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PurposeThis study aims to examine the impact of AI service robots on restaurant customers' engagement and acceptance and the moderating role of robot anthropomorphism on the relationship between AI robot service quality and customer engagement.Design/methodology/approachUsing a three-wave time-lagged design, 416 customers of service robots-enabled restaurants participated in the study. Mplus was used to examine the hypotheses.FindingsThe results confirmed that customers' perception regarding automation, personalization, efficiency and precision of robot service quality determine customer engagement, which further influences customer acceptance of AI service robots. Additionally, robot anthropomorphism moderates the relationships between AI robot service quality in terms of automation, personalization, efficiency and precision and customer engagement. This study confirms that AI service robots-customer engagement contributes to better acceptance of AI service robots.Practical implicationsThe proposed framework can be used as a diagnostic tool to enhance customer acceptance of AI service robots in restaurant settings. This research provides guidelines to restaurant owners to employ AI service robots in front-line services that provide better quality, ultimately enhancing customer engagement and acceptance.Originality/valueThis study fills the gap in the literature by investigating the influence of AI robot service quality on customer engagement and customer acceptance with the moderating effect of robot anthropomorphism in an emerging market context.

PurposeThis paper aims to identify the dimensions of service quality in the case of ride-sourcing services in Indian context.Design/methodology/approachThe service quality dimensions of ride-sourcing services are identified using an exploratory factor analysis (EFA). Further, the reliability and validity of the factors are established through confirmatory factor analysis (CFA) using AMOS.FindingsThe service quality dimensions of ride-sourcing services are identified: comfort, internal environment, safety and personnel, mobile convenience and reliability, mobile system efficiency and availability, mobile customer service and billing and mobile security and privacy.Research limitations/implicationsThe various dimensions are identified to measure service quality of ride-sourcing services in India. So, these dimensions can be tested for ride-sourcing services of countries having similar culture as India.Practical implicationsThe proposed dimensions can be used as a diagnostic tool to identify and compare important criteria for service quality of ride-sourcing services.Originality/valueMost relevant studies about dimensions of service quality for ride-sourcing services do not have stable factor structure. The dimensions identified include the traditional taxi service quality and mobile app service quality, which are not covered in current literature.

Purpose This paper aims to establish and empirically investigate a research model examining the effect of four dimensions of the technology readiness index – optimism, innovativeness, discomfort and insecurity – on customer engagement that further influences purchase intention in the context of online shopping through artificial intelligence voice assistants (AI VAs). Design/methodology/approach Data were collected in India from 429 customers in a self-administered online survey. Data analysis uses the structural equation modelling technique. Findings Technology readiness dimensions, e.g. optimism, innovativeness, discomfort and insecurity, are critical factors driving customer engagement. Customer engagement further results in purchase intention in online shopping through AI VAs. Research limitations/implications This study adds to the literature by understanding how customers’ technology readiness levels drive engagement and purchase intention. However, this study includes customer engagement as a unidimensional construct. Further research can consist of customer engagement as a multidimensional construct. Practical implications The findings offer guidelines for e-retailers to enhance customer engagement that matches their personality traits, thereby strengthening their purchase intention through AI VAs. Originality/value The research contributes to the literature by empirically investigating a research model, revealing optimism, innovativeness, discomfort and insecurity as crucial parameters for customer engagement and purchase intention.

