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Se i virus A/H5N1 acquisissero la capacità di diffondersi tra gli esseri umani potrebbe verificarsi una trasmissione su larga scala, ma a oggi la trasmissione da uomo a uomo non è mai stata confermata
Ecdc/Efsa, H5N1 ha già fatto passi verso l’adattamento ai mammiferi
‘Disponibili a essere parte attiva’. Anticorpi per prevenirlo
Objectives
An increased risk of stroke has been reported among patients with COVID-19 caused by SARS-CoV-2. We aimed to investigate the nationwide prevalence of SARS-CoV-2 among patients with acute ischaemic stroke and to study the impact on stroke severity, quality of care and mortality on an individual patient level.
Design
This was a nationwide register-based cohort study.
Setting
We used data from several Danish registers which were linked at an individual patient level using the unique civil registration number assigned to all Danish citizens. Patients were identified from the Danish Stroke Registry and information on SARS-CoV-2 infection status was collected from the Danish National COVID-19 Registry. Concurrent SARS-CoV-2 infection was defined as a positive PCR test within 31 days prior to, and 1 day after, stroke admission. Information on comorbidity was collected from the Danish National Patient Registry and information on vital status was collected from the Danish Civil Registration System.
Participants
A total of 11 502 patients admitted with acute ischaemic stroke from 10 March 2020 to 31 May 2021 were included in the study.
Results
Among the included patients, the majority (84.6%) were tested for SARS-CoV-2, but only 68 had a positive test. These patients were more prone to have atrial fibrillation and were more often treated with reperfusion therapy. They had a significantly increased risk of severe stroke (adjusted relative risk (aRR) 1.93, 95% CI: 1.22 to 3.04) and a significantly increased 30-day mortality risk (aRR 2.29, 95% CI: 1.19 to 4.39). There was no difference in the proportion of patients fulfilling relevant performance measures on quality of care.
Conclusion
In this nationwide study, only 0.6% of patients with acute ischaemic stroke were tested positive for a concurrent SARS-CoV-2 infection. The patients with SARS-CoV-2 presented with more severe strokes.
In una circolare. Secondo le raccomandazioni dell’Ecdc
Studio dell’Università di Trento pubblicato su ‘Science Advances
Seduta del Consiglio Marche. Bassetti, nel 2003 salvò il pianeta
Annals of Internal Medicine, Ahead of Print.
Annals of Internal Medicine, Ahead of Print.
Circulation, Ahead of Print. BACKGROUND:Viral infections can cause acute respiratory distress syndrome (ARDS), systemic inflammation, and secondary cardiovascular complications. Lung macrophage subsets change during ARDS, but the role of heart macrophages in cardiac injury during viral ARDS remains unknown. Here we investigate how immune signals typical for viral ARDS affect cardiac macrophage subsets, cardiovascular health, and systemic inflammation.METHODS:We assessed cardiac macrophage subsets using immunofluorescence histology of autopsy specimens from 21 patients with COVID-19 with SARS-CoV-2–associated ARDS and 33 patients who died from other causes. In mice, we compared cardiac immune cell dynamics after SARS-CoV-2 infection with ARDS induced by intratracheal instillation of Toll-like receptor ligands and an ACE2 (angiotensin-converting enzyme 2) inhibitor.RESULTS:In humans, SARS-CoV-2 increased total cardiac macrophage counts and led to a higher proportion of CCR2+(C-C chemokine receptor type 2 positive) macrophages. In mice, SARS-CoV-2 and virus-free lung injury triggered profound remodeling of cardiac resident macrophages, recapitulating the clinical expansion of CCR2+macrophages. Treating mice exposed to virus-like ARDS with a tumor necrosis factor α–neutralizing antibody reduced cardiac monocytes and inflammatory MHCIIloCCR2+macrophages while also preserving cardiac function. Virus-like ARDS elevated mortality in mice with pre-existing heart failure.CONCLUSIONS:Our data suggest that viral ARDS promotes cardiac inflammation by expanding the CCR2+macrophage subset, and the associated cardiac phenotypes in mice can be elicited by activating the host immune system even without viral presence in the heart.
