The impact of pre-operative depression on pain outcomes after major surgery: a systematic review and meta-analysis.

Symptoms of depression are common among patients before surgery. Depression may be associated with worse postoperative pain and other pain-related outcomes. This review aimed to characterise the impact of pre-operative depression on postoperative pain outcomes. We conducted a systematic review of observational studies that reported an association between pre-operative depression and pain outcomes after major surgery. Multilevel random effects meta-analyses were conducted to pool standardised mean differences and 95%CI for postoperative pain scores in patients with depression compared with those without depression, at different time intervals. A meta-analysis was performed for studies reporting change in pain scores from the pre-operative period to any time-point after surgery. Sixty studies (n = 501,962) were included in the overall review, of which 18 were eligible for meta-analysis. Pre-operative depression was associated with greater pain scores at < 72 h (standardised mean difference 0.97 (95%CI 0.37-1.56), p = 0.009, I2 = 41%; moderate certainty) and > 6 months (standardised mean difference 0.45 (95%CI 0.23-0.68), p < 0.001, I2 = 78%; low certainty) after surgery, but not at 3-6 months after surgery (standardised mean difference 0.54 (95%CI -0.06-1.15), p = 0.07, I2 = 83%; very low certainty). The change in pain scores from pre-operative baseline to 1-2 years after surgery was similar between patients with and without pre-operative depression (standardised mean difference 0.13 (95%CI -0.06-0.32), p = 0.15, I2 = 54%; very low certainty). Overall, pre-existing depression before surgery was associated with worse pain severity postoperatively. Our findings highlight the importance of incorporating psychological care into current postoperative pain management approaches in patients with depression.

Postoperative delirium, neuroinflammation, and influencing factors of postoperative delirium: A review.

Postoperative delirium (POD) is an acute cognitive dysfunction that is mainly characterized by memory impairment and disturbances in consciousness. POD can prolong the hospital stay and increase the 1-month mortality rate of patients. The overall incidence of POD is approximately 23%, and its prevalence can go up to 50% in high-risk surgeries. Neuroinflammation is an important pathogenic mechanism of POD that mediates microglial activation and leads to synaptic remodeling. Neuroinflammation, as an indispensable pathogenesis of POD, can occur due to a variety of factors, including aseptic inflammation caused by surgery, effects of anesthetic drugs, disruption of the blood-brain barrier, and epigenetics. Understanding these factors and avoiding the occurrence of risk factors may help prevent POD in time. This review provides a brief overview of POD and neuroinflammation and summarizes various factors affecting POD development mediated by neuroinflammation, which may serve as future targets for the prevention and treatment of POD.

Transcriptomic changes during stage progression of mycosis fungoides.

BACKGROUND: Mycosis fungoides (MF) is the most common cutaneous T-cell lymphoma, which in the early patch/plaque stages runs an indolent course. However, ~25% of patients with MF develop skin tumours, a hallmark of progression to the advanced stage, which is associated with high mortality. The mechanisms involved in stage progression are poorly elucidated. OBJECTIVES: We sought to address the hypothesis of MF cell trafficking between skin lesions by comparing transcriptomic profiles of skin samples in different clinical stages of MF. METHODS: We performed whole-transcriptome and whole-exome sequencing of malignant MF cells from skin biopsies obtained by laser-capture microdissection. We compared three types of MF lesions: early-stage plaques (ESP, n = 12) as well as plaques and tumours from patients in late-stage disease [late-stage plaques (LSP, n = 10) and tumours (TMR, n = 15)]. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to determine pathway changes specific for different lesions which were linked to the recurrent somatic mutations overrepresented in MF tumours. RESULTS: The key upregulated pathways during stage progression were those related to cell proliferation and survival (MEK/ERK, Akt-mTOR), T helper cell (Th)2/Th9 signalling [interleukin (IL)4, STAT3, STAT5, STAT6], meiomitosis (CT45A1, CT45A3, STAG3, GTSF1, REC8) and DNA repair (PARP1, MYCN, OGG1). Principal coordinate clustering of the transcriptome revealed extensive gene expression differences between early (ESP) and advanced-stage lesions (LSP and TMR). LSP and TMR showed remarkable similarities at the level of the transcriptome, which we interpreted as evidence of cell percolation between lesions via haematogenous self-seeding. CONCLUSIONS: Stage progression in MF is associated with Th2/Th9 polarization of malignant cells, activation of proliferation, survival, as well as increased genomic instability. Global transcriptomic changes in multiple lesions may be caused by haematogenous cell percolation between discrete skin lesions.

Effect of IL-1ra on human dental pulp cells and pulpal inflammation.

AIM: This study was conducted to investigate the effect of interleukin-1 receptor antagonist (IL-1ra) on the LPS-induced interleukin-1beta (IL-1beta) synthesis in human dental pulp cells and to assess the role of IL-1ra in pulpal inflammation. METHODS: IL-1beta from human dental pulp cells (HDP) was measured by sandwich ELISA; IL-1ra expression in pulpal tissue was detected by immunohistochemical staining. RESULTS: Stimulation of HDP with increasing concentrations of FnLPS resulted in dose-dependent IL-1beta production. The addition of IL-1ra reduced FnLPS-induced IL-1beta synthesis in human dental pulp cells. Significant inhibition of the FnLPS-induced IL-1beta synthesis was observed when IL-1ra was added before treating with FnLPS for 60 min. Large numbers of IL-1ra positive neutrophils, plasmacytes, endothelial cells and lymphocytes were observed in inflamed pulp tissue. CONCLUSIONS: IL-1ra could reduce LPS-stimulated IL-1beta synthesis, suggesting that IL-1ra may play a role in pulpitis.

Expression of amelogenins in developing embryonic and neonatal rat teeth.

OBJECTIVE: Tooth enamel is formed by ameloblasts, which are derived from epitheliums and secrete an extracellular matrix containing a complex arrangement of protein components. The epithelial component, referred to as the enamel organ, contains a layer of cells that secrete an organic matrix that biomineralizes to become tooth enamel. Adjacent ectomesenchyme cells differentiate to become dentinproducing odontoblasts. These two mineralized matrices form the crown of the vertebrate tooth. Therefore, amelogenins play a critical role in tooth enamel formation. We have examined the expression patterns and tissue distribution of amelogenins in their developmental stages in order to build a foundation for further study. METHODS: Amelogenin expression patterns and tissue distribution in developing teeth of embryonic (E17E19) and neonatal (1 to 9 days old) Wistar rats were examined by immunohistochemistry. RESULTS: Positive immunostaining for amelogenin was first observed in the late embryonic stage, E18. The highest level of amelogenin was noted in neonatal secretary ameloblasts, fully engaged in enamel matrix deposition (3 to 5 days old). After that, amelogenin expression continued at a lower level (6, 7, 8 days old). There was no amelogenin staining observed in the maturation stage of development (9 days old). CONCLUSIONS: Amelogenin expression occurs as early as the polarization stage of pre-ameloblasts. Amelogenin was also expressed, but at a low level, in post-secretary stages of amelogenesis. Odontoblasts did not contain detectable amelogenin.