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BMSCs-derived exosomes restrained apoptosis in hippocampal tissues of depressed rats. BMSCs-derived exosomes and upregulated miR-26a elevated SOD level, lessened MDA, LDH, TNF-α and IL-1β levels, boosted hippocampal neuron proliferation and suppressed apoptosis in depressed rats. CONCLUSION Collectively, our study reveals that miR-26a is lowly expressed in depressed rats, and BMSCs-derived exosomes improve hippocampal neuron injury of rat with depression by upregulating miR-26a. OBJECTIVES The anti-PD-1/PD-L1 therapy has been demonstrated safe and effective for cancer patients. However, our previous data showed that it had no obvious effects on gastric cardia adenocarcinoma (GCA). Thus, we investigated how the expression level of the PD-L1 was affected by the anti-PD-1 therapy, because it has been demonstrated that the PD-L1 level affects the therapeutic efficient of the anti-PD-1 therapy. MATERIALS AND METHODS The mRNA and protein levels of PD-L1 in the GCA tissues and corresponding normal tissues were determined by qPCR and ELISA. Promoter methylation was analyzed by bisulfite sequencing. Finally the methylation of PD-L1 promoter was confirmed in the mice. RESULTS The level of PD-L1 was up-regulated in the GCA tissues when compared to the adjacent non-tumor tissues. The anti-PD1 therapy could reduce the PD-L1 levels in patients with cancer recurrence. The promoter of PD-L1 was more hypermethylated in the secondary GCA after the anti-PD-1 therapy when compared with the adjacent non-tumor tissues or the primary GCA without the anti-PD-1 therapy. Furthermore, the promoter methylation of PD-L1 could be induced by the anti-PD-1 therapy in the mice model. Finally, the anti-PD-1 plus DNA hypomethylating agent azacytidine could significantly suppressed the tumor growth better than the anti-PD-1 therapy. CONCLUSIONS Here we demonstrated that the unresponsiveness of GCA to the anti-PD-1 therapy might result from the promoter methylation and down-regulation of PD-L1. The anti-PD-1 plus azacytidine might be a more promising approach to treat GCA. We investigated the protective effect of the bioactive compound eckol on inflammatory-related skin lesions in vitro. HaCaT cells were stimulated with tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) mixture, and treated with various concentration of eckol (25, 50, and 100 µg/ml). The expression of pro-inflammatory cytokines and chemokines were analyzed by enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR), respectively. Mitogen-activated protein kinase (MAPKs) and nuclear factor-kappa B (NF-κB) signaling pathways regulate immune and inflammation responses. Phosphorylation of MAPKs and NF-κB, indicating activation of respective signaling pathways, was examined by western blot analysis. Treatment of TNF-α and IFN-γ promoted the mRNA expression and production of pro-inflammatory cytokines and chemokines in HaCaT cells. However, eckol significantly suppressed the these mediators. Furthermore, activation of TNF-α/IFN-γ-induced MAPKs and NF-κB signaling pathway was inhibited by eckol treatment. Eckol also hampered the TNF-α/IFN-γ-mediated nuclear translocation of NF-κB p65 in HaCaT cells. Taken together, our findings demonstrate that eckol shows effective protective activity against TNF-α/IFN-γ-induced skin inflammation. The present study investigated the association between preterm birth PT conditions, intrauterine growth restriction IUGR and the combination of both PT-IUGR with infant motor development. A cohort with 1006 children was monitored during prenatal, at birth, and two years of age. Bayley-III screening was used to evaluate of fine and gross motor skills. The data did not indicate an increased risk for motor delays in the PT or IUGR, composed mainly by mild cases. However, the combination of the conditions PT-IUGR increased the risk of delays in motor, which emphasizes the importance of monitoring the motor development of the group. The role of the medial olivocochlear (MOC) reflex has been investigated by assessing changes of cochlear responses (CR) in humans. The CR consists of pre-neural and neural potentials originating from the inner ear, and at high signal levels is dominated by cochlear microphonic (CM). The CM originates from the outer hair cells, where the MOC fibers synapse, and there is little research about using it to investigate the MOC reflex in humans. The current study aimed to investigate the effect of contralateral activation of the MOC reflex on the CR in humans. The CR was recorded in female adults (n = 16) to 500 and 2000 Hz tone burst stimuli presented at 80 dB nHL with and without contralateral broadband noise (CBBN) at 40 dB SPL. Two different methods were utilized to quantify and analyze the CR data peak amplitude and power spectrum. Results revealed enhancement of the CR amplitude with activation of the MOC reflex. selleck chemical Furthermore, on average, enhancement in the CR amplitude was observed to 500 Hz, but not 2000 Hz stimulus. The CR power spectrum findings revealed similar findings to the peak amplitude. These findings indicate the MOC effect is measurable when using a low frequency stimulus, but not high frequency. Moreover, the CR could be used as a potential tool to study the MOC reflex in humans. BACKGROUND Childhood primary angiitis of the central nervous system (cPACNS) is an increasingly recognized inflammatory brain disease in children. CASE PRESENTATION We present a case of a 17-year-old boy with recurrent ischemic events over a short time period. Diagnosis of angiography positive cPACNS was made based on neuroimaging findings while secondary causes or mimics of CNS vasculitis were meticulously excluded. The patient exhibited rapid deterioration of his condition with poor initial response to immunosuppressive treatment. CONCLUSIONS Recognition of cPACNS remains a challenge because of rarity of disease, unexplained etiopathogenesis, protean clinical presentation, as well as lack of specific laboratory and neuroimaging markers. Pregnanediol-3-glucuronide (PdG) is the major terminal metabolite of progesterone, playing an important role in physiological processes, such as the female menstrual cycle, pregnancy (supports gestation), embryogenesis and maternal immune response of humans and other species. Hence, accurate measurement of PdG in serum/plasma is needed for the evaluation of progesterone production. However, such high-specificity determination of PdG is lacking in clinical sample detection. In this study, a highly sensitive and accurate LC-MS/MS method was firstly established for subsequent measurement of PdG in serum of three different female groups thyroid cancer patients (TCs), healthy controls (HCs) and pregnant women. The factors affecting the sample preparation, MS/MS method, gradient elution program, selection of chromatographic column and internal standard (IS) have been optimized in this study. Compared with enzyme immunoassay (EIA) method, we used LC-MS/MS to shorten analysis time, increase sensitivity, raise specificity, simplify sample preparation, and reduce costs.