiae Proteins ; chemistry ; genetics ; metabolism

Mutations or inactivation of parkin, an E3 ubiquitin ligase, are associated with familial form or sporadic Parkinson's disease (PD), respectively, which manifested with the selective vulnerability of neuronal cells in substantia nigra (SN) and striatum (STR) regions. However, the underlying molecular mechanism linking parkin with the etiology of PD remains elusive. Here we report that p62, a critical regulator for protein quality control, inclusion body formation, selective autophagy and diverse signaling pathways, is a new substrate of parkin. P62 levels were increased in the SN and STR regions, but not in other brain regions in parkin knockout mice. Parkin directly interacts with and ubiquitinates p62 at the K13 to promote proteasomal degradation of p62 even in the absence of ATG5. Pathogenic mutations, knockdown of parkin or mutation of p62 at K13 prevented the degradation of p62. We further showed that parkin deficiency mice have pronounced loss of tyrosine hydroxylase positive neurons and have worse performance in motor test when treated with 6-hydroxydopamine hydrochloride in aged mice. These results suggest that, in addition to their critical role in regulating autophagy, p62 are subjected to parkin mediated proteasomal degradation and implicate that the dysregulation of parkin/p62 axis may involve in the selective vulnerability of neuronal cells during the onset of PD pathogenesis.
Adaptor Proteins, Signal Transducing ; chemistry ; metabolism ; Animals ; HEK293 Cells ; Heat-Shock Proteins ; chemistry ; metabolism ; Humans ; Lysine ; metabolism ; Mice ; Neurons ; metabolism ; pathology ; Oxidopamine ; pharmacology ; Parkinson Disease ; metabolism ; pathology ; Proteasome Endopeptidase Complex ; metabolism ; Protein Stability ; Proteolysis ; drug effects ; Sequestosome-1 Protein ; Ubiquitin-Protein Ligases ; metabolism ; Ubiquitination ; drug effects