How to improve technical and tactical actions of dominant and non-dominant players in children’s football?

As young football players develop important technical and tactical skills during competitive matches, this study investigated quantity and quality of technical and tactical actions in real game conditions in a 4v4 compared to the traditional 7v7 match format. In total, three matches of each format were played by 103 young football players (10.3±0.6 years) and video monitored for subsequent manual tagging of technical and tactical events. Based on the number of technical and tactical actions in the 7v7 matches, players were classified as dominant or non-dominant and changes in these subgroups were assessed during the 4v4 match format. The 4v4 match format significantly (P<0.001) increased total number of actions per player per minute compared to the 7v7 matches (5.59±1.44 and 2.78±0.73, respectively) and the number of successful (2.88±0.92 and 1.15±0.49, respectively) and unsuccessful (1.05±0.42 and 0.67±0.23, respectively) actions. Both dominant and non-dominant players increased their number of actions during the 4v4 compared to 7v7 match format. Despite a missing significant interaction effect, there was a larger percentage increase in number of actions for the non-dominant players (143%) compared to dominant players (72%) in 4v4. The 4v4 match format shows twice as many technical and tactical actions in real game conditions and, therefore, may improve players' skill development

Origins of Relative Age Effects in Youth Football - A Nationwide Analysis

Introduction: Relative age effects (RAEs) refer to the overrepresentation of players born earlier in the selection year compared to late-born players within the same age category. To date, the origins and mechanisms of RAEs are still unclear. To evaluate the development of RAEs in terms of age group and selection level, we analyzed data of all registered child and adolescent football players in Switzerland. Methods: Age category, selection level, and birthdate from all licensed 101,991 Swiss child and youth football players assigned to a specific team [9,149 girls (9.0%) and 92,842 boys (91.0%); age range: 4.6–19.6 years] were analyzed. Additionally, out of 1,128 clubs, 54 clubs provided their documented waiting lists (1,224 players). Birthdate distributions were split by age category, sex, and birth quarter (Q1 = January to March, Q4 = October to December). RAEs were calculated using odds ratios (Q1 vs. Q4) with 95% confidence intervals (95% CI). Results: We found small RAEs among U8 players (OR 1.44 [95% CI 1.31, 1.59]) and U10 (OR 1.24 [95% CI 1.16, 1.32]). The RAE was negligible in all other age categories, independent of gender. In children's football, 5,584 (71.3%) teams performed selections. In teams without selection, there were no obvious RAEs. However, teams with selections for the same age category showed small RAEs with an overrepresentation of Q1 athletes in the first team (OR = 1.29 [95% CI 1.24, 1.35]) and inverse RAEs with an underrepresentation of Q1 athletes in the last team (OR = 0.85 [95% CI 0.82, 0.89]). Only small RAEs were observed on the waiting lists for the U8 (OR = 1.48 [1.13, 1.95]). Discussion and Conclusion: RAEs have a small, but consistent effect on participation in Swiss children's football at the grassroots level. Contrary to expectations, no inverse RAEs were found on the waiting lists. Nonetheless, first time coach selections seem to be the origin of RAEs. To protect young athletes from discrimination, RAE biases should be analyzed and eliminated at all stages of sport participation, selection, and dropout situations. Modifications to the organizational structure of sport and athlete development systems are recommended to prevent RAE-related discrimination in youth sports

New Topoisomerase Inhibitors:Evaluating the Potency of Gepotidacin and Zoliflodacin in Fluoroquinolone-Resistant Escherichia coli upon tolC Inactivation and Differentiating Their Efflux Pump Substrate Nature

Inactivating tolC in multidrug-resistant Escherichia coli with differing sequence types and quinolone resistance-determining mutations reveals remarkably potentiated activity of the first-in-class topoisomerase inhibitors gepotidacin and zoliflodacin. Differences between both structurally unrelated compounds in comparison to fluoroquinolones regarding the selectivity of E. coli RND (resistance-nodulation-cell division)-type transporters, efflux inhibitors, and AcrB porter domain mutations were demonstrated. The findings should reinforce efforts to develop efflux-bypassing drugs and provide AcrB targets with critical relevance for this purpose

