We report a new fabrication method of a thin polymer film with regular array of micropores (honeycomb film). A honeycomb film was fabricated by depositing a dilute solution of an amphiphilic polymer on water surface. The honeycomb film transferred onto a solid substrate was characterized by atomic force microscopy. By this fabrication method, it was possible to control film area, pore diameter, and film thickness. The pore size depended upon the evaporation time of the polymer solution spread on water surface. The thickness of a honeycomb film was controlled by spreading area of the polymer solution. The spreading behavior was influenced by the water temperature. The film area was proportional to the volume of spread polymer solution and controlled by changing the sub-phase temperature, too. When the polymer solution was simply cast on a solid substrate, a thin polymer layer remained in the bottom of the honeycomb pores. On the other hand, the honeycomb film fabricated on water surface has no bottom layer in its pores. A self-standing honeycomb mesh is formed by the “on-water spreading” method.

We report that various geometric patterns can be formed upon mechanical deformation of hexagonal micro polymer mesh. The patterning of micromesh can be applied to the fabrication of micropatterned soft-materials for cell culturing. A microporous film was prepared from a viscoelastic polymer, poly(ε-caprolactone). The film was a hexagonal mesh of 4 μm diameter. Plastic deformation of the film was caused by loading tensile force in one direction. Geometrical patterns such as elongated hexagons, rectangles, squares, and triangles were found in the stretched microporous film. These four types of deformation were reproduced by computer simulations using a viscoelastic network of hexagonally connected viscoelastic bonds. On the stretched hexagonal mesh, cardiac myocytes formed fibrous tissue where cells were aligned along the direction of the long axis of micropores. The hierarchical structure of blood vessels could be modeled by the coculture of endothelial cells and smooth muscle cells using a stretched honeycomb film as a micropatterned substrate.

Isolated glucocorticoid deficiency (IGD) is an autosomal recessive disorder characterized by progressive primary adrenal insufficiency, without mineralocorticoid deficiency. The cDNA and gene of the human ACTH receptor were recently cloned. The gene encodes a 297-amino acid protein that belongs to the G protein-coupled superfamily of membrane receptors. We hypothesized that the ACIH receptor gene might be defective in IGD. To examine this, we studied its genomic structure by PCR and direct sequencing in a 5-yr-old proband with the disease, his parents, and grandparents. The proband was a compound heterozygote for two different point mutations, one in each allele: (a) a substitution (C --T), also found in one allele of the mother and maternal grandmother, which introduced a premature stop codon (TGA) at position 201 of the protein; this mutant receptor lacks its entire carboxy-terminal third and, if expressed, should be unable to transduce the signal; and (b) a substitution (C -G), also found in one of the paternal alleles, which changed neutral serine " in the apolar third transmembrane domain of the receptor to a positively charged arginine, probably disrupting the ligand-binding site. Standard ovine corticotropin releasing hormone (oCRH) test in the heterozygote parents and maternal grandmother revealed exaggerated and prolonged ACTH responses, suggestive of subclinical resistance to ACTH. We conclude that IGD in this family appears to be due to defects of the ACTH receptor gene. The oCRH test appears to be useful in ascertaining heterozygosity in this syndrome. (J. Clin. Invest. 1993Invest. .92:2458Invest. -2461

No abstract

No abstract

Ghrelin mRNA, in addition to GHSR mRNA, is expressed in various types of pituitary adenoma with different levels of expression in each type. Our findings suggest that ghrelin produced in pituitary adenoma may play some role in the mechanism underlying the development of adenoma cells through autocrine and/or paracrine pathways.

No abstract

No abstract