Mantle thermal pulses below the Mid-Atlantic Ridge and temporal variations in the formation of oceanic lithosphere

A 20-Myr record of creation of oceanic lithosphere is exposed along a segment of the central Mid-Atlantic Ridge on an uplifted sliver of lithosphere. The degree of melting of the mantle that is upwelling below the ridge, estimated from the chemistry of the exposed mantle rocks, as well as crustal thickness inferred from gravity measurements, show oscillations of approximately 3-4 Myr superimposed on a longer-term steady increase with time. The time lag between oscillations of mantle melting and crustal thickness indicates that the mantle is upwelling at an average rate of approximately 25 mm x yr(-1), but this appears to vary through time. Slow-spreading lithosphere seems to form through dynamic pulses of mantle upwelling and melting, leading not only to along-axis segmentation but also to across-axis structural variability. Also, the central Mid-Atlantic Ridge appears to have become steadily hotter over the past 20 Myr, possibly owing to north-south mantle flow.     

On the inhibitory action of endosperm on germination ofCercis siliquastrum seeds

Summary The endosperm inhibits the growth of embryos isolated fromCercis siliquastrum seeds. The inhibitory activity is present in autoclaved homogenates as well as in homogenates remaining after an extraction with chloroform or isobutanol.Acknowledgment. The authors wish to thank Prof. E. Marré, Milan University, for his help in preparation of this paper.     

Influence of prenatal X-radiation on brain lipid and cerebroside content in developing rats

Résumé Lorsque des rats sont irradiés par des rayons X au 14e jour de la gestation, le contenu en cérébrosides du cortex cérébral et du diencéphale est plus élevé que chez les témoins. Or il est bien connu que ce traitement entraîne d'une part une prolifération gliale et d'autre part une augmentation de la sensibilité du système nerveux central à une stimulation électrique. La possibilité d'une relation entre ces phénomènes est discutée.

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USPHS HD-101 fellow.     

Genetic dissection and prognostic modeling of overt stroke in sickle cell anemia

Sickle cell anemia (SCA) is a paradigmatic single gene disorder caused by homozygosity with respect to a unique mutation at the beta-globin locus. SCA is phenotypically complex, with different clinical courses ranging from early childhood mortality to a virtually unrecognized condition. Overt stroke is a severe complication affecting 6-8% of individuals with SCA. Modifier genes might interact to determine the susceptibility to stroke, but such genes have not yet been identified. Using Bayesian networks, we analyzed 108 SNPs in 39 candidate genes in 1,398 individuals with SCA. We found that 31 SNPs in 12 genes interact with fetal hemoglobin to modulate the risk of stroke. This network of interactions includes three genes in the TGF-beta pathway and SELP, which is associated with stroke in the general population. We validated this model in a different population by predicting the occurrence of stroke in 114 individuals with 98.2% accuracy.     

Modifications of myosin caused by adenosine-triphosphate,adenosinediphosphate, and pyrophosphate

Riassunto In presenza di ATP o ADP o pirofosfato, in concentrazioni da 10^–2 a 10⁴ M, la solubilità della miosina aumenta notevolmente a bassa forza ionica. Il legame che si forma fra la miosina e i polifosfati è tale che solo una dialisi prolungata può allontanarli interamente.     

Effects of estradiol and cortisol on neural tissue in culture

Résumé L'activité acétylcholinestérasique et la teneur globale en protéines de fragments de cervelet et de moelle d'embryon de poulet de 16 jours diminue lorsqu'ils sont maintenus en culture organotypique dans le milieu standard deEagle. Après addition de cortisol ou d'oestradiol au milieu, les caractéristiques des tissus ne sont pas alterées par la mise en culture.

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This work was partially supported by contract AT (11-1), Project 82, between U.S. Atomic Energy Commission and University of California, Berkeley.     

The N-terminal groups of glutamic aspartic transaminase

Riassunto Su una preparazione altamente purificata di glutammico aspartico transaminasi del cuore di porco sono stati determinati i gruppi N-terminali con il metodo diSanger. È stata dimostrata la presenza di una mole di alanina N-terminale per 58 000 g di proteina, cioè per una mole di coenzima. La transaminasi risulterebbe pertanto costituita da due catene polipeptidiche.     

The ABC protein turned chloride channel whose failure causes cystic fibrosis

CFTR chloride channels are encoded by the gene mutated in patients with cystic fibrosis. These channels belong to the superfamily of ABC transporter ATPases. ATP-driven conformational changes, which in other ABC proteins fuel uphill substrate transport across cellular membranes, in CFTR open and close a gate to allow transmembrane flow of anions down their electrochemical gradient. New structural and biochemical information from prokaryotic ABC proteins and functional information from CFTR channels has led to a unifying mechanism explaining those ATP-driven conformational changes.     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.