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The instability of organic field-effect transistors (OFETs) is one key obstacle to practical application and is closely related to the unstable aggregate state of organic semiconductors (OSCs). However, the underlying reason for this instability remains unclear, and no effective solution has been developed. Herein, we find that the intrinsic tensile and compressive strains that exist in OSC films are the key origins for aggregate state instability and device degradation. We further report a strain balance strategy to stabilize the aggregate state by regulating film thickness, which is based on the unique transition from tensile strain to compressive strain with increasing film thickness. Consequently, a strain-free and ultrastable OSC film is obtained by regulating the film thickness, with which an ultrastable OFET with a five-year lifetime is realized. This work provides a deeper understanding of and a solution to the instability of OFETs and sheds light on their industrialization.

Background Antihypertensive drug use is inconsistently associated with the risk of dementia, Alzheimer's disease, cognitive impairment, and cognitive decline. Therefore, we conducted a meta-analysis of available prospective cohort studies to summarize the evidence on the strength of these relationships. Methods Three electronic databases including MedLine, Embase, and the Cochrane Library were searched to identify studies from inception to April 2017. Only prospective cohort studies that reported effect estimates with corresponding 95% confidence intervals (CIs) of dementia, Alzheimer's disease, cognitive impairment, and cognitive decline for antihypertensive drug use versus not using antihypertensive drugs were included. Results We included 10 prospective cohort studies reporting data on 30,895 individuals. Overall, participants who received antihypertensive drugs had lower incidence of dementia (relative risk [RR]: 0.86; 95% CI: 0.75–0.99; p = 0.033), while there was no significant effect on the incidence of Alzheimer's disease (RR: 0.83; 95% CI: 0.64–1.09; p = 0.154), cognitive impairment (RR: 0.89; 95% CI: 0.57–1.38; p = 0.596), and cognitive decline (RR: 1.11; 95% CI: 0.86–1.43; p = 0.415). Further, the incidence of Alzheimer's disease might be affected by antihypertensive drug use in participants with specific characteristics. Conclusions Antihypertensive drug use was associated with a significantly reduced risk of dementia, but not with the risk of Alzheimer's disease, cognitive impairment, and cognitive decline.

This study aimed to explore the effects of astragaloside IV on metabolic syndrome induced by a high-fructose/high-fat diet in rats. Methods: Rats were randomized into four groups: normal control, metabolic syndrome, metabolic syndrome þ intraperitoneal astragaloside 0.5 mg/kg/day, and metabolic syndrome þ intraperitoneal astragaloside 2.0 mg/kg/day (n¼30 per group) for 14 continuous days. Left ventricular functions were evaluated by hemodynamic and echocardiographic parameters. Results: Metabolic syndrome rats had a thicker interventricular septum and left ventricular posterior wall, accompanied by a higher E/A wave ratio, reduced E 0 wave, increased A 0 wave, decreased E 0 /A 0 wave ratio, and higher E/E 0 wave ratio. Astragaloside decreased insulin and triglyceride levels and improved diastolic dysfunction with no effects on systolic function. A high-fructose/high-fat diet also increased oxidative stress and decreased the myocardial endothelial nitric oxide synthase (NOS) dimer ratio, thus impairing nitric oxide (NO) production and reducing cyclic guanosine monophosphate (cGMP) production. Astragaloside increased NO and cGMP production in the myocardium and improved diastolic function. Conclusions: Astragaloside alleviated oxidative stress and restored NO signaling, thus improving myocardial left ventricular diastolic dysfunction in rats with metabolic syndrome. The underlying mechanisms could be associated with alleviation of oxidative stress and activation of the endothelial NOS/NO/cGMP pathway.

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