Tongue pressure production against hard palate during supraglottic swallow and super supraglottic swallow

Introduction: Supraglottic swallow (SS) and super supraglottic swallow (SSS) are voluntary airway protection techniques which are widely used in the rehabilitation of patients with dysphagia. Although there have been some reports about the effect of these techniques on the pharyngeal stage of swallowing, little is known about that on the oral stage. The purpose of this study is to investigate the influence of SS and SSS on the state of tongue-palate contact by measuring tongue pressure production against hard palate. Materials and Methods: Nineteen healthy adults (six males and thirteen females, average age; 25.9 years) participated in this study. Tongue pressure during swallowing 5 ml water with normal swallow, SS and SSS was measured by using an ultra-thin tongue pressure sensor sheet with 5 pressure-sensing points attached to the hard palate. Maximal magnitude, duration and integrated value of tongue pressure were analyzed based on the tongue pressure waveform obtained. Results and Discussion: Maximal magnitude and integrated values during SS were higher at posterior part of the hard palate than those during normal swallow, and those during SSS were higher at each part of the hard palate than those during normal swallow. In addition, those during SSS were higher at anterior-median part and posterior circumferential part of the hard palate than those during SS. These results suggest that SS and SSS facilitated tongue-palate contact which might improve bolus driving force in the oral stage. SSS was more effective than SS in this respect

Retinoid-Induced Expression and Activity of an Immediate Early Tumor Suppressor Gene in Vascular Smooth Muscle Cells

Retinoids are used clinically to treat a number of hyper-proliferative disorders and have been shown in experimental animals to attenuate vascular occlusive diseases, presumably through nuclear receptors bound to retinoic acid response elements (RARE) located in target genes. Here, we show that natural or synthetic retinoids rapidly induce mRNA and protein expression of a specific isoform of A-Kinase Anchoring Protein 12 (AKAP12β) in cultured smooth muscle cells (SMC) as well as the intact vessel wall. Expression kinetics and actinomycin D studies indicate Akap12β is a retinoid-induced, immediate-early gene. Akap12β promoter analyses reveal a conserved RARE mildly induced with atRA in a region that exhibits hyper-acetylation. Immunofluorescence microscopy and protein kinase A (PKA) regulatory subunit overlay assays in SMC suggest a physical association between AKAP12β and PKA following retinoid treatment. Consistent with its designation as a tumor suppressor, inducible expression of AKAP12β attenuates SMC growth in vitro. Further, immunohistochemistry studies establish marked decreases in AKAP12 expression in experimentally-injured vessels of mice as well as atheromatous lesions in humans. Collectively, these results demonstrate a novel role for retinoids in the induction of an AKAP tumor suppressor that blocks vascular SMC growth thus providing new molecular insight into how retiniods may exert their anti-proliferative effects in the injured vessel wall

Deletion of a Csf1r enhancer selectively impacts CSF1R expression and development of tissue macrophage populations.

The proliferation, differentiation and survival of mononuclear phagocytes depend on signals from the receptor for macrophage colony-stimulating factor, CSF1R. The mammalian Csf1r locus contains a highly conserved super-enhancer, the fms-intronic regulatory element (FIRE). Here we show that genomic deletion of FIRE in mice selectively impacts CSF1R expression and tissue macrophage development in specific tissues. Deletion of FIRE ablates macrophage development from murine embryonic stem cells. Csf1r mice lack macrophages in the embryo, brain microglia and resident macrophages in the skin, kidney, heart and peritoneum. The homeostasis of other macrophage populations and monocytes is unaffected, but monocytes and their progenitors in bone marrow lack surface CSF1R. Finally, Csf1r mice are healthy and fertile without the growth, neurological or developmental abnormalities reported in Csf1r rodents. Csf1r mice thus provide a model to explore the homeostatic, physiological and immunological functions of tissue-specific macrophage populations in adult animals

STATISTICAL MODELLING OF DAMAGE EVOLUTION IN SPALLATION

En vue de comprendre le mécanisme d'initiation de l'écaillage dans les métaux laminés, un modèle statistique unidimensionnel de l'évolution des microfissures lors de l'écaillage est proposé. Pour cette description statistique la longueur de fissure semble être la variable fondamentale. Deux processus dynamiques, la nucléation des fissures et leur croissance, sont associés dans le modéle d'évolution du dommage. Un cas simplifié est examiné et des corrélations préliminaires avec les observations expérimentales de l'écaillage sont données.In order to understand the mechanism of the incipient spallation in rolled metals, a one dimensional statistical mode1 on evolution of microcracks in spallation was proposed. The crack length appears to be the fundamental variable in the statistical description. Two dynamic processes, crack nucleation and growth, were involved in the model of damage evolution. A simplified case was examined and preliminary correlation to experimental observations of spallation was made