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D increment, adjusted OR, 1.07; 95% CI 1.01, 1.14) and new-onset IFG (per SD increment, adjusted OR, 1.07; 95% CI 1.02, 1.14). Moreover, a stronger positive association between baseline ALP (per SD increment) with new-onset diabetes was found in participants with total homocysteine (tHcy)  less then  10 μmol/L (adjusted OR, 1.24; 95% CI 1.10, 1.40 vs. ≥ 10 μmol/L adjusted OR, 1.03; 95% CI 0.96, 1.10; P-interaction = 0.007) or FG ≥ 5.9 mmol/L (adjusted OR, 1.16; 95% CI 1.07, 1.27 vs.  less then  5.9 mmol/L adjusted OR, 1.00; 95% CI 0.93, 1.08; P-interaction = 0.009) CONCLUSIONS In this non-diabetic, hypertensive population, higher serum ALP was significantly associated with the increased risk of new-onset diabetes, especially in those with lower tHcy or higher FG levels. Clinical Trial Registration-URL Trial registration NCT00794885 (clinicaltrials.gov). Retrospectively registered November 20, 2008.Traumatic brain injury (TBI) is a subset of brain injury induced by external mechanical forces to the head or neck. this website TBI has been reported to be one of the leading causes of disability, and it causes a huge financial burden around the world. Aloin is the major anthraquinone glycoside extracted from Aloe species, and has presented anti-tumour, anti-oxidative and anti-inflammatory activities. However, few studies have focused the effect of aloin in treatment of TBI. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is the only subset of enzymes which produces solely the reactive oxygen species (ROS). A recent study showed that activation of NOX might aggravate the primary TBI, and among these members, NOX2 is the key member in regulation of uncontrolled ROS expression, and thus plays a critical role in development of inflammatory diseases. Here, we noticed that inhibition of NOX2 combined with aloin treatment promoted the recovery of brain function in a mice model as well as the viability rate in a cell model. A further study found that the inflammation response process was also inhibited after treatment. Then, we found that these effects might be mediated by the PI3K/AKT/mTOR signalling pathway and NOX2 might be a therapeutic target for TBI.Traumatic brain injury (TBI) is the leading cause of death and disability around the world in all age groups. The primary injury of TBI is exacerbated by secondary injury, leading to an increased inflammatory response, cell death and even impairment of neurological function. Bexarotene has been found to improve neurological function in mice in an ApoE-dependent manner, but the detailed mechanism is not fully clear. Upregulated expression of MAPT has been found in mouse models after TBI; therefore, we hypothesized that inhibition of MAPT might contribute to the effects of bexarotene treatment in TBI models. Herein, we found that inhibition of MAPT enhanced the effects of bexarotene in increasing cellular viability and restoring brain function, and expression of anti-oxidative and anti-apoptotic molecules were elevated in response to inhibition of MAPT. These effects might be mediated by activation of the Nrf2/HO-1 signalling pathway and inhibition of the MAPK/NF-kB signalling pathway. Thus, we concluded that inhibition of MAPT might represent a novel treatment target for TBI.The present study was performed to evaluate the protective effects of icariin on cognitive function in a hypoxia-induced neonatal epilepsy rat model. Neonatal epilepsy was induced in rat pups on postnatal day (PD) 20 by induction of hypoxia for 15 minutes. Rats were treated intraperitoneally with icariin at 75 mg/kg 1 hour before the induction of hypoxia. The effects of icariin were examined by estimating seizure stage, cognitive function and parameters of electroencephalography (EEG) in this neonatal epilepsy rat model. Parameters of oxidative stress and expression of proteins were examined in the brain tissue of the neonatal epilepsy rat model by histopathological study and Western blotting analysis, respectively. The results of this study suggest that treatment with icariin ameliorates the changes in seizure stage, number of seizures and parameters of EEG in hypoxia-induced neonatal epilepsy rats. Oxidative stress and apoptosis were decreased in the brain tissue of the icariin treatment group compared to the hypoxia group. Moreover, treatment with icariin ameliorated the altered expression of glutamate ionotropic receptor AMPA type subunit 2 (GluR2) and extracellular receptor kinase (ERK I/II) proteins in the brain tissue of hypoxia-induced epilepsy rats. Histopathological study also showed that icariin treatment improved the histopathology of brain tissue of hypoxia-induced epilepsy rats. In conclusion, the results of the present study suggest that icariin protects against neuronal injury and improves cognitive function in hypoxia-induced neonatal epilepsy rats by modulating the GluR2/ERK I/II pathway.A neuropeptide, Substance P (SP), has mitogenic action in many types of cancer cells mediated via the neurokinin-1 receptor (NK1R). Small molecular NK1R antagonists have been frequently shown to possess anticancer activity both in vivo and in vitro, but there are only a few papers on such activity regarding peptide antagonists. In order to extend the data on this class of compounds, we have compared the effects of a peptide antagonist, [D-Pro2, D-Trp7,9]-Substance P, and a small molecular antagonist, aprepitant on the proliferation of five cancer and three normal cell lines. The comparison was based on three assays cell proliferation test, MTT test and assay for colony formation. Consistently with earlier reports, aprepitant potently reduced cell proliferation in cancer cell lines in all assays, but in contrast to previous works, the compound was not selective and it affected normal cell lines to a similar degree. The studied peptide antagonist, [D-Pro2, D-Trp7,9]-Substance P, was able to decrease proliferation only in a few cell lines, and only in the highest concentration (100 µM). In a lower concentration, a slight pro-proliferative effect was observed in a few cell lines. No statistically significant effects on colony formation were found for this compound.

