Plasma levels of renin, angiotensin II, and 6-ketoprostaglandin F1 alpha in endurance athletes

Twelve male runners and 12 matched nonathletes performed a prolonged uninterrupted graded exercise test on the bicycle ergometer up to exhaustion to study blood pressure and plasma levels of renin (PRA), vasoconstrictor angiotensin II (ANG II), and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), a metabolite of the vasodilator prostacyclin. In the athletes work load was increased by 30 W/4 min, and in the control subjects the increments of work load were adjusted to their lower exercise capacity to equalize total exercise duration. Blood was drawn, and blood pressure and O2 uptake (VO2) were measured at rest and at the fourth, eighth, and last steps of exercise. Peak VO2 averaged 60 +/- 1.6 ml . min-1 . kg-1 in the runners and 46.8 +/- 1.5 in the nonathletes. To evaluate differences between athletes and controls, PRA, ANG II, and 6-keto-PGF1 alpha were first adjusted for significant confounding factors, such as age, weight, hematocrit, 24-h urinary sodium excretion, and O2 uptake. PRA was significantly lower in the athletes (F = 11.2; P less than 0.01); ANG II was not different at rest, but its rise with exercise was less steep in the runners (F = 8.2; P less than 0.01), whereas 6-keto-PGF1 alpha was not different between the groups (F = 1.3; NS). Despite the differences in PRA and ANG II, however, blood pressure was similar in athletes and nonathletes (F = 0.0; NS).     

Spleen protein tyrosine kinases TPK-IIB and CSK display different immunoreactivity and opposite specificities toward c-src-derived peptides.

Polyclonal antibodies have been raised against two synthetic peptides reproducing the 48-64 and 353-369 sequences of CSK, a protein tyrosine kinase implicated in the down-regulation of src-related protein kinases. Both antibodies specifically recognize recombinant CSK and a CSK-related 49 kDa protein tyrosine kinase present in spleen but they do not cross-react with purified TPK-IIB, a spleen protein tyrosine kinase sharing with CSK catalytic activity toward src kinases and incapability to autophosphorylate. CSK and TPK-IIB once resolved from each other by heparin-Sepharose affinity chromatography, display opposite specificities toward synthetic peptides reproducing the sequences around the main phosphoacceptor residues of pp60c-src, namely Tyr-416 and Tyr-527. These data support the view that TPK-IIB and CSK may exert opposite effects on the activity of src-related protein tyrosine kinases.     

The contribution of prenatal environment and genetic factors to the association between birth weight and adult grip strength

Low birth weight has been associated with reduced hand grip strength, which is a marker of future physical function and disease risk. The aim of this study was to apply a twin pair approach, using both ‘individual’ data and ‘within-pair’ differences, to investigate the influence of birth weight on hand grip strength and whether this association may be mediated through fat free mass (FFM). Participants from the East Flanders Prospective Twin Survey were included if born without congenital abnormalities, birth weight >500 g and ≥22 weeks of gestation. Follow up in adulthood (age: 18–34 year), included anthropometric measures and hand grip (n = 783 individuals, n = 326 same-sex twin pairs). Birth weight was positively associated with hand grip strength (β = 2.60 kg, 95% CI 1.52, 3.67, p<0.001) and FFM (β = 4.2, 95% CI 3.16, 5.24, p<0.001), adjusted for gestational age, sex and adult age. Using ‘within-pair’ analyses, the birth weight hand grip association was significant in DZ men only (β = 5.82, 95% CI 0.67, 10.97, p = 0.028), which was attenuated following adjustment for FFM. Within-pair birth weight FFM associations were most pronounced in DZ men (β = 11.20, 95% CI 7.18, 15.22, p<0.001). Our ‘individual’ analyses show that higher birth weight is associated with greater adult hand grip strength, which is mediated through greater adult FFM. The ‘within-pair’ analyses confirm this observation and furthermore show that, particularly in men, genetic factors may in part explain this association, as birth weight differences in DZ men result in greater differences in adult strength and FFM.     

The bacterial effector DspA/E is toxic in Arabidopsis thaliana and is required for multiplication and survival of fire blight pathogen

The type III effector DspA/E is an essential pathogenicity factor of the phytopathogenic bacterium Erwinia amylovora. We showed that DspA/E was required for transient bacterial growth in nonhost Arabidopsis thaliana leaves, as an E. amylovora dspA/E mutant was unable to grow. We expressed DspA/E in A. thaliana transgenic plants under the control of an oestradiol‐inducible promoter, and found that DspA/E expressed in planta restored the growth of a dspA/E mutant. DspA/E expression in these transgenic plants led to the modulation by at least two‐fold of the expression of 384 genes, mostly induced (324 genes). Both induced and repressed genes contained high proportions of defence genes. DspA/E expression ultimately resulted in plant cell death without requiring a functional salicylic acid signalling pathway. Analysis of A. thaliana transgenic seedlings expressing a green fluorescent protein (GFP):DspA/E fusion indicated that the fusion protein could only be detected in a few cells per seedling, suggesting the degradation or absence of accumulation of DspA/E in plant cells. Consistently, we found that DspA/E repressed plant protein synthesis when injected by E. amylovora or when expressed in transgenic plants. Thus, we conclude that DspA/E is toxic to A. thaliana: it promotes modifications, among which the repression of protein synthesis could be determinant in the facilitation of necrosis and bacterial growth.     

Radiolytic transformation of 2,2',4'-trihydroxychalcone

Radiolysis of 2,2',4'-trihydroxychalcone, a natural antioxidant present in fruit and vegetables, was performed in ethanol in the absence or in the presence of dioxygen. The degradation process of chalcone was followed in de-aerated solution by HPLC, NMR, FAB-LSIMS mass spectroscopy and analytical TLC. Under anaerobic conditions, six new products (three couples of diastereoisomers) were identified. Four of them kept the chalcone skeleton with OCH(2)CH(3), CH(OH)CH(3) and H substitutions on C(alpha) and C(beta). Thus the target was the alpha-beta double bond on which ethanol radicals were added. The two other compounds were formed in a second stage and exhibited a cyclization between the substituent on C(beta) and the carbonyl group. In the presence of dioxygen, these reactions were prevented and chalcone was protected. This study was the first step toward understanding of the behavior chalcone in irradiated fruits and vegetables.     

Erwinia amylovora type three-secreted proteins trigger cell death and defense responses in Arabidopsis thaliana

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2 ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.     

Systemic silencing signal(s)

Grafting experiments have revealed that transgenic plants that undergo co-suppression of homologous transgenes and endogenous genes or PTGS of exogenous transgenes produce a sequence-specific systemic silencing signal that is able to propagate from cell to cell and at long distance. Similarly, infection of transgenic plants by viruses that carry (part of) a transgene sequence results in global silencing (VIGS) of the integrated transgenes although viral infection is localized. Systemic PTGS and VIGS strongly resemble recovery from virus infection in non-transgenic plants, leading to protection against secondary infection in newly emerging leaves and PTGS of transiently expressed homologous transgenes. The sequence-specific PTGS signal is probably a transgene product (for example, aberrant RNA) or a secondary product (for example, RNA molecules produced by an RNA-dependent RNA polymerase with transgene RNA as a matrix) that mimics the type of viral RNA that is targeted for degradation by cellular defence. Whether some particular cases of transgene TGS could also rely on the production of such a mobile molecule is discussed.