Flexible and wearable biosensors have received tremendous attention over the past decade owing to their great potential applications in the field of health and medicine. Wearable biosensors serve as an ideal platform for real-time and continuous health monitoring, which exhibit unique properties such as self-powered, lightweight, low cost, high flexibility, detection convenience, and great conformability. This review introduces the recent research progress in wearable biosensors. First of all, the biological fluids often detected by wearable biosensors are proposed. Then, the existing micro-nanofabrication technologies and basic characteristics of wearable biosensors are summarized. Then, their application manners and information processing are also highlighted in the paper. Massive cutting-edge research examples are introduced such as wearable physiological pressure sensors, wearable sweat sensors, and wearable self-powered biosensors. As a significant content, the detection mechanism of these sensors was detailed with examples to help readers understand this area. Finally, the current challenges and future perspectives are proposed to push this research area forward and expand practical applications in the future.

To evaluate the effects on biochemicals, antioxidants, immune responses and disease resistance of the snakehead fish, following exposure to deltamethrin at 0.061, 0.121, 0.242, 0.485 and 0.970 μg/L. After 28 d, the biochemical, the levels of antioxidant enzymes and immune enzymes in liver, spleen, kidney and intestine were negatively related to the concentrations of deltamethrin exposure. Likewise, the survival rates of the fish after 7 d challenge with Aeromonas veronii were negatively related. The levels of IL-1β, IL-8, TNF-α, Hsp70 and malondialdehyde in liver, spleen, kidney and intestine were positively connected to the concentrations of deltamethrin exposure. Results demonstrated that environmentally relevant concentrations (0.121, 0.242, 0.485 and 0.970 μg/L) inhibited the biochemicals, antioxidants and immune responses and disease resistance of snakehead fish.

Cementogenesis is of great importance for normal teeth root development and is involved in the repair process of root resorption caused by orthodontic treatment. As highly differentiated mesenchymal cells, cementoblasts are responsible for this process under the regulation of many endogenous agents. Among these molecules, sclerostin has been much investigated recently for its distinct antagonism effect on bone metabolism. Encoded by the sost gene, sclerostin is expressed in osteocytes and cementocytes of cellular cementum. it is still unclear. In the current study, we investigated the effects of sclerostin on the processes of proliferation and differentiation; a series of experiments including MTT, apoptosis examination, alkaline phosphatase (ALP) activity, gene analysis, and alizarin red staining were carried out to evaluate the proliferation and differentiation of cementoblasts. Protein expression including osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) were also checked to analyze changes in osteoclastogenesis. Results show that sclerostin inhibits cementoblasts proliferation and differentiation, and promotes osteoclastogenesis. Interestingly, the monoclonal antibody for sclerostin has shown positive effects on osteoporosis, indicating that it may facilitate cementogenesis and benefit the treatment of cementum related diseases.

Ginsenoside Rh2 (G-Rh2), a rare ginsenoside isolated from red ginseng, has considerable anti-cancer activity and induces apoptosis in a variety of cancer cells, but its activity in esophageal cancer cells is unclear. In this study, we examined the cytotoxic activity of (20S) G-Rh2 in highly differentiated esophageal squamous ECA109 cells and poorly differentiated esophageal squamous TE-13 cells. (20S) G-Rh2 exerted intense cytotoxicity in ECA109 and TE-13 cells with an IC50 of 2.9 and 3.7 μg/mL, respectively. After treatment with G-Rh2, Bcl-2, and Bcl-xL, the two main anti-apoptosis Bcl-2 family proteins upregulated, and Bax and Bak, the two key pro-apoptosis proteins translocated to mitochondria in both cell lines. At the same time, cytochrome c and Smac released from mitochondria, followed by caspase-9 activation, indicating that a mitochondria-mediated intrinsic apoptosis pathway was activated in both cell lines upon treatment with (20S) G-Rh2. It is noteworthy that (20S) G-Rh2 upregulated the transcription and protein expression of two death receptors, Fas and DR5, and subsequently activated Caspase-8 in the TE-13 cells but not in the ECA109 cells. Taken together, we demonstrated the potent anti-esophageal cancer cell activity of (20S) G-Rh2 and showed its working mechanism in two differentiated esophageal cancer cells, which can provide important evidence for developing an effective strategy for anti-esophageal cancer treatment.