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El desarrollo de hipertensión portal va ligado a la evolución natural de la enfermedad hepática crónica, marcando el pronóstico de la misma. Cuando el gradiente de presión venosa hepática excede los 10mm Hg se considera hipertensión portal clínicamente significativa, hecho que marca la transición entre el estadio de cirrosis compensada y el de cirrosis descompensada, pues identifica una población con un alto riesgo de sufrir la primera descompensación (ascitis, hidrotórax hepático, encefalopatía hepática o hemorragia varicosa aguda). Gracias al desarrollo de métodos de diagnóstico no invasivo, como la elastografía, actualmente es más sencillo identificar a estos pacientes, lo que permite un tratamiento dirigido de forma individualizada. En este escenario, los bloqueadores beta-adrenérgicos no cardioselectivos cobran cada vez más importancia, ya que permiten la prevención tanto de la hemorragia como de otras complicaciones de la hipertensión portal.

La cirrosis hepática es una enfermedad muy prevalente a nivel mundial, asociada a una importante morbimortalidad derivada de sus complicaciones: descompensaciones agudas y hepatocarcinoma. En su etiología están implicadas causas diversas como el consumo crónico perjudicial de alcohol, infecciones víricas (virus de hepatitis B o C) o la enfermedad hepática grasa no alcohólica. Todas ellas provocan un daño del parénquima con fenómenos de inflamación y reparación anómalos que conducen finalmente al desarrollo de fibrosis y nódulos de regeneración que se traducen en el desarrollo de hipertensión portal e insuficiencia hepática. Fenómenos como la inflamación sistémica y la disfunción inmune asociada a la cirrosis, así como la alteración en el eje hígado-intestino, serán clave en su evolución. El proceso diagnóstico irá encaminado a identificar las causas de la enfermedad y evaluar el grado de fibrosis e hipertensión portal que determinarán el pronóstico de la enfermedad en los diferentes estadios. Las estrategias de manejo, por su parte, se enfocarán en el tratamiento etiológico, prevención/tratamiento de las complicaciones e incluso en el trasplante hepático como tratamiento definitivo. La identificación y tratamiento de los factores de riesgo y diagnóstico precoz de esta enfermedad permitirán en un futuro una mejoría del pronóstico.

Alonso-Callejo, A, García-Unanue, J, Guitart-Trench, M, Majano, C, Gallardo, L, and Felipe, J. Validity and reliability of the acceleration-speed profile for assessing running kinematics' variables derived from the force-velocity profile in professional soccer players. J Strength Cond Res38(3): 563–570, 2024—The aim of this research is to assess the validity and reliability of the acceleration-speed profile (ASP) for measuring the mechanical variables of running kinematics when compared with the force-velocity profile (FVP) obtained by reference systems. The ASP and FVP of 14 male players of an elite football club were assessed during a competitive microcycle. Three ASPs were tested according to the number and type of sessions included in its plotting (ASP1: 5 training sessions and competitive match; ASP2: 5 training sessions; ASP3: competitive match). Force-velocity profile was tested 4 days before match (MD-4) with a 30-m linear sprint using 3 previously validated devices (encoder, mobile App, and global positioning system). Level of significance was p< 0.05. Acceptable reliability (intraclass correlation coefficient > 0.5) was found between the ASP1 and the encoder for all variables (F0-A0, V0-S0, and Vmax). The more reliable ASP method was the ASP1 showing a lower bias than the ASP2 and ASP3 methods for almost all variables and reference systems. For ASP1, lower mean absolute error (MAE: 0.3–0.5) and higher correlation (P-M corr: 0.57–0.92) were found on variables related to the velocity in comparison with variables related to the early acceleration phase (F0-A0; MAE: 0.49–0.63; P-M corr: 0.13–0.41). Acceleration-speed profile, when computed with data from a complete competitive week, is a reliable method for analyzing variables derived from velocity and acceleration kinematics. From these results, practitioners could implement ASP and the applications of the FVP previously studied, such as resistance training prescription, performance assessment, and return-to-play management.

