Background: Acute right heart failure occurs in patients with pulmonary artery hypertension (PAH) with exposure to acute inflammation, the mortality rate is very high when right heart failure occurs. Biomarkers that can be used to detect acute right heart failure in patients with pulmonary hypertension need to be studied.Methods: A PAH rat model was established using monocrotaline, and lipopolysaccharide was used to induce acute right heart failure. The Agilent rat miRNA microarray, Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to assess the microRNA expression of PAH rats. The expression of up-and downregulated miRNAs in plasma from PAH patients with acute right heart failure was validated with quantitative reverse transcription polymerase chain reaction (qRT-PCR).Then, the Wilcoxon matched paired test and receiver operating characteristic (ROC) curve analysis were performed.Results: Thirty-three miRNAs were upregulated, and 7 miRNAs were downregulated in plasma of PAH rats with acute right heart failure. In the plasma of PAH patients, the miR-212-3p level was inversely correlated with the level of NT-pro BNP, and the area under the ROC curve was 0.751.Conclusions: These results suggest that the reduction of the expression of MIR-212-3p may be a biomarker for PAH patients with right heart dysfunction.

Background: The mechanism underlying delirium, a common acute fluctuating mental state, may be related to the activation of a neuroinflammatory response. In this study, we attempted to investigate whether plasma inflammatory response markers, vascular and cerebrovascular injury-related markers, and neurodegeneration-associated markers were associated with emergence delirium (ED). Methods: Patients aged 50 years or above who underwent elective laparoscopic surgery under general anesthesia were included in this study. Delirium was assessed postoperatively with the Richmond Agitation Sedation Scale (RASS) and the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) scale. Plasma samples were collected from ED patients and non-ED patients to test concentrations of inflammation markers, including interleukin 6 (IL-6), chitinase 3-like 1 (CHI3L1), S100 calciumbinding protein B (S100B), lipoprotein-associated phospholipase-A2 (Lp-PLA2), and macrophage migration inhibitory factor (MIF); vascular and cerebrovascular injury-related markers, including intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM-1); and neurodegeneration-associated markers, including alpha-synuclein (α-Syn) and β-secretase 1 (BACE1). Binary logistic regression analysis was performed to analyze the relationship between biomarkers and ED, and receiver operating characteristic (ROC) curves were used to analyze the diagnostic value of biomarkers. Results: A total of 104 patients were included in this study, with an average age of 63.69 ± 7.21. IL-6 (OR = 2.73, 95% CI: 1.66-6.44, P = 0.022), S100B (OR = 4.74, 95% CI: 1.88-11.95, P = 0.001), and BACE1 (OR = 6.54, 95% CI: 2.57-16.65, P < 0.000) were independent biological indicators for the occurrence of ED.CHI3L1, Lp-PLA2, MIF, ICAM-1, VCAM-1, and α-Syn were unrelated to ED. Plasma BACE1 level had a possible diagnostic value for ED [area under curve (AUC) = 0.75, 95% CI: 0.66-0.85], whereas plasma IL-6 (AUC = 0.62, 95% CI: 0.51-0.73) and S100B (AUC = 0.65, 95% CI: 0.54-0.76) levels had little diagnostic value for distinguishing ED vs. non-ED. Conclusion: Higher levels of systemic inflammation marker IL-6, cerebral inflammation marker S100B, and neurodegeneration-associated marker BACE1 are related to ED. Plasma BACE1 may be a potential diagnostic biomarker for ED.

Background: Inflammation promotes the progression of Alzheimer’s disease (AD). In this study, we explored the effect of dexmedetomidine on inflammation and cognitive function in a mouse model of AD.Methods: 5xFAD mice were intragastrically administered saline, dexmedetomidine, or dexmedetomidine and yohimbine for 14 days. The effects of dexmedetomidine on the acquisition and retention of memory in the Morris water-maze test and Y maze were evaluated. The deposition of amyloid beta protein (Abeta) and cytokine levels in the hippocampus were assessed. The expression of Bace1 protein and NFκB-p65 protein was assessed by Western blotting.Results: Compared with WT mice, 5xFAD mice exhibited cognitive impairment in the Morris water maze test and Y maze test. Cognitive decline was alleviated by dexmedetomidine and this was reversed by the α2 adrenoceptor antagonist yohimbine. Compared with saline treatment, dexmedetomidine led to a reduction in the Abeta deposition area (p &lt; 0.05) and in the mean gray value (p &lt; 0.01) in the hippocampus of 5xFAD mice. Compared with saline treatment, dexmedetomidine inhibited the activation of astrocytes and microglia in the hippocampal DG of 5xFAD mice and reduced the area of GFAP (p &lt; 0.01) and IBA1 (p &lt; 0.01). The level of IL-1β in the hippocampus decreased significantly after dexmedetomidine treatment compared with saline treatment in 5xFAD mice (p &lt; 0.01). Yohimbine neutralized the effects of dexmedetomidine. Dexmedetomidine inhibited the expression of BACE1 and NF-κB p65 (p &lt; 0.01), and these changes were reversed by yohimbine treatment.Conclusion: Dexmedetomidine alleviates cognitive decline, inhibits neuroinflammation, and prevents the deposition of Abeta in 5xFAD mice. The effect is mediated by the α2 adrenoceptor-mediated anti-inflammatory pathway. Dexmedetomidine may be effective for the treatment of AD and a better choice for the sedation of AD.