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Background Excessive blood loss in total joint arthroplasty (TJA) usually leads to an allogenic blood transfusion, which may cause adverse outcomes, prolonged length of hospitalization, and increased costs. The purpose of this study was to determine the incidence and risk factors for intraoperative and postoperative allogenic transfusion in patients undergoing primary unilateral total knee and hip arthroplasty (TKA and THA). Methods We conducted a retrospective study and enrolled consecutive patients undergoing primary unilateral TKA and THA at our institution between January 2010 and July 2014 ( n = 1534). Information about allogenic transfusion was collected from medical records to determine the incidence. We performed univariate analysis and multivariate logistic regression analysis to identify the independent risk factors. Results Total, intraoperative, and postoperative transfusion rates were 17.9%, 7.9%, and 11.3%, respectively. The preoperative lower level of hemoglobin (Hb) ( P < 0.001) and increased amount of intraoperative blood loss ( P < 0.001) were independently associated with transfusion in TKA. The independent risk factors for transfusion in THA were female ( P = 0.023), preoperative lower Hb level ( P < 0.001), prolonged operation time ( P < 0.001), and increased intraoperative blood loss ( P < 0.001). Conclusions Given the high prevalence and potential risk of transfusion in TJA, interventions for identified risk factors should be used during the perioperative period.

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Background Excessive blood loss caused by total joint arthroplasty (TJA) often increases the requirement for blood transfusion, which is associated with adverse outcomes. The purpose of this study was to determine the relationship between perioperative transfusion and postoperative DVT in TJA. Methods This retrospective study reviewed medical records of 715 patients, who consecutively underwent primary unilateral total knee arthroplasty (TKA) or total hip arthroplasty (THA) at our institution between September 2015 and March 2017. Demographic, clinical and surgical parameters were introduced into the univariate analysis to find risk factors for DVT within postoperative 30 days. In order to identify if allogenic blood transfusion was independently associated with DVT, a multivariate logistic regression analysis was conducted to adjust for gender, age, body mass index (BMI), diagnosis, and type of surgery. Results The incidence of perioperative allogenic blood transfusion was 12.4% ( n = 89). Fifty-seven patients (8.0%) developed DVT after surgery. Univariate analysis demonstrated that there were differences between DVT group and non-DVT group in gender ( P = 0.045), age ( P < 0.001), BMI ( P = 0.026), primary diagnosis ( P = 0.001), type of surgery ( P < 0.001), and transfusion rates ( P = 0.040). After adjustment by using multivariate logistic regression analysis, transfusion appeared to be the independent risk factor for DVT in TJA ( P = 0.001; OR = 3.9, 95%CI 1.8–8.4). Conclusion We found that perioperative allogenic blood transfusion was significantly associated with DVT following TJA. In order to reduce the risk of DVT and other adverse outcomes, methods to decrease transfusion rates should be used in clinical practice.

Background: Protein phosphatase 2A (PP2A) controls most cell signaling, but the current understanding of its many isoforms, e.g. as tumor suppressors, is limited. Results: Differentiation was controlled by the small fraction of PP2A using the A␤ scaffold. Conclusion: PP2A A␤ regulates Akt. Significance: Given the extreme importance of Akt in cancer, these findings help explain why A␤ is a tumor suppressor.

Cordycepin, 3'-deoxyadenosine, is an effective component isolated from the rare Chinese caterpillar fungus Cordyceps militaris. It exerts potent anti-inflammatory actions in different cell and animal models. However, its action remains unclear on the TNF-α-induced inhibition of osteogenic differentiation of adipose-derived mesenchymal stem cells (ADMSCs). In the present study, we demonstrated that cordycepin induced cell death at 20 and 40 μg/mL. Interestingly, 10 μg/mL cordycepin abrogated the cell death induced by 20 ng/mL TNF-α. Meanwhile, cordycepin exhibited a dosedependent regulation of the osteogenesis of human ADMSCs: it promoted the differentiation at 10 μg/mL, whereas inhibited differentiation at 40 μg/mL. Furthermore, we discovered that 10 μg/mL cordycepin protected against the TNF-α (induced inhibition of osteogenic differentiation of human ADMSCs. It was also revealed that 10 μg/mL cordycepin restored Runx2 and Osx mRNA levels, which were significantly inhibited by TNF-αduring osteogenesis. At the same time, we found that 10 μg/mL cordycepin suppressed TNF-α-activated NF-κB signaling, by inhibiting IκBα phosphorylation and subsequent p65 release and translocation into the cell nucleus. Of clinical interest, the present study revealed mechanisms involved in inflammatory cytokine-inhibited osteogenesis, and it highlights the potential of cordycepin to promote the osteogenesis of human ADMSCs in cell-based therapy for inflammatory bone diseases.

Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or programmed cell death 1 ligand 1 (PD-L1) have enabled some patients with cancer to experience durable, complete treatment responses; however, reliable anti–PD-(L)1 treatment response biomarkers are lacking. Our research found that PD-L1 K162 was methylated by SETD7 and demethylated by LSD2. Furthermore, PD-L1 K162 methylation controlled the PD-1/PD-L1 interaction and obviously enhanced the suppression of T cell activity controlling cancer immune surveillance. We demonstrated that PD-L1 hypermethylation was the key mechanism for anti–PD-L1 therapy resistance, investigated that PD-L1 K162 methylation was a negative predictive marker for anti–PD-1 treatment in patients with non–small cell lung cancer, and showed that the PD-L1 K162 methylation:PD-L1 ratio was a more accurate biomarker for predicting anti–PD-(L)1 therapy sensitivity. These findings provide insights into the regulation of the PD-1/PD-L1 pathway, identify a modification of this critical immune checkpoint, and highlight a predictive biomarker of the response to PD-1/PD-L1 blockade therapy.