New York State Teacher Salary Report

Teachers are central to the success of any education system and the salaries paid to teachers are among the most important issues for both school districts and the unions that represent teachers. For school districts, teacher salaries are a major com- ponent of district budgets. Teacher salary levels are also a crucial factor in attracting and retaining quality educators. This report presents data on teacher salary levels based on teacher contracts throughout New York State. In addition to reporting overall statewide salary levels, it also documents the wide variation in teacher salary levels across New York State. This New York State Teacher Salary Report was prepared by the Bargaining for Better Schools (BBS) project, which is an initiative of the ILR School at Cornell University through the Scheinman Institute on Conflict Resolution and the Worker Institute. The data provided in this report comes from an analysis of the teacher contracts from every school district in the State of New York. The database of information came from two sources, both of which are publicly available on websites: DigitalCommons at ILR and SeeThroughNY, each of which contain the full text of teacher contracts, i.e. collective bargaining agreements and asso- ciated memoranda of understanding. The most recent contract from either website was selected for inclusion in this data

Konservierte und nicht-konservierte Funktionen der Lef/Tcf Transkriptionsfaktoren

Die Lef/Tcf Transkriptionsfaktoren sind die nukleären Mediatoren des Wnt-Signalwegs. In allen bisher untersuchten Invertebraten liegt je nur ein Ortholog vor. Dagegen sind in Vertebraten vier distinkte Vertreter der Lef/Tcfs zu finden, Lef-1, Tcf-1, Tcf-3 und Tcf-4. Diese weisen spezifische aber auch redundante Funktionen auf. Die funktionale Analyse in Xenopus sowie in Drosophila ergab, dass diese Transkriptionsfaktoren durch das evolutionäre Prinzip der Subfunktionalisierung entstanden sind

A novel role for the tumour suppressor Nitrilase1 modulating the Wnt/β-catenin signalling pathway

Nitrilase1 was classified as a tumour suppressor in association with the fragile histidine-triad protein Fhit. However, knowledge about nitrilase1 and its tumour suppressor function is still limited. Whereas nitrilase1 and Fhit are discrete proteins in mammals, they are merged in Drosophila melanogaster and Caenorhabditis elegans. According to the Rosetta-Stone hypothesis, proteins encoded as fusion proteins in one organism and as separate proteins in another organism may act in the same signalling pathway. Although a direct interaction of human nitrilase1 and Fhit has not been shown, our previous finding that Fhit interacts with β-catenin and represses its transcriptional activity in the canonical Wnt pathway suggested that human nitrilase1 also modulates Wnt signalling. In fact, human nitrilase1 forms a complex with β-catenin and LEF-1/TCF-4, represses β-catenin-mediated transcription and shows an additive effect together with Fhit. Knockdown of human nitrilase1 enhances Wnt target gene expression. Moreover, our experiments show that β-catenin competes away human nitrilase1 from LEF-1/TCF and thereby contributes to the activation of Wnt-target gene transcription. Inhibitory activity of human nitrilase1 on vertebrate Wnt signalling was confirmed by repression of Wnt-induced double axis formation in Xenopus embryogenesis. In line with this finding, the Drosophila fusion protein Drosophila NitFhit directly binds to Armadillo and represses the Wingless pathway in reporter gene assays. Genetic experiments confirmed the repressive activity of Drosophila NitFhit on Wingless signalling in the Drosophila wing imaginal disc. In addition, colorectal tumour microarray analysis revealed a significantly reduced expression of human nitrilase1 in poorly differentiated tumours. Taken together, repression of the canonical Wnt pathway represents a new mechanism for the human nitrilase1 tumour suppressor function

Left Ventricular Physiology and Ventricular‐Vascular Interactions in Young Patients After Heart Transplantation

