Trust not in money: The effect of financial conflict of interest disclosure on dietary behavioural intention

Purpose To determine the impact of financial conflict of interest (FCI) disclosure on dietary behavioural intention related to the glycaemic index (GI) of food. Design/methodology/approach Seventy-two participants were randomly allocated to two conditions by reading an academic journal article about GI that contained an FCI disclosure (conflict) or a statement detailing that the authors had no FCI to declare (no-conflict). Using a questionnaire, participants made judgments about the article and authors as well as intention to perform GI-related behaviour. These were then analysed for significant differences between the two conditions. Findings Although no significant differences emerged between group means of judgments about the article, those in the conflict condition judged the authors as significantly less trustworthy and credible than those in the conflict condition. Contrary to expectation, those in the conflict condition reported significantly higher intentions to perform GI-related behaviour. Research limitations/implications The present research must be conducted in other populations of interest in order to establish if the results can be generalised. Practical implications The results suggest that FCI disclosure might be best placed at the beginning of articles and that education about FCI be made available to the general public. Originality/value This paper examines the practical implications of FCI disclosure. It also focuses on a readership beyond an academic community who is well-acquainted with the subject area and issues pertaining to FCI

Neutrophil defensins enhance lung epithelial wound closure and mucin gene expression in vitro.

Contains fulltext : 58772.pdf (publisher's version ) (Closed access)Human airways are frequently exposed to potentially harmful agents that cause tissue injury. Upon such injury, a repair process is initiated that comprises cell migration, proliferation, and differentiation. We have previously shown that human neutrophil defensins (human neutrophil peptides 1-3 [HNP1-3]) induce airway epithelial cell proliferation. Because of the role of cell proliferation in epithelial wound repair, we investigated the effect of HNP1-3 on airway epithelial wound closure and mucin gene expression in vitro. Using NCI-H292 airway epithelial cell cultures, we demonstrated that HNP1-3 cause a dose- and time-dependent increase of wound closure as well as increased cell migration. Furthermore, HNP1-3 caused a biphasic activation of the mitogen-activated protein kinase extracellular-regulated kinase 1 and 2 (ERK1/2). Both the effects of HNP1-3 on wound closure and ERK1/2 activation were blocked by specific inhibitors of the mitogen-activated protein kinase kinase MEK, whereas inhibitors of epidermal growth factor receptor tyrosine kinase, phosphatidylinositol 3-kinase, and Src did block defensin-enhanced wound closure but not ERK1/2 activation. Finally, HNP1-3 increased mRNA encoding the mucins MUC5B and MUC5AC, suggesting a role for defensins in mucous cell differentiation. These results indicate that neutrophil defensins increase epithelial wound repair in vitro, which involves migration and proliferation, and mucin production. Neutrophil defensin-enhanced wound repair appears to require epidermal growth factor receptor activation and downstream signaling pathways

The role of monoclonal antibody affinity in tumor immunotherapy evaluated in in vivo models for minimal residual disease

Contains fulltext : 23197___.PDF (publisher's version ) (Open Access

Martensitic transformation and ordering in heat-resistant Ni-Co-Cr-AI β\beta/γ\gamma eutectics

The method of thin-foil transmission electron microscopy was used to examine phase transformations in the $\beta$-phase, representing the main heat-resistant component, of $\beta$/$\gamma$ eutectics of the Ni-Co-Cr-Al system (mass % : 0–15 Co, 14–20 Cr, 8.5–10.5 Al). The martensitic transformation $\beta\rm (B2)\to L1_{0}$ took place in all the alloys, except those with 20 mass % Cr, when they were quenched in water from 1200°C. It was found for the first time that high-rank superstructures A$_2$B (Ni$_2$Al) and A$_5$B$_3$ (Ni$_5$Al$_3$) could be formed in a complex-alloyed $\beta$ solid solution. Phase transformations L1$_{0}\to\rm A_5B_3$, $\rm L1_0\to 14M$, $\rm L1_0\to B2\to A_2B$, and $\rm L1_0\to B2\to A_5B_3$ were observed in the $\beta$-component of the eutectics when isothennal annealing temperature was increased from 250 to 600°C. At a temperature of 400°C and higher those transformations were accompanied by the decomposition of the $\beta$ solid solution and the appearance of dispersed $\alpha$-Cr particles. Structural features of the aforementioned phase transformations in heat-resistant quaternary eutectics were considered

Expression of Ep-cam in normal, regenerating, metaplastic, and neoplastic liver.

Contains fulltext : 186033.pdf (publisher's version ) (Closed access

Synthesis of hybrid compounds by benzylation of acylhydrazones with 3,5-di-tert-butyl-4-hydroxybenzyl acetate

N-Benzylation of acylhydrazones of the hydroxybenzaldehyde series with 3,5-di-tert-butyl-4-hydroxybenzyl acetate was performed at room temperature in the absence of acid or base catalysts. Carboxamides do not react with 3,5-di-tert-butyl-4-hydroxybenzyl acetate under similar conditions. N-Benzylation of isoniazid and (diphenylphosphoryl)acetic acid hydrazones was shown to be an efficient method for the synthesis of new hybrid compounds containing moieties of biologically active acylhydrazones and sterically hindered phenols. N-Benzyl derivatives of isoniazid and (diphenylphosphoryl)acetic acid hydrazones containing a hydroxy group at the ortho position of the aromatic ring are formed as individual E isomers with respect to the C-N double bond

Pathogenesis, Diagnosis, and Treatment of Hemostatic Disorders in COVID-19 Patients

The novel coronavirus infection named COVID-19 was first detected in Wuhan, China, in December 2019, and it has been responsible for significant morbidity and mortality in scores of countries. At the time this article was being written, the number of infected and deceased patients continued to grow worldwide. Most patients with severe forms of the disease suffer from pneumonia and pulmonary insufficiency; in many cases, the disease is generalized and causes multiple organ failures and a dysfunction of physiological systems. One of the most serious and prognostically ominous complications from COVID-19 is coagulopathy, in particular, decompensated hypercoagulability with the risk of developing disseminated intravascular coagulation. In most cases, local and diffuse macro- and microthromboses are present, a condition which causes multiple-organ failure and thromboembolic complications. The causes and pathogenic mechanisms of coagulopathy in COVID-19 remain largely unclear, but they are associated with systemic inflammation, including the so-called cytokine storm. Despite the relatively short period of the ongoing pandemic, laboratory signs of serious hemostatic disorders have been identified and measures for specific prevention and correction of thrombosis have been developed. This review discusses the causes of COVID-19 coagulopathies and the associated complications, as well as possible approaches to their early diagnosis, prevention, and treatment