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This chapter delves into critical components of the community building approach used by the EdTech team at Hostos Community College. These initiatives, such as iPads, lecture capture, ePortfolios together with the Bronx EdTech Showcase, are the focus of this chapter. The iPads initiative provided faculty with an opportunity to explore the true potential of mobile learning to improve the teaching and learning process in a classroom. The EdTech team also developed the lecture-capture system to help faculty use video recording as a tool to record the most difficult concepts of a lesson or the whole lesson and make them available to students. This chapter also covers the ePortfolios initiative, which aims to provide students with a venue to showcase the progress and achievements of their learning journey. Finally, this chapter explains the vision and goals behind the creation of the Bronx EdTech Showcase, a multi-campus collaboration that provides faculty with a space to share best practices, innovations in the classroom, and network and collaboration with other colleagues.

C-reactive protein (CRP) is a component of the acute phase response to infection, inflammation, and trauma. A major activity of acute phase proteins is to limit the inflammatory response. It has been demonstrated that CRP protects mice from lethal doses of LPS. In the mouse, CRP binds to the regulatory receptor, FcγRIIb, and to the γ-chain-associated receptor, FcγRI. The goal ofthis study was to determine whether FcγRs are necessary for the protective effect of CRP. The ability of CRP to protect mice from a lethal dose of LPS was confirmed using injections of 500 and 250 μg of CRP at 0 and 12 h. CRP treatment of FcγRIIb-deficient mice increased mortality after LPS challenge and increased serum levels of TNF and IL-12 in response to LPS. CRP did not protect FcR γ-chain-deficient mice from LPS-induced mortality. Treatment of normal mice, but not γ-chain-deficient mice, with CRP increased IL-10 levels following LPS injection. In vitro, in the presence of LPS, CRP enhanced IL-10 synthesis and inhibited IL-12 synthesis by bone marrow macrophages from normal, but not γ-chain-deficient mice. The protective effect of CRP appears to be mediated by binding to FcγRI and FcγRII resulting in enhanced secretion of the anti-inflammatory cytokine IL-10 and the down-regulation of IL-12. These results suggest that CRP can alter the cytokine profile of mouse macrophages by acting through FcγR leading to a down-regulation of the inflammatory response.

A pair of Black-vented Orioles (Icterus wagleri) successfully fledged young from a nest inside a log cabin in the Montecristo National Park, El Salvador. This is the first breeding record of the species for El Salvador. The nest was hammock-shaped, 18 × 20 cm outside, 6 cm deep inside, and contained four eggs. After the first clutch failed, the pair renested using the same nest, incubating and rearing three young over 34 days.

C-reactive protein (CRP) is a member of the pentraxin family of proteins and an acute phase reactant. CRP modulates the response to inflammatory stimuli including LPS and C5a. We recently demonstrated that CRP prevents and reverses proteinuria in accelerated nephrotoxic nephritis (NTN). NTN is a model of active inflammatory immune complex-mediated nephritis induced by injection of antiglomerular basement membrane. CRP treatment prevented the induction of NTN in C57BL/6 (B6) mice, increased survival, and reversed ongoing nephritis. Protection was associated with a decrease in IL-1β and chemokines in the kidney and peritoneal cells as measured by quantitative RT-PCR. However, IL-10−/− mice were not protected by CRP either when given before disease onset or when disease activity was maximal. FcγRI−/− mice developed NTN, but were only transiently protected by CRP treatment. This transient protection was abrogated by cobra venom factor depletion of complement from FcγRI−/− mice. However, complement depletion did not prevent CRP-mediated protection in B6 mice, and CRP was protective in C3−/− mice. The role of macrophages in the protection provided by CRP was tested by treating B6 mice with liposomes containing clodronate. Clodronate-containing liposomes deplete mice of splenic and hepatic macrophages for 5–7 days. Pretreatment of NTN mice with clodronate but not control liposomes completely prevented CRP-mediated protection. These studies suggest that CRP mediates protection from NTN through the induction of IL-10 and that macrophages are required. In addition, FcγRI plays an important role but is not the sole mediator of CRP-mediated protection.

Objective C-reactive protein (CRP) is an acute-phase serum protein with binding reactivity to nuclear autoantigens and immunomodulatory function. The MRL/lpr mouse is an important model of human systemic lupus erythematosus (SLE). These mice develop high-titer anti-DNA antibodies and immune complex–mediated nephritis and exhibit progressive lymphadenopathy. The mortality rate among these mice is 50% by age 18–20 weeks; the most frequent cause of death is glomerulonephritis. The present study was undertaken to determine whether treatment of mice with CRP would affect the course of lupus nephritis. Methods MRL/lpr mice were treated with a single 200-μg injection of CRP at either age 6 weeks (before disease onset) or age 13 or 15 weeks (when proteinuria had reached high levels). Proteinuria was measured weekly, and levels of anti–double-stranded DNA autoantibodies and blood urea nitrogen were determined monthly. Glomerular immune complex deposition and renal pathology were assessed in mice ages 15 weeks and 17 weeks. Results Early CRP treatment markedly delayed the onset of proteinuria and lymphadenopathy, increased survival, and reduced levels of autoantibodies to DNA. Treatment of mice with active disease reversed proteinuria and prolonged survival. Renal disease was decreased in CRP-treated mice, with a marked suppression of glomerular pathology, tubular degeneration, and interstitial inflammation, which correlated with the decrease in proteinuria and azotemia. Conclusion These findings demonstrate that systemic suppression of autoimmunity is initiated by a single injection of CRP. Long-term maintenance of CRP-mediated protection was reversed by injection of an anti-CD25 monoclonal antibody but not by macrophage depletion, suggesting that disease suppression is maintained by CD25-bearing T cells.

We discuss the solution of the integral Dirac–Fock equation in momentum space. “Balanced” momentum-space gaussian functions are used to expand the large and small components of the Dirac 4-spinors. We show that this approach, which has been successfully used in atomic Dirac–Fock calculations, works equally well in molecular Dirac–Fock calculations.

A major impediment to achieving accurate solutions of the momentum-space Hartree-Fock equation in fully numerical form lies in the error caused by the truncation of momentum space. We use a coordinate transformation, which is characterized by P = tan(α/2), thus avoiding this truncation to achieve accurate solutions of the Hartree-Fock equation. Using this approach, we have re-examined the He model problem previously analyzed by Delhalle and Defranceschi [Intern. J. Quantum Chem. Symp. 21 425 (1987)]: The kinetic, nuclear attraction and Coulomb repulsion energies of the He atom have been evaluated using both conventional spherical polar momentum coordinates, (p, θ, φ) and the transformed coordinates, (α,θ,φ) in order to compare their accuracies. We have performed a number of fully numerical calculations on the H ion in order to examine the influence of the number of points in the mesh on the accuracy of the computed total electronic energy of the diatomic molecule.

Using the H2+ ion as an example, we show that the algebraic approximation to the Dirac equation in momentum space is capable of giving accurate relativistic energies for molecular systems. A small number of Gaussians are sufficient for such calculations, and we examine in detail the selection of a proper basis.

Using the H2+ ion as an example, we discuss a fully numerical approach to the solution of the Hartree-Fock equation in momentum space which ensures accurate and stable solutions for polyatomic molecules. We made use of a “tangential” grid to solve the problems of truncation of momentum space and the lack of an appropriate discretization procedure, which currently limit the widespread applicability of this approach.