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Models are presented for the successive stages of aggregation and recombination of radiation-induced defects in alkali halides. The construction of our models is assisted by the calculation of defect energies. We concentrate on three main areas: firstly, we consider initial aggregation of H centres, where we propose the formation of a weakly bound di-H centre which collapses into a neutral halogen molecule occupying an interstitial site. Secondly, we consider the thermodynamics of formation of the interstitial loops detected in the electron microscope by Hobbs, Hughes and Pooley (1973). We confirm the previously proposed mechanism by which the loops are created; this involves the displacement of lattice ions to dislocation loops by halogen molecules which occupy the vacancy pairs created. Thirdly, we consider the mechanism of annealing of metal colloids, and suggest that the vacancy-molecule complexes, which are created together with the dislocation loops, may play an important role.

A thermodynamic model is presented to describe the combined freezing and thawing process for living cells. Continuous changes in the cell volume are predicted according to the thermal protocol imposed on the system. Experimental verification of the model is sought by monitoring continuously the volume of cells as frozen on a cryomicroscope. The volumes of individual cells are measured from sequential photomicrographs by a computerized image analysis technique. The model and experimental data are in quite close agreement for the freezing process, but upon thawing the experimentally measured volumes consistently increased much more rapidly than predicted by the model. The model can be made to conform to the data by accounting for a substantial influx of electrolyte to the cell at subfreezing temperatures.

The water permeability (Lp) of human granulocytes was measured for individual isolated cells with a novel, microscopic stopped-flow mixing system. Changes in volume were monitored as a cell was introduced suddently into an osmotically active solution. Permeability values were determined as a function of solution osmolality from the volume versus time curves for mixing into both hypotonic and hypertonic solutions within the range of 145 to 833 mOsm. The calculated reference permeability at 25°C was 1.15 μm/atm·min with an osmotic coefficient of 0.46 Osm/kg.

This paper investigates some of the numerical problems involved in simulating heat transfer in porous media in the presence of phase change. Applications of this type of simulation include modeling of certain metal forming processes, of biological tissues and organs during cryosurgery or cyropreservation, and of heat transfer in frozen soils subjected to transient environmental conditions. A two-dimensional finite element model was used in which the latent heat is treated directly as an energy source in the problem formulation. Several parameters addressed in this work are crucial to the successful implementation of numerical methods for nonlinear heat transport with phase change, including: the effect of nodal point spacing on the occurrence and magnitude of numerical oscillations in the temperature solution and the use of grid point spacing to control these oscillations; the limiting element size which should be used in order to insure stable temperature fields; and the effect which the range of temperatures over which latent heat is liberated has on the solution. The results indicate that numerical stability is achieved for combinations of the foregoing parameters which yield small values of the Stefan number.

Freezing procedures for preservation of living cells create osmotic stresses associated with the addition and removal of cryoprotective agents and with ice formation in the extracellular solution, causing a concomitant segregation of electrolytes into the remaining liquid phase. When these osmotic stresses are introduced, coupled flows of water and permeable solute are induced across the plasma membrane. A network thermodynamic model of this process is presented, based on development according to the principles of bond graphs. The model is a complete representation of the equations that describe the process, and the bond graph can be interpreted directly in terms of the relevant energy flows during membrane transport and the topology of the system. Determination of the transient cell volume during addition of glycerol to an erythrocyte suspension is used to demonstrate the model.

The effects of thermal insult on living tissue have been studied by direct microscopic observation of the circulatory system’s response to a controlled trauma regimen. An experimental apparatus has been developed which utilizes a unique high and low temperature stage in conjunction with a precision thermal control system to examine the injury process in the microcirculation of the golden hamster cheek pouch. Unique features of this experimental apparatus are: (1) continuous monitoring of the injury processes at the cellular level, (2) capability for quantitative assay of thermal injury, (3) precise control over the thermal parameters that govern injury, (4) versatility in isolating the effects of these individual parameters. The important thermal parameters monitored using this experimental procedure are the time rates of change of temperature during burning and cooling, the maximum temperature reached, and the length of time the tissue was held at this temperature. With this type of experimental apparatus any portion of the burn protocol, such as the maximum temperature reached during burning, may be varied while holding all other parameters constant. It is well documented that the microvascular bed is a primary site for manifestation of burn wound injury. Burn injury occurs as a consequence of rate dependent physiochemical processes, and, therefore, develops over a finite period of time subsequent to trauma. The experimental technique is designed to determine the gross response of the microvascular system to burn trauma. Initial investigations on burn injury have demonstrated a direct dependency of the extent of damage upon both the maximum temperature attained and the duration of exposure. The minimum temperature required to produce stasis within 20 s after completion of the burn in 95 ±5 percent of the microcirculation decreased exponentially with burn duration between the extremes of 85°C for 1 s exposure and 60°C for 100 s exposure.

Many medical applications involving lasers rely upon the generation of heat within the tissue for the desired therapeutic effect. Determination of the absorbed light energy in tissue is difficult in many cases. Although UV wavelengths of the excimer laser and 10.6 μm wavelength of the CO2 laser are absorbed within the first 20 μm of soft tissue, visible and near infrared wavelengths are scattered as well as absorbed. Typically, multiple scattering is a significant factor in the distribution of light in tissue and the resulting heat source term. An improved model is presented for estimating heat generation due to the absorption of a collimated (axisymmetric) laser beam and scattered light at each point r and z in tissue. Heat generated within tissue is a function of the laser power, the shape and size of the incident beam and the optical properties of the tissue at the irradiation wavelength. Key to the calculation of heat source strength is accurate estimation of the light distribution. Methods for experimentally determining the optical parameters of tissue are discussed in the context of the improved model.