Throat cancer treatment involves surgical removal of the tumor, leaving patients with facial disfigurement as well as temporary or permanent loss of voice. Surface electromyography (sEMG) generated from the jaw contains lots of voice information. However, it is difficult to record because of not only the weakness of the signals but also the steep skin curvature. This paper demonstrates the design of an imperceptible, flexible epidermal sEMG tattoo-like patch with the thickness of less than 10 μm and peeling strength of larger than 1 N cm −1 that exhibits large adhesiveness to complex biological surfaces and is thus capable of sEMG recording for silent speech recognition. When a tester speaks silently, the patch shows excellent performance in recording the sEMG signals from three muscle channels and recognizing those frequently used instructions with high accuracy by using the wavelet decomposition and pattern recognization. The average accuracy of action instructions can reach up to 89.04%, and the average accuracy of emotion instructions is as high as 92.33%. To demonstrate the functionality of tattoo-like patches as a new human-machine interface (HMI) for patients with loss of voice, the intelligent silent speech recognition, voice synthesis, and virtual interaction have been implemented, which are of great importance in helping these patients communicate with people and make life more enjoyable.

Background. Intermediate coronary stenosis (ICS) is defined as a visually estimated percentage of diameter stenosis ranging between 40% and 70% by conventional coronary angiography (CAG). Whether to perform percutaneous coronary intervention (PCI) for these lesions is a challenge in clinical practice. The fractional flow reserve (FFR) can guide treatment by determining the functional significance of ICS. Studies have shown that some clinical indicators can be used to predict FFR. However, there is little research on this in the Chinese population. Methods. We retrospectively analyzed 690 patients who underwent FFR measurements to determine the functional significance of a single ICS. Patients were divided into 2 groups: FFR ≤0.8 (n = 280) and FFR >0.8 (n = 410). We compared the clinical factors between the two groups and performed multivariate logistic regression analyses to explore the risk factors. In addition, receiver-operating characteristic (ROC) curves were constructed for FFR ≤0.8 diagnoses. Results. The mean UHR (uric acid to high-density lipoprotein cholesterol ratio) level was significantly higher in the FFR ≤0.8 group ( p < 0.001 ). UHR corrects negatively with FFR (r = −0.44, p < 0.001 ). High-level UHR was an independent risk factor for the FFR ≤0.8 (OR = 7.17, 95% CI 4.17–12.34). The area under the curve (AUC) of the UHR diagnostic capacity for the FFR ≤0.8 is 0.77, with 77.3% sensitivity and 68.2% specificity. Conclusion. UHR levels were significantly increased in patients with hemodynamically significant coronary lesions. UHR is a novel predictor of functionally significant lesions in patients with a single-vessel disease of ICS.

Aging augments postischemic apoptosis via incomplete mechanisms. Our previous animal study suggests that in addition to proapoptotic effects, lncRNAs also exert antiapoptotic effects in cardiomyocytes. However, whether this unexpected phenomenon exists in humans is unknown. In the present study, we investigated the relationship between aging and apoptosis regulation in human blood samples and confirmed their role by utilizing the cardiomyocyte lines (AC16 cells). Human blood samples were collected from 20 pairs of older adult and young volunteers. Age-different apoptotic regulatory lncRNAs and miRNAs were identified by microarray and bioinformatics analysis. The results indicated that lncRNA (NONHSAT069381 and NONHSAT140844) and miRNA (hsa-miR-124-5p and hsa-miR-6507-5p) were increased in aging human blood, confirmed by both bioinformatics analysis and polymerase chain reaction (PCR). Overexpression of NONHSAT069381 in AC16 cells increased caspase-3 levels and increased cardiomyocyte apoptotic cell death (determined by TUNEL staining and caspase activity assays) after hypoxia/reoxygenation (H/R), while overexpression of NONHSAT140844 increased X-chromosome-linked inhibitor of apoptosis protein (XIAP) content and decreased the myocardial apoptotic cell death. Furthermore, luciferase reporter assay revealed that hsa-miR-124-5p might be a mediator between NONHSAT069381 and mCASP3 and hsa-miR-6507-5p might be a mediator between NONHSAT140844 and mXIAP. Overexpression of hsa-miR-124-5p decreased caspase-3 levels and overexpression of hsa-miR-6507-5p decreased XIAP content in AC16 cells. We have found evidence that lncRNAs are important regulatory molecules in aging-mediated effects upon apoptosis. More interestingly, besides apoptosis-promoting effects, aging also inhibits myocardial apoptosis after H/R. This phenomenon also exists in the human cardiomyocyte line.