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Background Serum procalcitonin and high-sensitivity C-reactive protein (hs-CRP) elevations have been associated with pneumonia in adults. Our aim was to establish their diagnostic usefulness in a cohort of hospitalized multimorbid patients ≥65 years old admitted to hospital with acute respiratory symptoms. Methods With a retrospective cohort study design, all multimorbid patients ≥65 years-old with acute respiratory symptoms admitted to an internal medicine hospital ward in Italy from January to August 2013 were evaluated. Pneumonia diagnosis, comorbidities expressed through Cumulative Illness Rating Scale (CIRS), setting of living, length of stay, serum hs-CRP and procalcitonin at admission were collected for each patient. Data were analyzed with Mann-Whitney’s U test and multivariate Cox logistic regression analysis. A Receiver Operating Characteristic (ROC) curve was used to verify each biomarker’s association with pneumonia diagnosis. Results Four hundred fifty five patients (227 M) were included in the study, of whom 239 with pneumonia (138 M, mean age 80 ± 13) and 216 without pneumonia (89 M, mean age 80 ± 14). After adjustment for age and sex, median levels of hs-CRP were significantly higher in patients with pneumonia (116 mg/L, IQR 46.5–179.0, vs 22.5 mg/dl, IQR 6.9–84.4, p 61 mg/L were independently associated with a 3.59-fold increased risk of pneumonia (OR 3.59, 95 % CI 2.35–5.48, p < 0.0001). Conclusion In elderly multimorbid patients who require hospital admission for respiratory symptoms, serum hs-CRP testing seems to be more useful than procalcitonin for guiding the diagnostic process when clinical suspicion of pneumonia is present. Procalcitonin testing might hence be not recommended in this setting.

Autophagy is involved in different degenerative diseases and it may control epigenetic modifications, metabolic processes, stem cells differentiation as well as apoptosis. Autophagy plays a key role in maintaining the homeostasis of cartilage, the tissue produced by chondrocytes; its impairment has been associated to cartilage dysfunctions such as osteoarthritis (OA). Due to their location in a reduced oxygen context, both differentiating and mature chondrocytes are at risk of premature apoptosis, which can be prevented by autophagy. AutophagomiRNAs, which regulate the autophagic process, have been found differentially expressed in OA. AutophagomiRNAs, as well as other regulatory molecules, may also be useful as therapeutic targets. In this review, we describe and discuss the role of autophagy in OA, focusing mainly on the control of autophagomiRNAs in OA pathogenesis and their potential therapeutic applications.

Under many inflammatory contexts, such as tumor progression, systemic and peripheral immune response is tailored by reactive nitrogen species (RNS)-dependent post-translational modifications, suggesting a biological function for these chemical alterations. RNS modify both soluble factors and receptors essential to induce and maintain a tumor-specific immune response, creating a "chemical barrier" that impairs effector T cell infiltration and functionality in tumor microenvironment and supports the escape phase of cancer. RNS generation during tumor growth mainly depends on nitric oxide production by both tumor cells and tumor-infiltrating myeloid cells that constitutively activate essential metabolic pathways of l-arginine catabolism. This review provides an overview of the potential immunological and biological role of RNS-induced modifications and addresses new approaches targeting RNS either in search of novel biomarkers or to improve anti-cancer treatment.

Abstract Mitochondria provide energy for cells via oxidative phosphorylation. Reactive oxygen species, a byproduct of this mitochondrial respiration, can damage mitochondrial DNA (mtDNA), and somatic mtDNA mutations have been found in all colorectal, ovarian, breast, urinary bladder, kidney, lung, and pancreatic tumors studied. The resulting altered mitochondrial proteins or tumor-associated mitochondrial Ags (TAMAs) are potentially immunogenic, suggesting that they may be targetable Ags for cancer immunotherapy. In this article, we show that the RENCA tumor cell line harbors TAMAs that can drive an antitumor immune response. We generated a cellular tumor vaccine by pulsing dendritic cells with enriched mitochondrial proteins from RENCA cells. Our dendritic cell–based RENCA mitochondrial lysate vaccine elicited a cytotoxic T cell response in vivo and conferred durable protection against challenge with RENCA cells when used in a prophylactic or therapeutic setting. By sequencing mtDNA from RENCA cells, we identified two mutated molecules: COX1 and ND5. Peptide vaccines generated from mitochondrial-encoded COX1 but not from ND5 had therapeutic properties similar to RENCA mitochondrial protein preparation. Thus, TAMAs can elicit effective antitumor immune responses, potentially providing a new immunotherapeutic strategy to treat cancer.

Abstract Background: Breast reconstruction after mastectomy using silicone implants is a surgical procedure that occasionally leads to capsular contracture formation. This phenomenon constitutes an important and persistent cause of morbidity, and no successful therapies are available to date. Recently, the use of acellular membranes as a protective material for silicone prostheses has been gaining attention due to their ability to prevent this adverse outcome. For this reason, the evaluation of the tissue-material integration and the induced biostimulation by acellular membranes results crucial. Evaluation of in vivo tissue integration and biostimulation induced by three different natural acellular collagen membranes. Methods: Scanning electron microscopy was performed to analyse the membrane porosity and cells-biomaterial interaction in vitro, both in dry and wet conditions. Adipose-derived stem cells were cultured in the presence of membranes, and the colonisation capacity and differentiation potential of cells were assessed. In vivo tests and ex vivo analyses have been performed to evaluate dermal integration, absorption degree and biostimulation induced by the evaluated membrane. Results: Analysis performed in vitro on the three different acellular dermal matrices evidenced that porosity and the morphological structure of membranes influence the liquid swelling ratio, affecting the cell mobility and the colonisation capacity. Moreover, the evaluated membranes influenced in different manner the adipose derived stem cells differentiation and their survival. In vivo investigation indicated that the absorption degree and the fluid accumulation surrounding the implant were membrane-dependent. Finally, ex vivo analysis confirmed the membrane-dependent behavior revealing different degree of tissue integration and biostimulation, such as adipogenic stimulation. Conclusion: The physico-chemical characteristics of the membranes play a key role in the biostimulation of the cellular environment inducing the development of well-organized adipose tissue.