Acute Effects of Muscular Fatigue on Vertical Jump Performance in Acrobatic Gymnasts, Evaluated by Instrumented Insoles: A Pilot Study

The study of fatigue during training is becoming a very useful tool to avoid possible injuries not only during the training sessions but also during recovery time. Many researches have proved that concepts such as muscular fatigue and postactivation potentiation have a close relationship. With this aim, vertical jump can provide a very important information that can help to analyze the muscular fatigue that happened during this type of activity, mainly if the monitoring system is able to measure jumping parameters during their regular training session in their natural training environment. This study was performed with instrumented insoles called ECnsole. These insoles were tested with a group of twelve volunteers. In a tumbling surface, the participants performed a jumping protocol in three conditions: rest, fatigue-induced, and recovery. Using these validated insoles, the acrobatic gymnasts showed an inability to use the stretch-shortening cycle for improving vertical jumping performance after fatigue condition, although no deterioration of jump performance was found.Junta de Andalucía European Commission P10-TIC5997European Commissio

Comparación de técnicas de entrenamiento de flexibilidad (FNP) con y sin electroestimulación

El objetivo de este estudio fue analizar el efecto de la técnica de estiramiento Contract-Relax Agonist Contract con (CRAC+EE) y sin (CRAC) electroestimulación sobre la mejora y retención del rango de movimiento activo (AROM) y pasivo (PROM) de cadera en flexión, en extremidad inferior dominante. 34 estudiantes universitarios fueron asignados a tres grupos: control, CRAC+EE y CRAC. AROM y PROM fueron evaluados antes, una vez finalizada y tras dos semanas de la finalización del entrenamiento. El entrenamiento tuvo una duración de cuatro semanas, a razón de tres sesiones semanales. El ANOVA mostró un aumento muy significativo de AROM (p<0,001 y p<0,005) y PROM (p<0,001 y p<0,01) en ambos grupos experimentales respectivamente. En la retención, se mantienen valores superiores con respecto a la medida pre-test. Como conclusión, la aplicación de CRAC+EE y CRAC mejoró AROM y PROM, siendo además efectivas en la retención de sendos rangos de movimiento

C3 glomerulopathy-associated CFHR1 mutation alters FHR oligomerization and complement regulation

C3 glomerulopathies (C3G) are a group of severe renal diseases with distinct patterns of glomerular inflammation and C3 deposition caused by complement dysregulation. Here we report the identification of a familial C3G-associated genomic mutation in the gene complement factor H–related 1 (CFHR1), which encodes FHR1. The mutation resulted in the duplication of the N-terminal short consensus repeats (SCRs) that are conserved in FHR2 and FHR5. We determined that native FHR1, FHR2, and FHR5 circulate in plasma as homo- and hetero-oligomeric complexes, the formation of which is likely mediated by the conserved N-terminal domain. In mutant FHR1, duplication of the N-terminal domain resulted in the formation of unusually large multimeric FHR complexes that exhibited increased avidity for the FHR1 ligands C3b, iC3b, and C3dg and enhanced competition with complement factor H (FH) in surface plasmon resonance (SPR) studies and hemolytic assays. These data revealed that FHR1, FHR2, and FHR5 organize a combinatorial repertoire of oligomeric complexes and demonstrated that changes in FHR oligomerization influence the regulation of complement activation. In summary, our identification and characterization of a unique CFHR1 mutation provides insights into the biology of the FHRs and contributes to our understanding of the pathogenic mechanisms underlying C3G

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Clinical and molecular characterization of Alzheimer disease-type dementiain a large kingred in Antioquia, Colombia.

