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Several letters to the editor are presented in response to articles in previous issues including "streams of translations" by W. H. Auden in the October 8, 1973 issue, "Episcopalian Backlash" in the October 15, 1973 issue and the political career of Spiro Agnew in the October 22, 1973 issue.

Thirty-seven critically ill infants and children were seen over a ten-year period with the diagnosis of complete "D" transposition of the great arteries. Since 1967, balloon atrial septostomy has been performed at the original diagnostic cardiac catheterization. Previously, palliative treatment was surgical. Considerable improvement immediately followed balloon septostomy, and eight of the ten infants seen since 1967 are alive and doing well. Death occurred following attempted banding of the pulmonary artery in two infants with ventricular septal defects. One, a 7-day-old, also had an associated coarctation of the aorta. The use of balloon septostomy has greatly improved the outlook for infants with transposition of the great arteries, and allows more of them to grow to an age and size when total physiological correction (Mustard operation) may be safely undertaken.

The modern techniques of the cardiology laboratory have resulted in marked improvement in diagnostic ability with concomitant refinement in diagnostic criteria.1-3 In aortic stenosis, these advances now permit precise differentiation into valvular, subvalvular, and supravalvular lesions.4,5Congenital supravalvular aortic stenosis, apparently first described by Archer in 1878,6 has recently been reviewed and given a comprehensive classification by Perou.7 The material and discussion presented below is limited to the true stenosis, or coarctation, of the supravalvular aorta under this classification, and is concerned with the familial incidence of this malformation. REPORT OF CASES Case 1.—Patient 1 (P1) is a 9-year-old white boy of Scandinavian ancestry in whom an aortic systolic murmur was discovered at 2 months of age, and who was asymptomatic until age 8. Since then, he has had mild exertional dyspnea and, occasionally, mild precordial pain. The family history is of considerable interest and will

Deoxycholate disruption of Micrococcus lysodeikticusprotoplast membranes resulted in solubilization of both l-malate and reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase enzymes (substrate: 2,6-dichlorophenolindophenol oxidoreductases). Insoluble residues contained cytochromes of the b, c, and atype. Solubilized dehydrogenases were reconstituted with insoluble residues by treatment of disrupted membranes with magnesium ions. Most of the solubilized l-malate and NADH dehydrogenase activities were precipitated by magnesium ions independent of enzyme reconstitution with insoluble residues. Reconstituted dehydrogenases explained the mechanism for restoration of disrupted l-malate and NADH oxidase activities (4). Black light irradiation inhibited oxidase activities of both native and reconstituted membranes. These irradiated membrane oxidases were partially restored by exogenous napthoquinones [K2(20)and K2(50)] but not by CoQ(6). Reconstitution experiments showed that native membrane napthoquinone was retained in the insoluble residues of deoxycholate-disrupted membranes.

On the basis of information available in the literature, gluconate dissimilation in Escherichia coliis thought to occur via the hexose monophosphate pathway. Evidence is presented in this study that gluconate is catabolized in this organism via an inducible Entner-Doudoroff pathway. This evidence is based on chromatographic examination of end products produced from 14C-labeled gluconate or glucose, distribution of 14C in the carbon atoms of pyruvate formed from specifically labeled 14C-glucose and 14C-gluconate, and the ability of cell-free extracts to produce pyruvate from 6-phosphogluconate. Degradation of gluconate by an Entner-Doudoroff pathway occurred simultaneously with a glycolytic cleavage of glucose. A relationship between gluconate-induced, Entner-Doudoroff pathway activity and catabolism of glucose in Escherichia coliand other bacterial species is discussed.

