Acute Impacts of Different Types of Exercise on Circulating α-Klotho Protein Levels.

Introduction: Elevated plasma α-klotho (αKl) protects against several ageing phenotypes and has been proposed as a biomarker of a good prognosis for different diseases. The beneficial health effects of elevated plasma levels of soluble αKl (SαKl) have been likened to the positive effects of exercise on ageing and chronic disease progression. It has also been established that molecular responses and adaptations differ according to exercise dose. The aim of this study is to compare the acute SαKl response to different exercise interventions, cardiorespiratory, and strength exercise in healthy, physically active men and to examine the behavior of SαKl 72h after acute strength exercise. Methods: In this quasi-experimental study, plasma SαKl was measured before and after a cardiorespiratory exercise session (CR) in 43 men, and strength exercise session (ST) in 39 men. The behavior of SαKl was also examined 24, 48, and 72h after ST. Results: Significant differences (time×group) were detected in SαKl levels (p=0.001; d=0.86) between CR and ST. After the ST intervention, SαKl behavior varied significantly (p=0.009; d=0.663) in that levels dropped between pre- and post-exercises (p=0.025; d=0.756) and were also significantly higher compared to pre ST values at 24h (p=0.033; d=0.717) and at 48h (p=0.015; d=0.827). Conclusions: SαKl levels increased in response to a single bout of cardiorespiratory exercise; while they decreased immediately after strength exercise, levels were elevated after 24h indicating different klotho protein responses to different forms of exercise.

Caracterización de las agresiones producidas al personal sanitario del servicio de urgencias en un hospital comarcal / Characterization of the personal aggressions caused emergency medical service in a regional hospital

Objetivo: La violencia ocupacional es un fenómeno emergente en los riesgos laborales y específicamente en el sector sanitario y servicios de urgencias. Nuestro objetivo es caracterizar las agresiones producidas al personal de urgencias de un hospital comarcal. Métodos: Estudio transversal. La población a estudio son los trabajadores del servicio de urgencias. Se excluyó personal con antigüedad inferior a un año. Se diseñó un cuestionario con variables sociodemográficas y características de las agresiones sufridas durante el 2011. La participación fue del 92,4%. Se realizó una estadística descriptiva con el programa SPSS 16. Resultados: El 58.2% del personal de urgencias fue agredido: enfermería sufrió el 39%, médicos el 19,5%, personal administrativo el 17,1%, auxiliares sanitarios el 12,2%, auxiliares de enfermería el 7,3 % y técnicos de radiología el 4,9%, con una asociación significativa entre categoría profesional y agresiones sufridas (p=0.004). El 40,4% de las agresiones se produjo por la noche, el 31,9% por la mañana y el 27,6% por la tarde. El 75% fueron agresiones verbales, el 25% físicas y verbales. El 27,5% sufrió 4 o más agresiones verbales. El 35,8% de agresiones fueron cometidas por acompañantes, el 18,9% por pacientes y el 45,3% por ambos. El 71,7% no notificó la agresión a su mando superior ni al servicio de prevención. Un 67,1% no recibió formación de prevención de violencia. El 69,9% no conoce el protocolo de la entidad. Conclusiones: Falta formación específica sobre el tema y difusión de los protocolos ya existentes(AU)

Objective: Workplace violence is an emerging phenomenon in occupational hazards and specifically in the health sector end emergency services. Our objective is to characterize the aggressions caused emergency personnel in a district hospital. Methods: Cross-sectional study. The study populations are workers in the emergency department. Staff was excluded under one year old. We designed a questionnaire with socio-demographic variables and characteristics of the aggressions in 2011. The response rate was 92.4%. Descriptive statistics were performed using SPSS 16. Results: The 58.2% of emergency personnel was attacked: 39% experienced nurses, doctors 19.5%, 17.1% administrative staff, 12.2% auxiliary sanitary, auxiliary nurses 7.3% technical of radiology 4.9%, with a significant association between professional and aggressions (p = 0.004). 40.4% of the aggressions took place in the night 31.9% in the morning and 27.6% in the afternoon.75% were verbal, 25% physical and verbal. 27.5% 4 or more suffered verbal abuse.35.8% of aggressions were committed by attendants, 18.9% of patients and 45.3% for both.71.7% did not report the attack on his high command or the prevention service.67.1% received no training in violence prevention. 69.9% do not know the protocol entity. Conclusions: Lack of specific training on the issue and dissemination of existing protocols(AU)

beta-Ureidopropionase deficiency: an inborn error of pyrimidine degradation associated with neurological abnormalities.

beta-Ureidopropionase deficiency is an inborn error of the pyrimidine degradation pathway, affecting the cleavage of N-carbamyl-beta-alanine and N-carbamyl-beta-aminoisobutyric acid. In this study, we report the elucidation of the genetic basis underlying a beta-ureidopropionase deficiency in four patients presenting with neurological abnormalities and strongly elevated levels of N-carbamyl-beta-alanine and N-carbamyl-beta-aminoisobutyric acid in plasma, cerebrospinal fluid and urine. No beta-ureidopropionase activity could be detected in a liver biopsy obtained from one of the patients, which reflected the complete absence of the beta-ureidopropionase protein. Analysis of the beta-ureidopropionase gene (UPB1) of these patients revealed the presence of two splice-site mutations (IVS1-2A>G and IVS8-1G>A) and one missense mutation (A85E). Heterologous expression of the mutant enzyme in Escherichia coli showed that the A85E mutation resulted in a mutant beta-ureidopropionase enzyme without residual activity. Our results demonstrate that the N-carbamyl-beta-amino aciduria in these patients is due to a deficiency of beta-ureidopropionase, which is caused by mutations in the UPB1 gene. Furthermore, an altered homeostasis of beta-aminoisobutyric acid and/or increased oxidative stress might contribute to some of the clinical abnormalities encountered in patients with a beta-ureidopropionase deficiency. An analysis of the presence of the two splice site mutations and the missense mutation in 95 controls identified one individual who proved to be heterozygous for the IVS8-1G>A mutation. Thus, a beta-ureidopropionase deficiency might not be as rare as is generally considered.