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.     

Increases in tyrosine phosphorylation are detectable before phospholipase C activation after T cell receptor stimulation.

Antiphosphotyrosine immunoblots were used to characterize tyrosine phosphorylated proteins after stimulation of the human TCR. Increased tyrosine phosphorylation was evident on at least 12 substrates within 2 min after ligation of the TCR with mAb. Analysis of the time course for increased tyrosine phosphorylation revealed distinct patterns. Increased phosphorylation of 135-kDa and 100-kDa substrates was evident within 5 s, whereas increased phosphorylation of the TCR-zeta-chain required several minutes after treatment with anti-CD3 mAb. This rapid cellular tyrosine phosphorylation occurred independent of the cell cycle, as it occurred after stimulation of resting T cells, T cell blasts, and the Jurkat T cell leukemia line. When the TCR complex was cross-linked together with the CD4 receptor by heteroconjugate anti-CD3/CD4 mAb, an increased magnitude of tyrosine phosphorylation occurred, although no new substrates could be detected. The increased tyrosine phosphorylation of the 135-kDa and 100-kDa substrates was specific in that anti-HLA class I, anti-CD6, anti-CD7, and anti-CD28 antibodies did not cause increased tyrosine phosphorylation. Anti-CD4 stimulation of resting T cells did not cause increased tyrosine phosphorylation of pp100 and pp135, suggesting that the CD4-associated kinase, lck, does not account for the tyrosine phosphorylation observed after TCR stimulation. Similarly, pharmacologic treatment of cells with phorbol ester and calcium ionophore did not cause increased tyrosine phosphorylation of these substrates, indicating that activation of protein kinase C or phospholipase C does not account for these early increases in tyrosine phosphorylation. The time of onset of pp100 phosphorylation, and the magnitude of phosphorylation correlated with the magnitude of calcium mobilization when cells were stimulated with different forms of TCR stimulation. When cells were labeled with [3H]myoinositol and analyzed after stimulation by anti-CD3 mAb, increased tyrosine phosphorylation of the 135-kDa and 100-kDa substrates preceded the activation of phospholipase C, as measured by the appearance of inositol 1,4,5-trisphosphate. This occurred in both T cell blasts and in the Jurkat T cell line. Thus, these findings show that increased tyrosine phosphorylation is the earliest yet detected signal observed after ligation of the TCR complex, and furthermore suggest that tyrosine phosphorylation might link the TCR to the phosphatidylinositolbisphosphate hydrolysis signaling pathway.     

In vitro RNA editing-like activity in a mitochondrial extract from Leishmania tarentolae.

A mitochondrial extract from Leishmania tarentolae directs the incorporation of uridylate (U) residues within the pre-edited domain of synthetic cytochrome b (CYb) and NADH dehydrogenase subunit 7 mRNA. This has several characteristics of an in vitro RNA editing activity, but no direct evidence for involvement of guide RNAs was obtained. Inhibition by micrococcal nuclease suggests a requirement for some type of endogenous RNA. The limitation of internal U-incorporation to the pre-edited region in the CYb mRNA and the inhibition by deletion or substitution of both mRNA anchor sequences for CYb gRNA-I and -II could be consistent either with a gRNA-mediated process or a secondary structure-mediated process. A low level of incorporation of [alpha-32P]CTP occurs at the same sites as UTP. Internal U-incorporation activity is selectively inhibited by heterologous RNAs, suggesting an involvement of low affinity RNA-binding proteins which can be competed by the added RNA.