Background In patients after heart transplantation, systemic arterial hypertension and enhanced central aortic stiffness contribute to increased ventricular afterload, which might lead to graft dysfunction. The aim of our study was to characterize systemic arterial elastance and its impact on left ventricular function and ventriculo‐arterial coupling in a cohort of children, adolescents, and young adults after heart transplantation using invasive conductance catheter technique. Methods and Results Thirty patients who had heart transplants (age, 20.0±6.5 years, 7 female) underwent invasive cardiac catheterization including pressure‐volume loop analysis. Load‐independent parameters of systolic (ventricular elastance [Ees]) and diastolic (ventricular compliance) function as well as systemic arterial elastance (Ea, end‐systolic pressure/stroke volume) and ventriculo‐arterial coupling (Ea/Ees) were assessed at baseline level and during dobutamine infusion (10 μg/kg/min). Ees showed an appropriate increase under inotropic stimulation from 0.43 (0.11–2.52) to 1.00 (0.20–5.10) mm Hg/mL/m2 (P<0.0001), whereas ventricular compliance remained rather unchanged (0.16±0.10 mm Hg/mL/m2 to 0.12±0.07 mm Hg/mL/m2; P=0.10). Ventriculo‐arterial coupling Ea/Ees was abnormal at rest and did not improve significantly under dobutamine (1.7 [0.6–6.7] to 1.3 [0.5–4.9], P=0.70) due to a simultaneous rise in Ea from 0.71 (0.37–2.82) to 1.10 (0.52–4.03) mm Hg/mL/m2 (P<0.0001). Both Ees and ventricular compliance were significantly associated with Ea at baseline and under dobutamine infusion. Conclusions Patients who underwent heart transplantation show impaired ventriculo‐arterial coupling at rest and under inotropic stimulation despite preserved left ventricular contractile reserve. An abnormal response in vascular function resulting in increased afterload seems to represent an important factor that may play a role for the development of late graft failure

Parvovirus B19-induced vascular damage in the heart is associated with elevated circulating endothelial microparticles

<div><p>Background</p><p>Diagnosis of viral myocarditis is difficult by clinical criteria but facilitated by detection of inflammation and viral genomes in endomyocardial biopsies. Parvovirus B19 (B19V) targets endothelial cells where viral nucleic acid is exclusively detected in the heart. Microparticles (MPs) are released after cell damage or activation of specific cells. We aimed to investigate whether circulating endothelial MPs (EMPs) in human and experimental models of myocarditis are associated with B19V myocarditis.</p><p>Methods</p><p>MPs were investigated in patients with myocarditis (n = 54), divided into two groups: B19V+ (n = 23) and B19V- (n = 31) and compared with healthy controls (HCTR, n = 25). MPs were also investigated in B19V transgenic mice (B19V-NS1+) and mice infected with coxsackievirus B3 (CVB3). MPs were analyzed with fluorescent activated cell sorting (FACS).</p><p>Results</p><p>In human samples, EMP subpopulation patterns were significantly different in B19V+ compared to B19V- and HCTR (p<0.001), with an increase of apoptotic but not activated EMPs. Other MPs such as platelet- (PMPs) leukocyte-(LMPs) and monocyte-derived MPs (MMPs) showed less specific patterns. Significantly different levels of EMPs were observed in transgenic B19V-NS1+ mice compared with CVB3-infected mice (p<0.001).</p><p>Conclusion</p><p>EMP subpopulations are different in B19V+ myocarditis in humans and transgenic B19V mice reflecting vascular damage. EMP profiles might permit differentiation between endothelial-cell-mediated diseases like myocardial B19V infection and other causes of myocarditis.</p></div

Murine endothelial microparticles (CVB3+ infected mice).

<p>Murine endothelial microparticles (EMPs) in CVB3+ infected mice (CVB3+) after 2, 8 and 28 days p.i. compared with controls (C57/Bl6). A: EMPs were increased in CVB3+ mice two days p.i. (p<0.001 vs. control) with a decline in the following 6 days (p<0.001 vs. control) and 28 days p.i. (p<0.001 vs. control). B: The increase of EMPs was due to apoptotic EMPs. C: Activated EMPs were not different between the groups.</p

Murine endothelial microparticles (B19V- transgenic mice).

<p>Murine endothelial microparticles (EMPs) in transgenic B19V-NS1-mice with induction by doxycycline (B19V+) after 2, 4 and 6 weeks p.i. compared with controls (C57/Bl6 and transgenic B19V-NS1 mice without doxycyclin). A: EMPs in C57/Bl6 mice compared to transgenic B19V-NS1-mice without doxycyclin showed about the same EMP numbers (p = 0.775). EMPs were significantly increased in transgenic B19V-NS1-mice with doxycyclin after 2, 4 and 6 weeks compared to controls such as C57/Bl6 (p<0.001) and transgenic B19V-NS1-mice without doxycylin (p<0.001, p = 0.003 and p = 0.029). The increase had its maximum after two weeks with a decline after four weeks. B: The increase of EMPs was due to apoptotic EMPs. C: Activated EMPs were not different between the groups.</p

Clinical parameters of human samples.

<p>Clinical parameters of human samples.</p