Exact and approximate boundary data interpolation in the finite element method

Matching boundary data exactly in an elliptic problem avoids one of Strang's "variational crimes". (Strang and Fix (1973)). Supporting numerical evidence for this procedure is given by Marshall and Mitchell (1973), who considered the solution of Laplace's equation with Dirichlet boundary data by bilinear elements over squares and measured the errors in the L2 norm. Then Marshall and Mitchell (1978) obtained some surprising results: for certain triangular elements, matching the boundary data exactly produced worse results than the usual procedure of interpolating the boundary data

Mapping of the Epstein-Barr virus and C3dg binding sites to a common domain on complement receptor type 2.

Complement receptor type 2 (CR2;CD21), a member of the superfamily of proteins containing short consensus repeats (SCRs), is the B cell receptor for both the gp350/220 envelope protein of Epstein-Barr virus (EBV), and for the C3dg protein of complement. By analysis of CR2 deletion mutants and chimeras formed with CR1 (CD35) we determined that of the 15 SCRs in CR2, the NH2-terminal two SCRs are necessary and sufficient to bind both gp350/220 and C3dg with affinities equivalent to those of the wild-type receptor. The epitope for OKB-7, a mAb that blocks binding of both EBV and C3dg and shares with these ligands B cell-activating capabilities, also requires both SCR-1 and SCR-2, whereas mAbs lacking these functions bind to other SCRs. Thus, EBV, a polyclonal activator of B cells, has selected a site that is proximate or identical to the natural ligand binding site in CR2, perhaps reflecting the relative immutability of that site as well as its signal transducing function

Delayed diagnosis of high proximal tracheoesophageal fistula in esophageal atresia and a novel approach to the treatment of tracheomalacia by submanubrial tracheopexy

An infant with esophageal atresia (EA) had delayed diagnosis of proximal tracheoesophageal fistula (TEF) and severe tracheomalacia. We recommend bronchoscopy via laryngeal mask or rigid bronchoscopy to rule out associated TEF in infants diagnosed with esophageal atresia, as flexible bronchoscopy via endotracheal tube may not provide complete visualization of the trachea. We also describe a novel cervical approach to tracheopexy via neck incision for treatment of associated severe tracheomalacia in this infant

Systematic study of constitutive cyclo-oxygenase-2 expression: role of NFκB and NFAT transcriptional pathways

Cyclooxygenase-2 (COX-2) is an inducible enzyme that drives inflammation and is the therapeutic target for widely used nonsteroidal antiinflammatory drugs (NSAIDs). However, COX-2 is also constitutively expressed, in the absence of overt inflammation, with a specific tissue distribution that includes the kidney, gastrointestinal tract, brain, and thymus. Constitutive COX-2 expression is therapeutically important because NSAIDs cause cardiovascular and renal side effects in otherwise healthy individuals. These side effects are now of major concern globally. However, the pathways driving constitutive COX-2 expression remain poorly understood. Here we show that in the kidney and other sites, constitutive COX-2 expression is a sterile response, independent of commensal microorganisms and not associated with activity of the inflammatory transcription factor NF-κB. Instead, COX-2 expression in the kidney but not other regions colocalized with nuclear factor of activated T cells (NFAT) transcription factor activity and was sensitive to inhibition of calcineurin-dependent NFAT activation. However, calcineurin/NFAT regulation did not contribute to constitutive expression elsewhere or to inflammatory COX-2 induction at any site. These data address the mechanisms driving constitutive COX-2 and suggest that by targeting transcription it may be possible to develop antiinflammatory therapies that spare the constitutive expression necessary for normal homeostatic functions, including those important to the cardiovascular-renal system

Masculinity, racism, social support, and colorectal cancer screening uptake among African American men: A systematic review

Colorectal cancer (CRC) is highly preventable when CRC screening is utilized, yet CRC screening completion among African American men is relatively low and their mortality rates remain 50% higher juxtaposed to their White counterparts. Since a growing body of literature indicates masculinity, racism, and social support each have strong influences on CRC screening uptake, this systematic review examined the connections between these three sociocultural factors and CRC screening uptake among African American men. Potential studies were retrieved from MEDLINE, CINAHL, EMBASE, and PsycINFO. Cited reference searching for the final sample was employed to identify and assess additional studies for inclusion using Scopus. The methodological quality of the reviewed evidence was also evaluated. Nineteen studies met inclusion/exclusion criteria. Thirteen studies employed nonexperimental research designs; a quasi-experimental design was present in four, and two utilized experimental designs. Studies were published between 2000 and 2014; the majority between 2009 and 2013. Social support was most frequently addressed (84%) while masculinity and racism were equally studied with paucity (11%) for their influence on CRC screening. After evaluating conceptual and methodological characteristics of the studies, 42% fell below average in quality and rigor. The need for increased attention to the sociocultural correlates of CRC screening for African American men are highlighted in this systematic review, and important recommendations for research and practice are provided. Alongside a call for more rigorous research, further research examining the influence of masculinity and racism on CRC screening completion among African American men is warrante

