Thermal attenuator channels model the decoherence of quantum systems interacting with a thermal bath, e.g., a two-level system subject to thermal noise and an electromagnetic signal traveling through ...a fiber or in free-space. Hence determining the quantum capacity of these channels is an outstanding open problem for quantum computation and communication. Here we derive several upper bounds on the quantum capacity of qubit and bosonic thermal attenuators. We introduce an extended version of such channels which is degradable and hence has a single-letter quantum capacity, bounding that of the original thermal attenuators. Another bound for bosonic attenuators is given by the bottleneck inequality applied to a particular channel decomposition. With respect to previously known bounds we report better results in a broad range of attenuation and noise: we can now approximate the quantum capacity up to a negligible uncertainty for most practical applications, e.g., for low thermal noise.
We extend the concept of transfer learning, widely applied in modern machine learning algorithms, to the emerging context of hybrid neural networks composed of classical and quantum elements. We ...propose different implementations of hybrid transfer learning, but we focus mainly on the paradigm in which a pre-trained classical network is modified and augmented by a final variational quantum circuit. This approach is particularly attractive in the current era of intermediate-scale quantum technology since it allows to optimally pre-process high dimensional data (e.g., images) with any state-of-the-art classical network and to embed a select set of highly informative features into a quantum processor. We present several proof-of-concept examples of the convenient application of quantum transfer learning for image recognition and quantum state classification. We use the cross-platform software library PennyLane to experimentally test a high-resolution image classifier with two different quantum computers, respectively provided by IBM and Rigetti.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glycemia by enhancing urinary glucose excretion. The physiologic response to pharmacologically induced acute or chronic glycosuria has not been ...investigated in human diabetes.
We evaluated 66 patients with type 2 diabetes (62 ± 7 years, BMI = 31.6 ± 4.6 kg/m(2), HbA1c = 55 ± 8 mmol/mol, mean ± SD) at baseline, after a single dose, and following 4-week treatment with empagliflozin (25 mg). At each time point, patients received a mixed meal coupled with dual-tracer glucose administration and indirect calorimetry.
Both single-dose and chronic empagliflozin treatment caused glycosuria during fasting (median, 7.8 interquartile range {IQR}, 4.4 g/3 hours and 9.2 IQR, 5.2 g/3 hours) and after meal ingestion (median, 29.0 IQR, 12.5 g/5 hours and 28.2 IQR, 15.4 g/5 hours). After 3 hours of fasting, endogenous glucose production (EGP) was increased 25%, while glycemia was 0.9 ± 0.7 mmol/l lower (P < 0.0001 vs. baseline). After meal ingestion, glucose and insulin AUC decreased, whereas the glucagon response increased (all P < 0.001). While oral glucose appearance was unchanged, EGP was increased (median, 40 IQR, 14 g and 37 IQR, 11 g vs. 34 IQR, 11 g, both P < 0.01). Tissue glucose disposal was reduced (median, 75 IQR, 16 g and 70 IQR, 21 g vs. 93 IQR, 18 g, P < 0.0001), due to a decrease in both glucose oxidation and nonoxidative glucose disposal, with a concomitant rise in lipid oxidation after chronic administration (all P < 0.01). β Cell glucose sensitivity increased (median, 55 IQR, 35 pmol • min(-1) • m(-2) • mM(-1) and 55 IQR, 39 pmol • min(-1) • m(-2) • mM(-1) vs. 44 IQR, 32 pmol • min(-1) • m(-2) • mM(-1), P < 0.0001), and insulin sensitivity was improved. Resting energy expenditure rates and those after meal ingestion were unchanged.
In patients with type 2 diabetes, empagliflozin-induced glycosuria improved β cell function and insulin sensitivity, despite the fall in insulin secretion and tissue glucose disposal and the rise in EGP after one dose, thereby lowering fasting and postprandial glycemia. Chronic dosing shifted substrate utilization from carbohydrate to lipid. Trial registration. ClinicalTrials.Gov NCT01248364 (EudraCT no. 2010-018708-99). Funding. This study was funded by Boehringer Ingelheim.
