Anaesthesia training designs across Europe: A survey-based study from the trainees committee of the European Society of Anaesthesiology and Intensive Care.

BACKGROUND: Anaesthesiology training programs in Europe vary in duration, content, and requirements for completion. This survey-based study conducted by the Trainees Committee of the European Society of Anaesthesiology and Intensive Care explores current anaesthesia training designs across Europe. METHODS: Between May and July 2018, we sent a 41-item online questionnaire to all National Trainee Representatives, members of the National Anaesthesiologists Societies Committee, and Council Representatives of the European Society of Anaesthesiology and Intensive Care (ESAIC) of all member countries. We cross-validated inconsistent data with different country representatives. RESULTS: Forty-three anaesthesiologists from all 39 associated ESAIC countries completed the questionnaire. Results showed considerable variability in teaching formats, frequency of teaching sessions during training, and differences in assessments made during and at the end of training. The reported duration of training was 60 months in 59% (n = 23) of participating countries, ranging from 24 months in Russia and Ukraine to 84 months in the UK. CONCLUSION: This study shows the significant differences in anaesthesiology training formats across Europe, and highlights the importance of developing standardised training programs to ensure a consistent level of training and to improve patient safety. This study provides valuable insights into European anaesthesia training, and underlines the need for further research and collaboration to improve requirements.

Analysis of cellular water content in T cells reveals a switch from slow metabolic water gain to rapid water influx prior to cell division.

Cell growth is driven by the acquisition and synthesis of both dry biomass and water mass. In this study, we examine the increase of water mass in T cell during cell growth. We found that T-cell growth is characterized by an initial phase of slow increase in cellular water, followed by a second phase of rapid increase in water content. To study the origin of the water gain, we developed a novel methodology we call cold aqua trap-isotope ratio mass spectrometry, which allows analysis of the isotope composition of intracellular water. Applying cold aqua trap-isotope ratio mass spectrometry, we discovered that glycolysis-coupled metabolism of water accounts on average for 11 fl out of the 20 fl of water gained per cell during the initial slow phase. In addition, we show that at the end of the rapid phase before initiation of cell division, a water influx occurs, increasing the cellular water mass by threefold. Thus, we conclude that activated T cells switch from metabolizing water to rapidly taking up water from the extracellular medium prior to cell division. Our work provides a method to analyze cell water content as well as insights into the ways cells regulate their water mass.

Restoration of energy homeostasis by SIRT6 extends healthy lifespan.

Aging leads to a gradual decline in physical activity and disrupted energy homeostasis. The NAD+-dependent SIRT6 deacylase regulates aging and metabolism through mechanisms that largely remain unknown. Here, we show that SIRT6 overexpression leads to a reduction in frailty and lifespan extension in both male and female B6 mice. A combination of physiological assays, in vivo multi-omics analyses and 13C lactate tracing identified an age-dependent decline in glucose homeostasis and hepatic glucose output in wild type mice. In contrast, aged SIRT6-transgenic mice preserve hepatic glucose output and glucose homeostasis through an improvement in the utilization of two major gluconeogenic precursors, lactate and glycerol. To mediate these changes, mechanistically, SIRT6 increases hepatic gluconeogenic gene expression, de novo NAD+ synthesis, and systemically enhances glycerol release from adipose tissue. These findings show that SIRT6 optimizes energy homeostasis in old age to delay frailty and preserve healthy aging.

Microleakage at the abutment-implant interface of osseointegrated implants: a comparative study.

Microleakage can occur at the abutment-implant (A-I) interface in osseointegrated implants and may cause malodor and inflammation of peri-implant tissues. The degree of microleakage at the A-I interface of 5 implant systems was comparatively assessed at varying closing torques. Using colored tracing probes driven by a 2-atm pressure system, the interface microleakage of Brånemark, Sulzer Calcitek, 3i, ITI, and Steri-Oss implants was determined spectrophotometrically. Microleakage through the A-I interface occurred in all systems, with variability between systems, samples, and closing torques. As closing torque increased from 10 Ncm to 20 Ncm to manufacturers' recommended closing torques, microleakage decreased significantly (P < .005) for all systems. Analysis of variance showed significant interaction between closing torques and the time course of microleakage, and between systems and the time course of microleakage (P < .001). The results indicate that fluids and small molecules are capable of passing through the interface of all the A-I assemblies studied. Presumably in an in situ situation, fluids containing bacterial byproducts and nutrients required for bacterial growth may pass through the interface gap, contributing in part to clinically observed malodor and peri-implantitis.