The Investment Decision in the Central City: A Consideration of a Property Tax Abatement Law

This article addresses an indirect policy approach to handling gray areas in large central cities where dilapidated and deteriorated housing go unresolved. Rather than focusing on abandonment and rebuilding, the article looks to fostering renewal of existing structures through property tax abatement programs. Using Pittsburgh as a model and experience to outline the framework for such a program, the article attempts to enhance ones understanding of the economic impacts that a property tax can have on the condition of city housing. The article concludes that for any city to embark on a tax abatement policy, it must understand the conditions necessary for success

FOCAL ADHESION KINASE INVOLVEMENT IN MODULATING THE PROLIFERATION OF TUMOR CELLS.

The focal adhesion kinase (FAK) is well characterized non-receptor tyrosine kinase, although it undergoes also to phosphorylation on serine residues whose role is not fully understood. FAK is ubiquitously expressed and plays a crucial role as integrator of signaling from either integrins or Receptor Tyrosine Kinases (RTKs) and has been linked to cell transformation and progression in many solid tumors. Among those, the Epithelial Ovarian Cancer (EOC) has a different behaviour during progression: it rarely metastasizes to distant sites but disseminate within the peritoneal cavity. Our attention was focused on the characterization of the role of FAK in different type of tumor cells and in particular on the phosphorylation (P) on the serine 732 of FAK (P-FAKSer732). We found that P-FAKSer732 was present at variable levels in cancer cell lines but its activation was independent from integrin engagement and from the kinase activity of FAK. P-FAKSer732 was not localized at the focal adhesion site during migration but it was accumulated in dividing cells, co-localizing with the tubulin of the spindle during mitosis and regulating microtubule (MT) polymerization and mitotic spindle formation. CDK5 was identified as the specific kinase responsible for FAK serine phosphorylation whose activation was induced by EGF stimulation of the EGFR/ERK signalling. Thus, we have identified for the first time the axis EGFR/MEK/ERK/CDK5/P-FAKSer732 as a novel pathway leading to mitosis of tumor cells. We next aimed to identify the mechanism governing the crosstalk between adhesion molecules and RTKs thus leading to proliferation, migration and invasion of tumor cells. I focused my analysis on EOC which is the main cancer histotype studied in our laboratory. We therefore investigated in EOC cells a possible role of E-cadherin (cadh) to contribute to the novel signalling pathway described above. Indeed, we found that E-cadh was the adhesion molecule necessary for the formation of the EOC multi-cellular aggregates (MCAs) present in the ascites. The E-cadh and CDK5 resulted to be necessary to the generation of FAKSer732 and this protein complex was necessary for the EGF-mediated EGFR activation likely due to the stabilization of EGFR protein on the cell membrane. In line with these results, E-cadh expressing EOC cells were more susceptible to the CDK5 inhibitor, roscovitine. These data demonstrated a pivotal role of E-cadh in contributing to the proliferation of EOC MCAs. To clarify the processes responsible for the switch from a proliferative to a more invasive phenotype of EOC MCAs necessary for tumor dissemination, we were studied another RTK, Axl whose expression has been already reported to be associated to a more invasive phenotype. We found that the stimulation of Axl by its ligand Gas6 required the engagement of \u3b23-integrin with components of the extra-cellular matrix (ECM). The crosstalk between Gas6/Axl and the integrin signallings was independent by FAK but required the contribution of p130Cas, a scaffold protein involved in the transmission of the ECM-integrin signalling, for adhesion, migration and invasion of EOC cells. Indeed, the lack of p130Cas decreased the level of Gas6-dependent Axl activation and inhibited Gas6-induced EOC cells adhesion, migration and invasion. In 56 out of 72 EOC biopsies, Axl and p130Cas were significantly co-expressed indicating of a collaborative signaling between Axl and p130Cas also in vivo. We have identified an Axl signalling which requires a p130Cas-mediated crosstalk with integrins for the dissemination of EOCs. Altogether, our investigation allowed the definition of two novel adhesion-dependent signalling pathways which drive the proliferation and the invasion of EOC cells, respectively. The inhibition of these pathways will likely affect EOC MCA growth as well as the invasion of EOC solid primary and secondary lesions

Evidence for clonal selection of gamma/delta T cells in response to a human pathogen.

