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Droplets splash when they impact dry, flat substrates above a critical velocity that depends on parameters such as droplet size, viscosity, and air pressure. By imaging ethanol drops impacting silicone gels of different stiffnesses, we show that substrate stiffness also affects the splashing threshold. Splashing is reduced or even eliminated: droplets on the softest substrates need over 70% more kinetic energy to splash than they do on rigid substrates. We show that this is due to energy losses caused by deformations of soft substrates during the first few microseconds of impact. We find that solids with Young's moduli ≲100  kPa reduce splashing, in agreement with simple scaling arguments. Thus, materials like soft gels and elastomers can be used as simple coatings for effective splash prevention. Soft substrates also serve as a useful system for testing splash-formation theories and sheet-ejection mechanisms, as they allow the characteristics of ejection sheets to be controlled independently of the bulk impact dynamics of droplets.

In human peripheral blood polymorphonuclear leukocytes and lymphocytes, GSH-oxidizing agents promote the movement of surface-bound concanavalin A (Con A) into caps and inhibit the assembly of microtubules (MT) that is normally induced by Con A binding. Con A capping and inhibition of MT assembly occur when GSH levels in cell suspensions are decreased by 30-70%, and return of GSH to control levels is accompanied by the appearance of cytoplasmic MT and by inhibition of the capping response with Con A. Oxidation of GSH markedly stimulates the hexose monophosphate shunt, and regeneration of GSH occurs rapidly.The data indicate that MT cannot be assembled or maintained in the face of decreased GSH levels. Thus, GSH homeostasis becomes critical during physiological events such as phagocytosis which simultaneously induce the assembly of MT and the production of agents like H202 that can oxidize GSH.Although a great deal of information is presently available about the conditions required for microtubule (MT) assembly in vitro, there is still no clear understanding of how assembly is regulated in vivo. Nath and Rebhun (21) have recently shown that oxidation of GSH in fertilized sea urchin eggs inhibits mitotic spindle formation and causes dissolution of preformed spindles. We proposed that intracellular GSH may also influence the organization and function of cytoplasmic MT. To test this hypothesis, we examined the effects of GSH oxidation on the assembly of MT in human peripheral blood polymorphonuclear leukocytes (PMN). Two relatively specific oxidizing agents were employed: diamide (diazene dicarboxylic and bis-N,N-dimethylamide) (15, 16) and BHP (tertiary butylhydroperoxide) (30).PMN were chosen for study first because MT assembly can be reproducibly induced by brief exposure of a variety of ligands including the plant lectin concanavalin A (Con A) (8,10,25), and second because the presence or absence of MT in Con A-treated PMN can be inferred from the distribution of surface-bound lectin. Thus, Con A shows a homogeneous surface distribution on cells that are competent to assemble MT but moves into a single aggregate-a cap-on the surface of cells treated with agents that bind with tubulin subunits and inhibit their polymerization (colchicine and the new carbamate anti-MT agent, R17934) (22-27).

Abstract

Aortic and inferior vena caval balloons were used to alter mean arterial blood pressure, pulse pressure ( PP ), and right atrial pressure ( RAP ) in unanesthetized rabbits and to reflexly evoke changes in heart period (pulse interval). Curves relating mean arterial blood pressure to heart period were compared in different groups of rabbits at similar Δ PP and Δ RAP . Median blood pressure ( BP 50 ), average gain (G), and heart period range (maximum to minimum heart period) were calculated from the S-shaped curves. The reflex was evoked from arterial baroreceptors and probably from cardiac and pulmonary baroreceptors. Curves relating mean arterial blood pressure and heart period differed with regard to BP 50 and G in sham-operated, thalamic, and pontine rabbits, indicating that suprabulbar centers normally play a role in the reflex. Curves from sham-operated and pontine rabbits treated with atropine also differed, suggesting suprabulbar control of sympathetic effectors. In intact rabbits, forebrain and diencephalic centers caused vagal and sympathetic effectors to respond over the same arterial blood pressure range, but, in pontine rabbits, the effectors responded over dissimilar ranges. In intact rabbits, changes in mean arterial blood pressure evoked reciprocal and nearly equal changes in vagal and sympathetic effectors, but, in pontine rabbits, a given pressure change altered heart period predominantly through one effector. In sham-operated rabbits, vagal effects on heart period were lower by a constant amount at every level of mean arterial blood pressure than they were in pontine rabbits, suggesting that suprabulbar centers exerted a tonic inhibitory effect on vagal motoneurons not involved in the reflex.

Antisera to neuropeptide Y (NPY) gave an intense immunohistochemical reaction of certain nerve cells in the myenteric and submucous plexuses of the guinea-pig small intestine. Each nerve cell had up to 20 branching, tapering processes that were less than approximately 50 micron long and a long process that could be followed for a considerable distance. This morphology corresponds to that of the type-III cells of Dogiel. The long process of each myenteric cell ran through the circular muscle to the submucosa, and in most cases the process could be traced to the mucosa. The submucous nerve cell bodies also had processes that extended to the mucosa. These cell bodies, in both plexuses, also stained with antisera raised against calcitonin gene-related peptide (CGRP), cholecystokinin (CCK), choline acetyltransferase (ChAT) and somatostatin (SOM), but did not stain with antibodies against enkephalin, substance P or vasoactive intestinal peptide. Thus, it has been possible for the first time to trace the processes of chemically specified neurons through the layers of the intestinal wall and to show by a direct method that CGRP/CCK/ChAT/NPY/SOM myenteric and submucous nerves cells provide terminals in the mucosa.

The initial stages of high-velocity droplet impact on a shallow water layer are described, with special emphasis given to the spray jet mechanics. Four stages of impact are delineated, with appropriate scalings, and the successively more important influence of the base is analysed. In particular, there is a finite time before which part of the water in the layer remains under the droplet and after which all of the layer is ejected in the splash jet.

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