Although Ti 3 C 2 T x MXene/fabric composites have shown promise as flexible pressure sensors, the effects of MXene composition and structure on piezoresistive properties and the effects of the textile structure on sensitivity have not been systematically studied. Herein, impregnation at room temperature was used as a cost-effective and scalable method to prepare composite materials using different fabrics [plain-woven fabric, twill-woven fabric, weft plain-knitted fabric, jersey cross-tuck fabric, and nonwoven fabric (NWF)] and MXene nanosheets (Ti 3 C 2 T x , Ti 2 CT x , Ti 3 CNT x , Mo 2 CT x , Nb 2 CT x , and Mo 2 TiC 2 T x ). The MXene nanosheets adhered to the fabric surface through hydrogen bonding, resulting in a conductive network structure. The Ti 3 C 2 T x @NWF composite was found to be the optimal flexible pressure sensor, demonstrating high sensitivity (6.31 kPa −1 ), a wide sensing range (up to 150 kPa), fast response/recovery times (300 ms/260 ms), and excellent durability (2000 cycles). Furthermore, the sensor was successfully used to monitor full-scale human motion, including pulse, and a 4 × 4 pixel flexible sensor array was shown to accurately locate pressure and recognize the pressure magnitude. These findings provide a basis for the rational design of MXene/textile composites as wearable pressure sensors for medical diagnosis, human−computer interactions, and electronic skin applications.

SummaryArterial stenosis results in a complex pattern of blood flow containing an extremely fast flow in the throat of stenosis and a post-stenosis low flow. The fast flow generates high shear stress that has been demonstrated in vitro to activate and aggregate platelets. One potential problem of these in vitro studies is that platelets are invariably exposed to a high shear stress for a period that is significantly longer than they would have experienced in vivo. More importantly, the role of the poststenosis low flow in platelet activation and aggregation has not been determined. By exposing platelets to a shear profile that contains both high and low shear segments, we found that platelets aggregate when they are exposed to a high shear stress of 100 dyn/cm2 for as short as 2.5 s, a period that is significantly shorter than those previously reported (30–120 s). Platelet aggregation under this condition requires a low shear exposure immediately after a high shear pulse, suggesting that post-stenosis low flow enhances platelet aggregation. Furthermore, platelet aggregation under this condition is not activation-dependent because the CD62P expression of sheared platelets is significantly less than that of platelets treated with ADP. Based on these findings, we propose that shear-induced platelet aggregation may be a process of mechanical crosslinking of platelets, requiring minimal platelet activation. This process may function as a protective mechanism to prevent in vivo irreversible platelet activation and aggregation under temporary high shear.

The increasing number of patients with chronic wounds caused by diseases, such as diabetes, malignant tumors, infections, and vasculopathy, has caused severe economic and social burdens. The main clinical treatments for chronic wounds include the systemic use of antibiotics, changing dressings frequently, operative debridement, and flap repair. These routine therapeutic strategies are characterized by a long course of treatment, substantial trauma, and high costs, and fail to produce satisfactory results. Biomaterial dressings targeting the different stages of the pathophysiology of chronic wounds have become an active research topic in recent years. In this review, after providing an overview of the epidemiology of chronic wounds, and the pathophysiological characteristics of chronic wounds, we highlight the functional biomaterials that can enhance chronic wound healing through debridement, anti-infection and antioxidant effects, immunoregulation, angiogenesis, and extracellular matrix remodeling. It is hoped that functional biomaterials will resolve the treatment dilemma for chronic wounds and improve patient quality of life.

We found that platelets are hyper-reactive to fluid shear stress at temperatures of 24, 32, and 35 degrees C as compared with at 37 degrees C. The hyperreactivity results in heightened aggregation through a platelet-activation independent mechanism. The enhanced platelet aggregation parallels with increased whole blood viscosity at these temperatures, suggesting that enhanced mechanical cross-linking may be responsible for the enhanced platelet aggregation.