Numerical Modeling and Analysis of a Cylindrical Reflector Antenna for Ground Penetrating Radar

Abstract -Since 1988, we have developed and commercialized various types of impulse ground penetrating radar (GPR) systems for locating buried structures and utility pipes. The performance of GPR systems depends mainly on the characteristics of radar antennas. In this paper, we propose a cylindrical reflector antenna fed by a resistively loaded Vshaped dipole as a new traveling wave antenna for GPR. We construct a numerical model of the antenna and analyze its characteristics using the method of moments based on RaoWilton-Glisson basis functions. The analysis results indicate that the new antenna's directivity is sharper and the ringing noise is less than in our commercialized GPR antennas, thus a weight saving can be achieved in the next GPR systems. Index Terms -Cylindrical reflector antenna, V-shaped dipole antenna, Ground penetrating radar

Olmesartan and temocapril prevented the development of hyperglycemia and the deterioration of pancreatic islet morphology in Otsuka-long-evans-Tokushima Fatty rats

We investigated the impact of olmesartan and temocapril on pancreatic islet beta-cells during the development of diabetes mellitus using Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats. Four-week-old male OLETF rats were fed standard chow (untreated:n5), or chow containing either 0.005% olmesartan(n5) or 0.01% temocapril (n5) until being sacrificed at 35 weeks of age. Pancreas sections were double-stained with anti-insulin and anti-glucagon antibodies. The percent areas of beta-cells, alpha-cells and non-alpha-non-beta-cells were compared among groups. In untreated OLETF rats, the fasting plasma glucose (FPG) level was elevated at the 18th week and remained elevated until the 35th week. On the other hand, no significant elevation in FPG levels was observed in olmesartan- or temocapril-treated rats. Pancreatic islets from olmesartan-treated rats were significantly smaller in size as compared with those from untreated OLETF rats. Furthermore, the average area occupied by beta-cells as a fraction of the total area of an individual islet was significantly higher in olmesartan- or temocapril-treated rats than that in untreated OLETF rats. Olmesartan and temocapril both prevented the development of hyperglycemia, possibly through the prevention of islet beta-cell loss in spontaneously diabetic OLETF rats.</p

Large-Area Resonance-Tuned Metasurfaces for On-Demand Enhanced Spectroscopy

We show an effective procedure for lateral structure tuning in nanoimprint lithography (NIL) that has been developed as a vertical top-down method fabricating large-area nanopatterns. The procedure was applied to optical resonance tuning in stacked complementary (SC) metasurfaces based on silicon-on-insulator (SOI) substrates and was found to realize structure tuning at nm precision using only one mold in the NIL process. The structure tuning enabled us to obtain fine tuning of the optical resonances, offering cost-effective, high-throughput, and high-precision nanofabrication. We also demonstrate that the tuned optical resonances selectively and significantly enhance fluorescence (FL) of dye molecules in a near-infrared range. FL intensity on a SC metasurface was found to be more than 450-fold larger than the FL intensity on flat Au film on base SOI substrate

Immunopathological Characterization of liposome Adjuvant Coated with Mannan

The adjuvant activity of liposomes coated with mannan-cholesterol was studied in mice. Ovalbumin (OVA) was reconstituted into liposomes as a model antigen. The adjuvant activity was assessed by the following two immunological responses: delayed-type hypersensitivity (DTH) footpad swelling responses and in vitro release of interferon-γ and interleukin-4 by regional lymph node cells. First, we studied dose effects on DTH responses of total lipid, mannan-cholesterol and OVA used for liposomes. The minimal doses per mouse required for the induction of optimal responses were as follows; 1μg of OVA, 10μg of mannan-cholesterol and 336μg of total lipid. Second, immunological and histopathological studies showed the following two points: 1) mannan-coated liposomes induced a tuberculintype DTH response while non-coated liposomes elicited a Jones-Mote reaction, and 2) mannan-coated liposomes induced obvious microabscesses but non-coated liposome did not. Third, the inoculation of mannan-coated liposomes rendered the regional lymph node cells to release a large amount of interferon-γ with little IL-4 against OVA while non-coated lipo-some released neither of the lymphokines. These results indicated that mannan-coated lipo-somes are a potent adjuvant to induce type 1 helper T cells but have a disadvantage to form microabscesses at the inoculation sites

Functionally confirmed compound heterozygous ADAM17 missense loss-of-function variants cause neonatal inflammatory skin and bowel disease 1

A disintegrin and metalloprotease 17 (ADAM17) is the major sheddase that processes more than 80 substrates, including tumour necrosis factor-α (TNFα). The homozygous genetic deficiency of ADAM17 causing a complete loss of ADAM17 expression was reported to be linked to neonatal inflammatory skin and bowel disease 1 (NISBD1). Here we report for the first time, a family with NISBD1 caused by functionally confirmed compound heterozygous missense variants of ADAM17, namely c.1699T>C (p.Cys567Arg) and c.1799G>A (p.Cys600Tyr). Both variants were detected in two siblings with clinical features of NISBD1, such as erythroderma with exudate in whole body, recurrent skin infection and sepsis and prolonged diarrhoea. In a cell-based assay using Adam10/17 double-knockout mouse embryonic fibroblasts (Adam10/17−/− mEFs) exogenously expressing each of these mutants, phorbol 12-myristate 13-acetate-stimulated shedding was strongly reduced compared with wild-type ADAM17. Thus, in vitro functional assays demonstrated that both missense variants cause the loss-of-function of ADAM17, resulting in the development of NISBD1. Our study further expands the spectrum of genetic pathology underlying ADAM17 in NISBD1 and establishes functional assay systems for its missense variants