THE EFFECT OF MECHANICAL TENSION UPON THE POLARITY OF GROWING FIBROBLASTS

These experiments seem to justify the conclusion that mechanical tension may determine the polarity of cell division and line of growth of developing fibroblasts, and further that a shift in tension may cause a shift in position of fibroblasts already formed.     

THE CONSTRICTING INFLUENCE OF ADRENALIN UPON THE HUMAN CORONARY ARTERIES

1. Adrenalin causes a marked constriction of the human coronary artery, although it undoubtedly produces a relaxation in some mammals; e. g., calf, sheep, pig, etc. 2. The human coronary artery is probably provided with sympathetic vasoconstrictors. 3. If human blood-vessels are obtained in a warm condition within a few hours after death, they are often suitable for biological and pharmacological study.     

THE INFLUENCE OF THE VAGUS NERVES UPON CONDUCTION BETWEEN AURICLES AND VENTRICLES IN THE DOG DURING AURICULAR FIBRILLATION

The experiments that have been reported indicate that stimulation of either the right vagus or the left vagus nerve is equally effectual in blocking impulses from the auricles to the ventricles when auricular fibrillation is present. Stimulation of the left vagus nerve is as effectual in blocking impulses from the normally beating auricles as from the auricles when in a state of fibrillation, and the type of auricular activity has apparently no influence on the effect which stimulation of the left vagus has on auriculoventricular conduction.     

EFFECT OF STIMULATION OF SENSORY NERVES UPON THE RATE OF LIBERATION OF EPINEPHRIN FROM THE ADRENALS

An attempt was made to determine whether stimulation of afferent nerves (sciatic and brachial) produced a detectable increase in the rate of liberation of epinephrin from the adrenals, as determined by testing adrenal vein blood on rabbit intestine and uterus segments. The result was negative.     

STUDIES WITH THE ELECTROCARDIOGRAPH ON THE ACTION OF THE VAGUS NERVE ON THE HUMAN HEART : I. THE EFFECT OF MECHANICAL STIMULATION OF THE VAGUS NERVE.

In hearts showing auricular fibrillation mechanical stimulation of the right vagus nerve causes, as a rule, marked slowing or stoppage of ventricular rhythm, without producing any appreciable effect in the electrocardiographic record of the auricular fibrillation. The ventricular pauses are apparently due to the blocking of stimuli from the auricles. The force of ventricular systole is distinctly weakened for several beats after vagus stimulation, and ectopic ventricular systoles have been seen in several instances, apparently the result of the vagus action. There may, in some cases, be lowered excitability of the ventricles, while no constant change is seen in the size of the electrical complexes representing ventricular systole.     

A STUDY OF HUMAN SKIN GRAFTED UPON THE CHORIO-ALLANTOIS OF CHICK EMBRYOS

Human skin grafted upon the chorio-allantoic membrane of chick embryos adheres and becomes nourished for as long as 10 days. Occasionally regrafts upon a second egg have succeeded and thus prolonged the vitality of the graft to 14 days. In successful experiments the epithelium of the chorio-allantois fuses with that of the graft, the collagen fibers of the corium interlace with those of the membrane after the separation or disappearance of the ectodermal layer, and the blood vessels of the chick anastomose, and unite by intervening pools of extravasated blood, with those of the graft. This vascular communication between the two tissues is largely responsible for the nourishment of the graft by affording a plasmatic circulation. Gradually there is a partial revascularization of the graft by an ingrowth of blood vessels from the chick membrane. Human skin grafts were susceptible to experimental infection by several viruses.     

EFFECTS OF MECHANICAL AGITATION AND OF TEMPERATURE UPON COMPLEMENT

1. Under certain conditions, mechanical agitation destroys the complementary activity of guinea pig serum. It is most injurious when carried out constantly at a temperature of 37° C., but it is extremely insignificant at 10° C. After the first few hours at 37° C., the destruction of complement proceeded much more rapidly, and after six hours it was almost complete. On the other hand, within one hour shaking had almost no destructive effect on complement, even at 37° C. From this we may conclude that the several shakings which are necessary for fixation experiments during incubation do not modify perceptibly the outcome of the reactions. 2. The rate of destruction of the complement of guinea pig serum at temperatures above 45° C. is progressively greater as it approaches 55° C., at which temperature the activity is reduced in thirty minutes to one-thirtieth to one-fortieth of the original strength of the unheated serum; but it is not completely destroyed, as is commonly assumed. The velocity of destruction of guinea pig complement when exposed to 55° C. for various lengths of time is found to be quite irregular, and not proportional to the length of time. This irregularity, however, presents a certain rhythm, a period of greater destruction alternating with one of less destruction.     

PROPERDIN FACTOR D: CHARACTERIZATION OF ITS ACTIVE SITE AND ISOLATION OF THE PRECURSOR FORM

The activity of properdin factor D was measured by the generation of the hemolytically active cellular intermediate, EAC43B(D), bearing the C3b-dependent alternate pathway C3 convertase. Treatment of factor D with DFP prevented formation of EAC43B(D); thus, a serine esterase is essential for the generation of the alternate pathway C3 convertase, a situation analogous to the role of C1 in the formation of the classical C3 convertase, C42. The definition of factor D as a serine esterase prompted a search for its proenzyme form, and resulted in the chromatographic isolation from plasma of a single peak of trypsin-inducible factor D activity, distinct from activated factor D. Analytical gel filtration indicated an apparent mol wt of 25,000. This protein from which trypsin elaborated factor D activity, as assessed by the formation of EAC43B(D), the generation of the CoVF-dependent C3 convertase, and the cleavage of factor B in the presence of C3b, was designated "precursor factor D." The DFP resistance of precursor factor D, and the susceptibility of its trypsin-activated form to inactivation by DFP is analogous to the behavior of other plasma serine esterases, including C1.