Shock protection against

We are currently pursuing our investigation into the heat-shock protection against heat-induced damage to the water-oxidizing complex of PSII. Since several heat-shock proteins are imported into chlorplasts, and since the most heat-labile component of the chloroplast is the watersplitting complex, we feel we have developed a system in which to address the mechanism of heat-shock protein protection of the photosynthetic apparatus. 

Selection and Erection Isolation and Switching Inspection and Testing Protection against Fire Protection against Electric Shock Protection against Overcurrent Special Locations Earthing and Bonding... 

Protection against Electric Shock. Protection against Overcurrent... 

The wide application of hydraulic systems has undoubtedly been stimulated by the increasing use of fully automatic controls for sequences of operations where the response to signals must be rapid and the controls themselves light and easily operated. These needs are met by hydraulic circuits that, in addition, provide infinitely variable speed control, reversal of high-speed parts without shock, full protection against damage from overhead and automatic lubrication. 

Protection against electrical shocks (device and or connections)... 

Lee, B.S., Chen, J., Angelidis, C., Jurivich, D.A., Morimoto, R.l. (1995). Pharmacological modulation of heat shock factor 1 by antiinflammatory drug results in protection against stress-induced cellular damage. Proc. Natl. Acad. Sci. USA 92, 7207-7211. 

Lukacs, K.V., Lowrie, D.B., Stokes, R.W., Colston, M.J. (1993). Tumor cells transfected with a bacterial heat shock gene lose tumorigenicity and induce protection against tumors. J. Exp. Med. 178,343-348. 

Margulis, B.A., Sandler, S., Eizirik, D.L., Welsh, N., Welsh, M. (1991). Liposomal delivery of purified heat shock protein hsp70 in rat pancreatic islets as protection against interleukin I beta-induced impaired beta cell function. Diabetes 40, 1418-1422. 

Matthews, R.C., Bumie, J.P., Howat, D., Rowland, T., Walton. F. (1991). Autoantibody to heat shock protein 90 can mediate protection against systemic candidosis. Immunology 74,20-24. 

Schuster, G., Even, D., Kloppstech, K. Ohad, I. (1988). Evidence for protection by heat-shock proteins against photoinhibition during heat-shock. EMBO Journal, 7, 1-6. 

The administration of Qio or quercetin to rats protected against endotoxin-induced shock in rat brain [252]. It was found that the pretreatment with these antioxidants diminished the shock-induced increase in brain MDA and nitric oxide levels. Interesting data have been obtained by Yamamura et al. [253] who showed that ubiquinone Qi0 is able to play a double role in mitochondria. It was found that on the one hand, Q10 enhanced the release of hydrogen peroxide from antimycin A- or calcium-treated mitochondria, but on the other hand, it inhibited mitochondrial lipid peroxidation. It was proposed that Q10 acts as a prooxidant participating in redox signaling and as an antioxidant suppressing permeability transition and cytochrome c release. 

Beech, J. T. et al., CD4+ Th2 cells specific for mycobacterial 65-kilodalton heat shock protein protect against pristane-induced arthritis. J. Immunol., 159, 3692, 1997. 

Gallily R, Yamin A, Waksmann Y, Ovadia H, Weidenfeld J, Bar-Joseph A, Biegon A, Mechoulam R, Shohami E. (1997). Protection against septic shock and suppression of tumor necrosis factor alpha and nitric oxide production by dexanabinol (HU-211), a nonpsychotropic cannabinoid. J Pharmacol Exp Ther. 283(2) 918-24. 

Acetyls alley lie acid was shown to prevent cirrhosis under certain experimental conditions [125]. Naproxen and indomethacin partially protected against LPS and D-galactosamine-in-duced hepatotoxicity [126] Acetylsalicylic acid and ibuprofen were also protective in endo-toxic shock [127]. Endotoxaemia is one of the complications in cirrhotic patients [128] and is probably caused by an impaired ability of the liver to take up and detoxify gut-derived LPS [116]. The presence of portosystemic shunts in cirrhotic patients may also contribute to this spill-over of LPS into the systemic circulation [129]. NSAIDs, however, are also reported to provoke deleterious effects on renal function in cirrhosis [130], and can therefore not be used in cirrhotic patients. Cell-specific delivery of NSAIDs to SECs and/or KCs may make application of these drugs in cirrhosis feasible by circumventing the renal side-effects. 

Mikami, K., Otaka, M., Watanabe, D., Goto, T., Endoh, A., Miura, K., Ohshima, S., Yoneyama, K., Sato, M., Shibuya, T., Segawa, D., Kataoka, E., et al. (2006). Zinc L-carnosine protects against mucosal injury in portal hypertensive gastropathy through induction of heat shock protein 72. ]. Gastroenterol. Hepatol. 21,1669-1674. 

Bovet and Staub first described agents that block histamine with the discovery that these agents provide protection against anaphylactic shock. Pyrilamine ma-leate was described as a specific and effective histamine antagonist in 1944. Diphenhydramine and tripelenna-mine soon followed (Babe and Serafin, 1996). 

If the deton wave is a shock wave initiating chem reaction and continuously supported by energy thus set free, then it must be protected against the rarefaction which will always follow. This is impossible, if the velocity of small disturbances behind the wave is greater than that of the wave itself. In other words, if (a ) is the velocity of sound at Xj relative to the fluid there, (which itself moves with velocity Wj), and if ai+Wf exceeds the wave cannot be steady but must loose velocity. If a + is less than D, the wave can apparently remain steady. However, the condition a + W < D must, by reason of continuity, persist some little way into Xj Xs, say up to a section X1 (not shown in Fig 5). Then the chem energy released within X Xp can have no influence on what happens ahead of X and is therefore ineffective from the point of view of supporting the wave front. 

Historically, antibodies have been obtained from the serum of animals. The serum contains a mixture of polyclonal antibodies. In 1890, Emil Behring immunized rabbits and mice against tetanus and diphtheria and reported that the antitoxin serum could protect against a lethal dose of the toxin. Since then, antisera have been used to protect from pathogens and toxins, but serum sickness was a major drawback for their clinical use. Antisera may produce immune responses, which could cause severe allergic reactions, and may even lead to anaphylactic shock and death. 

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