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Microporous, non-woven poly(ϵ-caprolactone) (PCL) scaffolds were made by electrostatic fiber spinning. In this process, polymer fibers with diameters down to the nanometer range, or nanofibers, are formed by subjecting a fluid jet to a high electric field. Mesenchymal stem cells (MSCs) derived from the bone marrow of neonatal rats were cultured, expanded and seeded on electrospun PCL scaffolds. The cell-polymer constructs were cultured with osteogenic supplements under dynamic culture conditions for up to 4 weeks. The cell-polymer constructs maintained the size and shape of the original scaffolds. Scanning electron microscopy (SEM), histological and immunohistochemical examinations were performed. Penetration of cells and abundant extracellular matrix were observed in the cell-polymer constructs after 1 week. SEM showed that the surfaces of the cell-polymer constructs were covered with cell multilayers at 4 weeks. In addition, mineralization and type I collagen were observed at 4 weeks. This suggests that electrospun PCL is a potential candidate scaffold for bone tissue engineering. [Copyright &y& Elsevier]

To expand designable circuit scale, we have developed a new cell-based circuit design for single flux quantum (SFQ) circuit. We call it CONNECT cell library. The CONNECT cell library has over 100 cells at present. Each CONNECT cell consists of a Verilog digital behavior model, circuit information, and a physical layout. All circuit parameter values have been optimized for obtaining the widest margins and minimizing interactions between cells. At the layout level, we have defined a minimum standard cell size and made cell height and width a multiple of the size. Using this cell library, we can easily expand circuit scale without the time-consuming dynamic simulations of whole circuits. For estimation of the reliability of the library, we designed and fabricated test circuits using CONNECT cells. We demonstrated experimentally correct operations, which means the CONNECT cell library is sufficiently reliable. [Copyright &y& Elsevier]

Abstract: Background: PRKAR1A gene encodes the type 1A regulatory subunit of protein kinase A. The mutation of this gene causes Carney complex which is an autosomal dominant multiple neoplasia syndrome characterized by spotty pigmentations, endocrine overactivity and cardiac myxoma. We hypothesized that cardiac myxoma may be associated with PRKAR1A gene mutation and determined whether mutation in the PRKAR1A gene is the cause of familial and sporadic cardiac myxoma. Methods: We studied seven patients (three males and four females) with cardiac myxoma. Two of them had familial cardiac myxoma complicated with Carney complex. The other five patients were characterized as sporadic cardiac myxomas. We analyzed the PRKAR1A gene of all patients by the polymerase chain reaction (PCR)–single-strand conformation method, followed with direct sequence analysis. Results: We identified a novel mutation (494delTG) in exon 4A of the PRKAR1A gene in the patients with Carney complex. A 16-year-old proband had a left atrial myxoma, pituitary adenoma and skin pigmentation. His father also had left atrial myxoma and skin pigmentation. In contrast, no mutations in the PRKAR1A gene were identified in the other five patients with sporadic cardiac myxomas. Conclusions: These results suggest that mutation of the PRKAR1A gene may be associated with familial cardiac myxoma in Carney complex but may not be associated with sporadic cardiac myxoma. [Copyright &y& Elsevier]