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Tracheostomy (TQT) has emerged as a valuable alternative for patients with orotracheal intubation, especially those under prolonged mechanical ventilation (VMP), as in the case of chronic obstructive pulmonary disease (COPD). This population presents additional challenges, and the available information regarding their progression in specialized centers is limited in Argentina.A descriptive, retrospective, and cross-sectional study was conducted at Santa Catalina Neurorehabilitation Clinic between August 2015 and December 2018. Patients with COPD referred to the Intensive Care Unit (ICU), tracheostomized, and subsequently referred to the Center for Ventilation Disconnection and Rehabilitation (CDVMR) were included. Cases with missing data or derived from other CDVMRs were excluded. Clinical records and interviews were employed to collect demographic and progression data.Out of the 27 COPD patients included (4.9% of 555), the majority were males (63%) with an average age of 68.1 years. Most were admitted with AVMi, and 11 (45.8%) were successfully disconnected, while 11 (40.7%) were decannulated. Survival and home discharge were more frequent in decannulated patients (81.8% were discharged) compared to non-decannulated ones (50% deceased, and none were discharged).COPD patients undergoing TQT and VMP, who succeed in being decannulated, seem to have better prospects for survival and home discharge compared to those who do not have the cannula removed. There is a suggestion for the need for additional analytical studies to confirm these findings and improve the understanding of this specific population., (Universidad Nacional de Córdoba)

PYHIN proteins are only found in mammals and play key roles in the defense against bacterial and viral pathogens. The corresponding gene locus shows variable deletion and expansion ranging from 0 genes in bats, over 1 in cows, and 4 in humans to a maximum of 13 in mice. While initially thought to act as cytosolic immune sensors that recognize foreign DNA, increasing evidence suggests that PYHIN proteins also inhibit viral pathogens by more direct mechanisms. Here, we examined the ability of all 13 murine PYHIN proteins to inhibit HIV-1 and murine leukemia virus (MLV). We show that overexpression of p203, p204, p205, p208, p209, p210, p211, and p212 strongly inhibits production of infectious HIV-1; p202, p207, and p213 had no significant effects, while p206 and p214 showed intermediate phenotypes. The inhibitory effects on infectious HIV-1 production correlated significantly with the suppression of reporter gene expression by a proviral Moloney MLV-eGFP construct and HIV-1 and Friend MLV LTR luciferase reporter constructs. Altogether, our data show that the antiretroviral activity of PYHIN proteins is conserved between men and mice and further support the key role of nuclear PYHIN proteins in innate antiviral immunity.

Dysregulated metabolic dynamics are evident in both cancer and diabetes, with metabolic alterations representing a facet of the myriad changes observed in these conditions. This review delves into the commonalities in metabolism between cancer and type 2 diabetes (T2D), focusing specifically on the contrasting roles of oxidative phosphorylation (OXPHOS) and glycolysis as primary energy-generating pathways within cells. Building on earlier research, we explore how a shift towards one pathway over the other serves as a foundational aspect in the development of cancer and T2D. Unlike previous reviews, we posit that this shift may occur in seemingly opposing yet complementary directions, akin to the Yin and Yang concept. These metabolic fluctuations reveal an intricate network of underlying defective signaling pathways, orchestrating the pathogenesis and progression of each disease. The Warburg phenomenon, characterized by the prevalence of aerobic glycolysis over minimal to no OXPHOS, emerges as the predominant metabolic phenotype in cancer. Conversely, in T2D, the prevailing metabolic paradigm has traditionally been perceived in terms of discrete irregularities rather than an OXPHOS-to-glycolysis shift. Throughout T2D pathogenesis, OXPHOS remains consistently heightened due to chronic hyperglycemia or hyperinsulinemia. In advanced insulin resistance and T2D, the metabolic landscape becomes more complex, featuring differential tissue-specific alterations that affect OXPHOS. Recent findings suggest that addressing the metabolic imbalance in both cancer and diabetes could offer an effective treatment strategy. Numerous pharmaceutical and nutritional modalities exhibiting therapeutic effects in both conditions ultimately modulate the OXPHOS-glycolysis axis. Noteworthy nutritional adjuncts, such as alpha-lipoic acid, flavonoids, and glutamine, demonstrate the ability to reprogram metabolism, exerting anti-tumor and anti-diabetic effects. Similarly, pharmacological agents like metformin exhibit therapeutic efficacy in both T2D and cancer. This review discusses the molecular mechanisms underlying these metabolic shifts and explores promising therapeutic strategies aimed at reversing the metabolic imbalance in both disease scenarios.