Stereopsis in sports: Visual skills and visuomotor integration models in professional and non-professional athletes

Visual skills in sport are considered relevant variables of athletic performance. However, data on the specific contribution of stereopsis—as the ability to perceive depth—in sport performance are still scarce and scattered in the literature. The aim of this review is therefore to take stock of the effects of stereopsis on the athletic performance, also looking at the training tools to improve visual abilities and potential differences in the visuomotor integration processes of professional and non-professional athletes. Dynamic stereopsis is mainly involved in catching or interceptive actions of ball sports, whereas strategic sports use different visual skills (peripheral and spatial vision) due to the sport-specific requirements. As expected, professional athletes show better visual skills as compared to non-professionals. However, both non-professional and professional athletes should train their visual skills by using sensory stations and light boards systems. Non-professional athletes use the visual inputs as the main method for programming motor gestures. In contrast, professional athletes integrate visual information with sport expertise, thus, they encode the match (or the athletic performance) through a more complex visuomotor integration system. Although studies on visual skills and stereopsis in sports still appear to be in their early stages, they show a large potential for both scientific knowledge and technical development

Thyroid-specific transcription factors control Hex promoter activity

The homeobox-containing gene Hex is expressed in several cell types, including thyroid follicular cells, in which it regulates the transcription of tissue-specific genes. In this study the regulation of Hex promoter activity was investigated. Using co-transfection experiments, we demonstrated that the transcriptional activity of the Hex gene promoter in rat thyroid FRTL-5 cells is ∼10-fold greater than that observed in HeLa and NIH 3T3 cell lines (which do not normally express the Hex gene). To identify the molecular mechanisms underlying these differences, we evaluated the effect of the thyroid-specific transcription factor TTF-1 on the Hex promoter activity. TTF-1 produced 3-4-fold increases in the Hex promoter activity. Gel-retardation assays and mutagenesis experiments revealed the presence of functionally relevant TTF-1 binding sites in the Hex promoter region. These in vitro data may also have functional relevance in vivo, since a positive correlation between TTF-1 and Hex mRNAs was demonstrated in human thyroid tissues by means of RT-PCR analysis. The TTF-1 effect, however, is not sufficient to explain the difference in Hex promoter activity between FRTL-5 and cells that do not express the Hex gene. For this reason, we tested whether Hex protein is able to activate the Hex promoter. Indeed, co-transfection experiments indicate that Hex protein is able to increase the activity of its own promoter in HeLa cells ∼4-fold. TTF-1 and Hex effects are additive: when transfected together in HeLa cells, the Hex promoter activity is increased 6-7-fold. Thus, the contemporary presence of both TTF-1 and Hex could be sufficient to explain the higher transcriptional activity of the Hex promoter in thyroid cells with respect to cell lines that do not express the Hex gene. These findings demonstrate the existence of direct cross-regulation between thyroid-specific transcription factors

Constraint-based modeling identifies new putative targets to fight colistin-resistant A. baumannii infections

Acinetobacter baumannii is a clinical threat to human health, causing major infection outbreaks worldwide. As new drugs against Gram-negative bacteria do not seem to be forthcoming, and due to the microbial capability of acquiring multi-resistance, there is an urgent need for novel therapeutic targets. Here we have derived a list of new potential targets by means of metabolic reconstruction and modelling of A. baumannii ATCC 19606. By integrating constraint-based modelling with gene expression data, we simulated microbial growth in normal and stressful conditions (i.e. following antibiotic exposure). This allowed us to describe the metabolic reprogramming that occurs in this bacterium when treated with colistin (the currently adopted last-line treatment) and identify a set of genes that are primary targets for developing new drugs against A. baumannii, including colistin-resistant strains. It can be anticipated that the metabolic model presented herein will represent a solid and reliable resource for the future treatment of A. baumannii infections

Different waters for different performances: Can we imagine sport-related natural mineral spring waters?

Preserving the hydration status means to balance daily fluids and salt losses with gains, where the losses depend on several physiological and environmental factors. Especially for athletes, these losses could be relevant and negatively influence the performance: therefore, their hydro-saline status must be preserved with personalized pre-and rehydration plans all along the performance period. Scientific literature in this field is mainly dedicated to artificial sport drinks. Different territories in most world areas are rich in drinking natural mineral spring waters with saline compositions that reflect their geological origin and that are used for human health (often under medical prescription). However, scarce scientific attention has been dedicated to the use of these waters for athletes. We therefore reviewed the existing literature from the innovative viewpoint of matching spring water mineral compositions with different athletic performances and their hydro-saline requirements

Anti-angiogenic activity of the flavonoid precursor 4-hydroxychalcone.

