Within-stand and seasonal variations of specific leaf area in a clonal Eucalyptus plantation in the Republic of Congo

Specific leaf area (SLA; m(leaf)(2) kg(leaf)(-1)) is a key ecophysiological parameter influencing leaf physiology, photosynthesis, and whole plant carbon gain. Both individual tree-based models and other forest process-based models are generally highly sensitive to this parameter, but information on its temporal or within-stand variability is still scarce. In a 2-4-year-old Eucalyptus plantation in Congo, prone to seasonal drought, the within-stand and seasonal variability in SLA were investigated by means of destructive sampling carried out at 2-month intervals, over a 2-year period. Within-crown vertical gradients of SLA were small. Highly significant relationships were found between tree-average SLA (SLA(t)) and tree size (tree height, H(t), or diameter at breast height, DBH): SLA(t) ranged from about 9 m(2) kg(-1) for dominant trees to about 14-15 m(2) kg(-1) for the smallest trees. The decrease in SLA(t) with increasing tree size was accurately predicted from DBH using power functions. Stand-average SLA varied by about 20% during the year, with lowest values at the end of the 5-month dry season, and highest values about 2-3 months after the onset of the wet season. Variability in leaf water status according to tree size and season is discussed as a possible determinant of both the within-stand and seasonal variations in SM. (C) 2009 Elsevier B.V. All rights reserved.

Ferrolysis induced soil transformation by natural drainage in Vertisols of sub-humid South India

In sub-humid South India, recent studies have shown that black soil areas (Vertisols and vertic Intergrades), located on flat valley bottoms, have been rejuvenated through the incision of streambeds, inducing changes in the pedoclimate and soil transformation. Joint pedological, geochemical and geophysical investigations were performed in order to better understand the ongoing processes and their contribution to the chemistry of local rivers. The seasonal rainfall causes cycles of oxidation and reduction in a perched watertable at the base of the black soil, while the reduced solutions are exported through a loamy sand network. This framework favours a ferrolysis process, which causes low base saturation and protonation of clay, leading to the weathering of 2:1 then 1:1 clay minerals. Maximum weathering conditions occur at the very end of the wet season, just before disappearance of the perched watertable. Therefore, the by-products of soil transformation are partially drained off and calcareous nodules, then further downslope, amorphous silica precipitate upon soil dehydration. The ferrolysed area is fringing the drainage system indicating that its development has been induced by the streambed incision. The distribution of (14)C ages of CaCO(3) nodules suggests that the ferrolysis process started during the late Holocene, only about 2 kyr B.P. at the studied site and about 5 kyr B.P. at the watershed outlet. The results of this study are applied to an assessment of the physical erosion rate (4.8x10(-3) m/kyr) since the recent reactivation of the erosion process. (C) 2010 Elsevier B.V. All rights reserved.

Novel inactivating mutations in the GH secretagogue receptor gene in patients with constitutional delay of growth and puberty

Background: A limited number of mutations in the GH secretagogue receptor gene (GHSR) have been described in patients with short stature. Objective: To analyze GHSR in idiopathic short stature (ISS) children including a subgroup of constitutional delay of growth and puberty (CDGP) patients. Subjects and methods: The GHSR coding region was directly sequenced in 96 independent patients with ISS, 31 of them with CDGP, in 150 adults, and in 197 children with normal stature. The pharmacological consequences of GHSR non-synonymous variations were established using in vitro cell-based assays. Results: Five different heterozygous point variations in GHSR were identified (c.-6 G>C, c.251G>T (p.Ser84Ile), c.505G>A (p.Ala169Thr), c.545 T>C (p.Val182Ala), and c.1072G>A (p.Ala358Thr)), all in patients with CDGP. Neither these allelic variants nor any other mutations were found in 694 alleles from controls. Functional studies revealed that two of these variations (p.Ser84Ile and p. Val182Ala) result in a decrease in basal activity that was in part explained by a reduction in cell surface expression. The p.Ser84Ile mutation was also associated with a defect in ghrelin potency. These mutations were identified in two female patients with CDGP (at the age of 13 years, their height SDS were -2.4 and -2.3). Both patients had normal progression of puberty and reached normal adult height (height SDS of -0.7 and -1.4) without treatment. Conclusion: This is the first report of GHSR mutations in patients with CDGP. Our data raise the intriguing possibility that abnormalities in ghrelin receptor function may influence the phenotype of individuals with CDGP.

Mechanisms Involved in 3 `,5 `-Cyclic Adenosine Monophosphate-Mediated Inhibition of the Ubiquitin-Proteasome System in Skeletal Muscle

Although it is well known that catecholamines inhibit skeletal muscle protein degradation, the molecular underlying mechanism remains unclear. This study was undertaken to investigate the role of beta(2)-adrenoceptors (AR) and cAMP in regulating the ubiquitin-proteasome system (UPS) in skeletal muscle. We report that increased levels of cAMP in isolated muscles, promoted by the cAMP phosphodiesterase inhibitor isobutyl methylxanthine was accompanied by decreased activity of the UPS, levels of ubiquitin-protein conjugates, and expression of atrogin-1, a key ubiquitin-protein ligase involved in muscle atrophy. In cultured myotubes, atrogin-1 induction after dexamethasone treatment was completely prevented by isobutyl methylxanthine. Furthermore, administration of clenbuterol, a selective beta(2)-agonist, to mice increased muscle cAMP levels and suppressed the fasting-induced expression of atrogin-1 and MuRF-1, atrogin-1 mRNA being much more responsive to clenbuterol. Moreover, clenbuterol increased the phosphorylation of muscle Akt and Foxo3a in fasted rats. Similar responses were observed in muscles exposed to dibutyryl-cAMP. The stimulatory effect of clenbuterol on cAMP and Akt was abolished in muscles from beta(2)-AR knockout mice. The suppressive effect of beta(2)-agonist on atrogin-1 was not mediated by PGC-1 alpha (peroxisome proliferator-activated receptor-gamma coactivator 1 alpha known to be induced by beta(2)-agonists and previously shown to inhibit atrogin-1 expression), because food-deprived PGC-1 alpha knockout mice were still sensitive to clenbuterol. These findings suggest that the cAMP increase induced by stimulation of beta(2)-AR in skeletal muscles from fasted mice is possibly the mechanism by which catecholamines suppress atrogin-1 and the UPS, this effect being mediated via phosphorylation of Akt and thus inactivation of Foxo3. (Endocrinology 150: 5395-5404, 2009)