Multi-Band Ultra-Sharp Transmission Response in All-Dielectric Resonant Structures Containing Kerr Nonlinear Media

All-dielectric resonant structure (ADRS) consisting of high-index nonlinear dielectrics has been theoretically and numerically demonstrated with multi-band ultra-sharp transmission response in this work. Bandwidth down to sub-nanometer and spectral Q-factor up to 920 are achieved in this ADRS-based metamaterial-like platform. Strong resonant electric field distributions by the high-index dielectric resonators and efficient coupling between the layered dielectric particles and the cavity mainly contribute to the multiple narrowband light transmission filtering. By using a Kerr nonlinear medium as the resonant dielectric, the positions of the transmission dips in the spectrum can be actively tuned by the incident light intensity. Due to the ultra-narrow spectral feature and the strong electric field distribution by the resonators, an efficient all-optical switching behavior with high spectral difference intensity and contrast ratio is obtained. Further study presents the observed multi-band transmission with high scalability by tuning the structural parameters. These optical features hold the predicted ADRS be potentially applied to constructing dielectric metamaterial-based all-optical switching or active subtractive transmission filtering with low power threshold at sub-diffraction scale.     

A novel common missense mutation G301C in the N-acetylgalactosamine-6-sulfate sulfatase gene in mucopolysaccharidosis IVA

Mucopolysaccharidosis IVA (MPS IVA) is an autosomal recessive lysosomal storage disorder caused by a genetic defect in N-acetylgalactosamine-6-sulfate sulfatase (GALNS). In previous studies, we have found two common mutations in Caucasians and Japanese, respectively. To characterize the mutational spectrum in various ethnic groups, mutations in the GALNS gene in Colombian MPS IVA patients were investigated, and genetic backgrounds were extensively analyzed to identify racial origin, based on mitochondrial DNA (mtDNA) lineages. Three novel missense mutations never identified previously in other populations and found in 16 out of 19 Colombian MPS IVA unrelated alleles account for 84.2% of the alleles in this study. The G301C and S162F mutations account for 68.4% and 10.5% of mutations, respectively, whereas the remaining F69V is limited to a single allele. The skewed prevalence of G301C in only Colombian patients and haplotype analysis by restriction fragment length polymorphisms in the GALNS gene suggest that G301C originated from a common ancestor. Investigation of the genetic background by means of mtDNA lineages indicate that all our patients are probably of native American descent. Received: 2 January 1997 / Accepted: 10 June 1997     

Hyperglycemic and Hyperlipidemic Conditions Alter Cardiac Cell Biomechanical Properties

Currently, many diabetic cardiomyopathy (DC) studies focus on either in vitro molecular pathways or in vivo whole-heart properties such as ejection fraction. However, as DC is primarily a disease caused by changes in structural and functional properties, such studies may not precisely identify the influence of hyperglycemia or hyperlipidemia in producing specific cellular changes, such as increased myocardial stiffness or diastolic dysfunction. To address this need, we developed an in vitro approach to examine how structural and functional properties may change as a result of a diabetic environment. Particle-tracking microrheology was used to characterize the biomechanical properties of cardiac myocytes and fibroblasts under hyperglycemia or hyperlipidemic conditions. We showed that myocytes, but not fibroblasts, exhibited increased stiffness under diabetic conditions. Hyperlipidemia, but not hyperglycemia, led to increased cFos expression. Although direct application of reactive oxygen species had only limited effects that altered myocyte properties, the antioxidant N-acetylcysteine had broader effects in limiting glucose or fatty-acid alterations. Changes consistent with clinical DC alterations occur in cells cultured in elevated glucose or fatty acids. However, the individual roles of glucose, reactive oxygen species, and fatty acids are varied, suggesting multiple pathway involvement.     

A wheat COP9 subunit 5‐like gene is negatively involved in host response to leaf rust

The COP9 (constitutive photomorphogenesis 9) signalosome (CSN) is a protein complex involved in the ubiquitin proteasome system and a common host target of diverse pathogens in Arabidopsis. The known derubylation function of the COP9 complex is carried out by subunit 5 encoded by AtCSN5A or AtCSN5B in Arabidopsis. A single CSN5‐like gene (designated as TaCSN5) with three homeologues was identified on the long arms of wheat (Triticum aestivum L.) group 2 chromosomes. In this study, we identified and characterized the function of TaCSN5 in response to infection by the leaf rust pathogen. Down‐regulation of all three TaCSN5 homeologues or mutations in the homeologues on chromosomes 2A or 2D resulted in significantly enhanced resistance to leaf rust. Enhanced leaf rust resistance corresponded to a seven‐fold increase in PR1 (pathogenesis‐related gene 1) expression. Collectively, the data indicate that the wheat COP9 subunit 5‐like gene acts as a negative regulator of wheat leaf rust resistance.