Effect of random fiber networks on bubble growth in gelatin hydrogels.

In hydrodynamics, the event of dynamic bubble growth in a pure liquid under tensile pressure is known as cavitation. The same event can also be observed in soft materials (e.g., elastomers and hydrogels). However, for soft materials, bubble/cavity growth is either defined as cavitation if the bubble growth is elastic and reversible or as fracture if the cavity growth is by material failure and irreversible. In any way, bubble growth can cause damage to soft materials (e.g., tissue) by inducing high strain and strain-rate deformation. Additionally, a high-strength pressure wave is generated upon the collapse of the bubble. Therefore, it is crucial to identify the critical condition of spontaneous bubble growth in soft materials. Experimental and theoretical observations have agreed that the onset of bubble growth in soft materials requires higher tensile pressure than pure water. The extra tensile pressure is required since the cavitating bubble needs to overcome the elastic and surface energy in soft materials. In this manuscript, we developed two models to study and quantify the extra tensile pressure for different gelatin concentrations. Both the models are then compared with the existing cavitation onset criteria of rubber-like materials. Validation is done with the experimental results of threshold tensile pressure for different gelatin concentrations. Both models can moderately predict the extra tensile pressure within the intermediate range of gelatin concentrations (3-7% [w/v]). For low concentration (∼1%), the network's non-affinity plays a significant role and must be incorporated. On the other hand, for higher concentrations (∼10%), the entropic deformation dominates, and the strain energy formulation is not adequate.

Enhanced sodium absorption by citrate: an in vivo perfusion study of rat small intestine.

The effect of citrate on sodium, potassium chloride, and water absorption in the presence of glucose from the whole rat small intestine was studied by an in vivo marker perfusion technique. The perfusion solutions contained glucose and were similar in their electrolyte composition to the currently recommended oral rehydration solution for the treatment and prevention of diarrheal dehydration. Significantly more sodium and water absorption occurred from the citrate-containing solution than from the one without citrate. It is concluded that citrate enhances net sodium absorption from a glucose electrolyte solution in the rat small intestine independent of glucose-stimulated absorption.

An animal model of haemolytic--uraemic syndrome in shigellosis: lipopolysaccharides of Shigella dysenteriae I and S. flexneri produce leucocyte-mediated renal cortical necrosis in rabbits.

To develop an animal model of the haemolytic-uraemic syndrome during shigellosis, rabbits were injected with lipopolysaccharides (LPS) extracted by the hot phenol-water method from Shigella dysenteriae I and from S. flexneri. Two intravenous injections of LPS spaced by 24 h elicited renal cortical necrosis in a generalized Shwartzman reaction characterized by fibrin deposition in glomerular capillaries and by elevated plasma creatinine concentration. Rabbits rendered leucopenic by busulphan treatment were protected against renal cortical necrosis after injection with LPS derived from S. dysenteriae I. Both LPS preparations derived from Shigella species were also active in producing fever in rabbits, death in rabbits, and gelation of limulus lysate with approximately the same potency as a standard LPS of E. coli 055:B5. These results demonstrated that the LPS of Shigella species given intravenously to rabbits produces renal cortical necrosis, which is caused by leucocyte-mediated intravascular fibrin deposition in renal blood vessels and which resembles histologically the renal lesion in the haemolytic-uraemic during shigellosis in humans.