FAK induces expression of Prx1 to promote tenascin-C–dependent fibroblast migration

Fibroblast migration depends, in part, on activation of FAK and cellular interactions with tenascin-C (TN-C). Consistent with the idea that FAK regulates TN-C, migration-defective FAK-null cells expressed reduced levels of TN-C. Furthermore, expression of FAK in FAK-null fibroblasts induced TN-C, whereas inhibition of FAK activity in FAK–wild-type cells had the opposite effect. Paired-related homeobox 1 (Prx1) encodes a homeobox transcription factor that induces TN-C by interacting with a binding site within the TN-C promoter, and it also promotes fibroblast migration. Therefore, we hypothesized that FAK regulates TN-C by controlling the DNA-binding activity of Prx1 and/or by inducing Prx1 expression. Prx1–homeodomain binding site complex formation observed with FAK–wild-type fibroblasts failed to occur in FAK-null fibroblasts, yet expression of Prx1 in these cells induced TN-C promoter activity. Thus, FAK is not essential for Prx1 DNA-binding activity. However, activated FAK was essential for Prx1 expression. Functionally, Prx1 expression in FAK-null fibroblasts restored their ability to migrate toward fibronectin, in a manner that depends on TN-C. These results appear to be relevant in vivo because Prx1 and TN-C expression levels were reduced in FAK-null embryos. This paper suggests a model whereby FAK induces Prx1, and subsequently the formation of a TN-C–enriched ECM that contributes to fibroblast migration

Hidden magnetic order in plutonium dioxide nuclear fuel

A thorough understanding of the chemistry of PuO2 is critical to the design of next-generation nuclear fuels and the long-term storage of nuclear materials. Despite over 75 years of study, the ground-state magnetic structure of PuO2 remains a matter of much debate. Experimental studies loosely indicate a diamagnetic (DM) ground-state, whereas theoretical methods have proposed either a collinear ferromagnetic (FM) or anti-ferromagnetic (AFM) ground-state, both of which would be expected to cause a distortion from the reported Fm[3 with combining macron]m symmetry. In this work, we have used accurate calculations based on the density functional theory (DFT) to systematically investigate the magnetic structure of PuO2 to resolve this controversy. We have explicitly considered electron-correlation, spin–orbit interaction and noncollinear magnetic contributions to identify a hereto unknown longitudinal 3k AFM ground-state that retains Fm[3 with combining macron]m crystal symmetry. Given the broad interest in plutonium materials and the inherent experimental difficulties of handling this compound, the results presented in this paper have considerable implications for future computational studies relating to PuO2 and related actinide structures. As the crystal structure is coupled by spin–orbit interactions to the magnetic state, it is imperative to consider relativity when creating computational models

Trombose venosa profunda: aspectos epidemiológicos, fisiopatológicos e manejo terapêutico

A Trombose Venosa Profunda (TVP) é uma condição médica grave caracterizada pela formação de um coágulo sanguíneo dentro das veias profundas do corpo, principalmente nas pernas. Quanto à epidemiologia, trata-se de uma doença comum em todo o mundo, afetando entre 2,5% a 5% da população. A prevalência da TVP aumenta com a idade e é maior em homens do que em mulheres. A fisiopatologia da TVP envolve a formação de coágulos sanguíneos nas veias profundas das pernas, o que pode ocorrer devido a uma variedade de fatores, incluindo imobilização prolongada, tabagismo, cirurgias, trauma, câncer, uso de contraceptivos orais, gravidez e pós-parto, fatores genéticos e obesidade. Quanto às manifestações clínicas, destacam-se dor, inchaço e vermelhidão nas pernas afetadas, bem como sensação de calor na pele sobre a veia afetada. No entanto, muitos casos de TVP são assintomáticos, o que torna o diagnóstico precoce desafiador. O diagnóstico da TVP envolve avaliação clínica, exames laboratoriais, exames de imagem, como ultrassonografia doppler, que podem detectar a presença de coágulos sanguíneos nas veias profundas das pernas. Já a abordagem terapêutica envolve o uso de medicamentos como anticoagulantes, que ajudam a prevenir a formação de novos coágulos sanguíneos e reduzem o risco de complicações graves. Em alguns casos, a remoção do coágulo pode ser necessária para prevenir complicações. A prevenção da TVP também é importante, especialmente em pessoas com fatores de risco, e pode envolver a mudança de estilo de vida e o uso de medicamentos preventivos

