THE EFFECT OF INSULIN, ALLOXAN DIABETES, AND ANOXIA ON THE ULTRASTRUCTURE OF THE RAT HEART

Hearts from normal and alloxan diabetic rats were perfused in vitro with a bicarbonate-buffered medium containing glucose. Transport of glucose through the cell membrane was stimulated with insulin or by induction of anaerobiosis. The organs were rapidly fixed and examined by electron microscopy. Transport stimulation was not associated with any increase in the number of sarcolemmal invaginations or subsarcolemmal cytoplasmic vesicles. It was concluded that glucose transport and the effects of insulin or anoxia do not involve pinocytosis. The relationship of pinocytosis to glucose transport is discussed. The appearance of numerous lipid inclusions at the Z line level of the sarcomeres in the diabetic and anoxic myocardia is described.     

An Analysis of the Striated Muscle Fiber Action Current

A method is presented for determining the magnitude of the ionic current associated with the propagated spike potential. Parameters of the action current are then compared to various aspects of the response as recorded in a phase plane. The findings also include evidence for (a) Na⁺ ion as the major inward current carrier, (b) a fairly constant membrane conductance during the terminal phase (~1 msec.) of the spike potential, and (c) the influence of Ca⁺⁺ ion concentration on the action current.     

Simian Virus 40 Transformation and the Period of Cellular Deoxyribonucleic Acid Synthesis

The antiviral agents interferon and statolon protected cells of the mouse line 3T3 against the transforming effect of simian virus 40. Loss of ability of these agents to protect when added some time after infection indicated that the transformation was already fixed. The cells of exponentially growing cultures became resistant to the protective effect of interferon at a linear rate after infection; after one cell generation, the whole population was resistant. By use of synchronous cultures, it was shown that, in cells passing though the G-1 period of the growth cycle, the transformation did not pass the interferon-sensitive stage, whereas cells in S [the period of cellular deoxyribonucleic acid (DNA) synthesis] readily passed this stage (i.e., became interferon-resistant). An irreversible step in transformation appeared to occur in cells synthesizing DNA, and it seems likely that replicating cellular DNA was the target of the viral action.     

Ventricular septal defect with bidirectional shunting: Mathematical considerations

Previously proposed formulae for the quantitative estimation of bidirectional shunts across ventricular septal defects require determination of the oxygen contents of mixed venous, pulmonary artery, pulmonary venous, and aortic blood. Because these formulae do not take into account the mixing of oxygenated with unoxygenated blood within the ventricles, their use must result in underestimation of shunt flows in each direction. A mathematical model for a ventricular defect is examined, in which it is assumed that mixing of blood occurs in each of six sites in the venae cavae or right atrium, right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. A total of fourteen streams of blood can flow from one to another of these mixing sites. As long as complete mixing occurs in the six specified mixing sites, any degree of mixing or non-mixing of the various streams is permitted. From the equations characterizing the model, formulae are derived in which the shunt flow in each direction is expressed in terms of the oxygen contents in the six mixing sites and the fractions of blood which enter the shunt from either side without prior mixing in a ventricular mixing site. The previously reported formulae, which apply when no ventricular mixing is allowed to occur, lead to theoretical minimum values for the shunt flows in each direction. At the opposite extreme where all the shunting blood is required to mix in a ventricle before entering the shunt, formulae for maximum possible shunt flows are also obtained. The absolute values for the left-to-right and right-to-left shunt flows, which must lie somewhere between the theoretical maximum and minimum values, cannot be computed from blood gas data alone. This work was supported in part by grant HE-07563 from the National Heart Institute of the National Institutes of Health and grants-in-aid from the American and North Carolina Heart Associations and the Life Insurance Medical Research Fund. Work completed during tenure as U.S.P.H.S. post-doctoral fellow.     

Thermodynamics of the binding of biotin and some analogues by avidin

1. The reaction between avidin and biotin was found to be exothermic, ΔH being −20·3kcal./mole of biotin bound. The corresponding value of ΔH for streptavidin was −23kcal./mole. 2. The heat evolved was independent of the pH (between 5 and 9), of the buffer (borate or ammonia) and of the fractional saturation of the avidin with biotin. 3. The entropy change for the reaction was zero, and it is suggested that the entropy increase to be expected from hydrophobic interactions was counterbalanced by a decrease in entropy accompanying the formation of buried hydrogen bonds. 4. Modification of the potential hydrogen-bonding sites of the imidazolidone ring led to a decreased heat output and a positive entropy of reaction.