Long-term labor market returns to upper secondary school track choice: Leveraging idiosyncratic variation in peers' choices.

Vocational education and training (VET) is theorized to play a dual role for inequality of labor market outcomes: the role of a safety net and the role of socioeconomic diversion. In this paper, we test these hypotheses by examining the long-term labor market returns to track choice in upper secondary education in Denmark using an instrumental variable approach that relies on random variation in school peers' educational decisions. We report two main findings. First, VET diverts students on the margin to the academic track away from higher-status but not higher-paying occupations. Second, VET protects students on the margin to leaving school from risks of non-employment and unskilled work, also leading to higher earnings. These results suggest that in countries with a highly compressed wage structure, a strong VET system benefits students unlikely to continue to college, while causing few adverse consequences for students on the margin to choosing academic education.

Multi-Camera Vessel-Speed Enforcement by Enhancing Detection and Re-Identification Techniques.

This paper presents a camera-based vessel-speed enforcement system based on two cameras. The proposed system detects and tracks vessels per camera view and employs a re-identification (re-ID) function for linking vessels between the two cameras based on multiple bounding-box images per vessel. Newly detected vessels in one camera (query) are compared to the gallery set of all vessels detected by the other camera. To train and evaluate the proposed detection and re-ID system, a new Vessel-reID dataset is introduced. This extensive dataset has captured a total of 2474 different vessels covered in multiple images, resulting in a total of 136,888 vessel bounding-box images. Multiple CNN detector architectures are evaluated in-depth. The SSD512 detector performs best with respect to its speed (85.0% Recall@95Precision at 20.1 frames per second). For the re-ID of vessels, a large portion of the total trajectory can be covered by the successful detections of the SSD model. The re-ID experiments start with a baseline single-image evaluation obtaining a score of 55.9% Rank-1 (49.7% mAP) for the existing TriNet network, while the available MGN model obtains 68.9% Rank-1 (62.6% mAP). The performance significantly increases with 5.6% Rank-1 (5.7% mAP) for MGN by applying matching with multiple images from a single vessel. When emphasizing more fine details by selecting only the largest bounding-box images, another 2.0% Rank-1 (1.4% mAP) is added. Application-specific optimizations such as travel-time selection and applying a cross-camera matching constraint further enhance the results, leading to a final 88.9% Rank-1 and 83.5% mAP performance.

How teachers form educational expectations for students: A comparative factorial survey experiment in three institutional contexts.

While schools are thought to use meritocratic criteria when evaluating students, research indicates that teachers hold lower expectations for students from disadvantaged backgrounds. However, it is unclear what the unique impact is of specific student traits on teacher expectations, as different traits are often correlated to one another in real life. Moreover, research has neglected the role of the institutional context, yet tracking procedures, financial barriers to education, and institutionalized cultural beliefs may influence how teachers form expectations. We conducted a factorial survey experiment in three contexts that vary with respect to these institutional characteristics (The United States, New York City; Norway, Oslo; the Netherlands, Amsterdam). We asked elementary school teachers to express expectations for hypothetical students whose characteristics were experimentally manipulated. Teachers in the different contexts used the same student traits when forming expectations, yet varied in the importance they attached to these traits. In Amsterdam - where teachers track students on the basis of their performance and tracking bears significant consequences for educational careers - we found a large impact of student performance. In Oslo - where institutions show an explicit commitment to equality of educational opportunity - teachers based their expectations less on student effort, and seemed to make more inferences about student performance by a student's socio-economic background. New York teachers seemed to make few inferences about student performance based on their socio-economic background.

Are universities left-wing bastions? The political orientation of professors, professionals, and managers in Europe.

Universities are accused of being left-wing bastions, unwelcoming to conservative and right-wing professors. However, we know little about the political orientation of professors in comparison to other professionals, which would be the right comparison group if we want to know whether universities are potentially hostile environments to conservatives. Examining culturally and economically oriented political orientations in Europe, it is demonstrated that professors are more liberal and left-leaning than other professionals. However, there is no greater homogeneity of political orientations among the professoriate relative to other specific professions, suggesting that there is a diversity of opinions which is similar to what professionals would find in other occupations. One exception concerns attitudes towards immigration, on which professors have more liberal orientations and comparatively low residual variance around that more liberal mean. Importantly, the difference between professors and other professionals is not so clear within graduates from the social sciences, but emerges more clearly among graduates with a medical, STEM, economics or law degree. An important political cleavage exists between professionals and managers, a group of similar social standing.

