Contextual modulation reported in early- to intermediate-level visual areas could be an essential component to signal border ownership (BO) that specifies the direction of figure along a contour. The surrounding regions that evoke significant suppression or facilitation are highly localized and asymmetric with respect to the center of the classical receptive field (CRF). We propose a hypothesis that such surrounding modulation is a basis for BO-selectivity. Although this idea has been discussed for several years, it is uncertain how many of a vast variety of surrounding organizations could signal correctly the direction of ownership, and how many could signal consistently for various stimuli. We carried out computationally a population study of the surrounding effects to investigate how many cells exhibit effective and consistent BO signals. We tested hundreds of various organizations, and found that most of the asymmetric, iso-orientation suppressive regions, regardless of position or size, lead to surprisingly high consistency in the direction of ownership for various stimuli. The combinations of iso-orientation suppression and cross-orientation facilitation indicate both high robustness and consistency in the ownership determination. We constructed a model for BO-selective neurons based on the surrounding effects, and investigated whether the model reproduces major characteristics of the neuronal responses, including a variety in the BO selectivity among neurons, consistency with respect to various stimuli, invariance to stimulus size, and co-selectivity to BO and contrast. The model reproduced successfully the major characteristics of BO-selective neurons.

OSTN might suppress the worsening of CHF after MI by inhibiting clearance of NP family peptides.

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The deformation mechanism of a polymer crystal has been directly clarified for the first time using an imaging-plate X-ray structural analysis system for a polydiacetylene single crystal subjected to a tensile stress at room temperature as well as at 122 K. That is to say, the small displacements of the constituent atoms of the planar-zigzag skeletal chain could be successfully detected. The change in the internal coordinates such as bond length and bond angle, which were induced by tensile stress, has been found to be consistent with the previously reported lattice-dynamical prediction. This first success in the accurate structural analysis of the deformed polymer crystal is considered to supply a new technique for investigating the deformation mechanism of polymer materials from the molecular level.

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Lack of photobleaching and blinking of new silicon nanocrystals allows direct observation of single-molecule receptor internalization and large-scale mosaicism in the plasma membrane.

Cardiac hypertrophy, which is commonly caused by hypertension, is a major risk factor for heart failure and sudden death. Endogenous ghrelin has been shown to exert a beneficial effect on cardiac dysfunction and postinfarction remodeling via modulation of the autonomic nervous system. However, ghrelin’s ability to attenuate cardiac hypertrophy and its potential mechanism of action are unknown. In this study, cardiac hypertrophy was induced by transverse aortic constriction in ghrelin knockout mice and their wild-type littermates. After 12 weeks, the ghrelin knockout mice showed significantly increased cardiac hypertrophy compared with wild-type mice, as evidenced by their significantly greater heart weight/tibial length ratios (9.2±1.9 versus 7.9±0.8 mg/mm), left ventricular anterior wall thickness (1.3±0.2 versus 1.0±0.2 mm), and posterior wall thickness (1.1±0.3 versus 0.9±0.1 mm). Furthermore, compared with wild-type mice, ghrelin knockout mice showed suppression of the cholinergic anti-inflammatory pathway, as indicated by reduced parasympathetic nerve activity and higher plasma interleukin-1β and interleukin-6 levels. The administration of either nicotine or ghrelin activated the cholinergic anti-inflammatory pathway and attenuated cardiac hypertrophy in ghrelin knockout mice. In conclusion, our results show that endogenous ghrelin plays a crucial role in the progression of pressure overload–induced cardiac hypertrophy via a mechanism that involves the activation of the cholinergic anti-inflammatory pathway.