SARS-CoV-2 is a single stranded RNA (ssRNA) virus and contains GU-rich sequences distributed abundantly in the genome. In COVID-19, the infection and immune hyperactivation causes accumulation of inflammatory immune cells, blood clots, and protein aggregates in lung fluid, increased lung alveolar wall thickness, and upregulation of serum cytokine levels. A serum protein called serum amyloid P (SAP) has a calming effect on the innate immune system and shows efficacy as a therapeutic for fibrosis in animal models and clinical trials. Here we show that aspiration of the GU-rich ssRNA oligonucleotide ORN06 into mouse lungs induces all of the above COVID-19-like symptoms. Men tend to have more severe COVID-19 symptoms than women, and in the aspirated ORN06 model, male mice tended to have more severe symptoms than female mice. Intraperitoneal injections of SAP starting from day 1 post ORN06 aspiration attenuated the ORN06-induced increase in the number of inflammatory cells and formation of clot-like aggregates in the mouse lung fluid, reduced ORN06-increased alveolar wall thickness and accumulation of exudates in the alveolar airspace, and attenuated an ORN06-induced upregulation of the inflammatory cytokines IL-1β, IL-6, IL-12p70, IL-23, and IL-27 in serum. SAP also reduced D-dimer levels in the lung fluid. In human peripheral blood mononuclear cells, SAP attenuated ORN06-induced extracellular accumulation of IL-6. Together, these results suggest that aspiration of ORN06 is a simple model for both COVID-19 as well as cytokine storm in general, and that SAP is a potential therapeutic for diseases with COVID-19-like symptoms and/or a cytokine storm.

Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and type 2 diabetes and is characterized by the accumulation of fat in the liver (steatosis). NAFLD can transition into non-alcoholic steatohepatitis (NASH), with liver cell injury, inflammation, and an increased risk of fibrosis. We previously found that injections of either 1866, a synthetic ligand for the lectin receptor CD209, or DANA, a sialidase inhibitor, can inhibit inflammation and fibrosis in multiple animal models. The methionine and choline-deficient (MCD) diet is a model of NASH which results in the rapid induction of liver steatosis and inflammation. In this report, we show that for C57BL/6 mice on a MCD diet, injections of both 1866 and DANA reversed MCD diet-induced decreases in white fat, decreases in adipocyte size, and white fat inflammation. However, these effects were not observed in type 2 diabetic db/db mice on a MCD diet. In db/db mice on a MCD diet, 1866 decreased liver steatosis, but these effects were not observed in C57BL/6 mice. There was no correlation between the ability of 1866 or DANA to affect steatosis and the effects of these compounds on the density of liver macrophage cells expressing CLEC4F, CD64, F4/80, or Mac2. Together these results indicate that 1866 and DANA modulate adipocyte size and adipose tissue macrophage populations, that 1866 could be useful for modulating steatosis, and that changes in the local density of 4 different liver macrophages cell types do not correlate with effects on liver steatosis.

Fibrosis involves increasing amounts of scar tissue appearing in a tissue, but what drives this is unclear. In fibrotic lesions in human and mouse lungs, we found extensive desialylation of glycoconjugates, and upregulation of sialidases. The fibrosis-associated cytokine TGF-β1 upregulates sialidases in human airway epithelium cells, lung fibroblasts, and immune system cells. Conversely, addition of sialidases to human peripheral blood mononuclear cells induces accumulation of extracellular TGF-β1, forming what appears to be a sialidase - TGF-β1 - sialidase positive feedback loop. Monocyte-derived cells called fibrocytes also activate fibroblasts, and we found that sialidases potentiate fibrocyte differentiation. A sialylated glycoprotein called serum amyloid P (SAP) inhibits fibrocyte differentiation, and sialidases attenuate SAP function. Injections of the sialidase inhibitors DANA and oseltamivir (Tamiflu) starting either 1 day or 10 days after bleomycin strongly attenuate pulmonary fibrosis in the mouse bleomycin model, and by breaking the feedback loop, cause a downregulation of sialidase and TGF-β1 accumulation. Together, these results suggest that a positive feedback loop involving sialidases potentiates fibrosis, and suggest that sialidase inhibitors could be useful for the treatment of fibrosis.

Concrete strength prediction is of great relevance for construction safety and quality assurance; however, these methods often trade-off their accuracy or interpretability, especially when it comes to the use of supplementary cementitious materials like fly ash in process. This study aims to build an interpretable, highly accurate model for predicting the compressive and tensile strength of concrete with a hybrid approach based on gradient boosting (XGBoost), deep neural networks (DNNs), and optimization via AutoGluon Process. The model is put into a multitask learning (MTL) framework that includes mix design variables, environmental factors, and non-destructive testing (NDT) data samples. The interpretation of model predictions is accomplished through SHAP and LIME to quantify global and local importance. Results show an impressive R² score of 0.91 on the test set with a 23% reduction in MSE and LIME fidelity exceeding 0.87. This shows a 10–15% increase in the mean-squared error, surpassing existing models. Feature analysis shows that fly ash percentage contributes around 25% to the predictions. The proposed solution thus offers a robust interpretability platform for concrete strength prediction and further shows great promise for optimization in material design and structural integrity assurances. This work serves as a landmark in bridging the gap between hybrid modeling with automated optimization and explainability for concrete strength predictions.