The varieties of remembered experience: Moving memory beyond the bounded self

We review the contributions to this Special Issue that highlight the diverse ways in which memory takes place that go beyond the standard personal autobiographical memory and its reliance on internal imagery. We look at how contributors explore a highly individual memory of trauma and re-consider it as a complex, socially contested phenomenon. We next turn to a discussion of shared memory within dyads and then look at a contribution that examines bodily and gestural alignment during shared recollection among group members and/or families. From there, contributors raise considerations of collective memory in prisoner-of-war survivors and among football fans attending a World Cup event. The next contribution illustrates how collective forgetting creates social bonds in a similar manner to collective remembering. Finally, we show how the boundaries of memory are being stretched by digital technology through its influence on how we recall and share memories. Methodological innovations are also discussed

Differential regulation of CCL-11/eotaxin-1 and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells

Background: Bacterial infections are a cause of exacerbation of airway disease. Airway smooth muscle cells (ASMC) are a source of inflammatory cytokines/chemokines that may propagate local airway inflammatory responses. We hypothesize that bacteria and bacterial products could induce cytokine/chemokine release from ASMC.Methods: Human ASMC were grown in culture and treated with whole bacteria or pathogen associated molecular patterns (PAMPs) for 24 or 48 h. The release of eotaxin-1, CXCL-8 or GMCSF was measured by ELISA.Results: Gram-negative E. coli or Gram-positive S. aureus increased the release of CXCL-8, as did IL-1β, LPS, FSL-1 and Pam3CSK4, whereas FK565, MODLys18 or Poly I:C did not. E. coli inhibited eotaxin-1 release under control conditions and after stimulation with IL-1β. S. aureus tended to inhibit eotaxin-1 release stimulated with IL-1β. E. coli or LPS, but not S. aureus, induced the release of GMCSF.Conclusion: Gram-positive or Gram-negative bacteria activate human ASMC to release CXCL-8. By contrast Gram-negative bacteria inhibited the release of eotaxin-1 from human ASMCs. E. coli, but not S. aureus induced GMCSF release from cells.Our findings that ASMC can respond directly to Gram-negative and Gram-positive bacteria by releasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about the role of neutrophil recruitment in bacterial infections in the lung. Our findings that bacteria inhibit the release of the eosinophil selective chemokine, eotaxin-1 may help to explain the mechanisms by which bacterial immunotherapy reduces allergic inflammation in the lung. © 2008 Issa et al; licensee BioMed Central Ltd

Differential regulation of CCL-11/eotaxin-1 and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells.

Background: Bacterial infections are a cause of exacerbation of airway disease. Airway smooth muscle cells (ASMC) are a source of inflammatory cytokines/chemokines that may propagate local airway inflammatory responses. We hypothesize that bacteria and bacterial products could induce cytokine/chemokine release from ASMC. Methods: Human ASMC were grown in culture and treated with whole bacteria or pathogen associated molecular patterns (PAMPs) for 24 or 48 h. The release of eotaxin-I, CXCL-8 or GMCSF was measured by ELISA. Results: Gram-negative E. coli or Gram-positive S. aureus increased the release of CXCL-8, as did IL-1 beta, LPS, FSL-1 and Pam(3)CSK4, whereas FK565, MODLys18 or Poly I:C did not. E. coli inhibited eotaxin-I release under control conditions and after stimulation with IL-1 beta. S. aureus tended to inhibit eotaxin-I release stimulated with IL-1 beta. E. coli or LPS, but not S. aureus, induced the release of GMCSF. Conclusion: Gram-positive or Gram-negative bacteria activate human ASMC to release CXCL-8. By contrast Gram-negative bacteria inhibited the release of eotaxin-I from human ASMCs. E. coli, but not S. aureus induced GMCSF release from cells. Our findings that ASMC can respond directly to Gram-negative and Gram-positive bacteria by releasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about the role of neutrophil recruitment in bacterial infections in the lung. Our findings that bacteria inhibit the release of the eosinophil selective chemokine, eotaxin-I may help to explain the mechanisms by which bacterial immunotherapy reduces allergic inflammation in the lung

Cardiovascular disease in women: Implications for improving health outcomes

Objective: To collate data on women and cardiovascular disease in Australia and globally to inform public health campaigns and health care interventions. Design: Literature review. Results: •Women with acute coronary syndromes show consistently poorer outcomes than men, independent of comorbidity and management, despite less anatomical obstruction of coronary arteries and relatively preserved left ventricular function. Higher mortality and complication rates are best documented amongst younger women and those with ST-segment-elevation myocardial infarction.•Sex differences in atherogenesis and cardiovascular adaptation have been hypothesised, but not proven.•Atrial fibrillation carries a relatively greater risk of stroke in women than in men, and anticoagulation therapy is associated with higher risk of bleeding complications.•The degree of risk conferred by single cardiovascular risk factors and combinations of risk factors may differ between the sexes, and marked postmenopausal changes are seen in some risk factors.•Sociocultural factors, delays in seeking care and differences in self-management behaviours may contribute to poorer outcomes in women.•Differences in clinical management for women, including higher rates of misdiagnosis and less aggressive treatment, have been reported, but there is a lack of evidence to determine their effects on outcomes, especially in angina.•Although enrolment of women in randomised clinical trials has increased since the 1970s, women remain underrepresented in cardiovascular clinical trials. Conclusions: Improvement in the prevention and management of CVD in women will require a deeper understanding of women's needs by the community, health care professionals, researchers and government. © 2011 Royal College of Nursing, Australia