Objective To investigate the diagnostic value and optimal threshold value of plasma 1,3-β-D-glucan test (G test)in the invasive fungal infections (IFI).Methods 46 patients diagnosed with IFI in our hospital from February 2012 to March 2014 were enrolled in this study,and 30 patients without IFI underwent surgical elective surgery in our hospital were selected as the neg-ative controls.The plasma 1,3-β-D-glucan content was quantitatively detected by using MB-80 microbial dynamic rapid detection system and its supporting G test kit.The results were evaluated by ROC curve for the determination of the optimal threshold value of G test.Results The plasma 1,3-β-D-glucan levels were (45.28±44.50)pg/mL in the IFI group and (8.62±4.85)pg/mL in the control group respectively,and the difference was statistically significant (P <0.05 ).The results of ROC curve analysis showed that the optimal threshold value of plasma 1 ,3-β-D-glucan used for diagnosis of IFI was 14.7 pg/mL;the area under the curve was up to 0.937;95% CI was between 0.888 and 0.990;the sensitivity and specificity were 88.9% and 90.3% respectively;G test had a better diagnostic efficiency.Conclusion The plasma 1 ,3-β-D-glucan test has a diagnostic application value for IFI,which can be used as the early warning indicator of IFI.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.
Anilides/pharmacology* ; Cerebral Hemorrhage/drug therapy* ; Hematoma/drug therapy* ; Humans ; Macrophages ; Microglia ; Neuroprotection ; PPAR gamma ; Retinoid X Receptor alpha