•Ketones serve as energy fuel during times of starvation.•Ketogenic diet has therapeutic benefits in some acute neurological disorders.•Randomized clinical trials in acute neurological disorders need to be conducted.•Standard protocols for treatment with Ketogenic diet need to be developed. The current review outlines the role of ketogenic diet (KD) in the management of acute neurological conditions namely traumatic brain injury, ischemic stroke, status epilepticus and primary aggressive brain tumor. An overview of the scientific literature- both clinical and pre-clinical studies is presented along with the proposed mechanism of ketogenic diet. The review also describes different formulations of commercially available ketogenic diets along with the common adverse effects and dosing recommendations.

Fibrosing diseases are a major medical problem, and are associated with more deaths per year than cancer in the US. Sialidases are enzymes that remove the sugar sialic acid from glycoconjugates. In this review, we describe efforts to inhibit fibrosis by inhibiting sialidases, and describe the following rationale for considering sialidases to be a potential target to inhibit fibrosis. First, sialidases are upregulated in fibrotic lesions in humans and in a mouse model of pulmonary fibrosis. Second, the extracellular sialidase NEU3 appears to be both necessary and sufficient for pulmonary fibrosis in mice. Third, there exist at least three mechanistic ways in which NEU3 potentiates fibrosis, with two of them being positive feedback loops where a profibrotic cytokine upregulates NEU3, and the upregulated NEU3 then upregulates the profibrotic cytokine. Fourth, a variety of NEU3 inhibitors block pulmonary fibrosis in a mouse model. Finally, the high sialidase levels in a fibrotic lesion cause an easily observed desialylation of serum proteins, and in a mouse model, sialidase inhibitors that stop fibrosis reverse the serum protein desialylation. This then indicates that serum protein sialylation is a potential surrogate biomarker for the effect of sialidase inhibitors, which would facilitate clinical trials to test the exciting possibility that sialidase inhibitors could be used as therapeutics for fibrosis.

Background Sialic acid is often the distal sugar on glycoconjugates, and sialidases are enzymes that remove this sugar. In fibrotic lesions in human and mouse lungs, there is extensive desialylation of glycoconjugates, and upregulation of sialidases including the extracellular sialidase NEU3. In the bleomycin model of pulmonary fibrosis, mice lacking NEU3 ( Neu3 −/− ) showed strongly attenuated bleomycin-induced weight loss, lung damage, inflammation, and fibrosis. This indicates that NEU3 is necessary for the full spectrum of bleomycin-induced pulmonary fibrosis. Methods To determine if NEU3 is sufficient to induce pulmonary fibrosis, recombinant murine NEU3 and a mutated inactive recombinant murine NEU3 protein were produced. Mice were given recombinant NEU3 proteins by oropharyngeal aspiration, either alone or 10 days after bleomycin challenge. Over the course of 21 days, mice were assessed for weight change, and after euthanasia, bronchoalveolar lavage fluid cells and lung tissue were assessed for inflammation and fibrosis. Results Aspiration of recombinant murine NEU3 caused inflammation and fibrosis in the lungs, while inactive NEU3 caused inflammation but not fibrosis. Mice were also treated with recombinant murine NEU3 starting 10 days after bleomycin. In male but not female mice, recombinant murine NEU3 increased inflammation and fibrosis. Inactive NEU3 did not enhance bleomycin-induced lung fibrosis. Conclusion These results suggest that NEU3 is sufficient to induce fibrosis in the lungs, that aspiration of NEU3 has a greater effect on male mice, and that this effect is mediated by NEU3’s enzymic activity.