A study of the hatching process in aquatic invertebrates. XVI. Events of eclosion in Calopsectra neoflavellus Malloch (Diptera,Tendipedidae). XVII. Hatching in Argulus megalops Smith (Crustacea,Branchiura)

Summary Hatching in the tendipedid, Calopsectra neoflavellus involves first a slow uptake of water by the embryo during development, whereby it increases in size and comes to fill entirely the space within the chorion. After completion of embryonic development, the prolarva increases still more in size by swallowing and absorbing water. Internal pressure thus generated results in the bursting of the chorion. The larva then frees itself by active movements.In the branchiuran, Argulus megalops, hatching is similar to that previously described for Copepoda, in that an inner egg membrane swells osmotically and splits the outer chorion. Subsequent bursting of the inner membrane throws the larva nearly out of the egg, but final emergence is by active struggle of the larva.

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Zusammenfassung Das Ausschlüpfen von Calopsectra neoflavellus enthält erstens eine langsame Wasseraufnahme durch den Embryo, wodurch der Embryo wächst und das Wasser den ganzen Raum zwischen Embryo und Chorion füllt. Nach Vollendung der Entwicklung quillt der Embryo noch mehr auf durch den Schluckakt und Aufnahme des Wassers. Dann zerreisst das Chorion durch den intraovularen Druck. Endlich befreit sich die Larve durch Sträuben.In Argulus megalops (Branchiura) gleicht das Ausschlüpfen dem vorher dargestellten für den Copepoden. Eine innere Membran schwillt osmotisch und zerreisst; das Chorion dann zerreist auch die innere Membran selbst and wirft die Larve nahezu aus dem Ei hinaus, aber die schliessiiche Befreiung geschieht durch Sträuben.

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Supported by National Science Foundation grant GB-219, entitled A study of hatching and of the ecology of egg masses of aquatic invertebrates.     

The Chilliwack Respiratory Survey, 1963: Part I. Methodology

In order to ascertain the prevalence of chronic respiratory disease in residents of a rural town and to determine the relative importance of tobacco smoking and air pollution, a survey was conducted of 726 persons living at Chilliwack, British Columbia, in May and June, 1963. Over 95% of a random sample of adults was interviewed and performed simple tests of respiratory function. The sample was selected from a commercial census. An analysis of the demographic characteristics of the sample indicated that the group, aged 25 to 74 years, was reasonably representative for detailed study of chronic respiratory disease.     

Heterozygotes for cystic fibrosis: models for study of airway and autonomic reactivity

Airway reactivity to cold air and methacholine, alpha-adrenergic and cholinergic reactivity measured as pupillary responses to phenylephrine and carbachol, respectively, and beta-adrenergic reactivity assessed by lymphocyte adenosine 3',5'-cyclic monophosphate (cAMP) response to isoproterenol were compared in 108 parents of patients with cystic fibrosis (CF) and 133 healthy adult controls. No differences were found between CF parents and controls in airway response to cold air or methacholine or in lymphocyte cAMP response to isoproterenol. Significant differences were found, however, in the response of the pupils to both phenylephrine and carbachol. Heterozygotes for CF have more reactive pupils; i.e., they require smaller doses of agonist for a 10% change in pupil size. In control subjects, the response of the pupils to phenylephrine and carbachol is highly correlated (r = 0.45, P less than 0.001), whereas in CF heterozygotes, the correlation is not significantly different from zero (r = -0.02). In controls, the pupil response to carbachol has a significant negative correlation with cold air response (r = 0.39, P less than 0.05), indicating that those whose pupils were most sensitive to carbachol had the greatest airway reactivity to cold air, but in CF heterozygotes the correlation is not significant (r = 0.10). A significant correlation exists between lymphocyte cAMP response and airway cold air response in CF heterozygotes (r = -0.32, P less than 0.05) (those whose beta-adrenergic responsiveness is low have greater airway reactivity), but not in controls. The CF parents with the most reactive airways tend to have lower beta-adrenergic responses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mutational analysis of a lactogenic hormone reveals a role for lactogen-specific amino acid residues in receptor binding and mitogenic activity

