Kasper K. S. Andersen

Calprotectin is released from human skeletal muscle tissue during exercise.

Skeletal muscle has been identified as a secretory organ. We hypothesized that IL‐6, a cytokine secreted from skeletal muscle during exercise, could induce production of other secreted factors in skeletal muscle. IL‐6 was infused for 3 h into healthy young males (n= 7) and muscle biopsies obtained at time points 0, 3 and 6 h in these individuals and in resting controls. Affymetrix microarray analysis of gene expression changes in skeletal muscle biopsies identified a small set of genes changed by IL‐6 infusion. RT‐PCR validation confirmed that S100A8 and S100A9 mRNA were up‐regulated 3‐fold in skeletal muscle following IL‐6 infusion compared to controls. Furthermore, S100A8 and S100A9 mRNA levels were up‐regulated 5‐fold in human skeletal muscle following cycle ergometer exercise for 3 h at ∼60% of in young healthy males (n= 8). S100A8 and S100A9 form calprotectin, which is known as an acute phase reactant. Plasma calprotectin increased 5‐fold following acute cycle ergometer exercise in humans, but not following IL‐6 infusion. To identify the source of calprotectin, healthy males (n= 7) performed two‐legged dynamic knee extensor exercise for 3 h with a work load of ∼50% of peak power output and arterial–femoral venous differences were obtained. Arterial plasma concentrations for calprotectin increased 2‐fold compared to rest and there was a net release of calprotectin from the working muscle. In conclusion, IL‐6 infusion and muscle contractions induce expression of S100A8 and S100A9 in skeletal muscle. However, IL‐6 alone is not a sufficient stimulus to facilitate release of calprotectin from skeletal muscle.

The Role of Inflammation in Vascular Insulin Resistance with Focus on IL-6

The present review focuses on the possible role of interleukin-(IL)-6 in vascular insulin resistance. The endothelium plays an important role in regulating the tone of the vasculature by releasing nitric oxide (NO) to the smooth muscles of the vessels, thereby regulating the distribution of blood flow to the various tissues in relation to their energy demand. A dysfunctioning endothelium has been associated with both initiation and progression of atherosclerotic cardiovascular (CV) disease and has been shown to predate the onset of hyperglycemia in the natural history of type 2 diabetes. It is likely that chronic low-level inflammation plays an important role in developing endothelial dysfunction mainly through proinflammatory actions of tumor necrosis factor alpha (TNF-alpha). TNF-alpha induces production of IL-6 and it has been suggested that a causal relationship exists between endothelial dysfunction and these cytokines. With regard to vascular insulin resistance, the available data point to a direct pathogenic role of TNF-alpha in mediating endothelial dysfunction, whereas with regard to IL-6 evidence is sparse and does not allow any firm conclusions.

Reduced, tame and exotic fusion systems

We define here two new classes of saturated fusion systems: reduced fusion systems and tame fusion systems. These are motivated by our attempts to better understand and search for exotic fusion systems: fusion systems which are not the fusion systems of any finite group. Our main theorems say that every saturated fusion system reduces to a reduced fusion system which is tame only if the original one is realizable and that every reduced fusion system which is not tame is the reduction of some exotic (nonrealizable) fusion system.

The classification of 2-compact groups

We prove that any connected 2-compact group is classified by its 2-adic root datum, and in particular the exotic 2-compact group DI(4), constructed by Dwyer-Wilkerson, is the only simple 2-compact group not arising as the 2-completion of a compact connected Lie group. Combined with our earlier work with Moller and Viruel for p odd, this establishes the full classification of p-compact groups, stating that, up to isomorphism, there is a one-to-one correspondence between connected p-compact groups and root data over the p-adic integers. As a consequence we prove the maximal torus conjecture, giving a one-to-one correspondence between compact Lie groups and finite loop spaces admitting a maximal torus. Our proof is a general induction on the dimension of the group, which works for all primes. It refines the Andersen-Grodal-Moller-Viruel methods by incorporating the theory of root data over the p-adic integers, as developed by Dwyer-Wilkerson and the authors. Furthermore we devise a different way of dealing with the rigidification problem by utilizing obstruction groups calculated by Jackowski-McClure-Oliver in the early 1990s. (Less)

A finite loop space not rationally equivalent to a compact Lie group

We construct a connected finite loop space of rank 66 and dimension 1254 whose rational cohomology is not isomorphic as a graded vector space to the rational cohomology of any compact Lie group, hence providing a counterexample to a classical conjecture. Aided by machine calculation we verify that our counterexample is minimal, i.e., that any finite loop space of rank less than 66 is in fact rationally equivalent to a compact Lie group, extending the classical known bound of 5.

The Steenrod problem of realizing polynomial cohomology rings

In this paper, we completely classify which graded polynomial R-algebras in finitely many even degree variables can occur as the singular cohomology of a space with coefficients in R, a 1960 question of N. E. Steenrod, for a commutative ring R satisfying mild conditions. In the fundamental case R=Z, our result states that the only polynomial cohomology rings over Z that can occur are tensor products of copies of

Automorphisms of p-compact groups and their root data

H^*(CP^\infty;Z)\cong Z[x_2]

Spaces with Noetherian cohomology

,

The classification of p-compact groups for p odd

H^*(BSU(n);Z)\cong Z[x_4, x_6, \ldots, x_{2n}]

The normalizer splitting conjecture for p-compact groups

, and