Serotonin Deficiency Increases Context-Dependent Fear Learning Through Modulation of Hippocampal Activity

Brain serotonin (5-hydroxytryptamine, 5-HT) system dysfunction is implicated in exaggerated fear responses triggering various anxiety-, stress-, and trauma-related disorders. However, the underlying mechanisms are not well understood. Here, we investigated the impact of constitutively inactivated 5-HT synthesis on context-dependent fear learning and extinction using tryptophan hydroxylase 2 ( ) knockout mice. Fear conditioning and context-dependent fear memory extinction paradigms were combined with c-Fos imaging and electrophysiological recordings in the dorsal hippocampus (dHip). mutant mice, completely devoid of 5-HT synthesis in brain, displayed accelerated fear memory formation and increased locomotor responses to foot shock. Furthermore, recall of context-dependent fear memory was increased. The behavioral responses were associated with increased c-Fos expression in the dHip and resistance to foot shock-induced impairment of hippocampal long-term potentiation (LTP). In conclusion, increased context-dependent fear memory resulting from brain 5-HT deficiency involves dysfunction of the hippocampal circuitry controlling contextual representation of fear-related behavioral responses.</p

Serotonin Deficiency Increases Context-Dependent Fear Learning Through Modulation of Hippocampal Activity

Brain serotonin (5-hydroxytryptamine, 5-HT) system dysfunction is implicated in exaggerated fear responses triggering various anxiety-, stress-, and trauma-related disorders. However, the underlying mechanisms are not well understood. Here, we investigated the impact of constitutively inactivated 5-HT synthesis on context-dependent fear learning and extinction using tryptophan hydroxylase 2 (Tph2) knockout mice. Fear conditioning and context-dependent fear memory extinction paradigms were combined with c-Fos imaging and electrophysiological recordings in the dorsal hippocampus (dHip). Tph2 mutant mice, completely devoid of 5-HT synthesis in brain, displayed accelerated fear memory formation and increased locomotor responses to foot shock. Furthermore, recall of context-dependent fear memory was increased. The behavioral responses were associated with increased c-Fos expression in the dHip and resistance to foot shock-induced impairment of hippocampal long-term potentiation (LTP). In conclusion, increased context-dependent fear memory resulting from brain 5-HT deficiency involves dysfunction of the hippocampal circuitry controlling contextual representation of fear-related behavioral responses

Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis

Previous reports indicate an association between autism spectrum disorders (ASD) and disorders of mitochondrial oxidative phosphorylation. One study suggested that children with both diagnoses are clinically indistinguishable from children with idiopathic autism. There are, however, no detailed analyses of the clinical and laboratory findings in a large cohort of these children. Therefore, we undertook a comprehensive review of patients with ASD and a mitochondrial disorder.We reviewed medical records of 25 patients with a primary diagnosis of ASD by DSM-IV-TR criteria, later determined to have enzyme- or mutation-defined mitochondrial electron transport chain (ETC) dysfunction. Twenty-four of 25 patients had one or more major clinical abnormalities uncommon in idiopathic autism. Twenty-one patients had histories of significant non-neurological medical problems. Nineteen patients exhibited constitutional symptoms, especially excessive fatigability. Fifteen patients had abnormal neurological findings. Unusual developmental phenotypes included marked delay in early gross motor milestones (32%) and unusual patterns of regression (40%). Levels of blood lactate, plasma alanine, and serum ALT and/or AST were increased at least once in 76%, 36%, and 52% of patients, respectively. The most common ETC disorders were deficiencies of complex I (64%) and complex III (20%). Two patients had rare mtDNA mutations of likely pathogenicity.Although all patients' initial diagnosis was idiopathic autism, careful clinical and biochemical assessment identified clinical findings that differentiated them from children with idiopathic autism. These and prior data suggest a disturbance of mitochondrial energy production as an underlying pathophysiological mechanism in a subset of individuals with autism