Impact of the Advanced Practice Provider in Adult Critical Care: A Systematic Review and Meta-Analysis.

OBJECTIVES: To evaluate the effects on quality and efficiency of implementation of the advanced practice provider in critical care. DATA SOURCES: PubMed, Embase, The Cochrane Library, and CINAHL were used to extract articles regarding advanced practice providers in critical care. STUDY SELECTION: Articles were selected when reporting a comparison between advanced practice providers and physician resident/fellows regarding the outcome measures of mortality, length of stay, or specific tasks. Descriptive studies without comparison were excluded. The methodological quality of the included studies was rated using the Newcastle-Ottawa scale. The agreement between the reviewers was assessed with Cohen's kappa. A meta-analysis was constructed on mortality and length of stay. DATA EXTRACTION AND SYNTHESIS: One-hundred fifty-six studies were assessed by full text. Thirty comparative cohort studies were selected and analyzed. These compared advanced practice providers with physician resident/fellows. All studies comprised adult intensive care. Most of the included studies showed a moderate to good quality. Over time, the study designs advanced from retrospective designs to include prospective and comparative designs. DATA SYNTHESIS: Four random effects meta-analyses on length of stay and mortality were constructed from the available studies. These meta-analyses showed no significant difference between performance of advanced practice providers on the ICU and physician residents/fellows on the ICU, suggesting the quality of care of both groups was equal. Mean difference for length of stay on the ICU was 0.34 (95% CI, -0.31 to 1.00; I = 99%) and for in hospital length of stay 0.02 (95% CI, -0.85 to 0.89; I = 91%); whereas the odds ratio for ICU mortality was 0.98 (95% CI, 0.81-1.19; I = 37.3%) and for hospital mortality 0.92 (95% CI, 0.79-1.07; I = 28%). CONCLUSIONS: This review and meta-analysis shows no differences between acute care given by advanced practice providers compared with physician resident/fellows measured as length of stay or mortality. However, advanced practice providers might add value to care in several other ways, but this needs further study.

Comparing peri-operative complications of paediatric and adult anaesthesia: A retrospective cohort study of 81 267 cases.

BACKGROUND: Comparisons of peri-operative complications associated with paediatric (≤16 years) and adult anaesthesia are poorly available, especially in which cardiac surgery, organ transplantation and neurosurgery are involved. OBJECTIVE: The aim of this study was to evaluate the nature and incidence of peri-operative complications that might be due to anaesthesia and to identify independent risk factors for complications in children and adults, including those undergoing cardiac surgery, organ transplantation and neurosurgery. DESIGN: Retrospective cohort study. SETTING: The study was performed at the University Medical Centre Groningen in the 4 years between 1 January 2010 and the 31 December 2013. MAIN OUTCOME MEASURES: Complications and their severity were graded according to the standard complication score (20 items) of the Dutch Society of Anaesthesia. Univariate and multivariate regression analysis was used to identify independent risk factors for the reported complications. RESULTS: A total of 81 267 anaesthetic cases were included. In the paediatric cohort, there were 410 (2.9%) complications and 1675 (2.5%) in the adults. In both cohorts age, American Society of Anaesthesiologists classification and emergency treatment were independent risk factors for complications. With respect to age, infants less than 1 year were at the highest risk, whereas in the adult cohort, increased age was related to a greater number of complications. The incidences of the specific complications were different between both cohorts. Upper airway obstruction was more frequently observed in paediatric patients (26%), whereas in the adults, complications with the highest incidence concerned conversion of regional-to-general anaesthesia (25%) and hypotension (17%). CONCLUSION: Risk factors for all peri-operative complications were similar for paediatric and adult anaesthesia. However, the incidence of specific complications differed between both age categories.

Upper tropospheric water vapour and its interaction with cirrus clouds as seen from IAGOS long-term routine in situ observations.

