Objective: Postoperative delirium is common after extensive surgery. This study aimed to collate and synthesize published literature on risk factors for delirium in patients with head and neck cancer surgery. Methods: Three databases were searched (MEDLINE, Embase, and Cochrane Library) between January 1987 and July 2016. The Newcastle Ottawa Scale (NOS) was adopted to evaluate the study quality. Pooled odds ratios or mean differences for individual risk factors were estimated using the Mantel-Haenszel and inverse-variance methods. Results: They provided a total of 1940 patients (286 with delirium and 1654 without), and predominantly included patients undergoing head and neck cancer surgery. The incidence of postoperative delirium ranged from 11.50% to 36.11%. Ten statistically significant risk factors were identified in pooled analysis. Old age, age >70 years, male sex, duration of surgery, history of hypertension, blood transfusions, tracheotomy, American Society of Anesthesiologists physical status grade at least III, flap reconstruction and neck dissection were more likely to sustain delirium after head and neck cancer surgery. Conclusion: Delirium is common in patients undergoing major head neck cancer surgery. Several risk factors were consistently associated with postoperative delirium. These factors help to highlight patients at risk of developing delirium and are suitable for preventive action.
Preeclampsia is a common pregnancy-specific disorder characterized by elevated blood pressure and proteinuria. Activation of the maternal immune system and impaired placental angiogenesis are thought to contribute to the pathogenesis of preeclampsia. TLR9 (Toll-like receptor 9) plays a role in innate immunity, defending the organism against infection. The purpose of this study was to determine whether TLR9 inhibits angiogenesis at the fetomaternal interface under conditions of preeclampsia. We confirmed the downregulation of VEGFA (vascular endothelial growth factor A) and upregulation of TLR9 and sFLT1 (soluble vascular endothelial growth factor receptor 1) in placentas from preeclamptic women. Then, we established a mouse model with preeclampsia-like symptoms using the synthetic TLR9 agonist CpG (cytidine-phosphate-guanosine)-ODN (oligodeoxynucleotide; ODN1826). We observed the downregulation of VEGFA and the upregulation of sFLT1 in placentas from the preeclampsia-like animal model and in trophoblasts treated with CpG-ODN (ODN2006). In addition, silencing TLR9 promoted the migration and invasion of HTR8/SVneo cells. In conclusion, TLR9 is capable of robustly suppressing angiogenesis by differentially regulating the expression of VEGFA and sFLT1 at the fetomaternal interface, potentially contributing to the development of preeclampsia.
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