Three-dimensional modular electronic interconnection system

A three-dimensional connection system uses a plurality of printed wiring boards with connectors completely around the printed wiring boards, and connected by an elastomeric interface connector. The device includes internal space to allow room for circuitry. The device is formed by stacking an electronics module, an elastomeric interface board on the electronics module such that the interface board's exterior makes electrical connection with the connectors around the perimeter of the interface board, but the internal portion is open to allow room for the electrical devices on the printed wiring board. A plurality of these devices are stacked between a top stiffener and a bottom device, and held into place by alignment elements

- INTER - An Examination of Potential

Nothing exists that we cannot perceive, nothing is ours that we have not made, and nothing has meaning that we have not given. In order to foster a more active participation in the collaborative act of creation in which mankind engages every day, we must engage in art practices that are completely dependent on interaction and investment. The value of artwork is not derived from its original material but from the energy invested in it and the significance that it gathers from each hand through which it passes. None of us exists in vacuum; instead, all creation relies on collaboration and exterior influence. Rather than try to isolate ourselves as individuals, we should embrace our dependency on the environment and each other. Our goal is not to make things that are new but to make anew that which already exists in our hands, our minds, and our hearts. As Roland Barthes famously said, “The author is dead.” He was born out of capitalism and a desire to protect a monetary claim to creative endeavors, distinction between those who appreciate art and those who profit from it. But in a post-industrial society, where tools of creation are widely available, the distinction between author and reader disappears completely. This allows us to see that which has always been true, that ownership of ideas does not exist. As any true creator knows, it is the integrity of the creation that matters. Rightness takes precedence over the artist\u27s ego, popular trends, personal whim, or even societal prescription. Thus it becomes imperative to make work that is larger than the self and that serves the greater society at large. But before we presume to do good for a community, we must first become part of that community. Before we reach out to the marginalized or estranged, we must become estranged ourselves. Before we can help the needy, we must experience helplessness. In April of the year 2012, we engage in project called “INTER,” a seven-day collaboration between two artists and the inhabitants of Syracuse\u27s Near West Side where the artists live and work for the duration of the project. The artists arrive on site with no supplies or food of any kind and they are strictly forbidden from using money, phones, or computers for the entire week. Through face-to-face interactions, they attempt to establish networks and infrastructures built solely on human capital. Armed only with a guitar, a drum, a video camera, the artists have exactly one week – 168 hours – to install an entire body of work in and around the gallery at 601 Tully using only materials they receive through the generosity of the Near West Side. This project examines the potential of human generosity and intent. No one among us has the power to create a world in 7 days, but by working together we might be able to discover one. The artists are not autonomous creators of their own narratives but instruments of art-makery whose function is to transform the material and social potentials of the Near West Side into a work of art. The irony of this project, and of every project, is that nothing new is created. Material is undeniably transformed, but the true art of the work is the illumination of relationships and connections already in existence. The artifacts themselves are merely manifestations of these relationships. The only thing that is truly created is a chain of new relationships that will continue to support the INTER mission long after the project has ended. → www.johncardone.co

PRINCIPAL PERCEPTIONS OF FACTORS THAT CONTRIBUTED TO ACADEMIC ACHIEVEMENT IN HIGH-MINORITY HIGH SCHOOLS: A CASE STUDY

This study seeks to develop an explanation for academic achievement in schools that have a high-minority population. The New York State Education Department (NYSED) collects a tremendous amount of information on New York State (NYS) schools. For the purposes of this study, quantitative NYSED data on enrollment and English Language and Mathematics Regents Examination scores are analyzed. Fifteen high schools in Long Island, New York, have a minimum 80% minority rate. Most of the minority subgroups in the schools under analysis are Black or African American and Hispanic or Latin American. Four Long Island high schools were chosen because most of their minority students are Black or African American and Hispanic or Latin American and scored in the top 33% on their Common Core English Language Arts and Algebra Regents Examinations compared to the other 11 high-minority high schools. This researcher developed a survey interview tool that is used to interview principals of each high-minority high school within the study. The survey questions developed were guided by the researcher’s conceptual framework, which includes six essential components to student achievement, namely, leadership, student factors, professional learning community, instruction, family community involvement, and teacher factors. A collective case study is conducted which includes all the schools in the study, and the data gained is then analyzed via a convergent mixed-methods design. This study examines the effective characteristics in these schools that has led to their academic achievement. By analyzing the success experienced by these schools, we can identify commonalities and differences that have assisted in academic achievement in these schools compared to others, thereby developing a framework to assist school districts and enabling leaders to meet and exceed the challenges they face

