Induced Stem Cells as a Novel Multiple Sclerosis Therapy.

Stem cell replacement is providing hope for many degenerative diseases that lack effective therapeutic methods including multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system. Transplantation of neural stem cells or mesenchymal stem cells is a potential therapy for MS thanks to their capacity for cell repopulation as well as for their immunomodulatory and neurotrophic properties. Induced pluripotent stem cell (iPSC), an emerging cell source in regenerative medicine, is also being tested for the treatment of MS. Remarkable improvement in mobility and robust remyelination have been observed after transplantation of iPSC-derived neural cells into demyelinated models. Direct reprogramming of somatic cells into induced neural cells, such as induced neural stem cells (iNSCs) and induced oligodendrocyte progenitor cells (iOPCs), without passing through the pluripotency stage, is an alternative for transplantation that has been proved effective in the congenital hypomyelination model. iPSC technology is rapidly progressing as efforts are being made to increase the efficiency of iPSC therapy and reduce its potential side effects. In this review, we discuss the recent advances in application of stem cells, with particular focus on induced stem/progenitor cells (iPSCs, iNSC, iOPCs), which are promising in the treatment of MS

Flexural capacity of overloading damaged RC T-beams strengthened with CFRP subjected to wet-dry cycles

Overweight trucks are common on the highways in China, which presents fatigue damage problem for the reinforced concrete (RC) bridges. Externally bonding CFRP sheets is increasingly being used to repair the damaged bridges. The degradation of adhesive bonding in a wet-dry environment, however, may have a significant adverse effect on the long term durability of the repaired bridges. This paper presents an experimental study on the flexural capacity of damaged RC T-beams strengthened with CFRP sheets subjected to the wet-dry cycles. A total of 19 specimens in 8 series were tested. The specimens were damaged by constant fatigue loading which were equivalent to the repetitive loadings caused by the overweight trucks across a bridge in one year. The specimens subjected to wet-dry environment were exposed to a period of 3 months or 6 months. A wet-dry cycle was 24 h including a wet cycle (salt water) of 10 h and a dry cycle (hot air at 40 ℃) of 14 h. The experimental results showed that a slight reduction in stiffness was observed for the strengthened beams due to overloading damage or wet-dry exposure. The residual deflection and cracks caused by overloading damage reduced the effect of CFRP strengthening. The wet-dry cycles induced degradation to bond at the concrete/FRP interface. Only in the first 3 months, however, the wet-dry environmental exposure can obvious reduce the strength of the retrofitted beams

μ-Adipato-bis­[chlorido(2,2′:6′,2′′-terpyridine)­copper(II)] tetra­hydrate

In the title compound, [Cu2(C6H8O4)Cl2(C15H11N3)2]·4H2O, the dinuclear copper complex is located on a crystallographic inversion centre. Each Cu atom is in a distorted square-pyramidal coordination environment, with one O atom of an adipate dianion and three N atoms from the 2,2′:6′,2′′-terpyridine ligand occupying the basal plane, and one chlorine in the apical site. In addition, there is weak Cu—O inter­action opposite of the chlorine with a distance of 2.768 (1) Å. The adipate ligand adopts a gauche–anti–gauche conformation. The inter­stitial water mol­ecules form hydrogen-bonded tertramers that are connected to the complexes via O—H⋯O and O—H⋯Cl hydrogen bonds, thus leading to the formation of tightly hydrogen-bonded layers extending perpendicular to the b-axis direction

FLEXURAL CAPACITY OF OVERLOADING DAMAGED RC T-BEAMS STRENGTHENED WITH CFRP SUBJECTED TO WET-DRY CYCLES

ABSTRACT Overweight trucks are common on the highways in China, which presents fatigue damage problem for the reinforced concrete (RC) bridges. Externally bonding CFRP sheets is increasingly being used to repair the damaged bridges. The degradation of adhesive bonding in a wet-dry environment, however, may have a significant adverse effect on the long term durability of the repaired bridges. This paper presents an experimental study on the flexural capacity of damaged RC T-beams strengthened with CFRP sheets subjected to the wet-dry cycles. A total of 19 specimens in 8 series were tested. The specimens were damaged by constant fatigue loading which were equivalent to the repetitive loadings caused by the overweight trucks across a bridge in one year. The specimens subjected to wet-dry environment were exposed to a period of 3 months or 6 months. A wet-dry cycle was 24 h including a wet cycle (salt water) of 10 h and a dry cycle (hot air at 40 ℃) of 14 h. The experimental results showed that a slight reduction in stiffness was observed for the strengthened beams due to overloading damage or wet-dry exposure. The residual deflection and cracks caused by overloading damage reduced the effect of CFRP strengthening. The wet-dry cycles induced degradation to bond at the concrete/FRP interface. Only in the first 3 months, however, the wet-dry environmental exposure can obvious reduce the strength of the retrofitted beams

N-Benzyl-2-(2-chloro-5-methyl­phen­oxy)acetamide

The asymmetric unit of the title compound, C16H16ClNO2, contains two crystallographically independent mol­ecules, which differ mainly in the orientation of the benzyl group with respect to the rest of the mol­ecule. In the crystal packing, centrosymmetrically related mol­ecules are linked into dimers via inter­molecular C—H⋯O hydrogen-bond inter­actions

FSD-C10, a Fasudil derivative, promotes neuroregeneration through indirect and direct mechanisms.

FSD-C10, a Fasudil derivative, was shown to reduce severity of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), through the modulation of the immune response and induction of neuroprotective molecules in the central nervous system (CNS). However, whether FSD-C10 can promote neuroregeneration remains unknown. In this study, we further analyzed the effect of FSD-C10 on neuroprotection and remyelination. FSD-C10-treated mice showed a longer, thicker and more intense MAP2 and synaptophysin positive signal in the CNS, with significantly fewer CD4(+) T cells, macrophages and microglia. Importantly, the CNS of FSD-C10-treated mice showed a shift of activated macrophages/microglia from the type 1 to type 2 status, elevated numbers of oligodendrocyte precursor cells (OPCs) and oligodendrocytes, and increased levels of neurotrophic factors NT-3, GDNF and BDNF. FSD-C10-treated microglia significantly inhibited Th1/Th17 cell differentiation and increased the number of IL-10(+) CD4(+) T cells, and the conditioned medium from FSD-C10-treated microglia promoted OPC survival and oligodendrocyte maturation. Addition of FSD-C10 directly promoted remyelination in a chemical-induced demyelination model on organotypic slice culture, in a BDNF-dependent manner. Together, these findings demonstrate that FSD-C10 promotes neural repair through mechanisms that involved both immunomodulation and induction of neurotrophic factors