Anomalous scaling behavior in Takens-Bogdanov bifurcations

A general algorithm is presented for estimating the nonlinear instability threshold, $\sigma_c$, for subcritical transitions in systems where the linearized dynamics is significantly non-normal (i.e. subcritical bifurcations of {\em Takens-Bogdanov} type). The $N$-dimensional degenerate node is presented as an example. The predictions are then compared to numerical studies with excellent agreement.Comment: 6 page

Liberalism and Communitarism: On Certain Aphorias of Contemporary Theretical Discourse

Autor sa stajališta sociologije znanja razmatra političke, historijske i intelektualne začetke debate o liberalizmu i komunitarizmu u SAD. Zatim ukratko opisuje recepciju te debate u Europi, da bi se ne kraju opširnije opisao njezin tijek u Republici Njemačkoj. Smisao čitave analize svodi se na preispitivanje mogućnosti transfera teoretskih i političkih rasprava iz jedne u drugu nacionalnu i socio-političku hermeneutičku situaciju. Autor je, s jedne strane, skeptičan prema takvim transferima, koji su redovito i vrlo smione transformacije, a s druge strane, ukazuje i na zajedničke ekonomsko-političke karakteristike suvremenih industrijskih društava Zapada, koje takve transfere omogućuju i čine razumljivim.The author looks into the political, historical and intellectual begginings of the debate about liberalism and communitarianism in the USA from the standpoint of sociology. Then he goes on to describe its reception in Europe and finally to depict in greater detail its course in Germany. The purpose of the whole analysis may be reduced to the investigation of the possibilities for a transfer of theoretical and political debates from one into another national and social and political hermeneutical situation. On one hand, the author is sceptical towards such transfers since they are at the same time very courageous transformations, while on the other this points to the common economic and political characteristics of contemporary industrial societies of the West which enable such transfers and make them understandable

Interview with Dick Gephardt and Tom O’Donnell by Diane Dewhirst

Biographical NoteRichard Andrew “Dick” Gephardt was born on January 31, 1941, in St. Louis, Missouri. He earned a B.S. from Northwestern University in 1962 and a law degree from the University of Michigan Law School in 1965. He was active in local Democratic politics and city government until 1976, when he was elected the U.S. House of Representatives, representing Missouri’s 3rd District until 2004, when he retired from the House and sought, unsuccessfully, the Democratic nomination for president, a nomination he also sought but failed to win in 1977. He served as House majority leader from 1989 to 1995 and minority leader from 1995 to 2003. After leaving the House, he founded the consulting and lobbying firm Gephardt Group Government Affairs, where he served as president and CEO at the time of this interview. Thomas J. “Tom” O’Donnell, a Brooklyn native, earned a B.A. in political science at SUNY Brockport and a Ph.D. from American University. He served as House Majority Leader Dick Gephardt’s chief of staff from 1989-1997, acting as Gephardt’s lead strategist for the Budget Summit Agreement of 1990 and the Omnibus Budget Reconciliation Act of 1993, among other legislative affairs. From 1997-2007, O’Donnell served as a partner at Doak, Carrier, O’Donnell and Goldman (DCO), a political consulting media firm. At the time of this interview, he was managing partner of Gephardt Government Affairs. SummaryInterview includes discussion of: first impressions on meeting Mitchell; 1990 budget summit, tax reform, and “Read my lips—no new taxes”; legislative initiatives during the Clinton administration; health care proposals from the Clinton White House in 1994; Edward Kennedy’s and Patrick Moynihan’s roles in the health care debate; Mitchell’s attributes and his abilities as majority leader; crime bill of 1994