Structure of a Protozoan Virus from the Human Genitourinary Parasite Trichomonas vaginalis

The flagellated protozoan Trichomonas vaginalis is an obligate human genitourinary parasite and the most frequent cause of sexually transmitted disease worldwide. Most clinical isolates of T. vaginalis are persistently infected with one or more double-stranded RNA (dsRNA) viruses from the genus Trichomonasvirus, family Totiviridae, which appear to influence not only protozoan biology but also human disease. Here we describe the three-dimensional structure of Trichomonas vaginalis virus 1 (TVV1) virions, as determined by electron cryomicroscopy and icosahedral image reconstruction. The structure reveals a T = 1 capsid comprising 120 subunits, 60 in each of two nonequivalent positions, designated A and B, as previously observed for fungal Totiviridae family members. The putative protomer is identified as an asymmetric AB dimer consistent with either decamer or tetramer assembly intermediates. The capsid surface is notable for raised plateaus around the icosahedral 5-fold axes, with canyons connecting the 2- and 3-fold axes. Capsid-spanning channels at the 5-fold axes are unusually wide and may facilitate release of the viral genome, promoting dsRNA-dependent immunoinflammatory responses, as recently shown upon the exposure of human cervicovaginal epithelial cells to either TVV-infected T. vaginalis or purified TVV1 virions. Despite extensive sequence divergence, conservative features of the capsid reveal a helix-rich fold probably derived from an ancestor shared with fungal Totiviridae family members. Also notable are mass spectrometry results assessing the virion proteins as a complement to structure determination, which suggest that translation of the TVV1 RNA-dependent RNA polymerase in fusion with its capsid protein involves −2, and not +1, ribosomal frameshifting, an uncommonly found mechanism to date

Asparaginyl endopeptidase (Legumain) supports human Th1 induction via cathepsin L-mediated intracellular C3 activation

Autocrine activation of the complement receptors C3aR and CD46 by complement activation components C3a and C3b produced through C3 cleavage by the protease cathepsin L (CTSL) during T cell stimulation is a requirement for IFN-γ production and Th1 induction in human CD4+ T cells. Thus, lack of autocrine CD46 activation, such as in CD46-deficient patients, is associated with defective Th1 responses and recurrent infections. We have identified LGMN [the gene coding for legumain, also known as asparaginyl endopeptidase (AEP)] as one of the key genes induced by CD46 co-stimulation during human CD4+ T cell activation. AEP processes and activates a range of proteins, among those α1-thymosin and CTSL, which both drive intrinsically Th1 activity—but has so far not been described to be functionally active in human T cells. Here we found that pharmacological inhibition of AEP during activation of human CD4+ T cells reduced CTSL activation and the CTSL-mediated generation of intracellular C3a. This translated into a specific reduction of IFN-γ production without affecting cell proliferation or survival. In line with these findings, CD4+ T cells isolated from Lgmn−/− mice also displayed a specific defect in IFN-γ secretion and Th1 induction. Furthermore, we did not observe a role for AEP-driven autocrine α1-thymosin activation in T cell-derived IFN-γ production. These data suggest that AEP is an “upstream” activator of the CTSL-C3-IFN-γ axis in human CD4+ T cells and hence an important supporter of human Th1 induction

