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Mortality is high in Coronavirus disease 2019 patients with pre-existing comorbidities and advanced age. learn more Associated complications have added to the negative prognosis. Nevertheless, many have fully recovered, even among the most fragile. Factors associated with their survival was investigated.

Retrospective study of patients aged ≥90 years admitted for COVID-19 to the Internal Medicine wards of two hospitals in Lombardy, Italy.

Among 34 patients with SARS-CoV-2 pneumonia, 33 (97.1%) had respiratory failure. Eighteen patients (52.9%) survived and 16 (47.1%) died during hospital stay. Survivors compared to deceased had a significantly longer hospitalization (19 vs. 10 days respectively; p=0.02), a better PaO2FiO2 ratio (241 vs. 171 respectively; p=0.003), higher lymphocyte counts (p=0.01) and lower serum LDH levels (p<0.001) at admission. At multivariate analysis only higher PaO2FiO2 was associated with survival (OR 1.06 [95%CI 1.0-1.03]; p=0.02). Kaplan-Meier analysis showed a significant difference in event-free survival between patients treated or not with LMWH (p<0.0001) and between those treated or not with beta-blockers (p=0.008). Cox regression, performed in the subgroup of patients who received LMWH, did not show significant difference for sex (HR 2.7 [95% CI 0.53-14.3], p=0.23), CCI (HR 0.7 [95% CI 0.37-1.45], p=0.38), PaO2FiO2 ratio (HR 0.98 [95% CI 0.97-1.0], p=0.07), corticosteroid therapy (HR 0.99 [95% CI 0.22-4.5], p=0.99) and beta-blocker therapy (HR 2.8 [95% CI 0.56-14,7], p=0.21).

Despite higher mortality in elderly, treatment with LMWH and betablockers might be associated with better survival. Dedicated studies are required to confirm our result.

Despite higher mortality in elderly, treatment with LMWH and betablockers might be associated with better survival. Dedicated studies are required to confirm our result.Wound healing is a complex process based on the coordinated signaling molecules and dynamic interactions between the engineered scaffold and newly formed tissue. So far, most of the engineered scaffolds used for the healing of full-thickness skin wounds do not mimic the natural extracellular matrix (ECM) complexity and therefore are not able to provide an appropriate niche for endogenous tissue regeneration [1]. To address this gap and to accelerate the wound healing process, we present biomimetic bilayer scaffolds compositing of gelatin nanofibers (GFS) and photocrosslinkable composite hydrogels loaded with epidermal growth factors (EGF). The nanofibers operate as the dermis layer, and EGF-loaded composite hydrogels acted as the epidermis matrix for the full-thickness wound healing application. The hydrogels are composed of gelatin metacryloyl (GelMA) modified with silicate nanoplatelets (Laponite). To overcome the challenges of transdermal delivery of EGF, including short half-life and lack of efficient formulation precise, controlled delivery was attained by immobilization of EGF on Laponite. It is shown that the addition of 1wt% silicate nanoplatelet increases the compressive modulus of the hydrogels by 170%. In vitro wound closure analysis also demonstrated improved adhesion of the scaffolds to the native tissue by 3.5 folds. Moreover, the tunable hemostatic ability of the scaffolds due to the negatively charged nanoplatelets is shown. In an established excisional full-thickness wound model, an enhanced wound closure (up to 93.1 ± 1.5%) after 14 days relative to controls (GFS and saline-treated groups) is demonstrated. The engineered adhesive and hemostatic scaffolds with sustained release of the growth factors have the potential to stimulate complete skin regeneration for full-thickness wound healing.Tendon adhesion formation describes the development of fibrotic tissue between the tendon and its surrounding tissues, which commonly occurs as a reaction to injury or surgery. Its impact on function and quality of life varies from negligible to severely disabling, depending on the affected area and extent of adhesion formed. Thus far, treatment options remain limited with prophylactic anti-inflammatory medications and revision surgeries constituting the only tools within the doctors' armamentarium - neither of which provides reliable outcomes. In this review, the authors aim to collate the current understanding of the pathophysiological mechanisms underlying tendon adhesion formation, highlighting the significant role ascribed to the inflammatory cascade in accelerating adhesion formation. The bulk of this article will then be dedicated to critically appraising different therapeutic structures like nanoparticles, hydrogels and fibrous membranes fabricated by various cutting-edge technologies for adhesion formation prophylaxis. Emphasis will be placed on the role of the fibrous membranes, their ability to act as drug delivery vehicles as well as the combination with other therapeutic structures (e.g., hydrogel or nanoparticles) or fabrication technologies (e.g., weaving or braiding). Finally, the authors will provide an opinion as to the future direction of the prevention of tendon adhesion formation in view of scaffold structure and function designs.The tendon interfascicular matrix (IFM) binds tendon fascicles together. As a result of its low stiffness behaviour under small loads, it enables non-uniform loading and increased overall extensibility of tendon by facilitating fascicle sliding. This function is particularly important in energy storing tendons, with previous studies demonstrating enhanced extensibility, recovery and fatigue resistance in the IFM of energy storing compared to positional tendons. However, the compositional specialisations within the IFM that confer this behaviour remain to be elucidated. It is well established that the IFM is rich in elastin, therefore we sought to test the hypothesis that elastin depletion (following elastase treatment) will significantly impact IFM, but not fascicle, mechanical properties, reducing IFM resilience in all samples, but to a greater extent in younger tendons, which have a higher elastin content. Using a combination of quasi-static and fatigue testing, and optical imaging, we confirmed our hypothesis, demonstrating that elastin depletion resulted in significant decreases in IFM viscoelasticity, fatigue resistance and recoverability compared to untreated samples, with no significant changes to fascicle mechanics.