1,793 research outputs found
Análisis del rendimiento en salto vertical, agilidad,
Objetivo
Analizar la influencia de la categoría de edad en la capacidad de salto, sprint, agilidad y velocidad de golpeo en futbolistas jóvenes.
Método
Estudio transversal en el que participaron 36 jugadores de nivel subélite provenientes de las categorías inferiores (cadete y juvenil) de equipos de fútbol andaluces (edad: 15,87 ± 1,43 años; masa corporal: 65,38 ± 10,84 kg; altura: 1,71 ± 0,06 m). Se evaluó la composición corporal, el rendimiento en salto vertical (CMJ), la agilidad mediante el test de Balsom, velocidad de sprint en 5, 10, 20 y 30 m y la velocidad de golpeo con ambas piernas.
Resultados
Los análisis mostraron que los jugadores juveniles tienen mayor rendimiento en los test de CMJ, agilidad y velocidad de golpeo con ambas piernas que los cadetes. No se aprecian diferencias significativas (p ≥ 0,05) en la prueba de velocidad, aunque se evidencia una clara tendencia a favor de los juveniles.
Conclusión
Existe efecto de la edad durante la etapa de la adolescencia sobre la capacidad de salto, la agilidad, la velocidad de golpeo y, en menor medida, sobre la velocidad de jóvenes jugadores de fútbol, además de asociación entre las capacidades condicionales más influyentes en el rendimiento del futbolista
Anàlisi del rendiment en el salt vertical, agilitat i velocitat
Objectiu
Analitzar la influència de la categoria d’edat en la capacitat de salt, esprint, agilitat i velocitat de xut de futbolistes joves.
Mètode
Estudi transversal en què participaren 36 jugadors de nivell subelit provinents de les categories inferiors (cadet i juvenil) d’equips de futbol andalusos (edat: 15,87 ± 1,43 anys; massa corporal: 65,38 ± 10,84 kg; alçada: 1,71 ± 0,06 m). S’avaluà la composició corporal, el rendiment en el salt vertical (CMJ), l’agilitat mitjançant el test de Balsom, la velocitat d’esprints en 5, 10, 20 i 30 m i la velocitat del xut amb ambdues cames.
Resultats
Les anàlisis mostraren que els jugadors juvenils tenien un rendiment major en els tests del CMJ, agilitat i velocitat de xut amb ambdues cames que els cadets. No s’aprecien diferències significatives (p ≥ 0,05) en la prova de velocitat, tot i que s’evidencia una tendència clara a favor dels juvenils.
Conclusió
Existeix l’efecte de l’edat durant l’etapa de l’adolescència sobre la capacitat de salt, l’agilitat, la velocitat de xut i, en menor mesura, sobre la velocitat dels jugadors de futbol joves, a més d’associació entre les capacitats condicionals, més influents en el rendiment del futbolista
Porous beta titanium alloy coated with a therapeutic biopolymeric composite to improve tribomechanical and biofunctional balance
Tooth loss is common in patients struggling with dental cavities, periodontal diseases, and tumors, as well as those
who abuse tobacco or drugs. In this scenario, dental implants have become the primary treatment option for
complete or partial tooth loss. Dental implant failure can be caused by stress shielding phenomenon, poor
osseointegration, or to bacterial infections. In the present study, a joint solution to these limitations is proposed
using a variety of porous β-titanium substrates using powder Ti35Nb7Zr5Ta alloy and employing the spacer-holder
approach (ammonium bicarbonate) to obtain a variety of porosity percentage (30, 40, and 50 vol%), and pore
diameters in 100–200 μm, that has been characterized in terms of its size distribution, density, morphology,
chemical composition, compaction ability and Vickers micro-hardness. Furthermore, porosity, microstructure
(Archimedes and image analysis) and tribomechanical behavior (P-h curves and scratch tests) experiments were
performed to study and characterize the porous substrates. Polyvinyl alcohol (PVA)/poly-ε-caprolactone (PCL)
containing silver nanoparticles (AgNPs), as antibacterial composite, was employed to infiltrate β-Ti disks. Scanning
electron microscopy was used to determine the coating morphology, thickness, and infiltration of the porous
substrates. Wettability and SBF experiments were also carried out to investigate hydrophobicity and potential biofunctionality.
