1.Pathogens causing healthcare-associated urinary tract infection in intensive care unit patients
Denghui LU ; Xia WAN ; Chan LI ; Julan XUE ; Yongquan DU
Chinese Journal of Infection Control 2015;(1):63-64,72
Objective To understand healthcare-associated urinary tract infection (HA-UTI)and pathogens causing HA-UTI in intensive care unit (ICU)patients,so as to provide scientific basis for the prevention and control of HA-UTI. Methods Targeted surveillance data about HA-UTI in 32 hospitals in 2013 were analyzed.Results A total of 23 680 ICU patients were monitored,157 cases of HA-UTI occurred,HA-UTI rate was 0.66%;the usage rate of urinary tract cathe-ter was 80.83%,catheter-associated UTI was 1.25‰.A total of 162 pathogenic strains were detected,the percentage of fungi,gram-negative bacteria,and gram-positive bacteria was 40.74% (n=66);31.48 % (n=51),and 27.78% (n=45)respectively.Conclusion The main pathogens causing HAI-URI are fungi,comprehensive intervention measures should be taken to control HA-UTI in ICU patients.
2.Protective effect of coenzyme Q10 on renal injury in diquat poisoned rats by inhibiting the expression of IL-17/NF-κB protein
Denghui YANG ; Jin WU ; Jie HU ; Jiangshan ZHAN ; Anjing LU ; Fuping LAI ; Yingmao JIA ; Yuanlan LU
Chinese Journal of Emergency Medicine 2024;33(9):1249-1256
Objective:To explore whether antioxidant coenzyme Q10 (CoQ10) is involved in the regulation of renal injury induced by diquat poisoning (DQ) in rats through anti-oxidative stress and inhibition of interleukin (IL)-17 and nuclear factor kappa-B (NF-κB) signaling pathway, and whether this mechanism is related to alleviating mitochondrial dysfunction.Methods:The expressions of NF-κB inhibitory protein α (IKB-α), phosphorylated nuclear factor κB (P-NF-κB), JNK-related leucine zipper protein (JLP) and neuroprotective protein PTEN-induced putative kinase 1(PINK1) pathway proteins were detected in vivo and in vitro. Biochemical detection of renal injury markers and inflammatory cytokines: serum urea nitrogen (BUN), serum creatinine (Cr), Cystatin C (CysC), renal injury molecule 1, Malondialdehyde, Supemxidedismutase (SOD), neutrophil gelatinase-associated lipocalin (NGAL), etc. Renal pathology HE staining was used to observe the degree of renal injury and pathological score under light microscope. The expression of reactive oxygen species (ROS) was detected by immunofluorescence. CCK-8 experiment was used to observe the level of cell proliferation after administration.Results:In vivo experiment, the indexes of renal function injury (Cr, BUN, CysC, NAGL, KIM-1) in plasma and kidney samples were significantly increased after 72 h of exposure in DQ group, and there were significant histopathological changes and pathological scores increased. In vitro experiment HK-2 cells were exposed to DQ for 48 h, and the cell viability decreased by half. After exposure to DQ, serum SOD decreased, MDA increased, and the immunofluorescence value of ROS in renal tissue increased. Intervention with CoQ10 can alleviate the pathological damage induced by DQ in rats, enhance the vitality of HK-2 cells, alleviate renal injury and reduce the level of oxidative stress. In addition, the expression of pro-inflammatory cytokines (IL-6, TNF-α and IL-17) increased in DQ group in vivo, the expression of P-NF-κBp65 protein in DQ group in vivo and HK-2 cell DQ group in vitro increased significantly, the expression of mitochondrial dysfunction index PINK1 protein increased significantly, and the expression of JLP protein and IκB-α protein decreased significantly. After intervention with CoQ10, the expression of P-NF-κBp65 protein and PINK1 can be decreased, while the expression of IκB-α protein can be increased and the degradation of JLP could be alleviated, and CoQ10 could improve the mitochondrial dysfunction after DQ poisoning.Conclusions:CoQ10 can alleviate the kidney injury induced by DQ poisoning in rats, and its mechanism may be related to the fact that CoQ10 regulates the expression of IL-17 and NF-κB signaling pathway through anti-oxidative stress, and further improves mitochondrial dysfunction.
3.Modified Latarjet splitting subscapularis muscle under arthroscopy: an anatomical study based on axillary nerve, glenoid, and subscapularis muscle.
Xinzhi LIANG ; Daqiang LIANG ; Zhihe QIU ; Sheng LI ; Bing WU ; Hao LI ; Gang HUANG ; Wei LU ; Denghui XIE ; Haifeng LIU
Chinese Journal of Reparative and Reconstructive Surgery 2023;37(5):556-560
OBJECTIVE:
To testify the spatial relationship between the subscapularis muscle splitting window and the axillary nerve in modified arthroscopic Latarjet procedure, which could provide anatomical basis for the modification of the subscapularis muscle splitting.
METHODS:
A total of 29 adult cadaveric shoulder specimens were dissected layer by layer, and the axillary nerve was finally confirmed to walk on the front surface of the subscapularis muscle. Keeping the shoulder joint in a neutral position, the Kirschner wire was passed through the subscapularis muscle from back to front at the 4 : 00 position of the right glenoid circle (7 : 00 position of the left glenoid circle), and the anterior exit point (point A, the point of splitting subscapularis muscle during Latarjet procedure) was recorded. The vertical and horizontal distances between point A and the axillary nerve were measured respectively.
RESULTS:
In the neutral position of the shoulder joint, the distance between the point A and the axillary nerve was 27.37 (19.80, 34.55) mm in the horizontal plane and 16.67 (12.85, 20.35) mm in the vertical plane.
CONCLUSION
In the neutral position of the shoulder joint, the possibility of axillary nerve injury will be relatively reduced when radiofrequency is taken from the 4 : 00 position of the right glenoid (7 : 00 position of the left glenoid circle), passing through the subscapularis muscle posteriorly and anteriorly and splitting outward.
Adult
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Humans
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Shoulder
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Rotator Cuff/surgery*
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Arthroscopy/methods*
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Scapula/surgery*
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Shoulder Joint/surgery*
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Cadaver
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Joint Instability/surgery*