A Novel Role for CD46 in Wound Repair

The intestinal epithelium not only provides a vital physical barrier between the host and environment but is also required for uptake of nutrients and the induction of tolerance against commensals. Deregulation of any of these functions leads to several disease states including chronic infection, inflammatory bowel disease, and cancer. Here, we describe a novel role for the complement regulator CD46 in the regulation of intestinal epithelial cell (IEC) barrier function. We found that CD46 directly interacts in IECs with the cytoplasmic kinase SPAK and with transmembrane E-cadherin, both proteins necessary for epithelial cell junction and barrier formation. Further, CD46 activation on Caco-2 cells induced rapid and significant decrease in transepithelial resistance with concomitant increase in paracellular permeability. Importantly, though CD46 activation of IEC layers allowed for increased transgression of pathogenic E. coli, it also increased epithelial cell proliferation and accelerated wound repair. These data suggest a previously unappreciated role for CD46 in the maintenance of epithelial cell barrier integrity as well as barrier repair. However, this role for CD46 as “gate keeper” of the epithelium could also provide reason as to why so many pathogens bind to CD46 as such event would facilitate infection

Dysfunctional CD39(POS) Regulatory T Cells and Aberrant Control of T-Helper Type 17 Cells in Autoimmune Hepatitis

Autoimmune hepatitis (AIH) is an important cause of severe liver disease and is associated with both quantitative and qualitative regulatory T-cell (Treg) impairments. Tregs express CD39, an ectonucleotidase responsible for extracellular nucleotide hydrolysis, culminating in the production of immunosuppressive adenosine. Here, we describe multiple CD39(pos) Treg defects that potentially contribute to the impaired immunoregulation that is characteristic of AIH. We have examined the frequency and phenotype of CD39(pos) Tregs by flow cytometry and measured their ectonucleotidase activity. The capacity of CD4(pos)CD25(high), CD4(pos)CD25(high)CD39(pos), and CD4(pos)CD25(high)CD39(neg) subsets to suppress both proliferation of effector T cells and interleukin (IL)-17 production was evaluated. In AIH, CD39(pos) Tregs are decreased in frequency, exhibit limited adenosine triphosphate/adenosine diphosphate hydrolysis activity, and fail to suppress IL-17 production by effector CD4 T cells. Moreover, these CD39(pos) Tregs display a more proinflammatory profile in AIH, which is characterized by elevated CD127 positivity, and a greater propensity to produce interferon-gamma or IL-17 upon challenge with proinflammatory stimuli. Conclusions: In AIH, CD39(pos) Tregs are decreased in number, fail to adequately hydrolyze proinflammatory nucleotides and do not efficiently suppress IL-17 production by effector CD4 T cells. CD39(pos) Tregs show plasticity and are unstable upon proinflammatory challenge, suggesting that defective immunoregulation in AIH might result not only from reduced Treg number and function, but also from increased conversion of Tregs into effector cells.</p

In autoimmune hepatitis type 1 or the autoimmune hepatitis-sclerosing cholangitis variant defective regulatory T-cell responsiveness to IL-2 results in low IL-10 production and impaired suppression

Defective immune regulation plays a permissive role enabling effector cells to initiate and perpetuate tissue damage, eventually resulting in autoimmune disease. Numerical and functional regulatory T-cell (Treg) impairment has been previously reported in autoimmune liver disease (AILD; including autoimmune hepatitis and autoimmune sclerosing cholangitis ASC). However, in these early reports, Tregs were phenotypically defined as CD4+CD25+ or CD4+CD25high cells. In the current study, we reexamined phenotypic and functional properties of Tregs by adopting a more refined definition of these cells that also includes negativity or low level of expression of CD127. We studied 43 AILD patients and 22 healthy subjects (HSs) and found that CD4+CD25+CD127− Tregs were decreased in the former. This decrease was more marked in patients with active disease than in those in remission. In AILD, Treg frequencies correlated inversely with parameters of disease activity and were not affected by immunosuppressive treatment. We also document, for the first time, that, in AILD, bona-fide Tregs produce less interleukin (IL)−10 and are impaired in their ability to suppress CD4+CD25− target cell proliferation, a feature that in HSs, but not in AILDs, is dependent, at least in part, on IL-10 secretion. Decreased IL-10 production by Tregs in AILD is linked to poor responsiveness to IL-2 and phospho signal transducer and activator of transcription 5 up-regulation. Conclusion: Tregs are numerically impaired in AILD, this impairment being more prominent during active disease. Notably, defective IL-10 production, resulting from low Treg responsiveness to IL-2, contributes to Treg functional impairment