Time course of strength and power recovery after resistance training with different movement velocities

The purpose of this study was to evaluate the time course of strength and power recovery after a single bout of strength training designed with fast and slow contraction velocities. Nineteen male subjects were randomly divided into 2 groups: the slow-velocity contraction (SV) group and the fast velocity contraction (FV) group. Resistance training protocols consisted of 5 sets of 12 repetition maximum (5 × 12RM) with 50 seconds of rest between sets and 2 minutes between exercises. Contraction velocity was controlled by the execution time for each repetition (SV-6 seconds to complete concentric and eccentric phases and for FV-1.5 seconds). Leg Press 45° 1RM (LP 1RM), horizontal countermovement jump (HCMJ), and right thigh circumference (TC) were accessed in 6 distinct moments: base (1 week before exercise), 0 (immediately after exercises), 24, 48, 72, and 96 hours after exercise protocol. The SV and FV presented significant LP 1RM decrements at 0, and these were still evident 24-48 hours postexercise. The magnitude of decline was significantly (p < 0.05) higher for FV. The SV and FV presented significant HCMJ decrements at 0, but only for FV were these still evident 24-72 hours postexercise. The SV and FV presented significant TC increments at 0, and these were still evident 24-48 hours postexercise for SV but for FV it continued up to 96 hours. The magnitude of increase was significantly (p < 0.05) higher for FV. In conclusion, the fast contraction velocity protocol resulted in greater decreases in LP 1RM and HCMJ performance, when compared with slow velocity. The results lead us to interpret that this variable may exert direct influence on acute muscle strength and power generation capacity.     

Functional analysis of Burkholderia cepacia genes bceD and bceF, encoding a phosphotyrosine phosphatase and a tyrosine autokinase, respectively: role in exopolysaccharide biosynthesis and biofilm formation

The biosynthesis of the exopolysaccharide (EPS) cepacian by Burkholderia cepacia complex strains requires the 16.2-kb bce cluster of genes. Two of the clustered genes, bceD and bceF, code for two proteins homologous to phosphotyrosine phosphatases and tyrosine kinases, respectively. We show experimental evidence indicating that BceF is phosphorylated on tyrosine and that the conserved lysine residue present at position 563 in the Walker A ATP-binding motif is required for this autophosphorylation. It was also proved that BceD is capable of dephosphorylating the phosphorylated BceF. Using the artificial substrate p-nitrophenyl phosphate (PNPP), BceD exhibited a V(max) of 8.8 mumol of PNPP min(-1) mg(-1) and a K(m) of 3.7 mM PNPP at 30 degrees C. The disruption of bceF resulted in the abolishment of cepacian accumulation in the culture medium, but 75% of the parental strain's EPS production yield was still registered for the bceD mutant. The exopolysaccharide produced by the bceD mutant led to less viscous solutions and exhibited the same degree of acetylation as the wild-type cepacian, suggesting a lower molecular mass for this mutant biopolymer. The size of the biofilm produced in vitro by bceD and bceF mutant strains is smaller than the size of the biofilm formed by the parental strain, and this phenotype was confirmed by complementation assays, indicating that BceD and BceF play a role in the establishment of biofilms of maximal size.     

Diet of the twaite shad Alosa fallax (Lacépède) (Clupeidae) in the River Tagus Estuary, Portugal

The diet of Alosafallax was studied by means of the frequency of occurrence of prey items. In the Tagus Estuary, shads feed preferentially on fish, with mysids, shrimp, isopods and insects occurring as secondary prey.     

Spatial genetic structure of <Emphasis Type=Italic>Coccoloba cereifera</Emphasis> (Polygonaceae), a critically endangered microendemic species of Brazilian rupestrian fields

Coccoloba cereifera (Polygonaceae) is an extremely rare endemic shrub found exclusively in the rupestrian fields of Serra do Cipó, southeastern, Brazil. We assessed the genetic diversity and structure across the single occurrence area of C. cereifera. The genetic variation at 13 microsatellite loci was estimated from 139 individuals sampled in nine patches. The number of alleles per locus varied from two to ten; the expected and observed heterozygosity ranged from 0.324 to 0.566 and 0.337 to 0.529, respectively. Microsatellites detected low but statistically significant levels of differentiation among patches (F _ST = 0.123, R _ST = 0.105), whereas Mantel test results showed a weak but significant pattern of isolation by distance (r ² = 0.31, P < 0.002). Bayesian clustering indicated two subdivisions connected via admixture. Habitat heterogeneity across the drainage basin of the Rio Indequicé is likely limiting gene flow within patches of the geographically restricted population. While there is currently no evidence for a direct genetic risk to species survival, the apparent natural segregation occurring within the species could be exacerbated by future land use changes and the influx of alien species which could lead to demographic reductions in population size leading to a reduction in genetic diversity and an increase in population subdivision. We suggest that maintaining the integrity of the habitat within the small range of the species and continued monitoring of the effects of alien species would be the wisest use of management resources.     

