Regression of the pupillary membrane (PM) and hyaloid vessels - hyaloid arteries (HAs), tunica vasculosa lentis (TVL), and vasa hyaloidea propria (VHP) - in mice aged from 0 to 16 days was observed using stereomicroscopy and transmission electron microscopy. Whole-mount stereomicroscopy revealed that the pattern of normal developed vessels was basically the same as that reported in rats and rabbits and that the VHP and PM disappeared between 12 and 16 days and 10 and 12 days, respectively, while certain examples of the TVL and HA remained even at 16 days. In the TVL, VHP and PM, regression occurred segmentally and resulted in a decreased number of interconnections. The ultrastructure of the vessels in the VHP, TVL and PM was consistent with a typical capillary with pericyte covering and no fenestrations. HAs had tunica media and adventitia in the older stages. Some endothelial cells in the TVL and PM attaching to the lens capsule were thin at the side of the lens. Many macrophages were observed in the vitreous and around vessels in the whole-mount specimens at all stages. Some macrophages remained linearly arranged even after vessels became vestigial and disappeared. In transmission electron microscopy, most of these macrophages were seen to possess vacuoles and/or processes, and some of them had phagosomes. Electron microscopic findings from regressing ocular vessels were consistent with the apoptosis of both endothelia and pericytes. Obstruction of the vessels was noted at older stages. These results add further anatomical information to previous studies and suggest that the VHP and TVL as well as PM regress via apoptosis. The precise mechanisms of regression of hyaloid vessels and the role of macrophages remain for further studies.

Patients with a complete section of the corpus callosum have been observed to exhibit strong left-ear suppression when different speech stimuli are presented to both ears simultaneously (so-called dichotic listening). Data concerning the locus of corpus callosum damage that causes strong left-ear suppression remains scanty. In the present investigation, a consonant-vowel syllable dichotic listening test was given to five right-handed patients with partial sections of the corpus callosum, which were located using MRI and accurately defined measurement procedures. The following two measurement methods were used: (i) the genu-splenium (G-S) method, in which a lesion was localized in the anteroposterior dimension relative to the total length of the corpus callosum, defined as the distance between the most anterior point of the genu to the most posterior point of the splenium; and (ii) the rostrum-splenium (R-S) method, which takes into account the curvature of the corpus callosum, and in which a lesion was localized relative to the total length of the corpus callosum, defined as the length of the curved line from the tip of the rostrum to the end of the splenium. Results were compared with scores from 50 normal control subjects. Strong left-ear suppression was observed in two patients, who had surgical sections of the posterior 15.5-18.5% of the corpus callosum as measured with the G-S method, or the posterior 20-24% of the corpus callosum as measured with the R-S method. The suppression phenomenon persisted for more than 10 years post-surgery. On the other hand, the remaining three patients, who had lesions anterior to the posterior 17-28% of the corpus callosum as measured with the G-S method or 20-33% as measured with the R-S method exhibited no left-ear extinction. Despite the common assumption that damage to the posterior part of the trunk of the corpus callosum causes strong left-ear suppression, the results from the G-S method indicated that damage to the splenium defined as the posterior one-fifth of the segment between the anterior-most and posterior-most points of the corpus callosum, cause strong left-ear suppression. By the R-S method, results showed that damage to the splenium (the posterior one-fifth of the curvature of the corpus callosum) and possibly the part extending to the most posterior part of the trunk (the posterior one-quarter of the curvature) causes strong left-ear suppression.

The synthesis, characterization, and carrier generation mechanism of self-doping in a tetrathiafulvalene (TTF) conductor, ammonium tetrathiafulvalene-2-carboxylate (TTFCOO(-)NH(4)(+)), are described together with molecular orbital characteristics. Insulating TTFCOOH changes into a hole-doped conductor TTFCOO(-)NH(4)(+) with a conductivity of sigma = 2.0 x 10(-4) S/cm (300 K), upon salt formation with NH(3). A radical species, TTF(*+)COO(-)NH(4)(+), is generated via protonation of the TTF moiety as demonstrated by UV-vis, ESR, and (1)H NMR spectra. The X-ray crystallographic structure of TTFCOO(-)NH(4)(+) reveals supramolecular arrays of TTFCOO(-) moieties with short S...S contact, assisted by the one-dimensional hydrogen-bonding network composed of the ammonium and carboxylate ions. Molecular orbital calculations of cluster models show that the singly occupied molecular orbital (SOMO) of TTF(*+)COO(-)NH(4)(+) in the supramolecular array is not at the highest energy level, which is characterized as a quasi-closed-shell state. The ab initio periodic calculation with a one-dimensional boundary condition reveals that TTF(*+)COO(-)NH(4)(+) behaves as a dopant leading to the semiconducting behavior of the stacked TTF moieties assembled by the hydrogen-bonding network. Namely, TTFCOO(-)NH(4)(+) can be described as a "hydrogen-bonding-assisted self-doped conductor". The contribution of the hydrogen-bonding interaction to the electron conduction is experimentally supported by a large isotope effect in the ac conductivity of TTFCOO(-)NH(4)(+) at low temperature.