Red LED light treatment promotes cognitive learning through up-regulation of trpm4 in zebrafish.

Although light emitting diodes (LEDs) are widely used in our daily lives, there is little research regarding LED light's possible effects on biological functions. We used a zebrafish animal model to investigate the long-term effects of white, blue and red LED lights on cognitive learning and memory recall. Our data suggest that these treatments had not only an impact on learning but also surprisingly long-lasting effects, particularly with regard to individuals treated with red light. The qPCR results revealed that the expression levels of trpm4, trpa1b, grin2aa and dlg4 in the skin were increased after monochromatic light treatment. Furthermore, the up-regulation of trpm4 in the brain may correlate to enhanced learning and memory following red-light treatment. Our results identify a light-based stimulation system for enhancing zebrafish learning, which has the potential to provide important insights into the relationship between LED lighting and animal behaviour.

Synthesis and Hydration Behavior of a Hydrolysis-Resistant Quasi-Choline Phosphate Zwitterionic Polymer.

A hydrolysis-resistant polymer bearing new quasi-choline phosphate (quasi-CP) structures as side groups, poly(2-methacryloyloxyethyl choline methylphosphonate) (PMCPm), was designed and synthesized. Radical polymerization and sub-surface-initiated radical polymerization were used to prepare homopolymer and polymer brush on polymer substrates. Hydrolytic stability and hydrophilicity of the polymer were confirmed by nuclear magnetic resonance and contact angle measurements. Furthermore, the hydration states were investigated using Fourier-transform infrared spectroscopy and differential scanning calorimetry. The similar hydration behavior of PMCPm to poly(2-methacryloyloxyethyl phosphorylcholine) (PMPC) sheds light on understanding the interfacial functions of quasi-CP-bearing zwitterionic biomaterials.

Synthesis of a conductive polymer thin film having a choline phosphate side group and its bioadhesive properties.

A conductive polymer thin film having choline phosphate as the side group was prepared. Quartz crystal microbalance (QCM) was employed to evaluate the adsorption of the model protein, bovine serum albumin (BSA), on the films deposited on indium tin oxide (ITO) electrodes. Cell adsorption on the film was evaluated by a fibroblast NIH3T3.

Direct Evaluation of Local Dynamic Viscoelastic Properties of Isotactic Polypropylene Films Based on a Dynamic µ-Beam X-ray Diffraction Method.

The local mechanical properties of crystalline polymer were evaluated using synchrotron radiation X-ray diffraction with 10 µm lateral resolution. A nonoriented isotactic polypropylene (iPP) film with isolated spherulites in a crystallized matrix was used as a model sample. In situ wide-angle X-ray diffraction (WAXD) measurement was performed on the iPP film using a microbeam synchrotron radiation X-ray under sinusoidal strain. The lattice spacing of the crystal planes increased and decreased in response to the applied sinusoidal strain. Local dynamic viscoelastic functions (dynamic storage and loss moduli (E' and E″)) were calculated at room temperature from the relationship between the calculated applied stress and the response strain obtained by dynamic µ-beam WAXD measurement inside and outside of the spherulites. The E' values inside and outside of spherulite obtained from the change in spacing of the (110) plane were 1.8 and 1.1 GPa, respectively. Furthermore, the E' value inside of spherulite obtained from the change in spacing of the (1̅13) plane was 6.0 GPa. These values can be explained by the deformation of crystallite, which depends on the direction of crystal planes. The results obtained here revealed that synchrotron radiation X-ray diffraction measurement gives not only structural information but also the local mechanical properties of the materials E'.

Block-copolymer-assisted synthesis of hydroxyapatite nanoparticles with high surface area and uniform size.

We report the synthesis of hydroxyapatite nanoparticles (HANPs) by the coprecipitation method using calcium D-gluconate and potassium hydrogen phosphate as the sources of calcium and phosphate ions, respectively, and the triblock copolymer F127 as a stabilizer. The HANPs were characterized using scanning electron microscopy, x-ray diffraction, and nitrogen adsorption/desorption isotherms. Removal of F127 by solvent extraction or calcination alters the structure of HANPs. The solvent-extracted HANPs were single crystals with their 〈001〉 axis oriented along the rod axis of the HANP, whereas the calcined HANPs contained two crystal phases that resulted in a spherical morphology. The calcined HANPs had much higher surface area (127 m2 g-1) than the solvent-extracted HANPs (44 m2 g-1).

Mitochondrial GLUT10 facilitates dehydroascorbic acid import and protects cells against oxidative stress: mechanistic insight into arterial tortuosity syndrome.

Mutations in glucose transporter 10 (GLUT10) alter angiogenesis and cause arterial tortuosity syndrome (ATS); however, the mechanisms by which these mutations cause disease remain unclear. It has been reported that in most cells, mitochondria are the major source of reactive oxygen species (ROS). Moreover, mitochondria are known to incorporate as well as recycle vitamin C, which plays a critical role in redox homeostasis, although the molecular mechanism(s) underlying mitochondrial vitamin C uptake are poorly understood. We report here that GLUT10 localizes predominantly to the mitochondria of smooth muscle cells and insulin-stimulated adipocytes, where GLUT10 is highly expressed. We further demonstrate that GLUT10 facilitates transport of l-dehydroascorbic acid (DHA), the oxidized form of vitamin C, into mitochondria, and also increases cellular uptake of DHA, which in turn protects cells against oxidative stress. This protection is compromised when GLUT10 expression in mitochondria is inhibited. In addition, we found that aortic smooth muscle cells from GLUT10-mutant mice have higher ROS levels than those from wild-type mice. Our results identify the physiological role of GLUT10 as the mitochondrial DHA transporter, and demonstrate that GLUT10 protects cells from oxidative injury. Furthermore, our findings provide a mechanism to explain the ascorbate in mitochondria and show how loss-of-function GLUT10 mutations may lead to arterial abnormalities in ATS. These results also reinforce the importance of vitamin C and ROS in degenerative diseases.

Mutations in the SLC2A10 gene cause arterial abnormalities in mice.

AIMS: Glucose transporter 10 (GLUT10), encoded by the SLC2A10 gene, is a member of the class III facilitative glucose transporter family. Mutations in the SLC2A10 gene cause arterial tortuosity syndrome (ATS) in humans. To further study the pathogenesis of the disease, we generated mice carrying GLUT10 mutations. METHODS AND RESULTS: Using a gene-driven N-ethyl-N-nitrosourea (ENU)-mutagenesis approach, we generated mice carrying GLUT10 mutations c.383G>A and c.449C>T, which resulted in missense mutations of glycine to glutamic acid (p.G128E) and serine to phenylalanine (p.S150F), respectively. Both mutant strains appeared normal at birth, gained weight appropriately and survived to adulthood (>18 months). Blood and urine glucose were normal. Echocardiogram and electrocardiogram were also normal and brain magnetic resonance angiography revealed normal cerebral arteries without tortuosity, stenosis/dilatation, or aneurysm. Histopathology revealed thickening and irregular vessel wall shape of large and medium size arteries characterized by markedly increased elastic fibres, both in number and size. There was also intima endothelial hypertrophy and deranged elastic fibres that resulted in disruption of internal elastic lamina in the aorta of older mice. CONCLUSION: Abnormal elastogenesis with early elastic fibre proliferation provides a clue to the pathogenesis of arterial tortuosity in human ATS. Availability of this mouse model will allow testing of the relationship between diabetes and its vascular complications, including diabetic retinopathy, nephropathy and peripheral vascular disease.