1.Research in using cycle of Lu Wofu lubricant preservation
Yuping LI ; Zhen WANG ; Qingyun NI ; Zhan LIN
Chinese Journal of Practical Nursing 2011;27(8):54-56
Objective To explore the effective using cycle of Lu Wofu lubricant preservation with different cleaning methods,and provide basis for change time of lubricant preservation.Methods 20 000 bricant was ensured under sterile conditions.400 pieces of the same equipment were extracted from surgical instruments every day,and they were randomly divided into the manual cleaning group and the mechanical cleaning group with 200 pieces in each group,each group adopted manual cleaning and mechanical cleaning.The Lu Wofu lubricant was reused and preserved for one week.Lubricant preservation was extracted and sent to do bacterial culture with fixed people,time and quantity.Results of two groups were compared.Results The qualified rate of the two groups at 24-hour was 100%,at 48-hour the manual cleaning group was 92%,the mechanical cleaning group was 77%,at 72-hour the manual cleaning group was 81%,the mechanical cleaning group was 19%,above 72 hours; both the manual cleaning group and the mechanical group was zero.Over 48 hours in the mechanical group and above 72 hours in the manual cleaning group appeared more than 10 million bacterial colonies.There was significant difference between the two groups.Conclusions The effective using cycle of Lu Wofu lubricant preservation was 72 hours for manual cleaning and 48 hours for mechanical cleaning,the manual cleaning delays one day over mechanical cleaning to change lubricant,which can reduce the waste of resources and cost savings.
2.Dual roles of p62/SQSTM1 in the injury and recovery phases of acetaminophen-induced liver injury in mice.
Hui QIAN ; Qingyun BAI ; Xiao YANG ; Jephte Y AKAKPO ; Lili JI ; Li YANG ; Thomas RÜLICKE ; Kurt ZATLOUKAL ; Hartmut JAESCHKE ; Hong-Min NI ; Wen-Xing DING
Acta Pharmaceutica Sinica B 2021;11(12):3791-3805
Acetaminophen (APAP) overdose can induce liver injury and is the most frequent cause of acute liver failure in the United States. We investigated the role of p62/SQSTM1 (referred to as p62) in APAP-induced liver injury (AILI) in mice. We found that the hepatic protein levels of p62 dramatically increased at 24 h after APAP treatment, which was inversely correlated with the hepatic levels of APAP-adducts. APAP also activated mTOR at 24 h, which is associated with increased cell proliferation. In contrast, p62 knockout (KO) mice showed increased hepatic levels of APAP-adducts detected by a specific antibody using Western blot analysis but decreased mTOR activation and cell proliferation with aggravated liver injury at 24 h after APAP treatment. Surprisingly, p62 KO mice recovered from AILI whereas the wild-type mice still sustained liver injury at 48 h. We found increased number of infiltrated macrophages in p62 KO mice that were accompanied with decreased hepatic von Willebrand factor (VWF) and platelet aggregation, which are associated with increased cell proliferation and improved liver injury at 48 h after APAP treatment. Our data indicate that p62 inhibits the late injury phase of AILI by increasing autophagic selective removal of APAP-adducts and mitochondria but impairs the recovery phase of AILI likely by enhancing hepatic blood coagulation.