IAGOS (In-service Aircraft for a Global Observing System) performs long-term routine in situ observations of atmospheric chemical composition (O3, CO, NOx, NOy, CO2, CH4), water vapour, aerosols, clouds, and temperature on a global scale by operating compact instruments on board of passenger aircraft. The unique characteristics of the IAGOS data set originate from the global scale sampling on air traffic routes with similar instrumentation such that the observations are truly comparable and well suited for atmospheric research on a statistical basis. Here, we present the analysis of 15 months of simultaneous observations of relative humidity with respect to ice (RHice) and ice crystal number concentration in cirrus (Nice) from July 2014 to October 2015. The joint data set of 360 hours of RHice-Nice observations in the global upper troposphere and tropopause region is analysed with respect to the in-cloud distribution of RHice and related cirrus properties. The majority of the observed cirrus is thin with Nice < 0.1 cm-3. The respective fractions of all cloud observations range from 90% over the mid-latitude North Atlantic Ocean and the Eurasian Continent to 67% over the subtropical and tropical Pacific Ocean. The in-cloud RHice distributions do not depend on the geographical region of sampling. Types of cirrus origin (in situ origin, liquid origin) are inferred for different Nice regimes and geographical regions. Most importantly, we found that in-cloud RHice shows a strong correlation to Nice with slightly supersaturated dynamic equilibrium RHice associated with higher Nice values in stronger updrafts.

Use of Postoperative Peak Arterial Lactate Level to Predict Outcome After Cardiac Surgery.

OBJECTIVES: In the present study, the authors investigated the predictive value of postoperative peak arterial lactate levels for early and late mortality after cardiac surgery. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Single-center study in an academic hospital. PARTICIPANTS: Adult patients who underwent cardiac surgery between 2004 and 2014 (n = 16,376). INTERVENTIONS: Different cardiac surgical procedures. MEASUREMENTS AND RESULTS: Patients were classified according to the peak arterial lactate level (PALL) within 3 days postoperatively. Logistic regression analysis and Cox regression analysis were performed to identify postoperative peak arterial lactate level as a predictor for early and late mortality respectively. In 8460 patients (51.7%), lactate was not measured postoperatively because these patients were managed according to the fast-track protocol. These patients constituted group 1 in our population but were excluded from the regression analysis. The remaining patients (n = 7,916; 48.3%) were divided according to the postoperative peak arterial lactate level (PALL): PALL<5 mmol/L (group 2), PALL 5 to 10 mmol/L (group 3), and PALL of>10 mmol/L (group 4). Early mortality was 3.7%, 20.4%, and 62.9% in groups 2, 3, and 4 respectively (p<0.0001). This mortality rate was significantly higher than that of group 1 (1.6%); p<0.0001. Multivariate regression analyses revealed postoperative peak arterial lactate as a significant predictor of 30-day mortality (odds ratio = 1.44 [1.39-1.48], p<0.001) as well as for late mortality (hazard ratio = 1.05 [1.01-1.10], p<0.025). CONCLUSIONS: Postoperative peak arterial lactate level in patients undergoing cardiac surgery is an independent predictor for both early and late mortality.

Nox2 mediates skeletal muscle insulin resistance induced by a high fat diet.

Inflammation and oxidative stress through the production of reactive oxygen species (ROS) are consistently associated with metabolic syndrome/type 2 diabetes. Although the role of Nox2, a major ROS-generating enzyme, is well described in host defense and inflammation, little is known about its potential role in insulin resistance in skeletal muscle. Insulin resistance induced by a high fat diet was mitigated in Nox2-null mice compared with wild-type mice after 3 or 9 months on the diet. High fat feeding increased Nox2 expression, superoxide production, and impaired insulin signaling in skeletal muscle tissue of wild-type mice but not in Nox2-null mice. Exposure of C2C12 cultured myotubes to either high glucose concentration, palmitate, or H2O2 decreases insulin-induced Akt phosphorylation and glucose uptake. Pretreatment with catalase abrogated these effects, indicating a key role for H2O2 in mediating insulin resistance. Down-regulation of Nox2 in C2C12 cells by shRNA prevented insulin resistance induced by high glucose or palmitate but not H2O2. These data indicate that increased production of ROS in insulin resistance induced by high glucose in skeletal muscle cells is a consequence of Nox2 activation. This is the first report to show that Nox2 is a key mediator of insulin resistance in skeletal muscle.