The results suggested how the porosity of the β-Ti alloy affects the mechanical characteristics and the
wettability of the substrate that was successfully infiltrated to exert an antimicrobial behavior
Regulation of cell death receptor S-nitrosylation and apoptotic signaling by Sorafenib in hepatoblastoma cells
Nitric oxide (NO) plays a relevant role during cell death regulation in tumor cells. The overexpression of nitric oxide synthase type III (NOS-3) induces oxidative and nitrosative stress, p53 and cell death receptor expression and apoptosis in hepatoblastoma cells. S-nitrosylation of cell death receptor modulates apoptosis. Sorafenib is the unique recommended molecular-targeted drug for the treatment of patients with advanced hepatocellular carcinoma. The present study was addressed to elucidate the potential role of NO during Sorafenib-induced cell death in HepG2 cells. We determined the intra- and extracellular NO concentration, cell death receptor expression and their S-nitrosylation modifications, and apoptotic signaling in Sorafenib-treated HepG2 cells. The effect of NO donors on above parameters has also been determined. Sorafenib induced apoptosis in HepG2 cells. However, low concentration of the drug (10nM) increased cell death receptor expression, as well as caspase-8 and -9 activation, but without activation of downstream apoptotic markers. In contrast, Sorafenib (10 µM) reduced upstream apoptotic parameters but increased caspase-3 activation and DNA fragmentation in HepG2 cells. The shift of cell death signaling pathway was associated with a reduction of S-nitrosylation of cell death receptors in Sorafenib-treated cells. The administration of NO donors increased S-nitrosylation of cell death receptors and overall induction of cell death markers in control and Sorafenib-treated cells. In conclusion, Sorafenib induced alteration of cell death receptor S-nitrosylation status which may have a relevant repercussion on cell death signaling in hepatoblastoma cells.Instituto de Salud Carlos III PI13/00021Ministerio de Economía y Competitividad BFU2012-32056Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía BIO-0216Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía CTS-6264Consejería de Salud, Junta de Andalucía PI13/ 0002
Clinical and pathological characteristics of peripheral T‐cell lymphomas in a Spanish population: a retrospective study
We investigated the clinicopathological features and prognostic factors of patients with peripheral T-cell lymphoma (PTCL) in 13 sites across Spain. Relevant clinical antecedents, CD30 expression and staining pattern, prognostic indices using the International Prognostic Index and the Intergruppo Italiano Linfomi system, treatments, and clinical outcomes were examined. A sizeable proportion of 175 patients had a history of immune-related disorders (autoimmune 16%, viral infections 17%, chemo/radiotherapy-treated carcinomas 19%). The median progression-free survival (PFS) and overall survival (OS) were 7·9 and 15·8 months, respectively. Prognostic indices influenced PFS and OS, with a higher number of adverse factors resulting in shorter survival (P 15% of cells were positive in anaplastic lymphoma kinase-positive and -negative anaplastic large-cell lymphoma and extranodal natural killer PTCL groups. We observed PTCL distribution across subtypes based on haematopathological re-evaluation. Poor prognosis, effect of specific prognostic indices, relevance of histopathological sub-classification, and response level to first-line treatment on outcomes were confirmed. Immune disorders amongst patients require further examination involving genetic studies and identification of associated immunosuppressive factors
Clinical and pathological characteristics of peripheral T-cell lymphomas in a Spanish population: a retrospective study
We investigated the clinicopathological features and prognostic factors of patients with peripheral T-cell lymphoma (PTCL) in 13 sites across Spain. Relevant clinical antecedents, CD30 expression and staining pattern, prognostic indices using the International Prognostic Index and the Intergruppo Italiano Linfomi system, treatments, and clinical outcomes were examined. A sizeable proportion of 175 patients had a history of immune-related disorders (autoimmune 16%, viral infections 17%, chemo/radiotherapy-treated carcinomas 19%). The median progression-free survival (PFS) and overall survival (OS) were 7·9 and 15·8 months, respectively. Prognostic indices influenced PFS and OS, with a higher number of adverse factors resulting in shorter survival (P 15% of cells were positive in anaplastic lymphoma kinase-positive and -negative anaplastic large-cell lymphoma and extranodal natural killer PTCL groups. We observed PTCL distribution across subtypes based on haematopathological re-evaluation. Poor prognosis, effect of specific prognostic indices, relevance of histopathological sub-classification, and response level to first-line treatment on outcomes were confirmed. Immune disorders amongst patients require further examination involving genetic studies and identification of associated immunosuppressive factors.This study was sponsored by Takeda
Acute Kidney Injury is Aggravated in Aged Mice by the Exacerbation of Proinflammatory Processes
