About Massachusetts Colleges Online June 2006 Sharing Best Practices Conference

This paper summarizes trends and issues in online learning in the United States of America as reflected in the presentations of the Massachusetts Colleges Online “Sharing Best Practices in E-Learning” Conference held on June 13-14, 2006

Adenosine signaling in airways: Toward a promising antiasthmatic approach

Adenosine participates to asthma physiopathology by signaling through more than just one receptor subtype. Defining the role of each receptor is complicated by evidence that often results obtained on rodents do not coincide with human studies, but what emerges is that an important condition to establish hyperresponsiveness to adenosine in any species of sensitized animals is the exposure to allergen; this feature appears to be very similar to the human situation, since allergic humans regularly undergo exposure to allergen. Furthermore, A2B in humans, but A3 receptor in rodents, would mediate, indirectly, the bronchoconstriction in response to adenosine and would play the main role in adenosine-induced airway inflammation and airway hyperreactivity. On the other hand, A1 receptor over-expressed on asthmatic airways would mediate a direct adenosine bronchoconstrictor effect. Antagonists and agonists to adenosine receptors have been considered as antiasthmatic drugs but often their development has been limited by unwanted effects. Preventing adenosine accumulation in airways should be considered as a novel promising antiasthmatic strategy

Macrophage autophagy in atherosclerosis

Macrophages play crucial roles in atherosclerotic immune responses. Recent investigation into macrophage autophagy (AP) in atherosclerosis has demonstrated a novel pathway through which these cells contribute to vascular inflammation. AP is a cellular catabolic process involving the delivery of cytoplasmic contents to the lysosomal machinery for ultimate degradation and recycling. Basal levels of macrophage AP play an essential role in atheroprotection during early atherosclerosis. However, AP becomes dysfunctional in the more advanced stages of the pathology and its deficiency promotes vascular inflammation, oxidative stress, and plaque necrosis. In this paper, we will discuss the role of macrophages and AP in atherosclerosis and the emerging evidence demonstrating the contribution of macrophage AP to vascular pathology. Finally, we will discuss how AP could be targeted for therapeutic utility

Return to Play Following Shoulder Stabilization: A Systematic Review and Meta-analysis.

BackgroundAnterior shoulder instability can be a disabling condition for the young athlete; however, the best surgical treatment remains controversial. Traditionally, anterior shoulder instability was treated with open stabilization. More recently, arthroscopic repair of the Bankart injury with suture anchor fixation has become an accepted technique.HypothesisNo systematic reviews have compared the rate of return to play following arthroscopic Bankart repair with suture anchor fixation with the Bristow-Latarjet procedure and open stabilization. We hypothesized that the rate of return to play will be similar regardless of surgical technique.Study designSystematic review; Level of evidence, 4.MethodsWe performed a systematic review and meta-analysis focused on return to play following shoulder stabilization. Inclusion criteria included studies in English that reported on rate of return to play and clinical outcomes following primary arthroscopic Bankart repair with suture anchors, the Latarjet procedure, or open stabilization. Statistical analyses included Student t tests and analyses of variance.ResultsSixteen papers reporting on 1036 patients were included. A total of 545 patients underwent arthroscopic Bankart repair with suture anchors, 353 with the Latarjet procedure, and 138 with open repair. No significant difference was found in patient demographic data among the studies. Patients returned to sport at the same level of play (preinjury level) more consistently following arthroscopic Bankart repair (71%) or the Latarjet procedure (73%) than open stabilization (66%) (P < .05). Return to play at any level and postoperative Rowe scores were not significantly different among studies. Recurrent dislocation was significantly less following the Latarjet procedure (3.5%) than after arthroscopic Bankart repair (6.6%) or open stabilization (6.7%) (P < .05).ConclusionThis systematic review demonstrates a greater rate of return to play at the preinjury level following arthroscopic Bankart repair and the Latarjet procedure than open stabilization. Despite this difference, >65% of all treated athletes returned to sport at their preinjury levels, with other outcome measures being similar among the treatment groups. Therefore, arthroscopic Bankart repair, the Latarjet procedure, and open stabilization remain good surgical options in the treatment of the athlete with anterior shoulder instability

Mapping the interaction of B cell Leukemia 3 (BCL-3) and nuclear factor κB (NF-κB) p50 identifies a BCL-3-mimetic anti-inflammatory peptide