Mathematical modeling in the field of glucose metabolism has a longstanding tradition. The use of models is motivated by several reasons. Models have been used for calculating parameters of ...physiological interest from experimental data indirectly, to provide an unambiguous quantitative representation of pathophysiological mechanisms, to determine indices of clinical usefulness from simple experimental tests. With the growing societal impact of type 2 diabetes, which involves the disturbance of the glucose homeostasis system, development and use of models in this area have increased. Following the approaches of physiological and clinical investigation, the focus of the models has spanned from representations of whole body processes to those of cells, i.e., from
to
research. Model-based approaches for linking
to
research have been proposed, as well as multiscale models merging the two areas. The success and impact of models has been variable. Two kinds of models have received remarkable interest: those widely used in clinical applications, e.g., for the assessment of insulin sensitivity and β-cell function and some models representing specific aspects of the glucose homeostasis system, which have become iconic for their efficacy in describing clearly and compactly key physiological processes, such as insulin secretion from the pancreatic β cells. Models are inevitably simplified and approximate representations of a physiological system. Key to their success is an appropriate balance between adherence to reality, comprehensibility, interpretative value and practical usefulness. This has been achieved with a variety of approaches. Although many models concerning the glucose homeostasis system have been proposed, research in this area still needs to address numerous issues and tackle new opportunities. The mathematical representation of the glucose homeostasis processes is only partial, also because some mechanisms are still only partially understood. For
research, mathematical models still need to develop their potential. This review illustrates the problems, approaches and contribution of mathematical modeling to the physiological and clinical investigation of glucose homeostasis and diabetes, focusing on the most relevant and stimulating models.
Excessive insulin secretion may lead to glucose dysregulation. Our aim was to identify primary (independent of insulin resistance) insulin hypersecretion in subjects with normal glucose tolerance and ...its role in the progression of dysglycemia.
In 1,168 adults, insulin secretion rate (ISR) and β cell function were estimated by C-peptide modeling during an oral glucose tolerance test (OGTT) and an i.v. glucose tolerance test. Whole-body insulin sensitivity was measured by a hyperinsulinemic-euglycemic clamp. After regressing ISR on insulin sensitivity, subjects in the upper tertile of the distribution of residuals were defined as primary hypersecretors. This approach was applied to a biethnic cohort of 182 obese adolescents, who received an OGTT, a hyperglycemic, and a euglycemic clamp.
Adult hypersecretors showed older age, more familial diabetes, sedentary lifestyle, increased fat mass, and worse lipid profile compared with the rest of the cohort, despite virtually identical BMI and insulin sensitivity. Insulin secretion was increased by 53% due to enhanced (+23%) β cell glucose sensitivity. Despite the resulting hyperinsulinemia, glucose tolerance was worse in hypersecretors among both adults and adolescents, coupled with higher indices of liver insulin resistance and increased availability of gluconeogenic substrates. At the 3-year follow-up, adult hypersecretors had increased incidence of impaired glucose tolerance/type 2 diabetes.
Primary insulin hypersecretion, independent of insulin resistance, is associated with a worse clinical and metabolic phenotype in adults and adolescents and predicts deterioration of glucose control over time.
The relationship between insulin sensitivity and cardiovascular disease (RISC) Study was partly supported by EU grant QLG1-CT-2001-01252.
A gene mutation of the Wnt/β-catenin signaling cascade is present in rare patients with the insulin resistance syndrome. Sclerostin is a circulating peptide inhibiting Wnt/β-catenin signaling. Our ...aims were to evaluate serum sclerostin in subjects with prediabetes and to analyze its relationship with insulin resistance and β-cell function.
We performed a cross-sectional study including 43 healthy normal glucose-tolerant (NGT) individuals and 79 individuals with impaired glucose regulation (IGR), which included subjects with impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and combined IFG-IGT, undergoing oral glucose tolerance test (OGTT) and dual-energy X-ray absorptiometry. A subgroup of 18 with NGT and 30 with IGR also underwent a euglycemic-hyperinsulinemic clamp with tracer.
Sclerostin levels were higher in IGR compared with NGT (50.8 ± 2.4 vs. 38.7 ± 2.3 pmol/L; P = 0.01), positively correlated with HOMA-insulin resistance (IR) (r = 0.62; P < 0.001), and negatively correlated with insulin-mediated total body glucose disposal (r = -0.40; P < 0.001). Fasting endogenous glucose production (EGP) and hepatic and adipose tissue insulin resistance indexes were positively correlated with sclerostin levels (r = 0.48, r = 0.62, and r = 0.61, respectively; P < 0.001). Fasting and OGTT insulin clearance were inversely correlated with sclerostin serum levels (r = -0.52 and r = -0.44, respectively; both P < 0.001). Sclerostin levels were not correlated with β-cell function parameters. In multiple linear regression analysis, the addition of sclerostin levels to the traditional risk factors for insulin resistance improved the r(2) associated with HOMA-IR (r(2) change: 0.055; F change: 28.893; P = 0.001) and insulin-mediated total body glucose disposal (r(2) change: 0.059; F change: 4.938; P = 0.033).
Sclerostin levels are increased in individuals with prediabetes and correlated with insulin resistance in skeletal muscle, liver, and adipose tissue. The correlation between sclerostin and insulin clearance at fasting state and during OGTT is novel; thus, studies are needed to explore the potential causal relationship.
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