T Cells in Vascular Inflammatory Diseases

Inflammation of the human vasculature is a manifestation of many different diseases ranging from systemic autoimmune diseases to chronic inflammatory diseases, in which multiple types of immune cells are involved. For both autoimmune diseases and chronic inflammatory diseases several observations support a key role for T lymphocytes in these disease pathologies, but the underlying mechanisms are poorly understood. Previous studies in several autoimmune diseases have demonstrated a significant role for a specific subset of CD4(+) T cells termed effector memory T (T-EM cells. This expanded population of T-EM cells may contribute to tissue injury and disease progression. These cells exert multiple pro-inflammatory functions through the release of effector cytokines. Many of these cytokines have been detected in the inflammatory lesions and participate in the vasculitic reaction, contributing to recruitment of macrophages, neutrophils, dendritic cells, natural killer cells, B cells, and T cells. In addition, functional impairment of regulatory T cells paralyzes anti-inflammatory effects in vasculitic disorders. Interestingly, activation of T-EM cells is uniquely dependent on the voltage-gated potassium Kv1.3 channel providing an anchor for specific drug targeting. In this review, we focus on the CD4+ T cells in the context of vascular inflammation and describe the evidence supporting the role of different T cell subsets in vascular inflammation. Selective targeting of pathogenic T-EM cells might enable a more tailored therapeutic approach that avoids unwanted adverse side effects of generalized immunosuppression by modulating the effector functions of T cell responses to inhibit the development of vascular inflammation

The immunopathology of ANCA-associated vasculitis.

The small-vessel vasculitides are a group of disorders characterised by variable patterns of small blood vessel inflammation producing a markedly heterogeneous clinical phenotype. While any vessel in any organ may be involved, distinct but often overlapping sets of clinical features have allowed the description of three subtypes associated with the presence of circulating anti-neutrophil cytoplasmic antibodies (ANCA), namely granulomatosis with polyangiitis (GPA, formerly known as Wegener's Granulomatosis), microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (eGPA, formerly known as Churg-Strauss syndrome). Together, these conditions are called the ANCA-associated vasculitidies (AAV). Both formal nomenclature and classification criteria for the syndromes have changed repeatedly since their description over 100 years ago and may conceivably do so again following recent reports showing distinct genetic associations of patients with detectable ANCA of distinct specificities. ANCA are not only useful in classifying the syndromes but substantial evidence implicates them in driving disease pathogenesis although the mechanism by which they develop and tolerance is broken remains controversial. Advances in our understanding of the pathogenesis of the syndromes have been accompanied by some progress in treatment, although much remains to be done to improve the chronic morbidity associated with the immunosuppression required for disease control

ANCA-associated vasculitis.

The anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAVs) are a group of disorders involving severe, systemic, small-vessel vasculitis and are characterized by the development of autoantibodies to the neutrophil proteins leukocyte proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA). The three AAV subgroups, namely granulomatosis with polyangiitis (GPA), microscopic polyangiitis and eosinophilic GPA (EGPA), are defined according to clinical features. However, genetic and other clinical findings suggest that these clinical syndromes may be better classified as PR3-positive AAV (PR3-AAV), MPO-positive AAV (MPO-AAV) and, for EGPA, by the presence or absence of ANCA (ANCA+ or ANCA-, respectively). Although any tissue can be involved in AAV, the upper and lower respiratory tract and kidneys are most commonly and severely affected. AAVs have a complex and unique pathogenesis, with evidence for a loss of tolerance to neutrophil proteins, which leads to ANCA-mediated neutrophil activation, recruitment and injury, with effector T cells also involved. Without therapy, prognosis is poor but treatments, typically immunosuppressants, have improved survival, albeit with considerable morbidity from glucocorticoids and other immunosuppressive medications. Current challenges include improving the measures of disease activity and risk of relapse, uncertainty about optimal therapy duration and a need for targeted therapies with fewer adverse effects. Meeting these challenges requires a more detailed knowledge of the fundamental biology of AAV as well as cooperative international research and clinical trials with meaningful input from patients

Chemokine receptor co-expression reveals aberrantly distributed T-H effector memory cells in GPA patients

Linear regression analysis for percentages of CD4 + TEM cells, TEM1, and TEM17 cells between r-GPA patients and HCs. (PDF 208 kb