Acute kidney injury (AKI) is more frequent in elderly patients. Mechanisms contributing to AKI (tubular cell death, inflammatory cell infiltration, impaired mitochondrial function, and prolonged cell-cycle arrest) have been linked to cellular senescence, a process implicated in regeneration failure and progression to fibrosis. However, the molecular and pathological basis of the age-related increase in AKI incidence is not completely understood. To explore these mechanisms, experimental AKI was induced by folic acid (FA) administration in young (3-months-old) and old (1-year-old) mice, and kidneys were evaluated in the early phase of AKI, at 48 h. Tubular damage score, KIM-1 expression, the recruitment of infiltrating immune cells (mainly neutrophils and macrophages) and proinflammatory gene expression were higher in AKI kidneys of old than of young mice. Tubular cell death in FA-AKI involves several pathways, such as regulated necrosis and apoptosis. Ferroptosis and necroptosis cell-death pathways were upregulated in old AKI kidneys. In contrast, caspase-3 activation was only found in young but not in old mice. Moreover, the antiapoptotic factor BCL-xL was significantly overexpressed in old, injured kidneys, suggesting an age-related apoptosis suppression. AKI kidneys displayed evidence of cellular senescence, such as increased levels of cyclin dependent kinase inhibitors p16ink4a and p21cip1, and of the DNA damage response marker γH2AX. Furthermore, p21cip1 mRNA expression and nuclear staining for p21cip1 and γH2AX were higher in old than in young FA-AKI mice, as well as the expression of senescence-associated secretory phenotype (SASP) components (Il-6, Tgfb1, Ctgf, and Serpine1). Interestingly, some infiltrating immune cells were p21 or γH2AX positive, suggesting that molecular senescence in the immune cells (“immunosenescence”) are involved in the increased severity of AKI in old mice. In contrast, expression of renal protective factors was dramatically downregulated in old AKI mice, including the antiaging factor Klotho and the mitochondrial biogenesis driver PGC-1α. In conclusion, aging resulted in more severe AKI after the exposure to toxic compounds. This increased toxicity may be related to magnification of proinflammatory-related pathways in older mice, including a switch to a proinflammatory cell death (necroptosis) instead of apoptosis, and overactivation of cellular senescence of resident renal cells and infiltrating inflammatory cells
The Sinorhizobium fredii HH103 Lipopolysaccharide is not only relevant at early soybean nodulation stages but also for symbiosome stability in mature nodules
In this work we have characterised the Sinorhizobium fredii HH103 greA lpsB lpsCDE genetic region and analysed for the first time the symbiotic performance of Sinorhizobium fredii lps mutants on soybean. The organization of the S. fredii HH103 greA, lpsB, and lpsCDE genes was equal to that of Sinorhizobium meliloti 1021. S. fredii HH103 greA, lpsB, and lpsE mutant derivatives produced altered LPS profiles that were characteristic of the gene mutated. In addition, S. fredii HH103 greA mutants showed a reduction in bacterial mobility and an increase of auto-agglutination in liquid cultures. RT-PCR and qPCR experiments demonstrated that the HH103 greA gene has a positive effect on the transcription of lpsB. Soybean plants inoculated with HH103 greA, lpsB or lpsE mutants formed numerous ineffective pseudonodules and showed severe symptoms of nitrogen starvation. However, HH103 greA and lps mutants were also able to induce the formation of a reduced number of soybean nodules of normal external morphology, allowing the possibility of studying the importance of bacterial LPS in later stages of the S. fredii HH103-soybean symbiosis. The infected cells of these nodules showed signs of early termination of symbiosis and lytical clearance of bacteroids. These cells also had very thick walls and accumulation of phenolic-like compounds, pointing to induced defense reactions. Our results show the importance of bacterial LPS in later stages of the S. fredii HH103-soybean symbiosis and their role in preventing host cell defense reactions. S. fredii HH103 lpsB mutants also showed reduced nodulation with Vigna unguiculata, although the symbiotic impairment was less pronounced than in soybean
The Latin American experience of allografting patients with severe aplastic anaemia: real-world data on the impact of stem cell source and ATG administration in HLA-identical sibling transplants
We studied 298 patients with severe aplastic anaemia (SAA) allografted in four Latin American countries. The source of cells
was bone marrow (BM) in 94 patients and PBSCs in 204 patients. Engraftment failed in 8.1% of recipients with no difference
between BM and PBSCs (P = 0.08). Incidence of acute GvHD (aGvHD) for BM and PBSCs was 30% vs 32% (P = 0.18), and for grades
III–IV was 2.6% vs 11.6% (P = 0.01). Chronic GvHD (cGvHD) between BM and PBSCs was 37% vs 59% (P = 0.002) and extensive 5% vs
23.6% (P = 0.01). OS was 74% vs 76% for BM vs PBSCs (P = 0.95). Event-free survival was superior in patients conditioned with
anti-thymocyte globulin (ATG)-based regimens compared with other regimens (79% vs 61%, P = 0.001) as excessive secondary graft
failure was seen with other regimens (10% vs 26%, P = 0.005) respectively. In multivariate analysis, aGvHD II–IV (hazard ratio (HR)
2.50, confidence interval (CI) 1.1–5.6, P = 0.02) and aGvHD III–IV (HR 8.3 CI 3.4–20.2, Po0.001) proved to be independent negative
predictors of survival. In conclusion, BM as a source of cells and ATG-based regimens should be standard because of higher GvHD
incidence with PBSCs, although the latter combining with ATG in the conditioning regimen could be an option in selected high-risk
patient
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