Effects of Smart City Construction on the Quality of Public Occupational Health: Empirical Evidence From Guangdong Province, China.

This article takes the Guangdong Province of China as the research object and uses the difference-in-difference model to evaluate the impact of smart city construction on the quality of public occupational health and intercity differences. The obtained results show that smart city construction significantly improves the quality of public occupational health, and it is still valid after a series of robustness tests. The effect of this policy is stronger in cities that belong to the Pearl River Delta region or sub-provincial level cities. This study indicates that the central government should improve the pilot evaluation system and the performance appraisal mechanism of smart cities from the perspective of top-level design during the process of promoting smart city construction, which aims to correctly guide local governments to promote the construction of smart cities. To achieve the full improvement effect of smart city construction on the quality of public occupational health, local governments should implement smart city strategies in a purposeful and planned way according to the actual situation of the development of the jurisdiction.

Combined therapy of intensive statin plus intravenous rt-PA in acute ischemic stroke: the INSPIRE randomized clinical trial.

OBJECTIVE: To investigate the safety and efficacy of intensive statin in the acute phase of ischemic stroke after intravenous thrombolysis therapy. METHODS: A total of 310 stroke patients treated with rt-PA were randomly scheduled into the intensive statin group (rosuvastatin 20 mg daily × 14 days) and the control group (rosuvastatin 5 mg daily × 14 days). The primary clinical endpoint was excellent functional outcome (mRS ≤ 1) at 3 months, and the primary safety endpoint was symptomatic intracranial hemorrhage (sICH) in 90 days. RESULTS: The intensive statin users did not achieve a favorable outcome in excellent functional outcome (mRS ≤ 1) at 3 months compared with controls (70.3% vs. 66.5%, p = 0.464). Intensive statin also not significantly improved the overall distribution of scores on the modified Rankin scale, as compared with controls (p = 0.82 by the Cochran-Mantel-Haenszel test). The incidence of primary safety endpoint events (sICH) in 90 days did not significantly differ between the intensive statin group and control group (0.6% vs. 1.3%, p > 0.999). CONCLUSION: The INSPIRE study indicated that intensive statin therapy may not improve clinical outcomes compared with the low dose of statin therapy in AIS patients undergoing intravenous thrombolysis, and the two groups had similar safety profile. CLINICAL TRIAL REGISTRATION: URL: http://www.chictr.org . Unique identifier: ChiCTR-IPR-16008642.

Association of aquaporin­1 with tumor migration, invasion and vasculogenic mimicry in glioblastoma multiforme.

The present study aimed to assess the expression and functional role of aquaporin-1 (AQP1) in glioblastoma multiforme (GBM) migration, invasion and vasculogenic mimicry (VM). In the primary human gliomas and human glioma­derived cell lines tested, it was observed that the expression of AQP1 was upregulated. In addition, it was demonstrated that silencing of AQP1 expression resulted in decreased migration and invasion, in addition to vasculogenic mimicry in vitro. It was additionally observed that silencing of AQP1 expression resulted in in vivo inhibition of tumor growth, a decrease in the expression of invasion­associated protein, and suppression of VM formation. Based on these data, it was concluded that AQP1 may serve a role in GBM migration, invasion and VM formation, and that it may serve as a novel diagnostic/prognostic biomarker and a potential therapeutic target.

Liraglutide Ameliorates ß-Amyloid Deposits and Secondary Damage in the Ipsilateral Thalamus and Sensory Deficits After Focal Cerebral Infarction in Rats.

Focal cerebral infarction causes ß-amyloid (Aß) deposition and secondary neuronal degeneration in the ipsilateral thalamus. Thalamus is the subcortical center of sensory, the damage of thalamus could cause sensory deficits. The present study aimed to investigate the protective effects of liraglutide, a long-acting glucagon-like peptide-1 (GLP)-1 receptor agonist, on Aß deposits and secondary damage in the ipsilateral thalamus after focal cerebral infarction. In addition, this study was conducted to investigate whether liraglutide could improve sensory function after focal cerebral infarction. Forty-two male Sprague-Dawley rats were subjected to distal middle cerebral artery occlusion (MCAO) and then randomly divided into liraglutide and vehicle groups, and 14 sham-operated rats as control. At 1 h after MCAO, rats in the liraglutide and vehicle groups were subcutaneously injected with liraglutide (100 µg/kg/d) and isopyknic vehicle, respectively, once a day for 7 days. Sensory function and secondary thalamic damage were assessed using adhesive-removal test and Nissl staining and immunostaining, respectively, at 7 days after MCAO. Terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick end labeling and Western blot were used to detect neuronal apoptosis. The results showed that liraglutide improved sensory deficit compared to the controls. Liraglutide treatment significantly reduced Aß deposition compared with the vehicle treatment. Liraglutide treatment decreased the neuronal loss, astroglial and microglial activation, and apoptosis compared with the vehicle treatment. Liraglutide significantly down-regulated the expression of Bcl-2 and up-regulated that of Bax in the ipsilateral thalamus compared with the vehicle group. These results suggest that liraglutide ameliorates the deposition of Aß and secondary damage in the ipsilateral thalamus, potentially contributing to improve sensory deficit after focal cerebral infarction.

Hyperphosphorylation of tau protein in the ipsilateral thalamus after focal cortical infarction in rats.

Hyperphosphorylation of tau has been considered as an important risk factor for neurodegenerative diseases. It has been found also in the cortex after focal cerebral ischemia. The present study is aimed at investigating changes of tau protein expression in the ipsilateral thalamus remote from the primary ischemic lesion site after distal middle cerebral artery occlusion (MCAO). The number of neurons in the ventroposterior thalamic nucleus (VPN) was evaluated using Nissl staining and neuronal nuclei (NeuN) immunostaining. Total tau and phosphorylated tau at threonine 231 (p-T231-tau) and serine 199 (p-S199-tau) levels, respectively, in the thalamus were measured using immunostaining and immunoblotting. Moreover, apoptosis was detected with terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling (TUNEL) assay. It was found that the numbers of intact neurons and NeuN(+) cells within the ipsilateral VPN were reduced significantly compared with the sham-operated group, but the levels of p-T231-tau and p-S199-tau in the ipsilateral thalamus were increased significantly in rats subjected to ischemia for 3 days, 7 days and 28 days. Furthermore, the number of TUNEL-positive cells was increased in the ipsilateral VPN at 7 days and 28 days after MCAO. Thus, hyperphosphorylated tau protein is observed in ipsilateral thalamus after focal cerebral infarction in this study. Our findings suggest that the expression of hyperphosphorylated tau protein induced by ischemia may be associated with the secondary thalamic damage after focal cortical infarction via an apoptotic pathway.