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The topological group $\mathcal{D}^k(\mathbb{S})$ of diffeomorphisms of the unit circle $\mathbb{S}$ of Sobolev class$H$^{$k$}, for$k$large enough, is a Banach manifold modeled on the Hilbert space $H^k(\mathbb{S})$ . In this paper we show that the$H$^{1}right-invariant metric obtained by right-translation of the$H$^{1}inner product on $T_{\rm id}\mathcal{D}^k(\mathbb{S})\simeq H^k(\mathbb{S})$ defines a smooth Riemannian metric on $\mathcal{D}^k(\mathbb{S})$ , and we explicitly construct a compatible smooth affine connection. Once this framework has been established results from the general theory of affine connections on Banach manifolds can be applied to study the exponential map, geodesic flow, parallel translation, curvature etc. The diffeomorphism group of the circle provides the natural geometric setting for the Camassa–Holm equation – a nonlinear wave equation that has attracted much attention in recent years – and in this context it has been remarked in various papers how to construct a smooth Riemannian structure compatible with the$H$^{1}right-invariant metric. We give a self-contained presentation that can serve as a detailed mathematical foundation for the future study of geometric aspects of the Camassa–Holm equation.

Inflammatory response following central nervous system (CNS) injury contributes to progressive neuropathology and reduction in functional recovery. Axons are sensitive to mechanical injury and toxic inflammatory mediators, which may lead to demyelination. Although it is well documented that degenerated myelin triggers undesirable inflammatory responses in autoimmune diseases such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), there has been very little study of the direct inflammatory consequences of damaged myelin in spinal cord injury (SCI), i.e., there is no direct evidence to show that myelin debris from injured spinal cord can trigger undesirable inflammation in vitro and in vivo. Our data showed that myelin can initiate inflammatory responses in vivo, which is complement receptor 3 (CR3)-dependent via stimulating macrophages to express pro-inflammatory molecules and down-regulates expression of anti-inflammatory cytokines. Mechanism study revealed that myelin-increased cytokine expression is through activation of FAK/PI3K/Akt/NF-B signaling pathways and CR3 contributes to myelin-induced PI3K/Akt/NF-B activation and cytokine production. The myelin induced inflammatory response is myelin specific as sphingomyelin (the major lipid of myelin) and myelin basic protein (MBP, one of the major proteins of myelin) are not able to activate NF-B signaling pathway. In conclusion, our results demonstrate a crucial role of myelin as an endogenous inflammatory stimulus that induces pro-inflammatory responses and suggest that blocking myelin-CR3 interaction and