Salvage of Monoblock Metal-on-Metal Acetabular Components Using a Dual-Mobility Bearing.

BACKGROUND: Large-diameter, monoblock acetabular components have been used for both hip resurfacing arthroplasty and metal-on-metal (MoM) total hip arthroplasty (THA). If revision is required, one solution is to retain the shell and use a dual-mobility bearing. METHODS: We reviewed the results of 25 revision THAs including 11 hip resurfacing arthroplasty and 14 MoM THAs where a monoblock acetabular component was mated to a dual-mobility bearing. RESULTS: At a mean of 29 months, there was one failure, an intraprosthetic dislocation of the dual-mobility bearing. There was a significant decrease in serum metal ion levels postoperatively. CONCLUSION: Retention of a well-fixed, monoblock MoM acetabular shell and mating it to a dual-mobility bearing in the setting of revision surgery seems to be a reasonable, low-morbidity option at short-term follow-up in appropriately positioned cups.

Alternating Hemiplegia of Childhood mutations have a differential effect on Na(+),K(+)-ATPase activity and ouabain binding.

De novo mutations in ATP1A3, the gene encoding the α3-subunit of Na(+),K(+)-ATPase, are associated with the neurodevelopmental disorder Alternating Hemiplegia of Childhood (AHC). The aim of this study was to determine the functional consequences of six ATP1A3 mutations (S137Y, D220N, I274N, D801N, E815K, and G947R) associated with AHC. Wild type and mutant Na(+),K(+)-ATPases were expressed in Sf9 insect cells using the baculovirus expression system. Ouabain binding, ATPase activity, and phosphorylation were absent in mutants I274N, E815K and G947R. Mutants S137Y and D801N were able to bind ouabain, although these mutants lacked ATPase activity, phosphorylation, and the K(+)/ouabain antagonism indicative of modifications in the cation binding site. Mutant D220N showed similar ouabain binding, ATPase activity, and phosphorylation to wild type Na(+),K(+)-ATPase. Functional impairment of Na(+),K(+)-ATPase in mutants S137Y, I274N, D801N, E815K, and G947R might explain why patients having these mutations suffer from AHC. Moreover, mutant D801N is able to bind ouabain, whereas mutant E815K shows a complete loss of function, possibly explaining the different phenotypes for these mutations.

Biochemical characterization of sporadic/familial hemiplegic migraine mutations.

Sporadic hemiplegic migraine type 2 (SHM2) and familial hemiplegic migraine type 2 (FHM2) are rare forms of hemiplegic migraine caused by mutations in the Na(+),K(+)-ATPase α2 gene. Today, more than 70 different mutations have been linked to SHM2/FHM2, randomly dispersed over the gene. For many of these mutations, functional studies have not been performed. Here, we report the functional characterization of nine SHM2/FHM2 linked mutants that were produced in Spodoptera frugiperda (Sf)9 insect cells. We determined ouabain binding characteristics, apparent Na(+) and K(+) affinities, and maximum ATPase activity. Whereas membranes containing T345A, R834Q or R879W possessed ATPase activity significantly higher than control membranes, P796S, M829R, R834X, del 935-940 ins Ile, R937P and D999H membranes showed significant loss of ATPase activity compared to wild type enzyme. Further analysis revealed that T345A and R879W showed no changes for any of the parameters tested, whereas mutant R834Q possessed significantly decreased Na(+) and increased K(+) apparent affinities as well as decreased ATPase activity and ouabain binding. We hypothesize that the majority of the mutations studied here influence interdomain interactions by affecting formation of hydrogen bond networks or interference with the C-terminal ion pathway necessary for catalytic activity of Na(+),K(+)-ATPase, resulting in decreased functionality of astrocytes at the synaptic cleft expressing these mutants.

Familial hemiplegic migraine mutations affect Na,K-ATPase domain interactions.