Objective
Dipeptidase-1 (DPEP-1) is a recently discovered leucocyte adhesion receptor for neutrophils and monocytes in the lungs and kidneys and serves as a potential therapeutic target to attenuate inflammation in moderate-to-severe COVID-19. We aimed to evaluate the safety and efficacy of the DPEP-1 inhibitor, LSALT peptide, to prevent specific organ dysfunction in patients hospitalised with COVID-19.
Design
Phase 2a randomised, placebo-controlled, double-blinded, trial.
Setting
Hospitals in Canada, Turkey and the USA.
Participants
A total of 61 subjects with moderate-to-severe COVID-19.
Interventions
Randomisation to LSALT peptide 5 mg intravenously daily or placebo for up to 14 days.
Primary and secondary outcome measures
The primary endpoint was the proportion of subjects alive and free of respiratory failure and/or the need for renal replacement therapy (RRT). Numerous secondary and exploratory endpoints were assessed including ventilation-free days, and changes in kidney function or serum biomarkers.
Results
At 28 days, 27 (90.3%) and 28 (93.3%) of subjects in the placebo and LSALT groups were free of respiratory failure and the need for RRT (p=0.86). On days 14 and 28, the number of patients still requiring more intensive respiratory support (O2 ≥6 L/minute, non-invasive or invasive mechanical ventilation or extracorporeal membrane oxygenation) was 6 (19.4%) and 3 (9.7%) in the placebo group versus 2 (6.7%) and 2 (6.7%) in the LSALT group, respectively (p=0.14; p=0.67). Unadjusted analysis of ventilation-free days demonstrated 22.8 days for the LSALT group compared with 20.9 in the placebo group (p=0.4). LSALT-treated subjects had a significant reduction in the fold expression from baseline to end of treatment of serum CXCL10 compared with placebo (p=0.02). Treatment-emergent adverse events were similar between groups.
Conclusion
In a Phase 2 study, LSALT peptide was demonstrated to be safe and tolerated in patients hospitalised with moderate-to-severe COVID-19.
Trial registration number
NCT04402957.
In a meta-analysis, testing reduced antibiotic use in some test-positive patients, but not in patients overall.
Basato su Omvs ricombinanti, colma lacune prodotti precedenti
Studio apre prospettive sul Long Covid
We read Kennedy et al1’s findings with interest, and report in-depth analyses of antibody and T cell responses in patients with inflammatory bowel disease (IBD) to COVID-19 vaccination. We prospectively recruited 100 SARS-CoV-2-uninfected patients with IBD on varying treatments at the Royal Melbourne Hospital (HREC/74403/MH-2021). Healthcare workers who did not have IBD and were not on immunosuppressive medication were enrolled as controls with approvals from Melbourne Health (HREC/68355/MH-2020) and University of Melbourne (HREC 22268, 21626). Participant characteristics are outlined in table 1. IBD medication regimens needed to be stable for at least 8 weeks prior to enrolment. Only one participant was on concomitant low-dose systemic corticosteroids with anti-TNF combination therapy. Eighty-nine patients received BNT162b2 (Pfizer–BioNTech), and 11 received ChAdOx1 nCoV-19 (Oxford–AstraZeneca). No participants had a clinical history of SARS-CoV-2 infection at enrolment. Anti-S1/2 and anti-RBD SARS-CoV-2-specific antibodies were measured at baseline and at five time…
Although safe and effective vaccines against HBV (hepatitis B virus) are available, there are worldwide more than 2 billion people who had an HBV infection and about 250 million people suffering from chronic HBV infection. Chronic HBV infection is a major cause for liver diseases such as fibrosis, cirrhosis and hepatocellular carcinoma (HCC). It is estimated that about 800 000–1 000 000 people die each year due to the consequences of chronic HBV infection.1 Moreover, in almost all HBV-associated HCCs integrated HBV-DNA is found. Therapy options at present are limited and based on nucleoside/nucleotide analogues and interferon alpha. Since persistence of HBV infection frequently can be attributed to an insufficient cellular immune response approaches to rescue host immune response may help to eliminate infected cells and to suppress virus replication. A recent development are HBV-specific CARs (chimeric antigen receptors) human T-cells that are intended to recognise and eliminate HBV positive…
