Idempotent residuated structures : some category equivalences and their applications

This paper concerns residuated lattice-ordered idempotent commutative monoids that are subdirect products of chains. An algebra of this kind is a generalized Sugihara monoid (GSM) if it is generated by the lower bounds of the monoid identity; it is a Sugihara monoid if it has a compatible involution :. Our main theorem establishes a category equivalence between GSMs and relative Stone algebras with a nucleus (i.e., a closure operator preserving the lattice operations). An analogous result is obtained for Sugihara monoids. Among other applications, it is shown that Sugihara monoids are strongly amalgamable, and that the relevance logic RMt has the projective Beth de nability property for deduction.http://www.ams.org//journals/tran/hb201

Diminished trk A receptor signaling reveals cholinergic‐attentional vulnerability of aging

The cellular mechanisms underlying the exceptional vulnerability of the basal forebrain ( BF ) cholinergic neurons during pathological aging have remained elusive. Here we employed an adeno‐associated viral vector‐based RNA interference ( AAV ‐ RNA i) strategy to suppress the expression of tropomyosin‐related kinase A (trk A ) receptors by cholinergic neurons in the nucleus basalis of M eynert/substantia innominata ( nMB / SI ) of adult and aged rats. Suppression of trk A receptor expression impaired attentional performance selectively in aged rats. Performance correlated with trk A levels in the nMB / SI . trk A knockdown neither affected nMB / SI cholinergic cell counts nor the decrease in cholinergic cell size observed in aged rats. However, trk A suppression augmented an age‐related decrease in the density of cortical cholinergic processes and attenuated the capacity of cholinergic neurons to release acetylcholine ( AC h). The capacity of cortical synapses to release AC h in vivo was also lower in aged/trk A ‐ AAV ‐infused rats than in aged or young controls, and it correlated with their attentional performance. Furthermore, age‐related increases in cortical pro NGF and p75 receptor levels interacted with the vector‐induced loss of trk A receptors to shift NGF signaling toward p75‐mediated suppression of the cholinergic phenotype, thereby attenuating cholinergic function and impairing attentional performance. These effects model the abnormal trophic regulation of cholinergic neurons and cognitive impairments in patients with early A lzheimer's disease. This rat model is useful for identifying the mechanisms rendering aging cholinergic neurons vulnerable as well as for studying the neuropathological mechanisms that are triggered by disrupted trophic signaling. The cellular mechanisms underlying the exceptional vulnerability of the basal forebrain ( BF ) cholinergic neurons during pathological aging have remained elusive. Here we employed an adeno‐associated viral vector‐based RNA interference ( AAV ‐ RNA i) strategy to suppress the expression of trk A receptors by cholinergic neurons in the nucleus basalis of M eynert/substantia innominata (n MB / SI ) of adult and aged rats. This study provides novel evidence that reduced trkA receptors is not sufficient to trigger cholinergic dysfunction. Rather, aging interacts with disrupted trkA signaling to escalate the vulnerability of BF cholinergic neurons and the manifestation of age‐related attentional impairments.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/96365/1/ejn12090-sup-0001-SupportingInformation.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/96365/2/ejn12090.pd

Security in peer-to-peer communication systems

P2PSIP (Peer-to-Peer Session Initiation Protocol) is a protocol developed by the IETF (Internet Engineering Task Force) for the establishment, completion and modi¿cation of communication sessions that emerges as a complement to SIP (Session Initiation Protocol) in environments where the original SIP protocol may fail for technical, ¿nancial, security, or social reasons. In order to do so, P2PSIP systems replace all the architecture of servers of the original SIP systems used for the registration and location of users, by a structured P2P network that distributes these functions among all the user agents that are part of the system. This new architecture, as with any emerging system, presents a completely new security problematic which analysis, subject of this thesis, is of crucial importance for its secure development and future standardization. Starting with a study of the state of the art in network security and continuing with more speci¿c systems such as SIP and P2P, we identify the most important security services within the architecture of a P2PSIP communication system: access control, bootstrap, routing, storage and communication. Once the security services have been identi¿ed, we conduct an analysis of the attacks that can a¿ect each of them, as well as a study of the existing countermeasures that can be used to prevent or mitigate these attacks. Based on the presented attacks and the weaknesses found in the existing measures to prevent them, we design speci¿c solutions to improve the security of P2PSIP communication systems. To this end, we focus on the service that stands as the cornerstone of P2PSIP communication systems¿ security: access control. Among the new designed solutions stand out: a certi¿cation model based on the segregation of the identity of users and nodes, a model for secure access control for on-the-¿y P2PSIP systems and an authorization framework for P2PSIP systems built on the recently published Internet Attribute Certi¿cate Pro¿le for Authorization. Finally, based on the existing measures and the new solutions designed, we de¿ne a set of security recommendations that should be considered for the design, implementation and maintenance of P2PSIP communication systems.Postprint (published version

Hypercapnia increases ACE2 expression and pseudo-SARS-CoV-2 entry in bronchial epithelial cells by augmenting cellular cholesterol

Patients with chronic lung disease, obesity, and other co-morbid conditions are at increased risk of severe illness and death when infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Hypercapnia, the elevation of CO2 in blood and tissue, commonly occurs in patients with severe acute and chronic lung disease, including those with pulmonary infections, and is also associated with high mortality risk. We previously reported that hypercapnia increases viral replication and mortality of influenza A virus infection in mice. We have also shown that culture in elevated CO2 upregulates expression of cholesterol synthesis genes in primary human bronchial epithelial cells. Interestingly, factors that increase the cholesterol content of lipid rafts and lipid droplets, platforms for viral entry and assembly, enhance SARS-CoV-2 infection. In the current study, we investigated the effects of hypercapnia on ACE2 expression and entry of SARS-CoV-2 pseudovirus (p-SARS-CoV-2) into airway epithelial cells. We found that hypercapnia increased ACE2 expression and p-SARS-CoV-2 uptake by airway epithelium in mice, and in cultured VERO and human bronchial epithelial cells. Hypercapnia also increased total cellular and lipid raft-associated cholesterol in epithelial cells. Moreover, reducing cholesterol synthesis with inhibitors of sterol regulatory element binding protein 2 (SREBP2) or statins, and depletion of cellular cholesterol, each blocked the hypercapnia-induced increases in ACE2 expression and p-SARS-CoV-2 entry into epithelial cells. Cigarette smoke extract (CSE) also increased ACE2 expression, p-SARS-CoV-2 entry and cholesterol accumulation in epithelial cells, an effect not additive to that of hypercapnia, but also inhibited by statins. These findings reveal a mechanism that may account, in part, for poor clinical outcomes of SARS-CoV-2 infection in patients with advanced lung disease and hypercapnia, and in those who smoke cigarettes. Further, our results suggest the possibility that cholesterol-lowering therapies may be of particular benefit in patients with hypercapnia when exposed to or infected with SARS-CoV-2