Shearing injuries

Epidermis Stratified squamous epithelium Stratum corneum Stratum spinosum Stratum basale Basement membrane Provides resistance to shear injury... 

Two types of polyvinylpyrrolidones (PVP-Bayer, Leverkusen, Germany) have been found beneficial to cell growth in spinner cultures, and a mixed molecular weight PVP has been found to protect hybridoma cells against shear injury in a bubble column reactor (Handa, 1986). 

Fig. 12.23. The classification of triradiate cartridge injuries based upon the Salter-Harris classification. (i)Shear injury (ii) fracture (iii) compressive injury...

This chapter is not concerned with other types of injuries, such as crushing and shearing injuries, that may occur as a consequence of, for example, a machine operating aberrantly because of a fault in its electrical control system. However, the safety integrity of electrotechnical machinery control systems is considered in Chapter 13. 

Shearing injuries. These injuries are associated with shearing processes and include tragedies such as amputation of fingers/hands. 

Compressed gases, therefore, present a unique hazard from their potential physical and chemical dangers. Unless cylinders are secured they may topple over, cause injury to operators, become damaged themselves and cause contents to leak. If the regulator shears off, the cylinder may rocket like a projectile or torpedo dangerously around the workplace. Other physical hazards stem from the high pressure of a cylinder s contents, e.g. accidental application of a compressed gas/air hose or jet onto an open cut or wound, whereby the gas can enter the tissue or bloodstream, is particularly dangerous. 

The specific platelet surface receptors that support these initial adhesive interactions are determined by the local fluid dynamic conditions of the vasculature and the extracellular matrix constituents exposed at the sites of vascular injury. Konstantopolous et al. (1998) and Alveriadou et al. (1993) demonstrated that under high shear conditions, the adhesion of platelets to exposed subendothelial surfaces of atherosclerotic or injured vessels presenting collagen and von Willebrand factor (vWF) is primarily mediated by the platelet glycoprotein (GP)Ib/IX/V complex. This primary adhesion to the matrix activates platelets, leading ultimately to platelet aggregation mediated... 

Aggregation of platelets involves a contact phase and an adhesive phase, shown diagram-matically in Fig. 7.44. There is good evidence that most thrombi forming within the arterial tree after endothelial injury consist initially of a mass of associated particles on the surface of the vessel. The shearing effects of blood may dislodge platelets. 

Literature reports have used the following reactor parameters to correlate the effects of agitation intensity with cell injury in bioreactors agitator rpm, impeller tip speed, integrated shear factor and Kolmogorov eddy size. Additional parameters have been used for microcarrier bioreactors (discussed below). All correlations of cell injury with a bioreactor parameter should be used only qualitatively. These correlations are, at present, indicative of various trends or mechanistic hypotheses and should not be used for quantitative bioreactor scale-up. In addition, such correlations are applicable to the specific cell type, because different cell types are likely to exhibit different responses to fluid forces. 

The extrinsic pathway is activated by tissue injury and is not of major concern in the clinical use of membrane devices. The intrinsic pathway, however, is initiated by a multitude of factors. Including interactions between serum proteins and exogenous materials. Hydrodynamic forces acting on platelets may also lead to the release of platelet factors that trigger the intrinsic pathway. Thus, the selection of membrane materials to minimize thrombogenesls cannot be fully separated from the design of devices to contain them because of this potential for shear forces to activate the clotting cascade. 

Perhaps the most satisfying hypothesis for the formation of atherosclerotic lesions is that of response to injury in which lesions are precipitated by some form of injury to endothelial cells. The injury may be caused by elevated plasma levels of LDL and modified LDL (oxidized LDL), free radicals (e.g., caused by cigarette smoking), diabetes mellitus, hypertension-induced shear stress, and other factors that lead to focal desquamation of endothelial cells such as elevated plasma homocysteine levels, genetic... 

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