The effect of cyclic stress on the physical properties of a poly(dimethylsiloxane) elastomer

The dynamic creep behavior of a filled poly(dimethylsiloxane) elastomer was studied under cyclic stress. The stress level was chosen such that the increase in the internal temperature was small and that microcracks were not observed. This work has demonstrated that cyclic stress in combination with high temperature accelerates the degradation of the elastomer. The results suggest that because of the applied force, breaks in the load-bearing chains of the network occur. These breaks, while relieving the mechanical stress, create highly reactive ionic fragments. It is believed that because of the subsequent reactions of the ionic fragments, changes in the specific gravity, storage modulus, effective crosslink density, and length of the sample (creep) are observed. The observed decrease in the storage modulus is thought to occur because of the reaction of the ionic fragments with moisture, which results in the formation of silanol chain ends that reduce the effective crosslink density. The results also show that contrary to the prediction of the Boltzmann's Superposition Principle, the rate of creep is greatly enhanced when the sample is subjected to a sinusoidally varying dynamic load as compared to a comparable static load. The polymer weight loss was found to be linear with time and strongly dependent on the level of applied dynamic and static force. In addition, the weight loss and rate of creep were also found to be strongly dependent upon temperature.     

Retrograde blood circulation and ischemic heart disease

The author performed experiments on 350 dogs and X-ray postmortem studies of 1520 corpses of subjects who had died of various diseases and injuries. It was found that in occlusive great vessels in the ischemic organs and tissues, retrograde circulation developed, which completely maintained their viability under definite conditions. Retrograde venous blood flow to diseased organs and tissues drastically increased in insufficient retrograde arterial blood circulation. Under certain conditions, surplus venous blood influx caused edema and their dysfunctions. The mechanisms of retrograde circulation account for asymptomatic occlusion of the great vessels.     

Comparative antagonism of kainate-activated kainate and AMPA receptors in hippocampal neurons

Native kainate receptors expressed by cultured hippocampal cells were studied in the whole-cell configuration of the patch-clamp technique by using a fast perfusion system. About 80% of the neurons expressed kainate receptors independently of the time in culture (0-4 days), which coincided with the number of cells immunoreactive for a monoclonal antibody against the GluR5/6/7 subunits. Three types of cells were considered: neurons in which the rapid application of kainate induced a rapidly desensitizing current, cells in which kainate induced a more slowly rising, non-desensitizing, response and those in which a mixture of both responses was apparent. Steady responses induced by 300 microM kainate were inhibited by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) in a dose-dependent manner (IC50 = 0.92 microM). CNQX was less potent in blocking transient kainate-induced responses (IC50 = 6.1 microM). Responses to kainate, whether steady or transient, were also inhibited by NS102, showing poor selectivity for the transient response (IC50 = 4.1 and 2.2 microM respectively). The new alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor antagonist NS394 was very potent in inhibiting steady kainate-induced currents (IC50 = 0.45 microM), but was even more effective in preventing peak responses (IC50 = 0.13 microM). In contrast, cyclothiazide did not affect transient kainate-induced responses but did potentiate current induced by activation of AMPA receptors by AMPA or kainate. These results demonstrate the lack of complete selectivity amongst some available competitive antagonists for AMPA and kainate receptors, and indicate that kainate receptors expressed by hippocampal cells lack the cyclothiazide modulatory site present at AMPA receptors. In addition, the present data support the idea that low-affinity kainate binding sites in the brain correspond to receptor channels selectively activated by kainate.     

Nonsulfhydryl-reactive phenoxyacetic acids increase aqueous humor outflow facility

PURPOSE: The phenoxyacetic acid, ethacrynic acid (ECA), has potential use in glaucoma therapy because it acts to increase aqueous outflow in vivo and in vitro. In human trabecular meshwork (HTM) cell culture, ECA acts to change cell shape and attachment, effects that have been correlated with microtubule (MT) alterations and chemical sulfhydryl (SH) reactivity. To further explore these actions, we evaluated two non-SH reactive phenoxyacetic acids, inadcrinone and ticrynafen, and the MT-disrupting drug vinblastine. METHODS: Excised bovine and porcine eyes were perfused and outflow facility measured. Calf pulmonary artery endothelial and HTM cells were grown in culture and cytoskeletal effects evaluated after drug treatment. RESULTS: Indacrinone, ticrynafen, and vinblastine all caused an increase in outflow facility. In contrast with ECA, the outflow effects of indacrinone and ticrynafen were not blocked by excess cysteine. Although indacrinone and ticrynafen produced changes in cell shape in vitro, the beta-tubulin staining pattern of treated cells was not altered. Vinblastine caused cell shape change and the expected MT disruption. CONCLUSIONS: Phenoxyacetic acids can increase aqueous outflow facility and alter HTM cell shape and attachment in vitro by a non-SH, non-MT mechanism (which is probably shared also by ECA). These findings suggest the possibility of a broader class of glaucoma drugs that may be directed at the HTM. An understanding of the cellular target for these drugs has implications both for potential glaucoma therapy and for the cytoskeletal mechanisms involved in normal outflow function.     

Simulation of sulfide buildup in wastewater and atmosphere of sewer networks.

A model concept for prediction of sulfide buildup in sewer networks is presented. The model concept is an extension to--and a further development of--the WATS model (Wastewater Aerobic-anaerobic Transformations in Sewers), which has been developed by Hvitved-Jacobsen and co-workers at Aalborg University. In addition to the sulfur cycle, the WATS model simulates changes in dissolved oxygen and carbon fractions of different biodegradability. The sulfur cycle was introduced via six processes: 1. sulfide production taking place in the biofilm covering the permanently wetted sewer walls; 2. biological sulfide oxidation in the permanently wetted biofilm; 3. chemical and biological sulfide oxidation in the water phase; 4. sulfide precipitation with metals present in the wastewater; 5. emission of hydrogen sulfide to the sewer atmosphere and 6. adsorption and oxidation of hydrogen sulfide on the moist sewer walls where concrete corrosion may take place.