How Does Income Inequality Influence Environmental Regulation in the Context of Corruption? A Panel Threshold Analysis Based on Chinese Provincial Data.

The question of how the income inequality of residents affects the level of environmental regulation in the context of official corruption was the core research issue of this study. We analyzed this problem using the panel threshold regression model from 26 provinces in China from 1995 to 2017. We found that when there is no official corruption, the widening of the residents' income inequality promotes stricter environmental regulations; when the corruption problem is serious, the expansion of the residents' income inequality leads to the decline in environmental standards; that is, the impact of residents' income inequality on environmental regulation has a threshold effect due to corruption. In addition, the threshold effect due to corruption of all residents' income inequality on environmental regulation is mainly generated by the urban residents' income inequality and the urban-rural income inequality. This paper contributes to the literature that concentrates on the relationship between income inequality and environmental regulation, and shows that corruption is a key factor that can deeply influence that relationship. The research conclusion shows that increasing anti-corruption efforts can not only maintain national political stability, social fairness, and justice, but also be a powerful measure for environmental pollution governance.

Tooth loss as a risk factor for dementia: systematic review and meta-analysis of 21 observational studies.

BACKGROUND: Tooth loss is suggested to be associated with an increased risk of dementia in many studies. But the relationship between tooth loss and dementia is not yet fully understood. This systematic review and meta-analysis aimed to determine the relative effect of tooth loss on dementia risk. METHODS: An electronic search of PubMed, Scopus, Embase, and Web of Knowledge was conducted in March 2018 to identify relevant observational studies with the English language restriction. Studies were included if they assessed the relationship between tooth loss and risk of dementia. Study quality was detected by the modified Downs and Black scale. Odds risks (ORs) were pooled using a random-effects model in the crude model. RESULTS: The literature search initially yielded 1574 articles, and 21 observational studies published between 1994 and 2017 were finally included for the analyses. The crude results with random-effects model showed that patients with multiple tooth loss had higher incidence of dementia (OR 2.62, 95% CI 1.90-3.61, P < 0.001, I2 = 90.40%). The association remained noted when only adjusted results were pooled from 18 studies (OR 1.55, 95% CI 1.41-1.70, P = 0.13, I2 = 28.00%). Meta-regression analysis showed that study design explained about 16.52% of heterogeneity in the crude model. The overall quality rating scores of studies ranged from 11 to 16. CONCLUSIONS: Findings from this review evidenced that tooth loss is positively associated with an increased risk of dementia in adults. Future well-designed longitudinal researches examining the direct and indirect relationship between tooth loss and dementia risk are encouraged.

Protective effects of DL­3­n­butylphthalide in the lipopolysaccharide­induced mouse model of Parkinson's disease.

DL­3­n­butylphthalide (NBP) is extracted from rapeseed and exhibits multiple neuroprotective effects, exerted by inhibiting the inflammatory process, including reducing oxidative stress, improving mitochondrial function and reducing neuronal apoptosis. The present study aimed to investigate the neuroprotective effects of NBP in a lipopolysaccharide (LPS)­induced mouse model of Parkinson's disease (PD). The behavior of mice was assessed using the rotarod test and open­field test, the amount of tyrosine hydroxylase in the substantia nigra pars compacta was evaluated by immunohistochemistry, and the levels of phosphorylated c­Jun N­terminal kinase (JNK), mitogen­activated protein kinase 14 (p38) and extracellular signal­regulated kinase 1 were determined by western blotting. It was demonstrated that the LPS­induced behavioral deficits were significantly improved. LPS­induced dopaminergic neurodegeneration was relieved following treatment with NBP, as determined from tyrosine hydroxylase­positive cells. Phosphorylation of JNK and p38 was significantly inhibited following treatment with NBP. Therefore in the present study, a role for NBP has been established in the treatment of a PD murine model, laying the experimental basis for the treatment of PD with this agent.