RESUMEN
We introduce a novel minimally disturbing method for sub-nK thermometry in a Bose-Einstein condensate (BEC). Our technique is based on the Bose polaron model; namely, an impurity embedded in the BEC acts as the thermometer. We propose to detect temperature fluctuations from measurements of the position and momentum of the impurity. Crucially, these cause minimal backaction on the BEC and hence, realize a nondemolition temperature measurement. Following the paradigm of the emerging field of quantum thermometry, we combine tools from quantum parameter estimation and the theory of open quantum systems to solve the problem in full generality. We thus avoid any simplification, such as demanding thermalization of the impurity atoms, or imposing weak dissipative interactions with the BEC. Our method is illustrated with realistic experimental parameters common in many labs, thus showing that it can compete with state-of-the-art destructive techniques, even when the estimates are built from the outcomes of accessible (suboptimal) quadrature measurements.
RESUMEN
Background: As people age, circulating levels of insulin-like growth factors (IGFs) and IGF binding protein 3 (IGFBP-3) decline. In rat cardiomyocytes, IGF-I has been shown to regulate sarcolemmal potassium channel activity and late sodium current thus impacting cardiac repolarization and the heart rate-corrected QT (QTc). However, the relationship between IGFs and IGFBP-3 with the QTc interval in humans, is unknown. Objectives: To examine the association of IGFs and IGFBP-3 with QTc interval in an older age population-based cohort. Methods: Participants were from the 1946 Medical Research Council (MRC) National Survey of Health and Development (NSHD) British birth cohort. Biomarkers from blood samples at age 53 and 60-64 years (y, exposures) included IGF-I/II, IGFBP-3, IGF-I/IGFBP-3 ratio and the change (Δ) in marker levels between the 60-64 and 53y sampled timepoints. QTc (outcome) was recorded from electrocardiograms at the 60-64y timepoint. Generalized linear multivariable models with adjustments for relevant demographic and clinical factors, were used for complete-cases and repeated after multiple imputation. Results: One thousand four hundred forty-eight participants were included (48.3% men; QTc mean 414 ms interquartile range 26 ms). Univariate analysis revealed an association between low IGF-I and IGF-I/IGFBP-3 ratio at 60-64y with QTc prolongation [respectively: ß -0.30 ms/nmol/L, (95% confidence intervals -0.44, -0.17), p < 0.001; ß-28.9 ms/unit (-41.93, -15.50), p < 0.001], but not with IGF-II or IGFBP-3. No association with QTc was found for IGF biomarkers sampled at 53y, however both ΔIGF-I and ΔIGF-I/IGFBP-3 ratio were negatively associated with QTc [ß -0.04 ms/nmol/L (-0.08, -0.008), p = 0.019; ß -2.44 ms/unit (-4.17, -0.67), p = 0.007] while ΔIGF-II and ΔIGFBP-3 showed no association. In fully adjusted complete case and imputed models (reporting latter) low IGF-I and IGF-I/IGFBP-3 ratio at 60-64y [ß -0.21 ms/nmol/L (-0.39, -0.04), p = 0.017; ß -20.14 ms/unit (-36.28, -3.99), p = 0.015], steeper decline in ΔIGF-I [ß -0.05 ms/nmol/L/10 years (-0.10, -0.002), p = 0.042] and shallower rise in ΔIGF-I/IGFBP-3 ratio over a decade [ß -2.16 ms/unit/10 years (-4.23, -0.09), p = 0.041], were all independently associated with QTc prolongation. Independent associations with QTc were also confirmed for other previously known covariates: female sex [ß 9.65 ms (6.65, 12.65), p < 0.001], increased left ventricular mass [ß 0.04 ms/g (0.02, 0.06), p < 0.001] and blood potassium levels [ß -5.70 ms/mmol/L (-10.23, -1.18) p = 0.014]. Conclusion: Over a decade, in an older age population-based cohort, declining levels and bioavailability of IGF-I associate with prolongation of the QTc interval. As QTc prolongation associates with increased risk for sudden death even in apparently healthy people, further research into the antiarrhythmic effects of IGF-I on cardiomyocytes is warranted.
RESUMEN
OBJECTIVE: To assess changes in metabolic risk factors and cancer-related growth factors associated with short-term abstinence from alcohol. DESIGN: Prospective, observational study. SETTING: Single tertiary centre. PARTICIPANTS: Healthy subjects were recruited based on intention to: (1) abstain from alcohol for 1 month (abstinence group), or (2) continue to drink alcohol (control group). Inclusion criteria were baseline alcohol consumption >64 g/week (men) or >48 g/week (women). Exclusion criteria were known liver disease or alcohol dependence. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was change in insulin resistance (homeostatic model assessment (HOMA) score). Secondary outcomes were changes in weight, blood pressure (BP), vascular endothelial growth factor (VEGF), epidermal growth factor (EGF) and liver function tests. Primary and secondary outcomes were adjusted for changes in diet, exercise and cigarette smoking. RESULTS: The abstinence group comprised 94 participants (mean age 45.5 years, SD ±1.2) and the control group 47 participants (mean age 48.7 years, SD ±1.8). Baseline alcohol consumption in the abstinence group was 258.2 g/week, SD ±9.4, and in the control group 233.8 g, SD ±19.0. Significant reductions from baseline in the abstinence group (all p<0.001) were found in: HOMA score (-25.9%, IQR -48.6% to +0.3%), systolic BP (-6.6%, IQR -11.8% to 0.0%), diastolic BP (-6.3%, IQR -14.1% to +1.3%), weight (-1.5%, IQR -2.9% to -0.4%), VEGF (-41.8%, IQR -64.9% to -17.9%) and EGF (-73.9%, IQR -86.1% to -36.4%). None of these changes were associated with changes in diet, exercise or cigarette smoking. No significant changes from baseline in primary or secondary outcomes were noted in the control group. CONCLUSION: These findings demonstrate that abstinence from alcohol in moderate-heavy drinkers improves insulin resistance, weight, BP and cancer-related growth factors. These data support an independent association of alcohol consumption with cancer risk, and suggest an increased risk of metabolic diseases such as type 2 diabetes and fatty liver disease.