IP 1115-04-040-95mulations in early onset AD families / Francisco Lopera. -'- en:Nature Genetics. -- Vol. 11 (Oct. 1995); p.;220-222. -- Complete analysis of the presenilin 1 gene inearlyonset Alzheimeris disease / Francisco Lopera.;... [et al.]. -- En: Neuro Report. -- Vol. 7, no. 3 (Feb.1996);p. 801-805. -- The E280A presenilin 1;Alzheimer mutation produces increased AB42 deposition andseverecerebellar pathology / Francisco Lopera. ...;[et al.]. -- En: Nature Medicine. -- Vol. 2, no. 10 (Oct.1996);p. 1146-1150. -- E280A PS-1 mutation causes;ARTICULO(S) EN REVISTA: The estructure of the presenilin 1(S182)gene andidentification of six novel;Human Mutation. -- Vol. 10 (1997); p. 186-195. -- Clinicalfeatures of early-onset Alzheimer disease in a;large kindred with an E280A presenilin-1 mutation / FranciscoLopera. ...[et al.]. -- En: Jama. -- Vol. 277,;no. 10 (Mar. 1997); p. 193-199. -- Descripcion de una familiacon demenciapresenil tipo Alzheimer / Francisco;Lopera, W. Cornejo y M. Salinas. -- En: Acta Medica Colombiana.-- Vol. 12, no. 2 (Mar.- Abr., 1987); p.;55-61. -- Demencia tipo Alzheimer con agregacion familiaren Antioquia, Colombia / Francisco Lopera. ... [et;al.]. -- En: Acta Neurologica Colombiana. -- Vol.10, no. 4(Oct.-Dic., 1994); p. 173-187. -- Plan de estudio;del paciente con demencia y diagnostico diferencial con elAlzheimer / Francisco Lopera. -- En: Iatreia. --;Alzheimer`sdisease but age of onset is not modified by ApoE alleles / Francisco Lopera. ... [et al.]. -- En:;Francisco Lopera Restrepo. ... [et al.]. -- En: Neurobiology ofAging. --Vol. 17, no. 4 (1996); p. 17. --;Molecular genetic analisis of chromosome 14 linked ad in fourColombian kindreds / Francisco Lopera Restrepo.;... [et al]. -- En: Brazilian Journal of Genetics. -- Vol.19no. 2 (Aug1996); p. 145. -- Identification of;three large early onset alzheimer's disease pedigrees fromColombia / Francisco Lopera Restrepo. ... [et al.].; En: Psychiatric Genetics. -- Vol. 5, no. 1 (1995); p. 73. --Linkage studies in three large early onset;of Human Genetics. -- Vol. 57, no. 1083. (1995); p. 189. -'- CaPITULO(S) ENLIBRO: Formas hereditarias de las;demencias / Francisco Lopera. -- p. 255-269. -- En: Demencia Enfoque Multidisciplinarios / Francisco Lopera. -;Argentina. Sagitario editores, 1997. -- 28 cm. -- ISBN 950438771.;alzheimer's disease pedigries from Colombia / Francisco LoperaRestrepo. ... [et al.]. -- En: American Society;Vol. 10, no. 3 (Sep.1997); p. 106-113. -- Aspectos molecularesde la enfermedad de Alzheimer / Andres;Villegas, Gabriel Bedoya. -- En: Iatreia. -- Vol.10, no.2(Jun.1997); p.82-88. -- A large geographical focus;of early onset familial alzheimer's disease in Antioquia,Colombia / Francisco Lopera Restrepo. ... [et al.].; En: Journal of the Neurological Sciences. -- Vol. 150,sup.1(Sep 1997); p. 156. -- ISSN 0022510X. --;Caracterizacion clinica y neuropsicologica del alzheimer familiar de Antioquia, Colombia / Francisco Lopera;Restrepo. -- En: Neuropsych Latina. -- Vol. 3, no. 2 (1997); p.108. -- Inmunocytochemical Characterizacition;of Plaques, Tangles, and Vascular Ayloid in the Brain of 2FADpatients With an Identified PS1 Mutations

Mediterranean diet, body esteem and anthropometric parameters in acrobatic teenage gymnasts / Dieta mediterránea, estima corporal y parámetros antropométricos en adolescentes practicantes de gimnasia acrobática

