Chinese Medical Sciences Journal最新文献

Objective

Total knee arthroplasty is one of the most common orthopedic surgeries. Readmission due to severe complications after total knee arthroplasty is a grave concern to surgeons. In this study, we evaluated the risk factors for severe complications after primary total knee arthroplasty.

Methods

We retrospectively collected clinical data of 2,974 patients who underwent primary total knee arthroplasty from July 2013 to June 2019 in our hospital. Postoperative complication > grade IE was defined as severe complication according to Clavien-Dindo classification system. Binary logistic regression was used to identify the predictive risk factors for severe complications.

Results

The complication rate after primary total knee arthroplasty was 6.8% and severe complication rate was 2.5%. Male (OR = 2.178, 95%CI: 1.324-3.585, P = 0.002), individuals above 75 years old (OR = 1.936, 95%CI: 1.155-3.244, P = 0.012), arrhythmia (OR = 2.913, 95%CI: 1.350-6.285, P = 0.006) and cerebrovascular disease (OR = 2.804, 95%CI: 1.432-5.489, P = 0.003) were predictive risk factors for severe complications after primary total knee arthroplasty.

Conclusion

Advanced age, male, arrhythmia, and cerebrovascular disease might be patients-related risk factors for postoperative severe complications after primary total knee arthroplasty. Special attention should be paid to patients with risk factors.

Renal amyloidosis secondary to anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is extremely rare. Here, we reported a 77-year-old woman with ANCA-associated vasculitis. Renal biopsy with Masson trichrome staining showed pauci-immune crescentic glomerulonephritis, and electron microscopy showed amyloid deposition in the mesangial area. Immunofluorescence revealed kappa light chain and lambda light chain negative. Bone marrow biopsy revealed no clonal plasma cell. Finally, she was diagnosed as ANCA-associated vasculitis with secondary renal amyloid A amyloidosis.

Objective

To investigate the expression of topoisomerase II α (TOP2α) in hepatocellular carcinoma (HCC) and its role in predicting prognosis of HCC patients.

Methods

We used HCC-related datasets in UALCAN, HCCDB, and cBioPortal databases to analyze the expression and mutation of TOP2α and its co-expressed genes in HCC tissues. GO function and KEGG pathway enrichment of TOP2α and its co-expressed genes were identified. The TIMER database was used to analyze infiltration levels of immune cells in HCC. The impacts of TOP2α and its co-expression genes and the infiltrated immune cells on the survival of HCC patients were assayed by Kaplan-Meier plotter analysis.

Results

TOP2α and its co-expression genes were highly expressed in HCC (P < 0.001) and detrimental to overall survival of HCC patients (P < 0.001). TOP2α and its co-expression genes were mainly involved in cell mitosis and proliferation, and cell cycle pathway (ID: hsa04110, P = 0.00194S). TOP2α and its co-expression genes were mutated in HCC and the mutations were significantly detrimental to overall survival (P = 0.0247) and disease-free survival (P = 0.026S) of HCC patients. High TOP2α expression was positively correlated with the infiltration of B cell (r = 0.4S9, P < 0.01), CD8⁺T cell (r = 0.312, P < 0.01), CD4⁺T cell (r = 0.370, P < 0.01), macrophage (r = 0.459, P < 0.01), neutrophil (r = 0.405, P < 0.01), and dendritic cell (r = 0.473, P < 0.01) in HCC. The CD8⁺T cell infiltration significantly prolonged the 3- and 5-year survival of HCC patients (all P < 0.05), and CD4⁺T cell infiltration significantly shortened the 3-, 5-, and 10-year survival of HCC patients (all P < 0.05)

Conclusion

TOP2α may be an oncogene, which was associated with poor prognosis of HCC patients and could be used as a biomarker for the prognostic prediction of HCC.

Objective

To study the effects of TYRO protein kinase-binding protein (TYROBP) deficiency on learning behavior, glia activation and pro-inflammatory cycokines, andTau phosphorylation of a new Alzheimer’s disease (AD) mouse model carrying a PSEN1 p.G378E mutation.

Methods

A new AD mouse model carrying PSEN1 p.G378E mutation was built based on our previously found AD family which might be ascribed to the PSEN1 mutation, and then crossed with TYROBP deficient mice to produce the heterozygous hybrid mice (PSEN1^G378E/WT; Tyrobp^+/–) and the homozygous hybrid mice (PSEN1^G378E/G378E; Tyrobp^–/–). Water maze test was used to detect spatial learning and memory ability of mice. After the mice were sacrificed, the hippocampus was excised for further analysis. Immunofluorescence was used to identify the cell that expresses TYROBP and the number of microglia and astrocyte. Western blot was used to detect the expression levels of Tau and phosphorylatedTau (p-Tau), and ELISA to measure the levels of pro-inflammatory cytokines.

Results

Our results showed that TYROBP specifically expressed in the microglia of mouse hippocampus. Absence of TYROBP in PSEN1^G378E mutation mouse model prevented the deterioration of learning behavior, decreased the numbers of microglia and astrocytes, and the levels of interleukin-6, interleukin-1β and tumor necrosis factor-α in the hippocampus (all P < 0.05). The ratios of AT8/Tau5, PHF1/Tau5, pT181/Tau5, pT231/ Tau5 and p-ERK/ERK were all higher in homozygous hybrid mice (PSEN1^G378E/G378E; Tyrobp^–/– mice) compared with PSEN1^G378E/G378E mice (all P < 0.05).

Conclusions

TYROBP deficiency might play a protective role in the modulation of neuroinflammation of AD. However, the relationship between neuroinflammation processes involving microglia and astrocyte activation, and release of pro-inflammatory cytokines, and p-Tau pathology needs further study.