Forkhead Box M1 (FOXM1) and aryl hydrocarbon receptor (AHR) signaling pathway participate in meningioma development, but their correlation was inadequately studied. The study is aimed to uncover their functions and correlation in malignant meningioma.

Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect FOXM1 expression in malignant meningioma and adjacent tissues. The viability, proliferation, apoptosis and tube formation of meningioma IOMM-Lee and CH157-MN cells transfected with overexpressed FOXM1 were examined with MTT assay, clone formation assay, flow cytometry and tube formation assay, respectively. The expressions of AHR and cytochrome P450 family 1 subfamily A member 1 (CYP1A1) in meningioma and adjacent tissues were detected using qRT-PCR, and the correlation of AHR with FOXM1 was analyzed with Pearson's correlation analysis. Western blot was conducted for measuring the expressions of vascular endothelial growth factor A (VEGFA), AHR and CYP1A1. The cell viability, proliferation, apoptosis and tube formation capability were further determined after treatment with StemRegenin 1 (SR1) (an AHR signaling pathway inhibitor), and transfected with or without overexpressed FOXM1.

FOXM1, AHR and CYP1A1 expressions were upregulated in malignant meningioma tissues. Overexpressed FOXM1 promoted meningioma cell viability, proliferation, tube formation, upregulated expressions of AHR, CYP1A1 and VEGFA, and inhibited the cell apoptosis. AHR was positively correlated with FOXM1. SR1 suppressed meningioma cell growth and the AHR signaling pathway, and also reversed the active effect of FOXM1 on meningioma cells.

FOXM1 may promote malignant meningioma via the AHR signaling pathway, which improved the current understanding of the role of FOXM1 in meningioma.

FOXM1 may promote malignant meningioma via the AHR signaling pathway, which improved the current understanding of the role of FOXM1 in meningioma.Brain ischaemia is one of the leading causes of mortality and disability worldwide, and the damage caused by ischaemia not only induces primary damage but also that induced by ischaemia-reperfusion (I/R) injury. Multiple processes including inflammation and oxidative stress response play important roles in the development of brain ischaemia injury. Sevoflurane is a well-known volatile anaesthetic, and a recent study discovered the role of sevoflurane in suppression of the inflammation response process via inhibition of inflammatory infiltrates and production, maintaining the balance of cytokine responses, although the possible mechanism was not fully clear. NLRC3 is a member of the nucleotide-binding domain and leucine-rich repeat containing (NLR) family, and it has been regarded as a regulator of the inflammation process via the regulation of inflammasome formation, which is an initiator of inflammatory events. In the present study, we found that overexpression of NLRC3 reduced the apoptosis in a cellular model of ischaemia reperfusion, and the expression of pro-inflammatory cytokines was also decreased. Further study found that these effects might be mediated by the TRAF6/TLR4/NF-kB signalling pathway. Thus, we speculate that overexpression might enhance the effect of sevoflurane in inhibiting the inflammatory response process in an ischaemia reperfusion model, which might be a new therapeutic strategy.

To investigate the effects of crocin on proliferation and migration of endogenous neural stem cells and the Notch1 signalling pathway in rats after cerebral ischemia reperfusion.

SD rats were randomly divided into the sham operation group, model group and administration group (crocin). Middle cerebral artery occlusion (MCAO/R) was used to establish the focal cerebral ischemia reperfusion model in rat. After surgical treatment, the treatment group was treated with crocin. Quantitative polymerase chain reaction (qPCR) was used to detect the changes in the expression of Notch1, Bax and bcl-2 proteins in rat endogenous neural stem cells after cerebral ischemia reperfusion. ELISA was used to detect changes in inflammatory factors. Neural stem cells were cultured in vitro, which were divided into the normal control group, the hypoglycaemic deprivation/reoxygenation group, hypoglycaemic deprivation/reoxygenation group with alow concentration of crocin, and hypoglycaemic deprivation/reoxygenation group with ahighng the Notch signalling pathway.

Despite the progress in current treatments, the event-free survival of high-risk neuroblastoma (HR-NB) patients does not exceed 40%-50%, and the prognosis of refractory or relapsed patients is poor, still representing a challenge for pediatric oncologist. Therapeutic Iodine-131 meta-iodobenzylguanidine (Th-

I-MIBG) is a recognized safe and potentially effective treatment for NB.

This retrospective study reports the outcomes of 28 MIBG-avid NB patients with advanced disease either refractory or relapsed, which was undertaken from 1996 to 2014. Th-

I-MIBG was administered shortly before (median 17 days) high-dose chemotherapy with busulfan and melphalan (HD-BuMel) and autologous stem cell rescue (ASCR) at the Gaslini Institute in Genoa, with the aim of analyzing the feasibility, safety, and efficacy of this approach.

Engraftment occurred in all patients after a median of 14 (11-29) and 30 days (13-80) from ASCR for neutrophils and platelets, respectively. No treatment-related deaths were observed. The main high-grade (3-4) toxicity observed was oral and gastrointestinal mucositis in 78.