Mackinnonwollesen6650

To determine its thermophysical and mechanical behavior at the micro and macro levels, in order to see the feasibility of substituting petroleum-based PCMs with a more environmentally friendly bio-based one, a section devoted to the excellent PCM with lightweight aggregate (PCM-LWA concrete) is presented due to the lack of description given in other reviews.Background and Objectives Laryngeal cancer is one of the most common cancers in the upper aerodigestive tract, and tobacco and alcohol habits are the most relevant risk factors. The role of these risk factors in the incidence of laryngeal carcinomas is well known, yet only a few studies have been conducted on their role as risk factors of prognosis. The aim of the study was to assess the impact of clinical-demographic data on overall survival (OS), disease-free survival (DFS), and disease-specific survival (DSS) in patients with advanced-stage laryngeal cancer (Stage III-IV) who underwent total laryngectomy. Materials and Methods This retrospective study was carried out on patients with Stage III-IV laryngeal squamous cell carcinoma treated with total laryngectomy between 2004 and 2014. For each patient, clinical and anamnestic data were collected and collated in a database, including alcohol and smoking habits. Results Considering the variable age, family history, alcohol, grading, subsite, stage, pT stage, pN stage, and adjuvant therapy, no statistical significance was found for five-year OS. Smoking was the only variable that was statistically significant (p = 0.0043). A relevant difference was noted in the five-year DFS between pN-negative and pN-positive tumors (74.3% vs. 55.26%, respectively; p = 0.056), and a statistically significant difference was found between non- and ≤20 cigarettes/day smokers and heavy smokers (77.78% vs. 53.66%, respectively; p = 0.021). The five-year disease-specific survival rate was 68.83%, and a significant difference was detected for the smoking and pN stage variables. Heavy smokers (43.90% died vs. 16.67% of the non- and ≤20 cigarettes/day smokers; p = 0.0057) and pN-positive (42.1% died vs. 20.51% of the pN-negative patients; p = 0.042) patients had a worse prognosis. Conclusion Smoking in our study was found to be an important independent risk factor for worse OS and DSS in patients with advanced laryngeal cancer.In the last few decades, the newly emerging field of epigenetic regulation of glycosylation acquired more importance because it is unraveling physiological and pathological mechanisms related to glycan functions. Glycosylation is a complex process in which proteins and lipids are modified by the attachment of monosaccharides. The main actors in this kind of modification are the glycoenzymes, which are translated from glycosylation-related genes (or glycogenes). The expression of glycogenes is regulated by transcription factors and epigenetic mechanisms (mainly DNA methylation, histone acetylation and noncoding RNAs). This review focuses only on these last ones, in relation to cancer and other diseases, such as inflammatory bowel disease and IgA1 nephropathy. In fact, it is clear that a deeper knowledge in the fine-tuning of glycogenes is essential for acquiring new insights in the glycan field, especially if this could be useful for finding novel and personalized therapeutics.Annexin A1 (ANXA1) is a calcium-dependent phospholipid-binding protein overexpressed in pancreatic cancer (PC). ANXA1 expression has been shown to take part in a wide variety of cancer biology, including carcinogenesis, cell proliferation, invasion, apoptosis, and metastasis, in addition to the initially identified anti-inflammatory effect in experimental settings. We hypothesized that ANXA1 expression is associated with cell proliferation and survival in PC patients. To test this hypothesis, we analyzed 239 PC patients in The Cancer Genome Atlas (TCGA) and GSE57495 cohorts. ANXA1 expression correlated with epithelial-mesenchymal transition (EMT) but weakly with angiogenesis in PC patients. ANXA1-high PC was significantly associated with a high fraction of fibroblasts and keratinocytes in the tumor microenvironment. ANXA1 high PC enriched multiple malignant gene sets, including hypoxia, tumor necrosis factor (TNF)-α signaling via nuclear factor-kappa B (NF-kB), and MTORC1, as well as apoptosis, protein secretion, glycolysis, and the androgen response gene sets consistently in both cohorts. ANXA1 expression was associated with TP53 mutation alone but associated with all KRAS, p53, E2F, and transforming growth factor (TGF)-β signaling pathways and also associated with homologous recombination deficiency in the TCGA cohort. ANXA1 high PC was associated with a high infiltration of T-helper type 2 cells in the TME, with advanced histological grade and MKI67 expression, as well as with a worse prognosis regardless of the grade. ANXA1 expression correlated with a sensitivity to gemcitabine, doxorubicin, and 5-fluorouracil in PC cell lines. In conclusion, ANXA1 expression is associated with EMT, cell proliferation, survival, and the drug response in PC.Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. The pathogenesis of psoriasis may involve the dysfunction of indoleamine 2,3-dioxygenase 2 or of UBA domain containing 1-mediated regulation of CARD14/CARMA2sh. The blood cells of psoriasis patients showed the enhanced oxidative stress/autophagy flux and decreased 20S proteasome activity. Elafin, clusterin, or selenoprotein P may act as biomarkers for psoriasis and comorbid metabolic diseases. The proteomic profile of psoriasis lesions showed the dysfunction of dermal fibroblasts; up-regulation of proinflammatory factors and signal transduction or down-regulation of structural molecules. The skin inflammation in psoriasis may populate certain gut bacteria, such as Staphylococcus aureus and Streptococcus danieliae, which worsen the skin inflammation in turn. Tasocitinib The psoriasis-associated pruritus may be caused by immune, nervous, or vascular mechanisms. In addition to current oral treatments and biologics, a new treatment option for psoriasis is now being developed, such as retinoic-acid-receptor-related orphan nuclear receptor γt inhibitors, IL-36 receptor antagonist, or aryl hydrocarbon receptor agonist. Antimicrobial peptides and innate immune cells, involved in the pathogenesis of psoriasis, may be novel therapeutic targets. The pathomechanisms and responses to drugs in collagen diseases are partially shared with and partially different from those in psoriasis. Certain nutrients can exacerbate or regulate the progress of psoriasis. The articles in this Special Issue will encourage attractive approaches to psoriasis by future researchers.