The input impedance of muscle fibers of the crab was determined with microelectrodes over the frequency range 1 cps to 10 kc/sec. Care was taken to analyze, reduce, and correct for capacitive artifact. One dimensional cable theory was used to determine the properties of the equivalent circuit of the membrane admittance, and the errors introduced by the neglect of the three dimensional spread of current are discussed. In seven fibers the equivalent circuit of an element of the membrane admittance must contain a DC path and two capacitances, each in series with a resistance. In two fibers, the element of membrane admittance could be described by one capacitance in parallel with a resistance. In several fibers there was evidence for a third very large capacitance. The values of the elements of the equivalent circuit depend on which of several equivalent circuits is chosen. The circuit (with a minimum number of elements) that was considered most reasonably consistent with the anatomy of the fiber has two branches in parallel: one branch having a resistance Re in series with a capacitance Ce; the other branch having a resistance Rb in series with a parallel combination of a resistance Rm and a capacitance Cm. The average circuit values (seven fibers) for this model, treating the fiber as a cylinder of sarcolemma without infoldings or tubular invaginations, are Re = 21 ohm cm2; Ce = 47 µf/cm2; Rb = 10.2 ohm cm2; Rm = 173 ohm cm2; Cm = 9.0 µf/cm2. The relation of this equivalent circuit and another with a nonminimum number of circuit elements to the fine structure of crab muscle is discussed. In the above equivalent circuit Rm and Cm are attributed to the sarcolemma; Re and Ce, to the sarcotubular system; and Rb, to the amorphous material found around crab fibers. Estimates of actual surface area of the sarcolemma and sarcotubular system permit the average circuit values to be expressed in terms of unit membrane area. The values so expressed are consistent with the dielectric properties of predominantly lipid membranes.

The resting ionic conductances of frog sartorius muscle fibers have been determined in a variety of conditions in order to measure the potassium conductance of the tubular and surface membranes (gKt and gKs) and the chloride conductance of the tubular and surface membranes (gClt and gCls). In both normal fibers and fibers without tubules, measurements of input resistance and diameter were made at normal pH and at low pH when the chloride conductance was very small. These measurements permitted the separation of the ionic conductances: gCls = 219 µmhos/cm2; gClt = 0 µmhos/cm2; gKs = 28 µmhos/cm2; gKt = 55 µmhos/cm2. Possible sources of systematic error are discussed and a statistical analysis of the effects of random error is presented. The implications of the nonuniformity of membrane properties are discussed along with possible anatomical explanations.

In frog sartorius muscle fibers in which the transverse tubular system has been disrupted by treatment with glycerol, action potentials which are unaccompanied by twitches can be recorded. These action potentials appear to be the same as those recorded in normal fibers except that the early afterpotential usually consists of a small hyperpolarization of short duration. After a train of action potentials no late afterpotential is seen even when the membrane potential is changed from the resting level. In fibers without transverse tubules hyperpolarizing currents do not produce a creep in potential. The interruption of excitation-contraction coupling, the changes in the afterpotentials, and the disappearance of creep are all attributed to the lack of a transverse tubular system.

The passive electrical properties of glycerol-treated muscle fibers, which have virtually no transverse tubules, were determined. Current was passed through one intracellular microelectrode and the time course and spatial distribution of the resulting potential displacement measured with another. The results were analyzed by using conventional cable equations. The membrane resistance of fibers without tubules was 3759 ± 331 ohm-cm2 and the internal resistivity 192 ohm-cm. Both these figures are essentially the same as those found in normal muscle fibers. The capacitance of the fibers without tubules is strikingly smaller than normal, being 2.24 ± 0.14 µF/cm2. Measurements were also made of the passive electrical properties of fibers in a Ringer solution containing 400 mM glycerol (which is used in the preparation of glycerol-treated fibers). The membrane resistance and capacitance are essentially normal, but the internal resistivity is somewhat reduced. These results show that glycerol in this concentration does not directly affect the membrane capacitance. Thus, the figure for the capacitance of glycerol-treated fibers, which agrees well with previous estimates made by different techniques, represents the capacitance of the outer membrane of the fiber. Estimates of the capacitance per unit area of the tubular membrane are made and the significance of the difference between the figures for the capacitance of the surface and tubular membrane is discussed.

To the Editor: Dr. Friedman's comment on the physical signs in supravalvular aortic stenosis is a useful one, and one which had escaped my notice. It was not present in either of the patients discussed. The abstract in Circulation 28 (part 2):760, 1964, by Lurie and Mandelbaum points out that in one patient with valvular stenosis, the pressure in the right arm was greater than in the left. In addition, it is well known that multiple anomalies of the great vessels are present and, therefore, a variation in pressure between the arms might be expected in this disease. The first patient discussed in this paper did, in fact, have a narrowing of the innominate artery, and on several occasions the pressure in the right arm was lower than the left. It seems more likely that the anatomic variations will take precedence over the hypothesis so neatly demonstrated by Drs. Lurie