 AbstractThe objective of this study was to evaluate the adherence to Mediterranean diet (AMD) and body esteem (BE) in acrobatic gymnasts and their relationships with anthropometric parameters. Participated 48 teenage gymnasts (32 girls and 16 boys) of 12-21old-years. The AMD was analyzed through Quality Test of Diet Mediterranean in Childhood and Adolescence (KIDMED test) and the Body Esteem Scale for Children (BES-C). The waist circumference was measured, as well as the height and weight, calculating BMI and waist-height ratio (WHR). The 69% of sample showed an optimal AMD with a BMI of 18.6 kg/ m2, waist circumference of 62.1 cm and WHR of 0.4 cm without sex differences. The AMD is not associated with BE and anthropometric parameters. In general, boys and girls showed good BE. Not significant relationships were found between values of KIDMED test, anthropometric variables and BE. In general, the eating habits of the gymnast were healthy, presenting to the most optimal AMD, normal values of BMI and a good perception of their body imagen. However, although these results are encouraging, it was evident that almost a third of the participants would need to improve their diet, which points to the need to strengthen nutritional education strategies in the sport field.ResumenEl objetivo de este estudio fue evaluar la adherencia a la dieta mediterránea (ADM) y la estima corporal (EC) en gimnastas acrobáticos, así como su relación con parámetros antropométricos. Participaron 48 gimnastas adolescentes (32 mujeres y 16 hombres), de 12-21 años de edad. La ADM fue evaluada a través del Índice de Calidad de la Dieta Mediterránea en la Infancia y Adolescencia (KIDMED) y la EC mediante la Escala de Estima Corporal para Niños (BES-C); además fueron medidos (talla, peso y perímetro de cintura) para calcular el índice de masa corporal (IMC) y la razón cintura-talla (RCT). El 69% de los participantes mostró alta ADM y buena EC, con IMC promedio de 18.6 kg/m2, perímetro de cintura de 62.1 cm y RCT de 0.4 cm, sin registrarse diferencias entre sexos. La ADM no se asoció con la EC o los parámetros antropométricos. En general, los hábitos alimentarios de los participantes fueron saludables, con alta o moderada ADM y satisfactoria imagen corporal. No obstante, aunque estos resultados son alentadores, fue evidente que casi un tercio de los participantes requeriría mejorar su dieta, lo que apunta a la necesidad de fortalecer las estrategias de educación nutricional en el ámbito deportivo

Taurine supplementation modulates glucose homeostasis and islet function

Taurine is a conditionally essential amino acid for human that is involved in the control of glucose homeostasis; however, the mechanisms by which the amino acid affects blood glucose levels are unknown. Using an animal model, we have studied these mechanisms. Mice were supplemented with taurine for 30 d. Blood glucose homeostasis was assessed by intraperitoneal glucose tolerance tests (IPGTT). Islet cell function was determined by insulin secretion, cytosolic Ca2+ measurements and glucose metabolism from isolated islets. Islet cell gene expression and translocation was examined via immunohistochemistry and quantitative real-time polymerase chain reaction. Insulin signaling was studied by Western blot. Islets from taurine-supplemented mice had: (i) significantly higher insulin content, (ii) increased insulin secretion at stimulatory glucose concentrations, (iii) significantly displaced the dose-response curve for glucose-induced insulin release to the left, (iv) increased glucose metabolism at 5.6 and 11.1-mmol/L concentrations; (v) slowed cytosolic Ca2+ concentration ([Ca2+]i) oscillations in response to stimulatory glucose concentrations; (vi) increased insulin, sulfonylurea receptor-1, glucokinase, Glut-2, proconvertase and pancreas duodenum homeobox-1 (PDX-1) gene expression and (vii) increased PDX-1 expression in the nucleus. Moreover, taurine supplementation significantly increased both basal and insulin stimulated tyrosine phosphorylation of the insulin receptor in skeletal muscle and liver tissues. Finally, taurine supplemented mice showed an improved IPGTT. These results indicate that taurine controls glucose homeostasis by regulating the expression of genes required for glucose-stimulated insulin secretion. In addition, taurine enhances peripheral insulin sensitivity.Peer Reviewe

C3 glomerulopathy-associated CFHR1 mutation alters FHR oligomerization and complement regulation

C3 glomerulopathies (C3G) are a group of severe renal diseases with distinct patterns of glomerular inflammation and C3 deposition caused by complement dysregulation. Here we report the identification of a familial C3G-associated genomic mutation in the gene complement factor H–related 1 (CFHR1), which encodes FHR1. The mutation resulted in the duplication of the N-terminal short consensus repeats (SCRs) that are conserved in FHR2 and FHR5. We determined that native FHR1, FHR2, and FHR5 circulate in plasma as homo- and hetero-oligomeric complexes, the formation of which is likely mediated by the conserved N-terminal domain. In mutant FHR1, duplication of the N-terminal domain resulted in the formation of unusually large multimeric FHR complexes that exhibited increased avidity for the FHR1 ligands C3b, iC3b, and C3dg and enhanced competition with complement factor H (FH) in surface plasmon resonance (SPR) studies and hemolytic assays. These data revealed that FHR1, FHR2, and FHR5 organize a combinatorial repertoire of oligomeric complexes and demonstrated that changes in FHR oligomerization influence the regulation of complement activation. In summary, our identification and characterization of a unique CFHR1 mutation provides insights into the biology of the FHRs and contributes to our understanding of the pathogenic mechanisms underlying C3G