Zebrafish miR-214 modulates Hedgehog signaling to specify muscle cell fate

Numerous microRNAs (miRNAs) have been discovered in the genomes of higher eukaryotes, and functional studies indicate that they are important during development. However, little is known concerning the function of individual miRNAs. We approached this problem in zebrafish by combining identification of miRNA expression, functional analyses and experimental validation of potential targets. We show that miR-214 is expressed during early segmentation stages in somites and that varying its expression alters the expression of genes regulated by Hedgehog signaling. Inhibition of miR-214 results in a reduction or loss of slow-muscle cell types. We show that su(fu) mRNA, encoding a negative regulator of Hedgehog signaling, is targeted by miR-214. Through regulation of su(fu), miR-214 enables precise specification of muscle cell types by sharpening cellular responses to Hedgehog.     

Cardiovascular development: towards biomedical applicability

Advances in our understanding of cardiac development have fuelled research into cellular approaches to myocardial repair of the damaged heart. In this collection of reviews we present recent advances into the basic mechanisms of heart development and the resident and non-resident progenitor cell populations that are currently being investigated as potential mediators of cardiac repair. Together these reviews illustrate that despite our current knowledge about how the heart is constructed, caution and much more research in this exciting field is essential. The current momentum to evaluate the potential for cardiac repair will in turn accelerate research into fundamental aspects of myocardial biology.     

Zur Blutdruckwirkung von Aludrin und Adrenalin

Summary The depressor action of small doses of adrenaline on the blood pressure (B.P.) of the decapitated cat may be abolished by pretreatment with pilocarpine; atropine restores the original depressor action. The fall in B.P. due to adrenaline after ergotamine once more becomes an increase when pilocarpine has been given earlier. After atropine a fall in B.P. again occurs. This effect of pilocarpine and atropine on a depressor response has already been described in the case of Aludrine (N-isopropyl-noradrenaline) byFromherz.     

Über ein Chromoplastin aus reifenden Tomaten

Summary (1) By precipitation with ammonium sulfate, streptomycin, or calcium salts, we obtained from the pulp of tomatoes a substance containing carotinoids. The behaviour of this substance was analogous to that of chloroplst-substance and to that of animal cytoplasmatic nucleoproteins. Like these it contains proteins, lipids, and very probably nucleic acids. We regard this substance as achromoplastine.(2) Experiments with slices of green tomatoes show that the changing over of the chlorophyll content into the carotinoid content is inhibited by the presence of streptomycin.(3) Streptomycin inhibits the formation of chlorophyll in etiolated separated cabbage leafs, just as this drug inhibits the formation of chlorophyll in growing seeds.(4) The development of anthocyanides is not influenced by streptomycin.     

Die Wirkung von synthetischen Antihistaminkörpern auf die Senfölchemosis am Kaninchenauge

Summary Intravenous or subcutaneous administration of pyribenzamine and other antihistaminics is able to decrease, and to delay the appearance of chemosis produced by mustard oils in the eye of the rabbit. Simultaneously occurring vascular reactions, on the other hand, are but slightly affected by antihistaminics. Intravenous or subcutaneous administration of rutin has no clear-cut effect on chemosis; it is however able to inhibit the vascular reaction.     

Die Wirkung des Toluidinblaus und der Thrombokinase auf den Vorgang der Thrombininaktivierung

Summary The disappearance of thrombin—formed in the blood, or added to serum-follows a manomolecular reaction-type. Heparin increases the reaction-velocity of this thrombin-inactivating process.Our investigation established that toluidine blue or kinase, which, according to the literature, bind heparin, strongly reduce the speed of thrombin-inactivation too. Therefore the heparin-binding capacity of these substances is also manifested in the decrease of thrombin-inactivation.