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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. 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. MMRi62 chemical structure 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. #link# 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.