Myocardial function and energy metabolism in carnitine-deficient rats

Carnitine is essential for mitochondrial metabolism of long-chain fatty acids and thus for myocardial energy production. Accordingly, carnitine deficiency can be associated with cardiomyopathy. To better understand this disease, we determined myocardial function and energy metabolism in a rat model of carnitine deficiency. Carnitine deficiency was induced by a 3- or 6-week diet containing N-trimethyl-hydrazine-3-propionate, reducing cardiac and plasma carnitine by 70-85%. Myocardial function was investigated in isolated isovolumic heart preparations. Carnitine-deficient hearts showed left ventricular systolic dysfunction, reduced contractile reserve, and a blunted frequency-force relationship independently of the substrate used (glucose or palmitate). After glycogen depletion, palmitate could not sustain myocardial function. Histology and activities of carnitine palmitoyl transferase, citrate synthase, and cytochrome c oxidase were unaltered. Thus, as little as 3-6 weeks of systemic carnitine deficiency can lead to abnormalities in myocardial function. These abnormalities are masked by endogenous glycogen and are not accompanied by structural alterations of the myocardium or by altered activities of important mitochondrial enzymes.     

Retinoic acid regulates avian lung branching through a molecular network

Retinoic acid (RA) is of major importance during vertebrate embryonic development and its levels need to be strictly regulated otherwise congenital malformations will develop. Through the action of specific nuclear receptors, named RAR/RXR, RA regulates the expression of genes that eventually influence proliferation and tissue patterning. RA has been described as crucial for different stages of mammalian lung morphogenesis, and as part of a complex molecular network that contributes to precise organogenesis; nonetheless, nothing is known about its role in avian lung development. The current report characterizes, for the first time, the expression pattern of RA signaling members (stra6, raldh2, raldh3, cyp26a1, rarα, and rarβ) and potential RA downstream targets (sox2, sox9, meis1, meis2, tgfβ2, and id2) by in situ hybridization. In the attempt of unveiling the role of RA in chick lung branching, in vitro lung explants were performed. Supplementation studies revealed that RA stimulates lung branching in a dose-dependent manner. Moreover, the expression levels of cyp26a1, sox2, sox9, rarβ, meis2, hoxb5, tgfβ2, id2, fgf10, fgfr2, and shh were evaluated after RA treatment to disclose a putative molecular network underlying RA effect. In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfβ2, and id2 spatial distribution; to increase rarβ, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Overall, these findings support a role for RA in the proximal–distal patterning and branching morphogenesis of the avian lung and reveal intricate molecular interactions that ultimately orchestrate branching morphogenesis.     

Migration intercinétique dans la placode olfactive chez l'embryon de poulet interkinetic nuclear migration in nasal placode

Summary Cells of nasal placode of chick embryos were studied with thymidine H³ and autoradiography. Our results shown, that the nuclei in the nasal placode synthesize DNA in the outer zone, then migrate toward the inner zone to undergo division and subsequently return to the outer zone.     

Amino acid accumulation by brain slices: Interactions among tryptophan,phenylalanine and histidine

Resumen La concentración de triptófano en cortes de cerebro incubados con este aminoácido durante 60 min, es disminuida por la presencia de fenilalanina pero aumentada por la histidina. El efecto de la histidina se puede explicar por intercambio a nivel de la membrana entre la histidina intracelular y el triptófano extracelular.     

Growth,development, feeding preference,and food consumption and utilization by tobacco hornworm on tobacco mosaic virus-infected and non-infected tobacco leaves

Summary Plant disease may cause a variety of changes in plants which influence their suitability to insect herbivores. The reported physiological changes in tobacco due to infection by tobacco mosaic virus have the potential to influence the feeding, growth and behavior of the tobacco hornworm,Manduca sexta. However, feeding on foliage of systematically infected plants had no statistically significant effects on development time, mean pupal weight or the amount of foliage consumed by 4th instars. Although an initial preference was exhibited by larvae for healthy leaves after about 72 h no differences were observed. These results do not support the results of previous research on the influence of tobacco mosaic virus-infected plants on the tobacco hornworm.Scientific contribution No. 8130, article No. A-5071, of the Maryland Agricultural Experiment Station, Department of Entomology