The NF-κB transcriptional response is tightly regulated by a number of processes including the phosphorylation, ubiquitination, and subsequent proteasomal degradation of NF-κB subunits. The IκB family protein BCL-3 stabilizes a NF-κB p50 homodimer·DNA complex through inhibition of p50 ubiquitination. This complex inhibits the binding of the transcriptionally active NF-κB subunits p65 and c-Rel on the promoters of NF-κB target genes and functions to suppress inflammatory gene expression. We have previously shown that the direct interaction between p50 and BCL-3 is required for BCL-3-mediated inhibition of pro-inflammatory gene expression. In this study we have used immobilized peptide array technology to define regions of BCl-3 that mediate interaction with p50 homodimers. Our data show that BCL-3 makes extensive contacts with p50 homodimers and in particular with ankyrin repeats (ANK) 1, 6, and 7, and the N-terminal region of Bcl-3. Using these data we have designed a BCL-3 mimetic peptide based on a region of the ANK1 of BCL-3 that interacts with p50 and shares low sequence similarity with other IκB proteins. When fused to a cargo carrying peptide sequence this BCL-3-derived peptide, but not a mutated peptide, inhibited Toll-like receptor-induced cytokine expression in vitro. The BCL-3 mimetic peptide was also effective in preventing inflammation in vivo in the carrageenan-induced paw edema mouse model. This study demonstrates that therapeutic strategies aimed at mimicking the functional activity of BCL-3 may be effective in the treatment of inflammatory disease

Some topics on permutable subgroups in infinite groups

The aim of this thesis is to study permutability in different aspects of the theory of infinite groups. In particular, it will be studied the structure of groups in which all the members of a relevant system of subgroups satisfy a suitable generalized condition of permutability

Deep Time Iterations: Familiarity, Horizons, and Pattern Among Finland's Nuclear Waste Safety Experts

This ethnography reconsiders nuclear waste risk’s deep time horizons’ often-sensationalized aesthetics of horror, sublimity, and awe. It does so by tracking how Finland’s nuclear energy and waste experts made visions of distant future Finlands appear more intelligible through mundane corporate, regulatory, financial, and technoscientific practices. Each chapter unpacks how informants iterated and reiterated traces of the very familiar to establish shared grounds of continuity for moving forward in time. Chapter 1 explores how Finland’s energy sector’s “mankala” cooperative corporate form was iterated and reiterated to give shape to political and financial time horizons. Chapter 2 explores how workplace role distinctions between recruit/retiree and junior/senior were iterated and reiterated to reckon nuclear personnel successions’ intergenerational horizons. Chapter 3 explores how input/output and part/whole distinctions were iterated and reiterated to help model distant future worlds in a portfolio of “Safety Case” evidence made to demonstrate the Olkiluoto repository’s safety to Finnish nuclear regulator STUK. Chapter 4 explores how Safety Case experts iterated and reiterated memories of a deceased predecessor figure in everyday engagements with deep time. What emerges are three insights about how futures attain discernible features – insights about the “continuity,” “thinkability,” and “extensibility” of expert thought – that, I argue, can help twenty-first century experts better navigate not only deep time, but also unknown futures of nuclear technologies, planetary environment, and expertise itself

Images in cardiovascular medicine : multiphoton microscopy for three-dimensional imaging of lymphocyte recruitment into apolipoprotein-E-deficient mouse carotid artery

Two recent elegant studies have shown that in apolipoprotein-E– deficient mice, the lamina adventitia is a major site of arterial wall inflammation associated with lymphocyte infiltration into atherosclerotic arteries and with formation of adventitial lymphoid-like tissues.1,2 These results suggest that lymphocyte responses in the lamina adventitia may play a crucial role in atherosclerosis development.1,

Perivascular mast cells regulate vein graft neointimal formation and remodeling

Objective. Emerging evidence suggests an important role for mast cells in vein graft failure. This study addressed the hypothesis that perivascular mast cells regulate in situ vascular inflammatory and proliferative responses and subsequent vein graft neointimal lesion formation, using an optimized local mast cell reconstitution method. Methods and Results. Neointimal hyperplasia was induced by insertion of a vein graft into the right carotid artery in wild type and mast cell deficient KitW−sh/W−sh mice. In some experiments, mast cells were reconstituted systemically (tail vein injection of bone marrow-derived mast cells) or locally (directly into the right neck area) prior to vein grafting. Vein graft neointimal lesion formation was significantly (P < 0.05) reduced in KitW−sh/W−sh mice. Mast cell deficiency reduced the number of proliferating cells, and inhibited L-selectin, CCL2, M-CSF and MIP-3α expression in the vein grafts. Local but not systemic mast cell reconstitution restored a perivascular mast cell population that subsequently promoted neointimal formation in mast cell deficient mice. Conclusion. Our data demonstrate that perivascular mast cells play a key role in promoting neointima formation by inducing local acute inflammatory and proliferative responses. These results suggest that ex vivo intraoperative targeting of mast cells may have therapeutic potential for the prevention of pathological vein graft remodeling