Rehabilitative treatment of patients with covid-19 infection: The p.a.r.m.a. evidence based clinical practice protocol

Background: The impact of the SARS-CoV-2 on the National Health System (NHS) required a reorganization of the various levels of care, which also involved the rehabilitation reality. Aim of the work: A clinical practice review of the literature was conducted to provide operational-rehabilitation guidelines adapt-ed to the local reality and to the recent corporate reorganization in the context of the COVID-19 emergency. Methods: A practice review of the available scientific evidence was regularly conducted from the start of the COVID-19 pandemic to periodically update the clinical practice guidelines. Articles that met the following inclusion criteria were included: studies conducted on human adult subjects with COVID-19 infection, un-dergoing rehabilitation in any hospitalization setting. Results: The results of this clinical practice update were periodically discussed with colleagues and collaborators in a multi-professional team, in order to guarantee a good clinical practice protocol, named P.A.R.M.A. Conclusions: The P.A.R.M.A. protocol is the result of a periodic review literature update, which has allowed us to take charge of patients affected by COVID-19 ac-cording to the most up-to-date clinical evidences, guaranteeing a shared and uniform treatment within a local reality in an era of health emergency. (www.actabiomedica.it)

Carrier-Induced Magnetic Circular Dichloism in the Magnetoresistive Pyrochlore Tl2Mn2O7

Infrared magnetic circular dichloism (MCD), or equivalently magneto-optical Kerr effect, has been measured on the Tl2Mn2O7 pyrochlore, which is well known for exhibiting a large magnetoresistance around the Curie temperature T_C ~ 120 K. A circularly polarized, infrared synchrotron radiation is used as the light source. A pronounced MCD signal is observed exactly at the plasma edge of the reflectivity near and below T_c. However, contrary to the conventional behavior of MCD for ferromagnets, the observed MCD of Tl2Mn2O7 grows with the applied magnetic field, and not scaled with the internal magnetization. It is shown that these results can be basically understood in terms of a classical magnetoplasma resonance. The absence of a magnetization-scaled MCD indicates a weak spin-orbit coupling of the carriers in Tl2Mn2O7. We discuss the present results in terms of the microscopic electronic structures of Tl2Mn2O7.Comment: 5 pages, 5 figures, submitted to J. Phys. Soc. Jp

Mechanisms of c-Myc Degradation by Nickel Compounds and Hypoxia

Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling. Recent studies reported that hypoxia signaling might either antagonize or enhance c-myc activity depending on cell context. We investigated the effect of nickel on c-myc levels, and demonstrated that nickel, hypoxia, and other hypoxia mimetics degraded c-myc protein in a number of cancer cells (A549, MCF-7, MDA-453, and BT-474). The degradation of the c-Myc protein was mediated by the 26S proteosome. Interestingly, knockdown of both HIF-1α and HIF-2α attenuated c-Myc degradation induced by Nickel and hypoxia, suggesting the functional HIF-1α and HIF-2α was required for c-myc degradation. Further studies revealed two potential pathways mediated nickel and hypoxia induced c-myc degradation. Phosphorylation of c-myc at T58 was significantly increased in cells exposed to nickel or hypoxia, leading to increased ubiquitination through Fbw7 ubiquitin ligase. In addition, nickel and hypoxia exposure decreased USP28, a c-myc de-ubiquitinating enzyme, contributing to a higher steady state level of c-myc ubiquitination and promoting c-myc degradation. Furthermore, the reduction of USP28 protein by hypoxia signaling is due to both protein degradation and transcriptional repression. Nickel and hypoxia exposure significantly increased the levels of dimethylated H3 lysine 9 at the USP28 promoter and repressed its expression. Our study demonstrated that Nickel and hypoxia exposure increased c-myc T58 phosphorylation and decreased USP28 protein levels in cancer cells, which both lead to enhanced c-myc ubiquitination and proteasomal degradation

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