Do Long-term Unemployed Workers Benefit from Targeted Wage Subsidies

Wage subsidies are often suggested as a particularly effective policy to improve labor market chances of economically disadvantaged groups. We empirically evaluate an employer-side wage subsidy scheme targeted at the long-term unemployed in Germany. Based on program regulations and a large data set we estimate the impact of program existence locally at the eligibility threshold using an RDD framework in differences. The results suggest no significant effect of the subsidy on exit rates out of unemployment or employment stability. Employment rates up to three years after eligibility show no significant improvement. In conclusion, our findings are in contrast to previous empirical results justifying such policies.Wage subsidy, Long-term unemployment, Regression discontinuity

Do Long-term Unemployed Workers Benefit from Targeted Wage Subsidies?

We evaluate a wage subsidy program that is targeted at long-term unemployed workers in Germany. We use an alternative identification procedure compared to empirical studies con­ducted so far. Exploiting the particular program regulations and large administrative data we estimate the impact of program availability using a regression discontinuity framework. Our results suggest no significant impact of the availability of the subsidy on labor market out­comes of the target group. Even though our analysis lacks some statistical power, our findings do not support the substantial positive effects obtained from matching studies. As our ap­proach does not require observability of all drivers of selection, previous empirical studies justifying government expenditures on wage subsidies based on matching methods should be reconsidered

Rassismus im Wandel - vom Rassebegriff zum Kulturbegriff

Die vorliegende Arbeit befasst sich mit der Transformation des Rassebegriffes hin zum Kulturbegriff. Dabei soll die nationalsozialistische Rassenideologie und die aktuelle ethnopluralistische Logik eines „Recht auf Differenz“ der Neuen Rechten Bewegung in Deutschland und Frankreich einem Vergleich unterzogen werden. Die Rolle der Wissenschaft – insbesondere Ethnologie, Evolutionspsychologie und Verhaltensforschung – scheint von enormer Bedeutung zu sein, um ein differentialistisches Menschheitsbild mit biologistischer Basis zu legitimieren. Daraus wird ersichtlich, dass die Diskursstrangtransformation des Rassismus, unter gegenseitiger Einflussnahme von Wissenschaft und rechtsextremer Politik, von einer Kontinuität im Wandel gekennzeichnet ist

Therapy of endocrine disease: Medical treatment of primary aldosteronism

In patients with primary aldosteronism, specific treatment provides prognostic benefit over optimal antihypertensive therapy and is therefore crucial to reduce mortality and morbidity in this subgroup of patients with hypertension. Prognostic relevance has been shown for adrenalectomy in unilateral disease and for medical treatment with mineralocorticoid receptor antagonists in bilateral adrenal hyperplasia. Collectively, evidence points to the superiority of surgical treatment compared to medical treatment. The causal approach of removing the mineralocorticoid excess, as well as the often-accompanying glucocorticoid excess, might provide one biologically plausible explanation for the observation of slightly better outcomes with surgical therapy. However, in patients living with primary aldosteronism, medical treatment is often insufficient for three major reasons. First and foremost, no marker of sufficient aldosterone blockade has yet been established and therefore adequate treatment of the aldosterone excess is often dismissed as a treatment goal. Second, side effects often limit patient compliance. Third, as recommendations differ from other indications like heart failure, drug dosing is often inadequate. The aim of this review is first to provide an overview over medical treatment options and second to review potential markers for treatment surveillance in patients with primary aldosteronism

Low-depth Circuit Implementation of Parity Constraints for Quantum Optimization

We present a construction for circuits with low gate count and depth, implementing three- and four-body Pauli-Z product operators as they appear in the form of plaquette-shaped constraints in QAOA when using the parity mapping. The circuits can be implemented on any quantum device with nearest-neighbor connectivity on a square-lattice, using only one gate type and one orientation of two-qubit gates at a time. We find an upper bound for the circuit depth which is independent of the system size. The procedure is readily adjustable to hardware-specific restrictions, such as a minimum required spatial distance between simultaneously executed gates, or gates only being simultaneously executable within a subset of all the qubits, for example a single line.Comment: 9 pages, 6 figure

Constructive plaquette compilation for the parity architecture

Parity compilation is the challenge of laying out the required constraints for the parity mapping in a local way. We present the first constructive compilation algorithm for the parity architecture using plaquettes for arbitrary higher-order optimization problems. This enables adiabatic protocols, where the plaquette layout can natively be implemented, as well as fully parallelized digital circuits. The algorithm builds a rectangular layout of plaquettes, where in each layer of the rectangle at least one constraint is added. The core idea is that each constraint, consisting of any qubits on the boundary of the rectangle and some new qubits, can be decomposed into plaquettes with a deterministic procedure using ancillas. We show how to pick a valid set of constraints and how this decomposition works. We further give ways to optimize the ancilla count and show how to implement optimization problems with additional constraints.Comment: 8 pages, 5 figure

De Novo Lipogenesis-Related Monounsaturated Fatty Acids in the Blood Are Associated with Cardiovascular Risk Factors in HFpEF Patients

