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Human coronaviruses (hCoVs) cause severe respiratory illness in the elderly. Age-related impairments in innate immunity and suboptimal virus-specific T cell and antibody responses are believed to cause severe disease upon respiratory virus infections. This phenomenon has recently received increased attention, as elderly patients are at substantially elevated risk for severe COVID-19 disease and experience increased rates of mortality following SARS-CoV-2 infection compared with younger populations. However, the basis for age-related fatal pneumonia following pathogenic hCoVs is not well understood. In this Review, we provide an overview of our current understanding of hCoV-induced fatal pneumonia in the elderly. We describe host immune response to hCoV infections derived from studies of young and aged animal models and discuss the potential role of age-associated increases in sterile inflammation (inflammaging) and virus-induced dysregulated inflammation in causing age-related severe disease. We also highlight the existing gaps in our knowledge about virus replication and host immune responses to hCoV infection in young and aged individuals.Cutaneous Lupus Erithematosus is one of the most common manifestation of Systemic Lupus Erithematosus and can be featured by the onset of cutaneous vasculitis which can bring to skin ulcers, expecially on the extremities. The "common" aetiopathogenesis can be summarized as following 1) an antiself response to the endothelial cells which brings to frequent ischemic or thrombotic episodes, 2) the drugs therapy; recently authors have been demostrated a correlation between Metalloproteinase Matrix (MMP) and Cutaneous LES. Here we present the case of a 33 y.o. woman affected by a rheumatic disorder, which has developed a chronic ulcer on her left leg. After several and different unsuccessful approaches, as homologous and autologous skin graft, and considering both the refusal of other surgery even if enhanced by Negative Pressure Therapy and the compromised vascularization which contraindicated the use of flaps, we decided to use a dressing based on the TLC-NOSF (Technology Lipido-Colloid plus Nano-Oligo Saccharide Factor) protease inhibitor, a metalloproteinase regulator. The dressing was changed 2 times/week for the first 2 months and 1 time/week for other 2 months. The ulcer became smaller at every session and we obtained a full coverage at 4th month. KEY WORDS Nano-oligo saccharide factor, Wound.

Intraabdominal schwannomas are rare benign tumors. In this study, we aimed to present our clinical experience in patients with intrabdominally located Schwannoma.

Patients who received the diagnosis of intrabdominal schwannoma between 2011-2019 were retrospectively examined. Demographic and clinical characteristics, treatment methods, short- and long-term results and immunohistochemical characteristics of the patients were analyzed.

A total of 7 patients were included in the study. Four patients were female and three were male. The mean age was 51.5 (31-63) years. The most common clinical presentation was abdominal pain (57.1%). Tumor location was stomach (n=2), pelvic region (n=2), rectum (n=1), retropancreas (n=1), and left juxtadrenal space (n=1). Postoperative wound infection developed in one patient and pancreatic fistula complication was seen in one patient. Re-admissions to the hospital were due to anemia and pleural effusion in two patients. The mean tumor diameter was 6 cm (0.3-13 cm). All patients were S 100 strongly positive Mitoses / 50 HPFs (high power field), <2 Ki67 <3%. The mean follow- up period was 60 months. Currently, 5 patients are being followed without disease, 1 patient survives despite recurrence and 1 patient has died due to non-cancer reasons.

Intrabdominal schwannomas are rare tumors which most commonly exhibit gastrointestinal involvement. Since these tumors are mostly benign, the long-term prognosis of patients is good. Schwannoma should be kept in mind in the differential diagnosis of intrabdominal masses. Radical resections with high morbidity and mortality should be avoided if preoperative diagnosis is made.

Abdominal tumor, Mesenchymal tumor, Nerve sheath tumor, Schwannoma.

Abdominal tumor, Mesenchymal tumor, Nerve sheath tumor, Schwannoma.Budding yeast, Saccharomyces cerevisiae, serves as a prime biological model to study mechanisms underlying asymmetric growth. Previous studies have shown that prior to bud emergence, polarization of a conserved small GTPase Cdc42 must be established on the cell membrane of a budding yeast. Additionally, such polarization contributes to the delivery of cell wall remodeling enzymes and hydrolase from cytosol through the membrane, to change the mechanical properties of the cell wall. This leads to the hypothesis that Cdc42 and its associated proteins at least indirectly regulate cell surface mechanical properties. Selleckchem N-butyl-N-(4-hydroxybutyl) nitrosamine However, how the surface mechanical properties in the emerging bud are changed and whether such change is important are not well understood. To test several hypothesised mechanisms, a novel three-dimensional coarse-grained particle-based model has been developed which describes inhomogeneous mechanical properties of the cell surface. Model simulations predict alternation of the levels of stretching and bending stiffness of the cell surface in the bud region by the polarized Cdc42 signals is essential for initiating bud formation. Model simulations also suggest that bud shape depends strongly on the distribution of the polarized signaling molecules while the neck width of the emerging bud is strongly impacted by the mechanical properties of the chitin and septin rings. Moreover, the temporal change of the bud mechanical properties is shown to affect the symmetry of the bud shape. The 3D model of asymmetric cell growth can also be used for studying viral budding and other vegetative reproduction processes performed via budding, as well as detailed studies of cell growth.Shelter-in-place and other confinement strategies implemented in the current COVID-19 pandemic have created stratified patterns of contacts between people close contacts within households and more distant contacts between the households. The epidemic transmission dynamics is significantly modified as a consequence. We introduce a minimal model that incorporates these household effects in the framework of mean-field theory and numerical simulations. We show that the reproduction number R 0 depends on the household size in a surprising way linearly for relatively small households, and as a square root of size for larger households. We discuss the implications of the findings for the lockdown, test, tracing, and isolation policies.

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