First observation of the decay B --> J/psistraight phiK

We present the first observation of the decay B-->J/psistraight phiK. Using 9.6x10(6) B&Bmacr; meson pairs collected with the CLEO detector, we have observed ten fully reconstructed B-->J/psistraight phiK candidates, whereas the estimated background is 0.5+/-0.2 event. We obtain a branching fraction of B(B-->J/psistraight phiK) = (8. 8(+3.5)(-3.0)[stat]+/-1.3[syst])x10(-5). This is the first observed B meson decay requiring the creation of an additional s&smacr; quark pair.

Staphylococcal scalded skin syndrome (SSSS) and consecutive septicaemia in a preterm infant.

Staphylococcal scaled-skin syndrome (SSSS) is a toxin-related epidermolytic disease that usually affects infants and children under 5 years. We report herein a case of a premature infant who had developed SSSS after an infection of the pharynx with staphylococci and who died of septicaemia due to pseudomonas aeruginosa. The primary mechanism of action of epidermolysin still remains unknown. We demonstrate that acantholysis is due to an early edema of the intercellular space with separation of ultrastructurally unaltered desmosomes.

Improving acute skin-flap survival through stress conditioning using heat shock and recovery.

We present our initial experience with a new method of increasing the survival of acute skin flaps through stress conditioning using heat shock and recovery. The heat-shock response is a basic form of stress response that exists on the cellular level. When cultured cells or whole organisms are exposed to supraphysiologic levels of heat, they respond by synthesizing a number of highly conserved proteins known as heat-shock proteins. These proteins have been shown to offer the cell or organism a survival advantage over nonstressed controls. The study demonstrates a significant survival advantage in acute dorsal skin flaps of Sprague-Dawley rats (p = 0.001). Study animals (n = 10) were subjected to a heating blanket set at 45 degrees C for 30 minutes and were allowed 6 hours' recovery before developing the flaps. Heat-shock protein was demonstrated in immunohistochemically stained sections of skin from the study animals but not in control animal skin (n = 14). We postulate that through stress conditioning a latent mechanism present within all cells was activated, thereby allowing the cells of our experimental flaps to better survive the stress of the acute flap model.