Enzyme-triggered model self-assembly in surfactant-cyclodextrin systems

We present here a host-guest approach to construct enzyme-triggered assembly systems on the basis of surfactant-cyclodextrin complexes and alpha-amylase. We realized enzyme-responsive model self-assembly systems including monolayers, micelles, and vesicles. The host-guest approach is expected to be extended to more complicated assembly systems with widespread applications.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000305792800003&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Chemistry, MultidisciplinarySCI(E)PubMed37ARTICLE597347-73494

Optimal remanufacturing strategies in name-your-own-price auctions with limited capacity

We study optimal pricing and production strategies faced by a manufacturer in a remanufacturing/manufacturing system. In the reverse channel, returns are collected under a name-your-own-price (NYOP) bidding mechanism. The manufacturer has a limited capacity to produce new and remanufactured products. We characterize the optimal decisions of the consumers and the manufacturer. We find that under the NYOP mechanism, the manufacturer׳s optimal strategies mainly depend on the bidding cost, the cost saving of remanufacturing, the production capacity, and the market scale. In addition, when remanufacturing needs more capacity than manufacturing , the manufacturer may adopt pure manufacturing strategy without remanufacturing. We also compare this mechanism with the traditional list-price mechanism and find that the manufacturer prefers the NYOP mechanism under the conditions of a low reverse market share, a high manufacturing cost, a sufficient capacity, or a low capacity requirement of remanufacturing. Numerical studies investigate the effect of key parameters on the manufacturer׳s profit and some managerial insights are obtained

Interleukin-10 Inhibits Bone Resorption: A Potential Therapeutic Strategy in Periodontitis and Other Bone Loss Diseases

Periodontitis and other bone loss diseases, decreasing bone volume and strength, have a significant impact on millions of people with the risk of tooth loss and bone fracture. The integrity and strength of bone are maintained through the balance between bone resorption and bone formation by osteoclasts and osteoblasts, respectively, so the loss of bone results from the disruption of such balance due to increased resorption or/and decreased formation of bone. The goal of therapies for diseases of bone loss is to reduce bone loss, improve bone formation, and then keep healthy bone density. Current therapies have mostly relied on longterm medication, exercise, anti-inflammatory therapies, and changing of the life style. However there are some limitations for some patients in the effective treatments for bone loss diseases because of the complexity of bone loss. Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine, and recent studies have indicated that IL-10 can contribute to the maintenance of bone mass through inhibition of osteoclastic bone resorption and regulation of osteoblastic bone formation. This paper will provide a brief overview of the role of IL-10 in bone loss diseases and discuss the possibility of IL-10 adoption in therapy of bone loss diseases therapy

Sliding wear of medium-carbon bainitic/martensitic/austenitic steel treated by short-term low-temperature austempering

A medium-carbon Si–Mn–Ni–Cr–Mo alloyed (300M) steel was austempered for various short periods at its martensite-starting temperature of 285 °C to seek improved sliding wear resistance as compared to the traditional martensitic and bainitic steels. Reciprocating sliding wear tests were performed against a WC/Co ball counterpart at a constant load of 49 N. The samples were characterised using field emission SEM, XRD and hardness testing. The associated wear mechanisms were analysed using SEM and cross-sectional TEM. The results revealed that a short austempering time of 6 min produced refined arrays of initial nano-bainitic ferrite laths and inter-lath filmy austenite and the majority martensite and retained austenite, while the majority of the microstructure remained martensitic with retained austenite. The hardness was unchanged to that of the as-quenched martensite of 6.4 GPa. Simultaneously the wear coefficient decreased by 41% from 2.67 to 1.58 × 10-15 m3N-1m-1, which is also superior to both the tempered martensite at 1.65 × 10-15 m3N-1m-1 and the lower bainite at 1.87 × 10-15 m3N-1m-1. Increasing the austempering time to 20 and 60 min resulted in wear coefficients of 1.38 and 2.18 × 10-15 m3N-1m-1, respectively. The improved wear resistance has been explained by the wear induced microstructure evolution, especially the carbon partitioning induced stabilisation of retained austenite. The high-stress sliding wear was found to be dominated by severe shear deformation, which resulted in a nano-laminate structured top layer. Delamination wear was found to take place within the embrittled nano-laminates

FUS Transgenic Rats Develop the Phenotypes of Amyotrophic Lateral Sclerosis and Frontotemporal Lobar Degeneration

Fused in Sarcoma (FUS) proteinopathy is a feature of frontotemporal lobar dementia (FTLD), and mutation of the fus gene segregates with FTLD and amyotrophic lateral sclerosis (ALS). To study the consequences of mutation in the fus gene, we created transgenic rats expressing the human fus gene with or without mutation. Overexpression of a mutant (R521C substitution), but not normal, human FUS induced progressive paralysis resembling ALS. Mutant FUS transgenic rats developed progressive paralysis secondary to degeneration of motor axons and displayed a substantial loss of neurons in the cortex and hippocampus. This neuronal loss was accompanied by ubiquitin aggregation and glial reaction. While transgenic rats that overexpressed the wild-type human FUS were asymptomatic at young ages, they showed a deficit in spatial learning and memory and a significant loss of cortical and hippocampal neurons at advanced ages. These results suggest that mutant FUS is more toxic to neurons than normal FUS and that increased expression of normal FUS is sufficient to induce neuron death. Our FUS transgenic rats reproduced some phenotypes of ALS and FTLD and will provide a useful model for mechanistic studies of FUS–related diseases