De novo lipogenesis (DNL)-related monounsaturated fatty acids (MUFAs) in the blood are associated with incident heart failure (HF). This observation's biological plausibility may be due to the potential of these MUFAs to induce proinflammatory pathways, endoplasmic reticulum stress, and insulin resistance, which are pathophysiologically relevant in HF. The associations of circulating MUFAs with cardiometabolic phenotypes in patients with heart failure with a preserved ejection fraction (HFpEF) are unknown. In this secondary analysis of the Aldosterone in Diastolic Heart Failure trial, circulating MUFAs were analysed in 404 patients using the HS-Omega-3-Index$^{®}$ methodology. Patients were 67 ± 8 years old, 53% female, NYHA II/III (87/13%). The ejection fraction was ≥50%, E/e' 7.1 ± 1.5, and the median NT-proBNP 158 ng/L (IQR 82-298). Associations of MUFAs with metabolic, functional, and echocardiographic patient characteristics at baseline/12 months follow-up (12 mFU) were analysed using Spearman's correlation coefficients and linear regression analyses, using sex/age as covariates. Circulating levels of C16:1n7 and C18:1n9 were positively associated with BMI/truncal adiposity and associated traits (dysglycemia, atherogenic dyslipidemia, and biomarkers suggestive of non-alcoholic-fatty liver disease). They were furthermore inversely associated with functional capacity at baseline/12 mFU. In contrast, higher levels of C20:1n9 and C24:1n9 were associated with lower cardiometabolic risk and higher exercise capacity at baseline/12 mFU. In patients with HFpEF, circulating levels of individual MUFAs were differentially associated with cardiovascular risk factors. Our findings speak against categorizing FA based on physicochemical properties. Circulating MUFAs may warrant further investigation as prognostic markers in HFpEF

Compensation for geometrical deviations in additive manufacturing

The design of additive manufacturing processes, especially for batch production in industrial practice, is of high importance for the propagation of new additive manufacturing technology. Manual redesign procedures of the additive manufactured parts based on discrete measurement data or numerical meshes are error prone and hardly automatable. To achieve the required final accuracy of the parts, often, various iterations are necessary. To address these issues, a data-driven geometrical compensation approach is proposed that adapts concepts from forming technology. The measurement information of a first calibration cycle of manufactured parts is the basis of the approach. Through non-rigid transformations of the part geometry, a new shape for the subsequent additive manufacturing process was derived in a systematic way. Based on a purely geometrical approach, the systematic portion of part deviations can be compensated. The proposed concept is presented first and was applied to a sample fin-shaped part. The deviation data of three manufacturing cycles was utilised for validation and verification

Lifestyle factors and high-risk atherosclerosis: Pathways and mechanisms beyond traditional risk factors

Despite major efforts to reduce atherosclerotic cardiovascular disease (ASCVD) burden with conventional risk factor control, significant residual risk remains. Recent evidence on non-traditional determinants of cardiometabolic health has advanced our understanding of lifestyle-disease interactions. Chronic exposure to environmental stressors like poor diet quality, sedentarism, ambient air pollution and noise, sleep deprivation and psychosocial stress affect numerous traditional and non-traditional intermediary pathways related to ASCVD. These include body composition, cardiorespiratory fitness, muscle strength and functionality and the intestinal microbiome, which are increasingly recognized as major determinants of cardiovascular health. Evidence points to partially overlapping mechanisms, including effects on inflammatory and nutrient sensing pathways, endocrine signalling, autonomic function and autophagy. Of particular relevance is the potential of low-risk lifestyle factors to impact on plaque vulnerability through altered adipose tissue and skeletal muscle phenotype and secretome. Collectively, low-risk lifestyle factors cause a set of phenotypic adaptations shifting tissue cross-talk from a proinflammatory milieu conducive for high-risk atherosclerosis to an anti-atherogenic milieu. The ketone body ß-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits. Adhering to low-risk lifestyle factors adds to the prognostic value of optimal risk factor management, and benefit occurs even when the impact on conventional risk markers is discouragingly minimal or not present. The aims of this review are (a) to discuss novel lifestyle risk factors and their underlying biochemical principles and (b) to provide new perspectives on potentially more feasible recommendations to improve long-term adherence to low-risk lifestyle factors

High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation

Current algorithms for assessing risk of atherosclerotic cardiovascular disease (ASCVD) and, in particular, the reliance on low-density lipoprotein (LDL) cholesterol in conditions where this measurement is discordant with apoB and LDL-particle concentrations fail to identify a sizeable part of the population at high risk for adverse cardiovascular events. This results in missed opportunities for ASCVD prevention, most notably in those with metabolic syndrome, prediabetes, and diabetes. There is substantial evidence that accumulation of ectopic fat and associated metabolic traits are markers for and pathogenic components of high-risk atherosclerosis. Conceptually, the subset of advanced lesions in high-risk atherosclerosis that triggers vascular complications is closely related to a set of coordinated high-risk traits clustering around a distinct metabolic phenotype. A key feature of this phenotype is accumulation of ectopic fat, which, coupled with age-related muscle loss, creates a milieu conducive for the development of ASCVD: atherogenic dyslipidemia, nonresolving inflammation, endothelial dysfunction, hyperinsulinemia, and impaired fibrinolysis. Sustained vascular inflammation, a hallmark of high-risk atherosclerosis, impairs plaque stabilization in this phenotype. This review describes how metabolic and inflammatory processes that are promoted in large measure by ectopic adiposity, as opposed to subcutaneous adipose tissue, relate to the pathogenesis of high-risk atherosclerosis. Clinical biomarkers indicative of these processes provide incremental information to standard risk factor algorithms and advanced lipid testing identifies atherogenic lipoprotein patterns that are below the discrimination level of standard lipid testing. This has the potential to enable improved identification of high-risk patients who are candidates for therapeutic interventions aimed at prevention of ASCVD