T cells bearing gamma/delta antigen receptors comprise a resident population of intraepithelial lymphocytes in organs such as skin, gut, and lungs, where they are strategically located to contribute to the initial defense against infection. An important unsolved question about antigen-driven gamma/delta T cell responses regards the breadth of their T cell receptor (TCR) repertoire, since many specific epithelial compartments in mice display limited diversity. We have examined the diversity of TCR delta gene expression among human gamma/delta T cells from skin lesions induced by intradermal challenge with Mycobacterium leprae. We show that the vast majority of gamma/delta cells from M. leprae lesions use either V delta 1-J delta 1 or V delta 2-J delta 1 gene rearrangements and, within a given region of the lesion, display limited junctional diversity. This contrasts markedly with the extensive diversity of gamma/delta T cells from peripheral blood of these same individuals, as well as skin from normal donors. These results indicate that the gamma/delta response to M. leprae involves the selection of a limited number of clones from among a diverse repertoire, probably in response to specific mycobacterial and/or host antigens

The NSF and the geosciences community: Rotating program officers

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95447/1/eost7407.pd

Performance of the ADAPT-Treated CardioCel® Scaffold in pediatric patients with congenital cardiac anomalies: Medium to Long-Term outcomes

Background: A Phase II Clinical Trial reviewed the performance (morbidity and calcification) of the tissue-engineered ADAPT® bovine pericardial scaffold (CardioCel®) in pediatric patients (n = 30) with congenital cardiac defects. In that study, CardioCel® demonstrated no graft-related morbidity and mortality in 25 patients, over 12 months. Five patients died due to non-graft-related events. Echocardiography revealed hemodynamically stable repairs with no calcification of the scaffold. Magnetic resonance imaging (MRI) at 12 months in 10 patients confirmed the absence of calcification. These patients were followed up for further up to 10 years. We present the results of this retrospective review of these patients that were followed for further medium to long-term (median 7.2 years, 25%: 3.6 years 75%: 9.25 years) postoperatively in these patients. Methods: Between April 2008 and September 2009, CardioCel® was implanted in 30 patients with congenital cardiac defects. Efficacy measures included graft-related mortality, morbidity and haemodynamic abnormalities. Calcification was assessed by standard 2D-M mode echocardiography and MRI at 12 months. Medium to long-term assessment included routine clinical assessments and echocardiography. Results: Median age at surgery was 18 months (27 days−13 years). Twenty-five patients (142 patient years) were followed for up to 10 years. The 10-year survival rate is estimated as 86.9% (95% CI 71.4–100.0%) over the entire follow-up period. One patient was lost to follow-up. No graft-related mortality was encountered up to a median follow-up of 7.2 years. Two patients died (pacemaker complications >5 years and arrhythmia >7 years postoperatively). No graft failure, thromboembolic events, infections or device-related reinterventions were recorded. Non-significant residual leaks occurred in 3 patients. Echocardiography demonstrated the absence of calcification in all implants. Conclusion: The tissue-engineered ADAPT® bovine pericardial scaffold demonstrated excellent medium to long-term performance (up to 10 years) when used as a scaffold for repair of congenital cardiac defects in children. Durability, acellularity, biostability and non-calcifying potential of CardioCel® makes it a very attractive tissue for congenital cardiac repair procedures

A variable absorption feature in the X-ray spectrum of a magnetar

Soft gamma-ray repeaters (SGRs) and anomalous X-ray pulsars (AXPs) are slowly rotating, isolated neutron stars that sporadically undergo episodes of long-term flux enhancement (outbursts) generally accompanied by the emission of short bursts of hard X-rays. This behaviour can be understood in the magnetar model, according to which these sources are mainly powered by their own magnetic energy. This is supported by the fact that the magnetic fields inferred from several observed properties of AXPs and SGRs are greater than - or at the high end of the range of - those of radio pulsars. In the peculiar case of SGR 0418+5729, a weak dipole magnetic moment is derived from its timing parameters, whereas a strong field has been proposed to reside in the stellar interior and in multipole components on the surface. Here we show that the X-ray spectrum of SGR 0418+5729 has an absorption line, the properties of which depend strongly on the star's rotational phase. This line is interpreted as a proton cyclotron feature and its energy implies a magnetic field ranging from 2E14 gauss to more than 1E15 gauss.Comment: Nature, 500, 312 (including Supplementary Information

Buying a herd boar

John W. Massey, R. K. Leavitt and John C. Rea (Department of Animal Science, College of Agriculture)Revised 12/81/8

Buying a herd boar

R. K. Leavitt, John C. Rea and John W. Massey (Department of Animal Husbandry, College of Agriculture)Rev. 5/78/10

An Innovative Approach to Action Research in Family Violence Prevention

Violence prevention remains a priority in the current public health agenda because of continuing high rates and debilitating effects of violence that exist across the globe (U.S. Department of Health and Human Services, Administration on Children, Youth and Families [USDHHS-ACF], 2009; World Health Organization [WHO], 2013). This article presents the use of an innovative qualitative study developed from community action research methods in the area of family violence. By applying the combined framework of force field analysis (Lewin, 1958) and the public health model (Centers for Disease Control, 2002; Knox & Aspy, 2011), the current study identified factors that positively and negatively influenced the ability of family violence prevention practitioners to apply research to their practice. Results from the current study led to the development of an action plan to increase the application of research to practice in the area of family violence prevention programming