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BackgroundThe COVID-19 epidemic has affected over 2.6 million people across 210 countries. Recent studies have shown that patients with COVID-19 experience relevant gastrointestinal (GI) symptoms. We aimed to perform a systematic review and meta-analysis on the GI symptoms of COVID-19.MethodsA literature search was conducted via electronic databases, including PubMed, Embase, Scopus, and Google Scholar, from inception until 20 March 2020. Data were extracted from relevant studies. A systematic review of GI symptoms and a meta-analysis comparing symptoms in severe and non-severe patients was performed using RevMan V.5.3.ResultsPooled data from 2477 patients with a reverse transcription-PCR-positive COVID-19 infection across 17 studies were analysed. Our study revealed that diarrhoea (7.8%) followed by nausea and/or vomiting (5.5 %) were the most common GI symptoms. We performed a meta-analysis comparing the odds of having GI symptoms in severe versus non-severe COVID-19-positive patients. 4 studies for nausea and/or vomiting, 5 studies for diarrhoea and 3 studies for abdominal pain were used for the analyses. There was no significant difference in the incidence of diarrhoea (OR=1.32, 95% CI 0.8 to 2.18, Z=1.07, p=0.28, I2=17%) or nausea and/or vomiting (OR=0.96, 95% CI 0.42 to 2.19, Z=0.10, p=0.92, I2=55%) between either group. However, there was seven times higher odds of having abdominal pain in patients with severe illness when compared with non-severe patients (OR=7.17, 95% CI 1.95 to 26.34, Z=2.97, p=0.003, I2=0%).ConclusionOur study has reiterated that GI symptoms are an important clinical feature of COVID-19. Patients with severe disease are more likely to have abdominal pain as compared with patients with non-severe disease.

In Crohn's disease, pathogenic Th17-cells express low levels of CD39 ectonucleotidase and are refractory to the immunosuppressive effects of unconjugated bilirubin (UCB), an endogenous ligand for aryl-hydrocarbon-receptor (AhR). This resistance to AhR ligation might be associated with alterations in responses to hypoxia. Limited exposure to hypoxia appears beneficial in acute tissue injury. However, in protracted inflammation, hypoxemia may paradoxically result in Th17-cell activation. We report here that in vitro exposure of Th17-cells from Crohn's disease patients to hypoxia limits responsiveness to AhR stimulation by UCB, as reflected by lower CD39 levels. Blockade of hypoxia-inducible-factor-1alpha (HIF-1α) upregulates CD39 and favors Th17-cell regulatory responses. Resistance of Th17-cells to AhR signaling results, in part, from HIF-1α-dependent induction of ATP-binding cassette (ABC) transporters: multidrug-resistance-protein-1 (MDR1) and multidrug-resistance-associated-protein-4 (MRP4). Increased ABC transporters promote efflux of suppressive AhR ligands, such as UCB, from Th17-cells. Inhibition of MDR1, MRP4 and/or HIF-1α with ritonavir (RTV) reconstitutes AhR function in Th17-cells, enhancing therapeutic effects of UCB in dextran-sulfate-sodium-induced experimental colitis. Deleterious effects of hypoxia on Th17-cells in Crohn's disease can be ameliorated either by inhibiting HIF-1α or by suppressing ABC transporters to increase UCB availability as an AhR substrate. Targeting HIF-1α-ABC transporters could provide innovative therapeutic pathways for IBD.

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Purpose This paper aims to examine the impact of key affective moments of a playful experience on consumers’ overall retrospective evaluations. Design/methodology/approach The authors build on past literature on hedonic psychology and sequential preferences and link it to specific characteristics of playful experiences to derive their hypotheses. The hypotheses are tested through two field experiments conducted at a videogame arcade. Findings Results demonstrated that consumers’ overall evaluations are better aligned with the affective intensity at the final or end moment of a playful experience. Findings also revealed the complexity of understanding playful experiences, for it is the meaningfulness of end moments rather than simply their recent position in the experience that underlies overall evaluations. When end moments cease to be meaningful, the trough or least affective intense moment impacts overall evaluations. Practical implications This research has implications for marketers who are deciding on which point of a playful experience to concentrate their resources for optimizing evaluations. Originality/value This research contributes to literature on playful consumption by illuminating how consumers rely on affective moments of a playful experience to construct overall evaluations. Additionally, it highlights the important role of meaningfulness of end moments, a relatively underexplored process, which extends literature on key moments and retrospective evaluations.

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Addiction does not begin with the harmful effects of being dependent on a particular consumption behaviour such as smoking, alcohol, or illegal drugs. Instead it starts with everyday seemingly benign behaviours that, through psychological, biophysical, and/or environmental triggers, can become harmful and morph into an addiction. We develop a framework based on harm and dependence that can help researchers better understand how consumers could become addicted to various types of everyday benign consumption behaviours (e.g., texting, shopping, plastic surgery, and other types of normally acceptable behaviours). Furthermore, the conceptual framework is based on expanding the concept of addiction to include the pre-addiction process with a focus on this continuum of benign to harmful behavioural consumption. This framework describes how consumers progress from a normal state of consumption into a state of addictive abuse and dependence. The framework discusses key issues and future research that can aid public policy researchers, practitioners, and marketers to better understand the entire pre-addiction process.

Inflammatory bowel disease (IBD) is a serious inflammatory condition of the gastrointestinal tract. Crohn's disease (CD) and ulcerative colitis (UC) are two of the most common IBD manifestations and are both associated with unfettered inflammation, often refractory to conventional immunosuppressive treatment. In both conditions, imbalance between effector and regulatory cell immune responses has been documented and is thought to contribute to disease pathogenesis. Purinergic signaling is a known modulator of systemic and local inflammation and growing evidences point to extracellular ATP/adenosine imbalance as a key determinant factor in IBD-associated immune dysregulation. In vitro and pre-clinical studies suggest a role for both ATP (P2) and adenosine (P1) receptors in dictating onset and severity of the disease. Moreover, our experimental data indicate ENTPD1/CD39 and CD73 ectoenzymes as pivotal modulators of intestinal inflammation, with clear translational importance. Here we will provide an updated overview of the current knowledge on the role of the purinergic signaling in modulating immune responses in IBD. We will also review and discuss the most promising findings supporting the use of purinergic-based therapies to correct immune dysregulation in CD and UC.