Familial hemiplegic migraine (FHM) is a monogenic variant of migraine with aura. One of the three known causative genes, ATP1A2, which encodes the α2 isoform of Na,K-ATPase, causes FHM type 2 (FHM2). Over 50 FHM2 mutations have been reported, but most have not been characterized functionally. Here we study the molecular mechanism of Na,K-ATPase α2 missense mutations. Mutants E700K and P786L inactivate or strongly reduce enzyme activity. Glutamic acid 700 is located in the phosphorylation (P) domain and the mutation most likely disrupts the salt bridge with Lysine 35, thereby destabilizing the interaction with the actuator (A) domain. Mutants G900R and E902K are present in the extracellular loop at the interface of the α and ß subunit. Both mutants likely hamper the interaction between these subunits and thereby decrease enzyme activity. Mutants E174K, R548C and R548H reduce the Na(+) and increase the K(+) affinity. Glutamic acid 174 is present in the A domain and might form a salt bridge with Lysine 432 in the nucleotide binding (N) domain, whereas Arginine 548, which is located in the N domain, forms a salt bridge with Glutamine 219 in the A domain. In the catalytic cycle, the interactions of the A and N domains affect the K(+) and Na(+) affinities, as observed with these mutants. Functional consequences were not observed for ATP1A2 mutations found in two sporadic hemiplegic migraine cases (Y9N and R879Q) and in migraine without aura (R51H and C702Y).

Na(+),K(+)-ATPase isoform selectivity for digitalis-like compounds is determined by two amino acids in the first extracellular loop.

Digitalis-like compounds (DLCs) comprise a diverse group of molecules characterized by a cis-trans-cis ring-fused steroid core linked to a lactone. They have been used in the treatment of different medical problems including heart failure, where their inotropic effect on heart muscle is attributed to potent Na(+),K(+)-ATPase inhibition. Their application as drugs, however, has declined in recent past years due to their small safety margin. Since human Na(+),K(+)-ATPase is represented by four different isoforms expressed in a tissue-specific manner, one of the possibilities to improve the therapeutic index of DLCs is to exploit and amend their isoform selectivity. Here, we aimed to reveal the determinants of selectivity of the ubiquitously expressed α1 isoform and the more restricted α2 isoform toward several well-known DLCs and their hydrogenated forms. Using baculovirus to express various mutants of the α2 isoform, we were able to link residues Met(119) and Ser(124) to differences in affinity between the α1 and α2 isoforms to ouabain, dihydro-ouabain, digoxin, and dihydro-digoxin. We speculate that the interactions between these amino acids and DLCs affect the initial binding of these DLCs. Also, we observed isoform selectivity for DLCs containing no sugar groups.

Solute diffusion is hindered in the mitochondrial matrix.

Intracellular chemical reactions generally constitute reaction-diffusion systems located inside nanostructured compartments like the cytosol, nucleus, endoplasmic reticulum, Golgi, and mitochondrion. Understanding the properties of such systems requires quantitative information about solute diffusion. Here we present a novel approach that allows determination of the solvent-dependent solute diffusion constant (D(solvent)) inside cell compartments with an experimentally quantifiable nanostructure. In essence, our method consists of the matching of synthetic fluorescence recovery after photobleaching (FRAP) curves, generated by a mathematical model with a realistic nanostructure, and experimental FRAP data. As a proof of principle, we assessed D(solvent) of a monomeric fluorescent protein (AcGFP1) and its tandem fusion (AcGFP1(2)) in the mitochondrial matrix of HEK293 cells. Our results demonstrate that diffusion of both proteins is substantially slowed by barriers in the mitochondrial matrix (cristae), suggesting that cells can control the dynamics of biochemical reactions in this compartment by modifying its nanostructure.

Subunit-specific incorporation efficiency and kinetics in mitochondrial complex I homeostasis.

