Low Serum Uric Acid Levels Promote Hypertensive Intracerebral Hemorrhage by Disrupting the Smooth Muscle Cell-Elastin Contractile Unit and Upregulating the Erk1/2-MMP Axis.

Intracerebral hemorrhage (ICH) is a catastrophic stroke with high mortality, and the mechanism underlying ICH is largely unknown. Previous studies have shown that high serum uric acid (SUA) levels are an independent risk factor for hypertension, cardiovascular disease (CVD), and ischemic stroke. However, our metabolomics data showed that SUA levels were lower in recurrent intracerebral hemorrhage (R-ICH) patients than in ICH patients, indicating that lower SUA might contribute to ICH. In this study, we confirmed the association between low SUA levels and the risk for recurrence of ICH and for cardiac-cerebral vascular mortality in hypertensive patients. To determine the mechanism by which low SUA effects ICH pathogenesis, we developed the first low SUA mouse model and conducted transcriptome profiling of the cerebrovasculature of ICH mice. When combining these assessments with pathological morphology, we found that low SUA levels led to ICH in mice with angiotensin II (Ang II)-induced hypertension and aggravated the pathological progression of ICH. In vitro, our results showed that p-Erk1/2-MMP axis were involved in the low UA-induce degradation of elastin, and that physiological concentrations of UA and p-Erk1/2-specific inhibitor exerted a protective role. This is the first report describing to the disruption of the smooth muscle cell (SMC)-elastin contractile units in ICH. Most importantly, we revealed that the upregulation of the p-Erk1/2-MMP axis, which promotes the degradation of elastin, plays a vital role in mediating low SUA levels to exacerbate cerebrovascular rupture during the ICH process.

Wireless Patrol Sign-In System with Mental Fatigue Detection.

Current sign-in methods of patrolling security guards mainly comprise signature, image identification, and fingerprint identification; notably, none of these methods indicate the physical and mental conditions of such guards. In particular, when patrolling security guards perform their duties consecutively for a long period of time, adequate attention should be directed toward their levels of mental fatigue. When a handwriting sign-in system is adopted, security guards may not record their sign-in time accurately, or they may fake signatures during long shifts. In addition, image identification systems cannot comprehensively reflect the physical and mental statuses of on-duty security guards, particularly their levels of fatigue. Monitor fatigue in patrolling security guards is important to avoid burnout and stress in the workplace. Therefore, in this study, a patrolling sign-in system that integrates physiological signals and images was designed. A thermometer, hand dynamometer, and electromyography sensor were combined to measure physiological signals. Results showed that hand grip strength and the median frequency of electromyography signals gradually reduced when muscle fatigue occurred. The system determined whether a security guard had signed in punctually and whether this person should stay on duty. Overall, this system was verified to operate effectively, and it is therefore applicable for monitoring the sign-in of patrolling security guards who work long shifts. This case series study proposed a conceptual prototype of the system; large-scale testing should be performed in subsequent research.