Mutant forms of mouse placental lactogen-II (PL-II) have been generated to assess the role of specific amino acid residues and protein regions in binding to the PRL receptor and in mitogenic activity. Conversion of any of three lactogen-specific residues significantly reduced both of these hormone functions; mutation of the two other lactogen-specific amino acids revealed only minimal effects unless these changes were coupled with a second mutation. Deletions within the PL-II protein all resulted in a complete loss of function, but switching regions between PL-II and proliferin, another member of the prolactin family in the mouse, did yield a chimeric protein with some PRL-like activity. This activity was increased substantially by conversion of one amino acid residue in the proliferin region to the corresponding lactogen-specific residue. The locations of the amino acids that have been found to affect hormone function are predicted to be closely apposed in the folded protein, suggesting that this region may be the site of interaction of this lactogenic hormone with the PRL receptor.     

Polyclonal antibodies against rat liver cytosolic casein kinase II (CK-2) cross-react with CK-2 from other tissues and nuclear form (PK-N2) of the enzyme

Casein kinase II (CK-2) is a ubiquitous serine/threonine protein kinase, and is localized to both the cell nucleus and cytoplasm. Despite extensive biochemical similarities in their properties, there is evidence that the two forms of the enzyme exhibit certain distinctions (1). This prompted us to produce antibodies against CK-2, which could be utilized as a possible tool for investigations of the various forms of this enzyme. Specific polyclonal antibodies against the rat liver cytosolic CK-2 were raised in egg yolk of laying hens; the enzyme had repeatedly failed to elicit an immunogenic response in rabbits. The purified polyclonal antibody (egg yolk immunoglobulin, IgY) recognized all three subunits (42, 38, and 28 kDa) of the enzyme in immunoblots. The antibody when bound to a matrix was capable of removing CK-2 from solution, and the bound enzyme could be recovered from the immunoaffinity matrix with 0.1 M diethylamine. The antibody exhibited a high affinity towards CK-2 prepared from cytosol of liver, ventral prostate, and several other rat tissues, but no immunoreactivity was detected towards a number of other protein kinases tested. The subunits of the nuclear form of CK-2 (PK-N2) migrated differently when electrophoresed in parallel in the same gel. However, the antibody did cross-react with the various subunits of PK-N2 suggesting a significant homology in the immunogenic domains in the various subunits of the two forms of the enzyme.     

Desensitization of the Neurokinin 1 Receptor Is Mediated by the Receptor Carboxy-Terminal Region, but Is Not Caused by Receptor Internalization

Abstract: The carboxy-terminal cytoplasmic regions of the rat neurokinin 1 (substance P) and neurokinin 2 (neurokinin A) receptors have been exchanged to determine if this region of the neurokinin 1 receptor is involved in its desensitization. When expressed at similar levels in stably transfected Chinese hamster ovary (CHO) cell lines, receptors containing the carboxy-terminal region of the neurokinin 1 receptor desensitized significantly more (as measured by reduction of the inositol 1,4,5-trisphosphate response) when preexposed for 1 min to 1 µ M neurokinin, indicating a role for the carboxy-terminal region of the neurokinin 1 receptor in its desensitization. Measurement of receptor internalization using radiolabeled neurokinins (0.3 n M ) indicated that ∼75–80% of the receptors were internalized in each cell line after 10 min at 37°C, with no observable correlation between neurokinin receptor desensitization and internalization. Measurement of loss of receptor surface sites for cell lines CHO NK1 and CHO NK1NK2 following exposure to 1 µ M substance P also indicated no obvious relationship between the percent desensitization and percent of receptors internalized. Also, two inhibitors of neurokinin 1 receptor internalization, phenylarsine oxide and hyperosmolar sucrose, did not inhibit neurokinin 1 receptor desensitization. The protein kinase inhibitors Ro 31-8220, staurosporine, and Zn²⁺ had no effect on neurokinin 1 receptor desensitization, indicating that the kinases affected by these agents are not rate-limiting in neurokinin 1 receptor desensitization in this system.