Angiogenesis, the growth of new blood vessels, is necessary for cancerous tumors to keep growing and spreading. Suppression of abnormal angiogenesis may provide therapeutic strategies for the treatment of angiogenesis-dependent disorders. In the present study, we describe the in vitro and in vivo anti-angiogenic activities of the flavonoid precursor 4-hydroxychalcone (Q797). This chalcone (22μg/ml) suppressed several steps of angiogenesis, including endothelial cell proliferation, migration and tube formation without showing any signs of cytotoxicity. Moreover, we found a selective effect on activated endothelial cells, in particular with resting endothelial cells and the human epithelial tumor cell lines (HeLa, MCF-7, A549). In addition, Q797 was able to modulate both vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (FGF)- induced phosphorylation of extracellular signal-regulated kinase (ERK)-1/-2 and Akt kinase. It did not influence the nuclear translocation of p65 subunit of the nuclear factor-κB (NF-κB) when human endothelial cells were stimulated with tumor necrosis factor (TNF)-α. Taken together this indicates that the Q797-mediated inhibition of in vitro angiogenic features of endothelial cells is most likely caused by suppression of growth factor pathways. The potent inhibitory effect of Q797 on bFGF-driven neovascularization was also demonstrated in vivo using the chick chorioallantoic membrane (CAM) assay. In summary, this chalcone could serve as a new leading structure in the discovery of new potent synthetic angiogenesis inhibitors

Gremlin is a novel agonist of the major pro-angiogenic receptor VEGFR2

The bone morphogenic protein antagonist gremlin is expressed during embryonic development and under different pathologic conditions, including cancer. Gremlin is a proangiogenic protein belonging to the cystine-knot superfamily that includes transforming growth factor-β proteins and the angiogenic vascular endothelial growth factors (VEGFs). Here, we demonstrate that gremlin binds VEGF receptor-2 (VEGFR2), the main transducer of VEGF-mediated angiogenic signals, in a bone morphogenic protein-independent manner. Similar to VEGF-A, gremlin activates VEGFR2 in endothelial cells, leading to VEGFR2-dependent angiogenic responses in vitro and in vivo. Gremlin thus represents a novel proangiogenic VEGFR2 agonist distinct from the VEGF family ligands with implications in vascular development, angiogenesis-dependent diseases, and tumor neovascularization

Buffering Adaptive Immunity by Hydrogen Sulfide

Abstract: T cell-mediated adaptive immunity is designed to respond to non-self antigens and pathogens through the activation and proliferation of various T cell populations. T helper 1 (Th1), Th2, Th17 and Treg cells finely orchestrate cellular responses through a plethora of paracrine and autocrine stimuli that include cytokines, autacoids, and hormones. Hydrogen sulfide (H2S) is one of these mediators able to induce/inhibit immunological responses, playing a role in inflammatory and autoimmune diseases, neurological disorders, asthma, acute pancreatitis, and sepsis. Both endogenous and exogenous H2S modulate numerous important cell signaling pathways. In monocytes, polymorphonuclear, and T cells H2S impacts on activation, survival, proliferation, polarization, adhesion pathways, and modulates cytokine production and sensitivity to chemokines. Here, we offer a comprehensive review on the role of H2S as a natural buffer able to maintain over time a functional balance between Th1, Th2, Th17 and Treg immunological responses

Kinetic Inductance Detectors for the OLIMPO experiment: design and pre-flight characterization

We designed, fabricated, and characterized four arrays of horn--coupled, lumped element kinetic inductance detectors (LEKIDs), optimized to work in the spectral bands of the balloon-borne OLIMPO experiment. OLIMPO is a 2.6 m aperture telescope, aimed at spectroscopic measurements of the Sunyaev-Zel'dovich (SZ) effect. OLIMPO will also validate the LEKID technology in a representative space environment. The corrected focal plane is filled with diffraction limited horn-coupled KID arrays, with 19, 37, 23, 41 active pixels respectively at 150, 250, 350, and 460$\:$GHz. Here we report on the full electrical and optical characterization performed on these detector arrays before the flight. In a dark laboratory cryostat, we measured the resonator electrical parameters, such as the quality factors and the electrical responsivities, at a base temperature of 300$\:$mK. The measured average resonator $Q$s are 1.7$\times{10^4}$, 7.0$\times{10^4}$, 1.0$\times{10^4}$, and 1.0$\times{10^4}$ for the 150, 250, 350, and 460$\:$GHz arrays, respectively. The average electrical phase responsivities on resonance are 1.4$\:$rad/pW, 1.5$\:$rad/pW, 2.1$\:$rad/pW, and 2.1$\:$rad/pW; the electrical noise equivalent powers are 45$\:\rm{aW/\sqrt{Hz}}$, 160$\:\rm{aW/\sqrt{Hz}}$, 80$\:\rm{aW/\sqrt{Hz}}$, and 140$\:\rm{aW/\sqrt{Hz}}$, at 12 Hz. In the OLIMPO cryostat, we measured the optical properties, such as the noise equivalent temperatures (NET) and the spectral responses. The measured NET$_{\rm RJ}$s are $200\:\mu\rm{K\sqrt{s}}$, $240\:\mu\rm{K\sqrt{s}}$, $240\:\mu\rm{K\sqrt{s}}$, and $\:340\mu\rm{K\sqrt{s}}$, at 12 Hz; under 78, 88, 92, and 90 mK Rayleigh-Jeans blackbody load changes respectively for the 150, 250, 350, and 460 GHz arrays. The spectral responses were characterized with the OLIMPO differential Fourier transform spectrometer (DFTS) up to THz frequencies, with a resolution of 1.8 GHz.Comment: Published on JCA

