THE BINDING OF BOTULINUM TOXIN TO MEMBRANE LIPIDS: SPHINGOLIPIDS, STEROIDS AND FATTY ACIDS

A number of lipids known to be constituents of nerve-ending membranes were tested for their ability to inactivate botulinum toxin. Inactivation of the toxin by a lipid was taken as presumptive evidence that the lipid might be the in vivo receptor for the toxin. Several sphingolipids (sphingosine, galactosylceramide, glucosylceramide, lactosylceramide, cytolipin K and cytolipin R), steroids (cholesterol and deoxycholic acid) and fatty acids (palmitic acid, stearic acid, prostaglandin E₁) did not affect the potency of botulinum toxin, and thus were discounted as potential toxin receptors. However, the gangliosides did inactivate botulinum toxin rapidly (in less than 5 min), within a temperature range of 2°-40°C, and at ionic strengths of 0.05-0.40. Inactivation diminished as pH fell below 6. The activity of gangliosides in suppressing the potency of botulinum toxin was a function of the number of sialic acid residues in the lipid. Thus, the data suggest that a molecule containing sialic acid may be the receptor for the toxin.     

THE FINE STRUCTURE OF SHEEP MYOCARDIAL CELLS; SARCOLEMMAL INVAGINATIONS AND THE TRANSVERSE TUBULAR SYSTEM

An electron microscope study of sheep myocardial cells has demonstrated the presence of a transverse tubular system, apparently forming a network across the cell at each Z band level. The walls of these tubules resemble the sarcolemma in consisting of two dense layers—plasma membrane and basement menbrane; continuity of the tubule walls with the sarcolemma can be seen when longitudinal sections of a cell are obtained between two subsarcolemmal myofibrils and at the same time perpendicular to the cell surface. The demonstration of communication between the lumen of the transverse tubular system and the extracellular space appears to be more definite in this study than in any work hitherto published. It provides anatomical evidence of a possible direct pathway for transmission of the activating impulse from the sarcolemma to the myofibril Z bands.     

The mechanism of honey-bee queen piping

Summary Queens breathed continuously while they were piping, and were able to pipe with all spiracles except one blocked, so the sound could not have been produced by air entering or leaving the spiracles. It is produced by operating the flight motor without spreading the wings, and is radiated partly by the substratum, to which the vibrations are communicated by pressing the thorax against it.

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Zusammenfassung Königinnen atmeten während des Tütens ununterbrochen, und waren zum Tüten fähig, wenn alle Atemlöcher bis auf eines blockiert waren, so daß der Laut nicht durch Ein oder Austreten der Luft durch die Atemlöcher hervorgerufen sein konnte. Er wird erzeugt, indem der flight motor ohne das Ausbreiten der Flügel funktioniert, und teilweise durch das Substrat verbreitet, auf das die Schwingungen durch Anpressen des Thorax übertragen werden.

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Piping in English includes both tüten and quaken in German. Both sounds are produced in the same way but quaken is heard when the queen is in her cell (Armbruster, 1922).     

Total Body Scanning with Strontium-85 in the Diagnosis of Metastatic Bone Disease

To demonstrate skeletal metastases before radiographic changes were apparent, Sr⁸⁵ scans were carried out on 46 patients who complained of sketetal pain but whose radiographs were negative. Positive scans were obtained in 34 patients, 20 of whom were subsequently shown to have metastases; three did not have skeletal metastases a year or more later; the outcome is unknown in 11 patients. Twelve patients had negative scans: three ultimately developed metastases, six did not, and three were inconclusive. Autoradiographs demonstrated Sr⁸⁵ concentrations in areas of reactive osteogenesis.Although not specific for skeletal metastases, Sr⁸⁵ scans are most helpful in substantiating this diagnosis when radiographic changes are absent.     

Early estrogen treatment of female zebra finches masculinizes the brain pathway for learned vocalizations

Telencephalic nucleus HVC and its two efferent targets, RA and X, play essential roles in the production of complex, learned vocalizations in the male zebra finch. Normal females do not produce these learned vocalizations; HVC, RA, and X are small in volume, and HVC and RA are not synaptically connected. We have shown that estrogen treatment during development causes females to learn and produce male-like vocalization. This article describes the neural masculinization of these E2 females, replicating and extending the work of others. Female zebra finches were treated with 17β-estradiol (E2) at hatching, at 14–22 days of age, or as adults. In adulthood, the volumes of nucleus RA and area X were measured and the efferent projections of nucleus HVC examined using the anterograde tracer PHA-L. Early, sustained E2 treatment caused the greatest increase in the volume of RA and X, the innervation of RA and X by HVC axons, and the masculinization of auditory responses of cells in RA. Treatments that lasted for a shorter period or started later in development resulted in different patterns of partial brain masculinization. E2 treatment in adulthood had no effect on the volume of RA or X or their innervation by HVC. Bilateral lesions of the tracheosyringeal nerves or of HVC had the same effects on the male-typical vocalizations produced by E2 females as they do on the vocalizations produced by males. These results demonstrate that the neural masculinization of telencephalic nuclei induced by E2 treatment sets up a functional circuit in females similar to one in males that enables the learning and production of complex vocalizations.     

Identification of a common molecular basis for combined 17α-hydroxylase/17,20-lyase deficiency in two Mennonite families

Summary During the course of studies to characterize mutations of the CYP17 gene that cause the 17-hydroxylase-deficient form of congenital adrenal hyperplasia we have discovered two ostensibly unrelated Mennonite families in which affected individuals are homozygous for the same mutation. The defect is a four-base duplication in exon 8 of the CYP17 gene, which alters the reading frame encoding the C-terminal 26 animo acids of cytochrome P450₁₇.