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The impact of corticosteroid withdrawal on medium-term graft histological changes in kidney transplant (KT) recipients under standard immunosuppression is uncertain. As part of an open-label, multicenter, prospective, phase IV, 24-month clinical trial (ClinicalTrials.gov, NCT02284464) in low-immunological-risk KT recipients, 105 patients were randomized, after a protocol-biopsy at 3 months, to corticosteroid continuation (CSC, n = 52) or corticosteroid withdrawal (CSW, n = 53). Both groups received tacrolimus and MMF and had another protocol-biopsy at 24 months. The acute rejection rate, including subclinical inflammation (SCI), was comparable between groups (21.2 vs. 24.5%). No patients developed dnDSA. Inflammatory and chronicity scores increased from 3 to 24 months in patients with, at baseline, no inflammation (NI) or SCI, regardless of treatment. CSW patients with SCI at 3 months had a significantly increased chronicity score at 24 months. HbA1c levels were lower in CSW patients (6.4 ± 1.2 vs. 5.7 ± 0.6%; p = 0.013) at 24 months, as was systolic blood pressure (134.2 ± 14.9 vs. 125.7 ± 15.3 mmHg; p = 0.016). Allograft function was comparable between groups and no patients died or lost their graft. An increase in chronicity scores at 2-years post-transplantation was observed in low-immunological-risk KT recipients with initial NI or SCI, but CSW may accelerate chronicity changes, especially in patients with early SCI. This strategy did, however, improve the cardiovascular profiles of patients.The clinical characteristics and laboratory values of patients with septic shock who experience in-hospital cardiac arrest (IHCA) have not been well studied. This study aimed to evaluate the prevalence of IHCA after admission into the emergency department and to identify the factors that increase the risk of IHCA in septic shock patients. This observational cohort study used a prospective registry of septic shock patients and was conducted at the emergency department of a university-affiliated hospital. The data of 887 adult (age ≥ 18 years) septic shock (defined using the Sepsis-3 criteria) patients who were treated with a protocol-driven resuscitation bundle therapy and were admitted to the intensive care unit between January 2010 and September 2018 were analyzed. The primary endpoint was the occurrence of sepsis-associated cardiac arrest. The patient mean age was 65 years, and 61.8% were men. Sepsis-associated cardiac arrest occurred in 25.3% of patients (n = 224). The 28-day survival rate after cardiac arrest was 6.7%. Multivariate logistic regression identified chronic pulmonary disease (odds ratio (OR) 2.06), hypertension (OR 0.48), unknown infection source (OR 1.82), a hepatobiliary infection source (OR 0.25), C-reactive protein (OR 1.03), and serum lactate level 6 h from shock (OR 1.34). Considering the high mortality rate of sepsis-associated cardiac arrest after cardiopulmonary resuscitation, appropriate monitoring is required in septic shock patients with major risk factors for IHCA.Nanoporous Shape Memory Alloys (SMA) are widely used in aerospace, military industry, medical and health and other fields. More and more attention has been paid to its mechanical properties. In particular, when the size of the pores is reduced to the nanometer level, the effect of the surface effect of the nanoporous material on the mechanical properties of the SMA will increase sharply, and the residual strain of the SMA material will change with the nanoporosity. In this work, the expression of Young's modulus of nanopore SMA considering surface effects is first derived, which is a function of nanoporosity and nanopore size. Based on the obtained Young's modulus, a constitutive model of nanoporous SMA considering residual strain is established. Then, the stress-strain curve of dense SMA based on the new constitutive model is drawn by numerical method. The results are in good agreement with the simulation results in the published literature. Finally, the stress-strain curves of SMA with different nanoporosities are drawn, and it is concluded that the Young's modulus and strength limit decrease with the increase of nanoporosity.The aim of the present special issue, proposed by two Co-Guest Editors with expertise in Clinical Microbiology and Medicinal Chemistry, is to collect and disseminate some of the most significant and innovative contributions focused on biofilm removal strategies, based on the use of natural or synthetic compounds/molecules/peptides or nanoparticles as well as biofilm formation inhibition aimed at both the control and monitoring of biofilm infections in medicine, food, industry, and natural environments [...].This study aimed to obtain and characterize extracted hemp oil enriched in cannabidiol (CBD) by decarboxylation of cannabidiolic acid (CBDA) and to give new insights into its antioxidant and anticancer effects. Optimization of CBDA decarboxylation in hemp oil was performed, and CBD and CBDA contents and purities were determined by flash chromatography, 1H- and 13C-NMR. The antioxidant properties of CBD-enriched oil were investigated by Fe2+ chelating activity, Fe3+ reducing antioxidant power assay, O2●- scavenging activity, HO● scavenging ability and lipid peroxidation inhibitory assay, and its cytotoxicity, apoptosis- and oxidative stress-inducing effects on NHDF, MeWo, HeLa, HepG2 and HOS cells were determined. The CBD concentration in hemp oil was increased by CBDA soft decarboxylation optimized at 90 °C, for 1 h and the resulting oil was capable of reducing iron, scavenging free radicals and inhibiting lipid peroxidation in cell-free oxidative conditions. EN450 ic50 CBD-enriched oil promoted NHDF proliferation at up to 15 µg CBD/mL, while inducing apoptosis and ROS production and modulating antioxidant enzymes' gene expression in cancer cells, being selective for osteosarcoma cells, and induced apoptosis by p53- and ROS-independent mechanisms. CBD-enriched hemp oil demonstrated antioxidant properties in oxidative conditions and promoted normal fibroblasts' proliferation, while inducing apoptosis and ROS production in cancer cells.
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