Fibroblast growth factor 2-antagonist activity of a long-pentraxin 3-derived antiangiogenic pentapeptide.

Fibroblast growth factor-2 (FGF2) plays a major role in angiogenesis. The pattern recognition receptor long-pentraxin 3 (PTX3) inhibits the angiogenic activity of FGF2. To identify novel FGF2-antagonistic peptide(s), four acetylated (Ac) synthetic peptides overlapping the FGF2-binding region PTX3-(97-110) were assessed for their FGF2-binding capacity. Among them, the shortest pentapeptide Ac-ARPCA-NH(2) (PTX3-[100-104]) inhibits the interaction of FGF2 with PTX3 immobilized to a BIAcore sensorchip and suppresses FGF2-dependent proliferation in endothelial cells, without affecting the activity of unrelated mitogens. Also, Ac-ARPCA-NH(2) inhibits angiogenesis triggered by FGF2 or by tumorigenic FGF2-overexpressing murine endothelial cells in chick and zebrafish embryos, respectively. Accordingly, the peptide hampers the binding of FGF2 to Chinese Hamster ovary cells overexpressing the tyrosine-kinase FGF receptor-1 (FGFR1) and to recombinant FGFR1 immobilized to a BIAcore sensorchip without affecting heparin interaction. In all the assays the mutated Ac-ARPSA-NH(2) peptide was ineffective. In keeping with the observation that hydrophobic interactions dominate the interface between FGF2 and the FGF-binding domain of the Ig-like loop D2 of FGFR1, amino acid substitutions in Ac-ARPCA-NH(2) and saturation transfer difference-nuclear magnetic resonance analysis of its mode of interaction with FGF2 implicate the hydrophobic methyl groups of the pentapeptide in FGF2 binding. These results will provide the basis for the design of novel PTX3-derived anti-angiogenic FGF2 antagonists

TR-644 a novel potent tubulin binding agent induces impairment of endothelial cells function and inhibits angiogenesis.

TR-644 is a novel combretastatin A-4 (CA-4) analogue endowed with potent microtubule depolymerizing activity superior to that of the lead compound and it also has high affinity to colchicines binding site of tubulin. We tested TR-644 anti-angiogenic effects in human umbilical endothelial cells (HUVEC). It showed no significant effects on the growth of HUVEC cells at concentrations below 1,000 nM, but at much lower concentrations (10-100 nM) it induced inhibition of capillary tube formation, inhibition of endothelial cell migration and affected endothelial cell morphology as demonstrated by the disruption of the microtubule network. TR-644 also increased permeability of HUVEC cells in a time dependent manner. The molecular mechanism for the anti-vascular activity of TR-644 was investigated in detail. TR-644 caused G2/M arrest in endothelial cells and this effect correlated with downregulation of the expression of Cdc25C and Cdc2Tyr15. Moreover TR-644 inhibited VEGF-induced phosphorylation of VE-cadherin but did not prevent the VEGF-induced phosphorylation of FAK. In chick chorioallantoic membrane in vivo assay, TR-644 (0.1-1.0 pmol/egg) efficiently counteracted the strong angiogenic response induced by FGF. Also CA-4, used as reference compound, caused an antagonistic effect, but in contrast, it induced per se, a remarkable angiogenic response probably due to an inflammatory reaction in the site of treatment. In a mice allogenic tumor model, immunohistochemical staining of tumors with anti-CD31 antibody showed that TR-644 significantly reduced the number of vessel, after 24 h from the administration of a single dose (30 mg/Kg)