Even if it looks like COVID-19, think again: the importance of differential diagnosis during a pandemic.

Introduction: Antisynthetase syndrome (ASSD) is a rare auto-immune condition that can present as interstitial lung disease (ILD) and progress into Acute Respiratory Distress Syndrome (ARDS).

Importance: The purpose of this clinical case is to highlight the importance of considering less prevalent causes of ARDS amid the COVID-19 pandemic.

Case Report: We present a 56-year-old Belgian female of African descent without past medical history who demonstrated typical signs of COVID-19 at the start of the pandemic.

Atriobronchial Fistula Complicated by Septic Cerebral Air Emboli After Pulmonary Vein Ablation.

Objective: To describe a case of an infected atriobronchial fistula as a late complication after pulmonary vein ablation, leading to septic air emboli and requiring urgent cardiac surgery.

Data Sources: Clinical observation.

Study Selection: Case report.

From therapeutic hypothermia towards targeted temperature management: a decade of evolution.

More than a decade after the first randomised controlled trials with targeted temperature management (TTM), it remains the only treatment with proven favourable effect on postanoxemic brain damage after out-of-hospital cardiac arrest. Other well-known indications include neurotrauma, subarachnoidal haemorrhage, and intracranial hypertension. When possible pitfalls are taken into consideration when implementing TTM, the side effects are manageable.

Dynamic recruitment of active proteasomes into polyglutamine initiated inclusion bodies.

Neurodegenerative disorders such as Huntington's disease are hallmarked by neuronal intracellular inclusion body formation. Whether proteasomes are irreversibly recruited into inclusion bodies in these protein misfolding disorders is a controversial subject. In addition, it has been proposed that the proteasomes may become clogged by the aggregated protein fragments, leading to impairment of the ubiquitin-proteasome system.

The DNAJB6 and DNAJB8 protein chaperones prevent intracellular aggregation of polyglutamine peptides.

Fragments of proteins containing an expanded polyglutamine (polyQ) tract are thought to initiate aggregation and toxicity in at least nine neurodegenerative diseases, including Huntington's disease. Because proteasomes appear unable to digest the polyQ tract, which can initiate intracellular protein aggregation, preventing polyQ peptide aggregation by chaperones should greatly improve polyQ clearance and prevent aggregate formation. Here we expressed polyQ peptides in cells and show that their intracellular aggregation is prevented by DNAJB6 and DNAJB8, members of the DNAJ (Hsp40) chaperone family.

Intracellular bacterial growth is controlled by a kinase network around PKB/AKT1.

With the emergence of multidrug resistant (MDR) bacteria, it is imperative to develop new intervention strategies. Current antibiotics typically target pathogen rather than host-specific biochemical pathways. Here we have developed kinase inhibitors that prevent intracellular growth of unrelated pathogens such as Salmonella typhimurium and Mycobacterium tuberculosis.

Concurrent infection with Schistosoma mansoni attenuates inflammation induced changes in colonic morphology, cytokine levels, and smooth muscle contractility of trinitrobenzene sulphonic acid induced colitis in rats.

Background And Aims: Crohn's disease, characterised by chronic T helper 1 (Th1) inflammation and dysmotility of the gut, is most prevalent in developed countries. Parasitic infections are most prevalent in developing countries and induce a T helper 2 (Th2) immune response. We hypothesised that this Th2 immune response protects against Th1 gut inflammation.

Effect of TNBS-induced morphological changes on pharmacological contractility of the rat ileum.

Intraluminal instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in ethanol is a classical model of colitis in the rat. Little is known about the time-related effect of TNBS on the contractility and morphology of the rat ileum. After 36 h, TNBS induced acute ileitis.