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ObjectivesNut consumption has been associated with a lower risk of type 2 diabetes, metabolic syndrome and insulin resistance. However, its effect on the risk of non-alcoholic fatty liver disease (NAFLD) is unknown. Therefore, we investigated the relationship between nut consumption and NAFLD risk.Setting and participantsWe conducted a retrospective case-control study including 534 patients diagnosed with NAFLD and 534 controls matched by sex and age (±5 years) from the Affiliated Nanping First Hospital of Fujian Medical University in China.Main outcome measuresInformation on dietary intake was collected using a semiquantitative food frequency questionnaire and nut consumption was calculated. Nut consumption was categorised using quartiles based on the distribution of daily nut intake of the controls. Binary logistic regression models were used to estimate ORs and the 95% CIs for the association between nut consumption and NAFLD risk.ResultsAfter adjusting for potential confounding variables, nut consumption was not associated with NAFLD risk in the overall sample. When the fully adjusted model was stratified by sex, a significant inverse association was found between high nut consumption and NAFLD only among the men in the highest quartile (OR=0.43; 95% CI 0.26 to 0.71;Ptrend =0.01). The inverse association of nut consumption with NAFLD risk in men remained significant after controlling for other known or suspected risk factors for NAFLD.ConclusionsDiets with a higher intake of nuts may be associated with a decreased risk of NAFLD, particularly in men.

Parkinson's disease (PD) is a neurodegenerative disease which results in damage in neuronal cells. Insulin-like growth factor (IGF)-1 was previously reported to play a role of neuroprotection in some diseases. Nitric oxide (NO) can also regulate neuronal cells. However, the mechanisms underlying IGF-1 and NO in PD still need to be elucidated. In present study, we explored the interaction between IGF-1 and inducible Nitric-Oxide Synthase (iNOS) in PD progression. We firstly constructed PD models by methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or MPP + treatment. Then RT-qPCR revealed that IGF-1 expression was downregulated while iNOS expression was upregulated in MPTP model. Moreover, IGF-1 elevation or iNOS depletion enhanced cell viability and blocked cell apoptosis. Rescue assay disclosed iNOS overexpression reversed the effect on viability and apoptosis mediated by IGF-1 upregulation. Furthermore, IGF-1 was identified to positively regulate miR-302b-5p which could target iNOS. MiR-302b-5p could abolish the inhibitory function IGF-1 exerted on cell apoptosis and iNOS could counteract miR-302b-5p upregulation-triggered inhibition on cell apoptosis as well. Besides, we observed the deficiency of miR-302b-5p improved the lesioned neurobehavior of MPTP-treated mice. To sum up, present study proved that miR-302b-5p enhanced the neuroprotective effect of IGF-1 in MPTP-induced PD by regulating iNOS, recommending a novel therapeutic target for PD treatment. Significance of the study: In this study, we mainly explored that IGF-1 was decreased while iNOS was boosted in MPTP-induced PD mice model; IGF-1 suppressed while iNOS promoted MPP +-induced toxicity and apoptosis in SH-SY5Y cells; miR-302b-5p ehanhced the neuroprotective effect of IGF-1 via targeting Inos; deficiency of miR-302b-5p improved the lesioned neurobehavior of MPTP-treated mice.

Correlation was sought between serum intestinal fatty acid binding protein (I-FABP), blood routine examination indexes, and necrotizing enterocolitis (NEC) disease classification. According to Bell-NEC grade, 86 children with NEC were divided into mild group (46 cases) and severe group (40 cases). Serum I-FBAP and blood routine indices including white blood cells (WBC), platelets (PLT), neutrophils and lymphocytes were determined. Serum levels of I-FABP and WBC in severe group were higher than those in mild group (both p <0.001), and serum level of PLT was lower than that in mild group (p <0.001). NEC grade was positively correlated with I-FABP and WBC (r=0. 930, p <0.001; r=0. 946, p <0.001), negatively correlated with PLT (r=-0. 602, p <0.001), and had weak correlation with neutrophils and lymphocytes (r=0. 186, p=0. 087; r=0. 072, p=0. 509). In conclusion, serum levels of I-FABP, WBC and PLT were correlated with the severity of NEC in children, which could be used as a reference index to judge prognosis of NEC children.

Parkinson’s disease (PD) is a common neurodegenerative disease that severely affects the quality of life of patients. There is no specific drug for PD up to now. Previous studies have shown that neuroinflammation plays an important role in the pathogenesis of PD. Isoliquiritigenin (ILG) is thought to have a variety of biological activities including anti-inflammatory. However, to date, no studies have reported the role of ILG on neuroinflammation in PD in vivo. This study aimed to investigate the effect of ILG on PD in vivo and its mechanism, and to provide an experimental basis for clinical treatment of PD. Our results showed that ILG at a concentration of 20 mg/kg was effective in reducing the number of rotations in PD mice. In addition, ILG increased the expression of tyrosine hydroxylase and decreased the expression of α-synuclein. The results also showed that ILG reduced the expression of Iba1, IL-1β, IL-6, and TNF-α. Not only that, ILG also upregulated the expression of Nrf2 and NQO-1 in vivo. Our results suggest that ILG significantly attenuates neurological deficits in PD, and the mechanism may be through the activation of the Nrf2/NQO-1 signaling pathway to reduce neuroinflammation. Moreover, our findings provide a new therapeutic strategy for PD.