Studies employing native PAGE suggest that most nDNA-encoded CI subunits form subassemblies before assembling into holo-CI. In addition, in vitro evidence suggests that some subunits can directly exchange in holo-CI. Presently, data on the kinetics of these two incorporation modes for individual CI subunits during CI maintenance are sparse. Here, we used inducible HEK293 cell lines stably expressing AcGFP1-tagged CI subunits and quantified the amount of tagged subunit in mitoplasts and holo-CI by non-native and native PAGE, respectively, to determine their CI incorporation efficiency. Analysis of time courses of induction revealed three subunit-specific patterns. A first pattern, represented by NDUFS1, showed overlapping time courses, indicating that imported subunits predominantly incorporate into holo-CI. A second pattern, represented by NDUFV1, consisted of parallel time courses, which were, however, not quantitatively overlapping, suggesting that imported subunits incorporate at similar rates into holo-CI and CI assembly intermediates. The third pattern, represented by NDUFS3 and NDUFA2, revealed a delayed incorporation into holo-CI, suggesting their prior appearance in CI assembly intermediates and/or as free monomers. Our analysis showed the same maximum incorporation into holo-CI for NDUFV1, NDUFV2, NDUFS1, NDUFS3, NDUFS4, NDUFA2, and NDUFA12 with nearly complete loss of endogenous subunit at 24 h of induction, indicative of an equimolar stoichiometry and unexpectedly rapid turnover. In conclusion, the results presented demonstrate that newly formed nDNA-encoded CI subunits rapidly incorporate into holo-CI in a subunit-specific manner.

Na,K-ATPase activity modulates Src activation: a role for ATP/ADP ratio.

Digitalis-like compounds (DLCs), specific inhibitors of Na,K-ATPase, are implicated in cellular signaling. Exposure of cell cultures to ouabain, a well-known DLC, leads to up- or down regulation of various processes and involves activation of Src kinase. Since Na,K-ATPase is the only known target for DLC binding an in vitro experimental setup using highly purified Na,K-ATPase from pig kidney and commercially available recombinant Src was used to investigate the mechanism of coupling between the Na,K-ATPase and Src. Digoxin was used as a representative DLC for inhibition of Na,K-ATPase. The activation of Src kinase was measured as the degree of its autophosphorylation. It was observed that in addition to digoxin, Src activation was dependent on concentrations of other specific ligands of Na,K-ATPase: Na(+), K(+), vanadate, ATP and ADP. The magnitude of the steady-state ATPase activity therefore seemed to affect Src activation. Further experiments with an ATP regenerating system showed that the ATP/ADP ratio determined the extent of Src activation. Thus, our model system which represents the proposed very proximal part of the Na,K-ATPase-Src signaling cascade, shows that Src kinase activity is regulated by both ATP and ADP concentrations and provides no evidence for a direct interaction between Na,K-ATPase and Src.

Metabolic consequences of NDUFS4 gene deletion in immortalized mouse embryonic fibroblasts.

Human mitochondrial complex I (CI) deficiency is associated with progressive neurological disorders. To better understand the CI pathomechanism, we here studied how deletion of the CI gene NDUFS4 affects cell metabolism. To this end we compared immortalized mouse embryonic fibroblasts (MEFs) derived from wildtype (wt) and whole-body NDUFS4 knockout (KO) mice. Mitochondria from KO cells lacked the NDUFS4 protein and mitoplasts displayed virtually no CI activity, moderately reduced CII, CIII and CIV activities and normal citrate synthase and CV (F(o)F(1)-ATPase) activity. Native electrophoresis of KO cell mitochondrial fractions revealed two distinct CI subcomplexes of ~830kDa (enzymatically inactive) and ~200kDa (active). The level of fully-assembled CII-CV was not affected by NDUFS4 gene deletion. KO cells exhibited a moderately reduced maximal and routine O(2) consumption, which was fully inhibited by acute application of the CI inhibitor rotenone. The aberrant CI assembly and reduced O(2) consumption in KO cells were fully normalized by NDUFS4 gene complementation. Cellular [NAD(+)]/[NADH] ratio, lactate production and mitochondrial tetramethyl rhodamine methyl ester (TMRM) accumulation were slightly increased in KO cells. In contrast, NDUFS4 gene deletion did not detectably alter [NADP(+)]/[NADPH] ratio, cellular glucose consumption, the protein levels of hexokinases (I and II) and phosphorylated pyruvate dehydrogenase (P-PDH), total cellular adenosine triphosphate (ATP) level, free cytosolic [ATP], cell growth rate, and reactive oxygen species (ROS) levels. We conclude that the NDUFS4 subunit is of key importance in CI stabilization and that, due to the metabolic properties of the immortalized MEFs, NDUFS4 gene deletion has only modest effects at the live cell level. This article is part of a special issue entitled: 17th European Bioenergetics Conference (EBEC 2012).