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Additional file 1: Fig. S1. Scanning electron microscopyimage of uncoated silicone surface. Fig. S2. Contact angle measurement ofuncoated,30-layer bionanomatrix coated, and60-layer bionanomatrix coatedsilicone implants.As per journal requirements, every additional file must have a corresponding caption. In this regard, please be informed that the caption was taken from the additional e-file itself. Please advise if the action taken is appropriate and amend if necessary.There is no problem with captions.

We recently reported that upregulation of the constitutively active ras homolog enriched in brain [Rheb(S16H)], which induces the activation of the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway, can protect adult neurons, mediated by the induction of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), in animal models of neurodegenerative diseases. Here we show that neuronal transduction of Rheb(S16H) using adeno-associated virus serotype 1 provides neuroprotection in a mouse model of photothrombosis-induced ischemic stroke. Rheb(S16H)-expressing neurons exhibited neurotrophic effects, such as mTORC1 activation, increases in neuronal size, and BDNF production, in mouse cerebral cortex. Moreover, the upregulation of neuronal Rheb(S16H) significantly attenuated ischemic damage and behavioral impairments as compared to untreated mice, suggesting that Rheb(S16H) upregulation in cortical neurons may be a useful strategy to treat ischemic stroke.

Neuropathic pain (NP) is caused by lesions of the peripheral fibers and central neurons in the somatosensory nervous system and affects 7–10% of the general population. Although the distinct cause of neuropathic pain has been investigated in primary afferent neurons over the years, pain modulation by central sensitization remains controversial. NP is believed to be driven by cell type-specific spinal synaptic plasticity in the dorsal horn. Upon intense afferent stimulation, spinothalamic tract neurons are potentiated, whereas GABAergic interneurons are inhibited leading to long-term depression. Growing evidences suggest that the inhibition of GABAergic neurons plays pivotal roles in the manifestation of neuropathic and inflammatory pain states. Downregulation of GABA transmission and impairment of GABAergic interneurons in the dorsal horn are critical consequences after spinal cord and peripheral nerve injuries. These impairments in GABAergic interneurons may be associated with dysfunctional autophagy, resulting in neuropathic pain. Here, we review an emerging number of investigations that suggest a pivotal role of impaired autophagy of GABAergic interneurons in NP. We discuss relevant research spurring the development of new targets and therapeutic agents of NP and emphasize the need for a multidisciplinary approach to manage NP in the future.

Unifying two notions of an action and coaction of a locally compact group on a $C^*$-cor\-re\-spond\-ence we introduce a coaction $(\sigma,\delta)$ of a Hopf $C^*$-algebra $S$ on a $C^*$-cor\-re\-spond\-ence $(X,A)$. We show that this coaction naturally induces a coaction $\zeta$ of $S$ on the associated Cuntz-Pimsner algebra $\mathcal{O}_X$ under the weak $\delta$-invariancy for the ideal $J_X$. When the Hopf $C^*$-algebra $S$ is defined by a well-behaved multiplicative unitary, we construct a $C^*$-cor\-re\-spond\-ence $(X\rtimes_\sigma\widehat{S},A\rtimes_\delta\widehat{S})$ from $(\sigma,\delta)$ and show that it has a representation on the reduced crossed product $\mathcal{O}_X\rtimes_\zeta\widehat{S}$ by the induced coaction $\zeta$. This representation is used to prove an isomorphism between the $C^*$-algebra $\mathcal{O}_X\rtimes_\zeta\widehat{S}$ and the Cuntz-Pimsner algebra $\mathcal{O}_{X\rtimes_\sigma\widehat{S}}$ under the covariance assumption which is guaranteed in particular if the ideal $J_{X\rtimes_\sigma\widehat{S}}$ of $A\rtimes_\delta\widehat{S}$ is generated by the canonical image of $J_X$ in $M(A\rtimes_\delta\widehat{S})$ or the left action on $X$ by $A$ is injective. Under this covariance assumption, our results extend the isomorphism result known for actions of amenable groups to arbitrary locally compact groups. The Cuntz-Pimsner covariance condition which was assumed for the same isomorphism result concerning group coactions is shown to be redundant., Comment: 37 pages; introduction is revised; section 4 is shortened