No abstract

In this work we reported a novel graphite doped conductive magnetorheological plastomer (GMRP) with magnetic field dependent electro-conductivity. The conductivity of the GMRPs increased by increasing the content of the graphite particles, while it decreased with the graphite size. When the graphite content reached 15 wt%, the conductivity of GMRPs is approximately 10 000 times higher than the non-doped MRP. Because the iron particles in the GMRPs were magnetic, the conductivity of the GMRPs was magnetically sensitive. Upon applying a 780 mT magnetic field, the electric conductivity could increase about 1000 times larger than the one under zero magnetic field. A particle-particle resistance model was developed to investigate the influence of the magnetic field and graphite doping on the conductivity, and the fitting curve matched the experimental results very well. Finally, a magnetically controllable on-off switch based on GMRPs was proposed and its working mechanism was discussed.

. Purpose:  To evaluate the effect of collagen cross‐linking induced by genipin in porcine sclera. Methods:  Porcine cadaver eyes were treated with genipin at concentrations (by w/v) of 0.01%, 0.03%, 0.1%, 0.3%, 1.0% for 15 and 30 min. Riboflavin/ultraviolet A(UVA)‐treated and untreated samples were used as controls. After treatment, scleral strips of 4.0 × 10.0 mm were cut. Twenty‐four hours later, the stress‐strain parameters of the strips were measured using a biomaterial microtester. The stress and Young’s modulus at 8% strain were evaluated. Results:  Compared with untreated groups, after treatment with genipin for 15 min, the stress was increased by 66–246%, depending on the concentration of genipin. As for the 30‐min groups, the stress was 171–444% higher than that of the control. The difference of the Young’s modulus between genipin 15‐min groups, except the 0.01% groups (p = 0.095), also had statistical significance (p < 0.05). The Young’s modulus had significant difference between the untreated group and the genipin 30‐min groups (all p < 0.05). Of 0.3% genipin for 15 min or 0.01% genipin for 30 min had a similar stress‐strain curve with those of eyes treated with the riboflavin/UVA group. The sclera exhibited a bluish colour which became deeper with increase concentration and cross‐linking time. Conclusions:  Collagen cross‐linking induced by genipin could increase the biomechanical strength in porcine sclera. The effect depends on the concentration and treatment time of genipin.

Respiratory syncytial virus (RSV) is the leading cause of acute respiratory tract viral infection in infants, causing bronchiolitis and pneumonia. The host antiviral response to RSV acts via retinoic acid-inducible gene I (RIG-I). We show here that RSV infection upregulates major histocompatibility complex class I (MHC-I Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection in infants and young children, causing bronchiolitis and pneumonia in infants and young children worldwide. Due to the highly infectious nature of the virus, roughly two-thirds of children are infected by their first birthday, and this reaches essentially 100% by the age of 2 (1, 2). RSV infection is a leading cause of infant hospitalization due to bronchiolitis (2, 3). In the United States alone, an estimated 2.1 million children under 5 years of age with RSV infection require medical attention each year (4). Importantly, lower respiratory tract infection by RSV early in life is a risk factor for persistent wheezing and asthma in later life (5, 6). There are no RSV vaccines available to prevent childhood infection. These factors create an urgent need to understand the mechanisms of RSV disease, the molecular mechanisms associated with immunoregulation, and the downstream association between RSV infection and allergic asthma.RSV belongs to the subfamily Pneumovirinae of the paramyxoviruses. A negative-sense, single-stranded RNA virus with a genome of approximately 15,000 nucleotides (7), the virus can infect a broad range of cells. In patients, however, infection is normally highly restricted to the superficial cells of the respiratory epithelium, the ciliated cells of the small bronchioles, and pneumocytes in the alveoli (8-10). Infection is initiated by cell surface binding via proteoglycans (11), followed by nucleolin-mediated fusion for RSV cell entry (9, 12) and infection. In response, the host initiates an early innate immune response at the site of infection. Receptors of innate immune recognition, like Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I), which are involved in detection of viral RNA, promote the activation of antiviral immunity and cytokine production, as well as the recruitment of proinflammatory cells (10,(13)(14)(15)(16). This increased expression of inflamma-