1.Intervention effect of chlorhexidine gargle on respiratory tract infection following general anesthesia
Ruili NIU ; Renguo GONG ; Xiangping ZHU
Chinese Journal of Infection Control 2015;(2):105-107
Objective To evaluate the effect of chlorhexidine gargle on respiratory tract infection (RTI)in patients following general anesthesia.Methods From January 2012 to June 2013,94 patients who received general anesthe-sia for removal of vertebral disc were randomly divided into two groups,with 47 cases in each group,control group gargled with normal saline,observation group accepted 2% chlorhexidine gargle.The occurrence of RTI and detec-tion of pharynx pathogens of two groups were compared.Results The incidence of RTI in observation group and control group was 8.51%(n=4)and 23.40%(n=11)respectively(χ2 = 12.95,P <0.05).4 patients in observation group were detected 4 isolates of pathogens,11 patients in control group were detected 26 isolates of pathogens,the detection rate of pharynx pathogens of observation group was lower than control group (χ2 =3.89,P <0.05).The main isolated pathogens were Pseudomonas aeruginosa ,Staphylococcus aureus ,Klebsiella pneumoniae and Esche-richia coli .Conclusion Chlorhexidine gargling can effectively reduce RTI following general anesthesia,it is worthy of clinical application.
2.The study of the colony formation of HPP-CFC from bone marrow-derived hematopoietic cells of psoriatic patients and the methylation of p21 gene promotor in HPP-CFC
Ruili ZHANG ; Xuping NIU ; Xinhua LI ; Kaiming ZHANG ; Guohua YIN
Chinese Journal of Immunology 2000;0(09):-
Objective:To investigate the colony formation of high-proliferative potential colony-forming cells(HPP-CFC) from bone marrow-derived hematopoietic cells of psoriatic patients and p21 gene promotor methylation in HPP-CFC,and probe into the relationship between the colony formation and the methylation status of p21 gene promoter.[WT5"HZ] Methods:[WT5"BZ]Bone marrow-derived mononuclear cells were separated by density gradient centrifugation.The cells were cultured in methycellulose semi-solid culture medium with SCF,GM-CSF,IL-3 and IL-6 for 14 days, and then high-proliferative potential colony-forming cells(HPP-CFC) were counted.The HPP-CFC were collected and their genomic DNA was isolated . DNA was subjected to bisulfite treatment,and the modified DNA was studied by using the methylation-specific polymerase chain reaction (MSP).[WT5"HZ]Results:[WT5"BZ]In methycellulose semi-solid culture system, the number of HPP-CFC in bone marrow of psoriatic patients was significantly less than that of normal control. The positive frequency of methylation of p21 gene promoter in HPP-CFC of normal contrasts was higher than that of psoriatic patients. [WT5"HZ]Conclusion:[WT5"BZ]The activity of methylation status of p21 gene promoter of bone marrow derived hematopoietic cells of psoriatic patients is abnomal. The lower positive frequency of methyllation of p21 gene promotor in HPP-CFC perhaps play a role in lower colony-forming capability of HPP-CFC of psoriatic patients.
3.High-throughput screening of novel TFEB agonists in protecting against acetaminophen-induced liver injury in mice.
Xiaojuan CHAO ; Mengwei NIU ; Shaogui WANG ; Xiaowen MA ; Xiao YANG ; Hua SUN ; Xujia HU ; Hua WANG ; Li ZHANG ; Ruili HUANG ; Menghang XIA ; Andrea BALLABIO ; Hartmut JAESCHKE ; Hong-Min NI ; Wen-Xing DING
Acta Pharmaceutica Sinica B 2024;14(1):190-206
Macroautophagy (referred to as autophagy hereafter) is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and organelles. Previous studies showed that autophagy protects against acetaminophen (APAP)-induced injury (AILI) via selective removal of damaged mitochondria and APAP protein adducts. The lysosome is a critical organelle sitting at the end stage of autophagy for autophagic degradation via fusion with autophagosomes. In the present study, we showed that transcription factor EB (TFEB), a master transcription factor for lysosomal biogenesis, was impaired by APAP resulting in decreased lysosomal biogenesis in mouse livers. Genetic loss-of and gain-of function of hepatic TFEB exacerbated or protected against AILI, respectively. Mechanistically, overexpression of TFEB increased clearance of APAP protein adducts and mitochondria biogenesis as well as SQSTM1/p62-dependent non-canonical nuclear factor erythroid 2-related factor 2 (NRF2) activation to protect against AILI. We also performed an unbiased cell-based imaging high-throughput chemical screening on TFEB and identified a group of TFEB agonists. Among these agonists, salinomycin, an anticoccidial and antibacterial agent, activated TFEB and protected against AILI in mice. In conclusion, genetic and pharmacological activating TFEB may be a promising approach for protecting against AILI.