Contact with or exposure to electricity continues to be one of the leading causes of workplace fatalities and injuries in the United States. Between 2011 and 2021, there was a total of 1,201 workplace fatalities involving electricity reported to the Occupational Safety and Health Administration (OSHA), accounting for 6% of all workplace deaths. During this period, 69% of all electrically related fatalities happened in nonelectrically related occupations. Further, there has not been a significant decrease in the number of electrical fatalities since 2011. This article reviews each electrical incident reported to OSHA during this period to find the commonalities in fatal electrical incidents, determine if engineering controls or behavioral changes could have avoided the injury, and propose changes that can be made in the workplace and training to reduce the number of electrically related injuries in the United States.

BackgroundDespite persistent reports of socioeconomic inequalities in colorectal cancer survival in England, the magnitude of survival differences has not been fully evaluated.MethodsPatients diagnosed with colon cancer (n=68 169) and rectal cancer (n=38 267) in England (diagnosed between January 2010 and March 2013) were analysed as a retrospective cohort study using the National Cancer Registry data linked with other population-based healthcare records. The flexible parametric model incorporating time-varying covariates was used to assess the difference in excess hazard of death and in net survival between the most affluent and the most deprived groups over time.ResultsSurvival analyses showed a clear pattern by deprivation. Hazard ratio of death was consistently higher in the most deprived group than the least deprived for both colon and rectal cancer, ranging from 1.08 to 1.17 depending on the model. On the net survival scale, the socioeconomic gap between the most and the least deprived groups reached approximately −4% at the maximum (−3.7%, 95% CI −1.6 to −5.7% in men, −3.6%, 95% CI −1.6 to −5.7% in women) in stages III for colon and approximately −2% (−2.3%, 95% CI −0.2 to −4.5% in men, −2.3%, 95% CI −0.2 to −4.3% in women) in stage II for rectal cancer at 3 years from diagnosis, after controlling for age, emergency presentation, receipt of resection and comorbidities. The gap was smaller in other stages and sites. For both cancers, patients with emergency presentation persistently had a higher excess hazard of death than those without emergency presentation.ConclusionSurvival disparities were profound particularly among patients in the stages, which benefit from appropriate and timely treatment. For the patients with emergency presentation, excess hazard of death remained high throughout three years from the diagnosis. Public health measures should be taken to reduce access inequalities to improve survival disparities.

Introduction:The promise of “precision medicine” is using therapeutic agents matched to the inferred biology of a patient's particular disease. In acute myeloid leukemia this approach demands fast and accurate assessment of the mutation and cytogenetic landscape of each AML case. The NCI Myeloid Malignancies Molecular Analysis for Therapy Choice program (“myeloMATCH”) is a precision medicine clinical trial initiative across the NCI National Clinical Trials Network for patients with newly diagnosed acute myeloid leukemia and myelodysplasia. In myeloMATCH the goal is to have cytogenetic and mutation assays performed within 72 hours of central lab receipt, allowing for a rapid assignment of the appropriate clinical trial from the myeloMATCH trial portfolio. Here we report analytic performance of rapid genomic profiling laboratory developed test based on the Thermo Fisher Genexus Oncomine Myeloid Panel GXv2 (NCI Myeloid Assay version 2, or “NMAv2”) which performs rapid sequencing of SNVs, indels, and gene fusions, capturing 1,661 hotspot variants (45 genes) and 779 fusions (35 genes) with a turnaround time of <48 hours from specimen receipt to clinical reporting.

AMA1and SPS1control distinct aspects of meiosis II spindle disassembly, with AMA1affecting the loss of Ase1 and Cin8 during meiosis II spindle disassembly, while SPS1affects Bim1. The Anaphase Promoting Complex and meiotic/mitotic exit pathways seem to regulate similar targets in meiosis as mitosis, despite utilizing meiosis-specific regulators in those pathways.