Use of glycoconjugates for trypanosomatid taxonomy

Glycoconjugates from five trypanosomatid genera—Crithidia, Herpetomonas, Endotrypanum, Leishmania, and Trypanosoma—were extracted with Triton X-114 and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis followed by periodic acid-Schiff staining. Most of the glycoconjugates were detected in the hydrophobic phase, indicating the presence of anchored glycoconjugates. All the trypanosomatids expressed a glycoconjugate with a low molecular weigh (below 20 kDa) in this phase. In each species, however, a characteristic and specific pattern of glycoconjugates was also observed in both phases. In the hydrophobic phase: 14–29 kDa lycoconjugates in C. guilhermei; 24–70 kDa in C. fasciculata, C. luciliae, E. schaudinni, and T. cruzi Y and G strains; 45–66 kDa in C. oncopelti and H. samuelpessoai; above 36 kDa in T. dionisii; 20–24 kDa, 36–45 kDa, and 70 kDa in L. tarentolae and T. mega. In the hydrophilic phase, typical glycoproteins were observed in some trypanosomatids: 60 kDa in T. mega and T. cruzi Y strain; 70 kDa in H. samuelpessoai; 66 kDa in C. oncopelti; 20–70 kDa in C. luciliae. These findings suggest that Triton X-114-extracted glycoconjugates could be useful markers for trypanosomatid taxonomy.     

Impact of continuous axenic cultivation in Leishmania infantum virulence

Experimental infections with visceral Leishmania spp. are frequently performed referring to stationary parasite cultures that are comprised of a mixture of metacyclic and non-metacyclic parasites often with little regard to time of culture and metacyclic purification. This may lead to misleading or irreproducible experimental data. It is known that the maintenance of Leishmania spp. in vitro results in a progressive loss of virulence that can be reverted by passage in a mammalian host. In the present study, we aimed to characterize the loss of virulence in culture comparing the in vitro and in vivo infection and immunological profile of L. infantum stationary promastigotes submitted to successive periods of in vitro cultivation. To evaluate the effect of axenic in vitro culture in parasite virulence, we submitted L. infantum promastigotes to 4, 21 or 31 successive in vitro passages. Our results demonstrated a rapid and significant loss of parasite virulence when parasites are sustained in axenic culture. Strikingly, the parasite capacity to modulate macrophage activation decreased significantly with the augmentation of the number of in vitro passages. We validated these in vitro observations using an experimental murine model of infection. A significant correlation was found between higher parasite burdens and lower number of in vitro passages in infected Balb/c mice. Furthermore, we have demonstrated that the virulence deficit caused by successive in vitro passages results from an inadequate capacity to differentiate into amastigote forms. In conclusion, our data demonstrated that the use of parasites with distinct periods of axenic in vitro culture induce distinct infection rates and immunological responses and correlated this phenotype with a rapid loss of promastigote differentiation capacity. These results highlight the need for a standard operating protocol (SOP) when studying Leishmania species.     

Modeling panic disorder in rodents

Panic disorder (PD) is a subtype of anxiety disorder in which the core phenomenon is the spontaneous occurrence of panic attacks. Although studies with laboratory animals have been instrumental for the understanding of its neurobiology and treatment, few review articles have focused on the validity of the currently used animal models for studying this psychopathology. Therefore, the aim of the present paper is to discuss the strengths and limits of these models in terms of face, construct and predictive validity. Based on the hypothesis that panic attacks are related to defensive responses elicited by proximal threat, most animal models measure the escape responses induced by specific stimuli. Some apply electrical or chemical stimulation to brain regions proposed to modulate fear and panic responses, such as the dorsal periaqueductal grey or the medial hypothalamus. Other models focus on the behavioural consequences caused by the exposure of rodents to ultrasound or natural predators. Finally, the elevated T-maze associates a one-way escape response from an open arm with panic attacks. Despite some limitations, animal models are essential for a better understanding of the neurobiology and pharmacology of PD and for discovering more effective treatments.     

MONITORING TRAINING LOADS,STRESS, IMMUNE-ENDOCRINE RESPONSES AND PERFORMANCE IN TENNIS PLAYERS

The study aim was to investigate the effect of a periodised pre-season training plan on internal training load and subsequent stress tolerance, immune-endocrine responses and physical performance in tennis players. Well-trained young tennis players (n = 10) were monitored across the pre-season period, which was divided into 4 weeks of progressive overloading training and a 1-week tapering period. Weekly measures of internal training load, training monotony and stress tolerance (sources and symptoms of stress) were taken, along with salivary testosterone, cortisol and immunoglobulin A. One repetition maximum strength, running endurance, jump height and agility were assessed before and after training. The periodised training plan led to significant weekly changes in training loads (i.e. increasing in weeks 3 and 4, decreasing in week 5) and post-training improvements in strength, endurance and agility (P < 0.05). Cortisol concentration and the symptoms of stress also increased in weeks 3 and/or 4, before returning to baseline in week 5 (P < 0.05). Conversely, the testosterone to cortisol ratio decreased in weeks 3 and 4, before returning to baseline in week 5 (P < 0.05). In conclusion, the training plan evoked adaptive changes in stress tolerance and hormonal responses, which may have mediated the improvements in physical performance.     

Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology

Mitochondria are uniquely poised to play a pivotal role in neuronal cell survival or death because they are regulators of both energy metabolism and cell death pathways. Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer's disease. This review discusses evidence indicating that mitochondrial dysfunction has an early and preponderant role in Alzheimer's disease. Furthermore, the link between mitochondrial dysfunction and autophagy in Alzheimer's disease is also discussed. As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy, neurons progressively accumulate lipofuscin that could exacerbate neuronal dysfunction. Since autophagy is the major pathway involved in the degradation of protein aggregates and defective organelles, an intense interest in developing autophagy-related therapies is growing among the scientific community. The final part of this review is devoted to discuss autophagy as a potential target of therapeutic interventions in Alzheimer's disease pathophysiology.