Seasonal and vertical demography of dead portions of shoots of smooth cordgrass in a south-temperate saltmarsh

Knowledge of the crop-size and vertical profile with respect to sea level of dead leaf blades and other shoot parts of saltmarsh grasses is a prerequisite for projections of seawater impact upon saltmarsh grass-shoot decomposers. We measured seasonal changes in quantities of leaf blade and leaf sheath+stem of smooth cordgrass in southern temperate saltmarshes of three types: low- (LD), mid- (MD), and high-drainage (HD) marshes (i.e., with low to high densities of drainage creeks). In each type of marsh, we took samples in the three characteristic subsites, short-shoot, intermediate-height, and tall-shoot. Wholly dead (brown) and living (some green) shoots were counted and their canopy heights measured, and the mass of all shoots was measured in 10-cm height increments (above sediment), with separation of living and dead parts. Detached material was also quantified, separated into that trapped in the canopy, and that prostrate on the sediment. Extent of marsh drainage did not affect the density of wholly dead shoots, which ranged from an average of 51 m⁻² in autumn to 103 m⁻² in spring, and 57 m⁻² in tall subsites to 89–96 m⁻² in short and intermediate subsites. The top of the dead-shoot canopy was about 20 cm taller than the living-shoot canopy in winter/spring, but was below it ( ≈50 cm) in summer/autumn. The mass of standing-dead leaf blades was 4- to 5-fold greater in winter than in summer, and it was about 2.5-fold greater at tall than at short sites. Detached litter trapped among shoots above the sediment averaged 26% of total dead-shoot mass, but litter lying on the sediment averaged only 6% of total dead-shoot mass. Since export of macrodetritus from marshgrass stands is inconsequential, the small prostrate-litter mass implies that breakdown of shoots to small particles takes place within the vegetated marsh, and that standing decay predisposes fallen material to rapid disintegration. Comparison of heights of usual tidal contact on shoots at the short- and tall-shoot subsites showed that projected impacts of seawater upon leaf-blade decay would be greater at short-shoot subsites (high marsh) than at tall-shoot subsites (low marsh). This was because the vertical profile of dead-blade mass resulted in more of the short-shoot dead-blade mass residing within the vertical span most regularly contacted by flooding tides.     

Adenyl cyclase activities in rat erythrocytes during stress erythropoiesis: localization of the enzyme in the reticulocytes

NaF- and isoproterenol-stimulated adenyl cyclase activity found in preparations from rat erythrocytes is obviously localized mainly in the reticulocytes. After treatment with acetylphenyl hydrazine, both reticulocyte counts and adenyl cyclase activity increase dose-dependently. Evidence is given that adenyl cyclase activity in the red blood cell is lost during the maturation process.     

Peptide degradation is a critical determinant for cell-penetrating peptide uptake

Cell-penetrating peptide mediated uptake of labels appears to follow an equilibrium-like process. However, this assumption is only valid if the peptides are stabile. Hence, in this study we investigate intracellular and extracellular peptide degradation kinetics of two fluorescein labeled cell-penetrating peptides, namely MAP and penetratin, in Chinese hamster ovarian cells. The degradation and uptake kinetics were assessed by RP-HPLC equipped with a fluorescence detector. We show that MAP and penetratin are rapidly degraded both extracellularly and intracellularly giving rise to several degradation products. Kinetics indicates that intracellularly, the peptides exist in (at least) two distinct pools: one that is immediately degraded and one that is stabile. Moreover, the degradation could be decreased by treating the peptides with BSA and phenanthroline and the uptake was significantly reduced by cytochalasin B, chloroquine and energy depletion. The results indicate that the extracellular degradation determines the intracellular peptide concentration in this system and therefore the stability of cell-penetrating peptides needs to be evaluated.     

Bacterial infection-mediated mucosal signalling induces local renal ischaemia as a defence against sepsis

Ascending urinary tract infections can cause extensive damage to kidney structure and function. We have used a number of advanced techniques including multiphoton microscopy to investigate the crucial early phases of uropathogenic Escherichia coli induced pyelonephritis within a living animal. Our results reveal a previously undescribed innate vascular response to mucosal infection, allowing isolation and eradication of the pathogen. The extremely rapid host response to mucosal infection was highlighted by the triggering of a cascade of events within 3-4 h. Epithelial signalling produced an increase in cellular O(2) consumption and affected microvascular flow by clotting, causing localized ischaemia. Subsequent ischaemic damage affected pathophysiology with actin re-arrangement and epithelial sloughing leading to paracellular bacterial movement. A denuded tubular basement membrane is shown to hinder immediate dissemination of bacteria, giving the host time to isolate the infection by clotting. Suppression of clotting by heparin treatment caused fatal urosepsis. Clinically these findings may be relevant in antibiotics delivery in pyelonephritis patients and to the use of anticoagulants in sepsis.     

Molecular diagnosis of Menkes disease: Genotype–phenotype correlation

Menkes syndrome is an X-linked, fatal neurodegenerative disorder of copper metabolism, caused by mutations in the ATP7A gene, encoding a copper-transporting P1B-type ATPase. To date, a total of approximately 160 different mutations have been reported worldwide. The clinical phenotypes observed in these patients include progressive neuro-degeneration, connective-tissue abnormalities and peculiar hair. There is phenotypic variability. While the majority of the patients do not survive early childhood, milder cases leading to longer survival have been reported. In this review we focus on mutations, identified in patients with milder forms of Menkes disease, and discuss the possibility of establishing a genotype–phenotype correlation. The presence of small amounts of normal protein, or the presence of partly functional protein variants containing a less essential amino acid substitution or a truncation of the N- or C-terminus, might all result in a milder, atypical phenotype. A clear phenotype–genotype correlation is however difficult to establish, clearly illustrated by the presence of inter- and even intra-familial variability.