No abstract

Background and aims COVID-19 is a dominant pulmonary disease, with multisystem involvement, depending upon comorbidities. Its profile in patients with pre-existing chronic liver disease (CLD) is largely unknown. We studied the liver injury patterns of SARS-Cov-2 in CLD patients, with or without cirrhosis. Methods Data was collected from 13 Asian countries on patients with CLD, known or newly diagnosed, with confirmed COVID-19. Results Altogether, 228 patients [185 CLD without cirrhosis and 43 with cirrhosis] were enrolled, with comorbidities in nearly 80%. Metabolism associated fatty liver disease (113, 61%) and viral etiology (26, 60%) were common. In CLD without cirrhosis, diabetes [57.7% vs 39.7%, OR = 2.1 (1.1-3.7), p = 0.01] and in cirrhotics, obesity, [64.3% vs. 17.2%, OR = 8.1 (1.9-38.8), p = 0.002] predisposed more to liver injury than those without these. Forty three percent of CLD without cirrhosis presented as acute liver injury and 20% cirrhotics presented with either acute-on-chronic liver failure [5 (11.6%)] or acute decompensation [4 (9%)]. Liver related complications increased (p < 0.05) with stage of liver disease; a Child-Turcotte Pugh score of 9 or more at presentation predicted high mortality [AUROC 0.94, HR = 19.2 (95 CI 2.3-163.3), p < 0.001, sensitivity 85.7% and specificity 94.4%). In decompensated cirrhotics, the liver injury was progressive in 57% patients, with 43% mortality. Rising bilirubin and AST/ALT ratio predicted mortality among cirrhosis patients. Conclusions SARS-Cov-2 infection causes significant liver injury in CLD patients, decompensating one fifth of cirrhosis, and worsening the clinical status of the already decompensated. The CLD patients with diabetes and obesity are more vulnerable and should be closely monitored.

This experiment explored how consumers evaluate electronic word-of-mouth (eWOM) messages about products. Each participant was exposed a 10-message set in a single board. Five groups were manipulated in terms of their ratios of positive and negative messages. The result showed significant differences across various sets of eWOM messages. Although more positive sets showed higher scores in many cases, this was not true in all situations, especially for the case of credibility. Involvement and prior knowledge partially moderated the relationship between the ratio of messages and the eWOM effect. The credibility of Web sites and eWOM messages can be damaged in the long run if all of the eWOM messages are positive.

No abstract

Environmental pollution arising from plastic waste is a major global concern. Plastic macroparticles, microparticles, and nanoparticles have the potential to affect marine ecosystems and human health. It is generally accepted that microplastic particles are not harmful or at best minimal to human health. However direct contact with microplastic particles may have possible adverse effect in cellular level. Primary polystyrene (PS) particles were the focus of this study, and we investigated the potential impacts of these microplastics on human health at the cellular level. We determined that PS particles were potential immune stimulants that induced cytokine and chemokine production in a sizedependent and concentration-dependent manner. Microplastic particles can be divided into two categories, primary and secondary. Plastic particles less than 5 mm in diameter are considered microplastics 1. Although local and national governments in North America took action in 2015 to regulate the manufacture of microbeads, microplastic particles are still produced in other parts of the world 2. Primary microplastic particles are intentionally manufactured at the microscale and are key ingredients in scrubs 3 , handwashing soaps 4 , cleansers 5 , toothpastes 6 , and biomedical products 7. Primary microplastic particles, particularly those between 1 and 5 µm in diameter, are spherical and often made of polypropylene (PP), polystyrene (PS), or polyethylene (PE). Unlike primary microplastic particles, secondary microplastic particles are generated through the fragmentation of plastic litter 8-10. Plastic debris is the primary source of secondary microplastic particles found in the ocean and soil, because the debris breaks down into mesoparticles and macroparticles. Ultraviolet (UV) radiation from the sun and physical forces degrade these particles into plastic microparticles and nanoparticles 11,12. A recent study investigated the fragmentation of PS coffee cup lids, disposable plates, and PS foams irradiated with simulated UV light to determine the degradation mechanism 13. Seafood is also a potential source of particulate plastic contaminants 14-18. Anthropogenic debris, including plastic particles and fibers, was found in over 20% of individual shellfish and the gastrointestinal (GI) tracts of fish in a 2015 study 19. The ingestion of microplastics by fish and shellfish has been demonstrated in several studies 16,18,20. Food, food containers, everyday products (personal care products), biomedical products, and drinking water are not the main sources of particulate plastic contaminants. However, they may be continuous sources of plastic particles 21-24. For example, one study found microplastic fragments in all types of returnable and single-use plastic bottles 24. Other examples include facial scrubs that are commonly used for exfoliation. It is estimated that 1.1 million women in the UK use these scrubs every day. A typical amount for daily use is 5 mL, which contains between 4,594 and 94,500 microplastic particles 4,5. Additio...

Tumor size and fibrosis are important factors related to complications during colorectal ESD. Younger age and development of abdominal pain can predict the hospital course in patients with perforation after ESD.

No abstract

Background and Aims: COVID-19 is a dominant pulmonary disease, with multisystem involvement, depending upon co morbidities. Its profile in patients with pre-existing chronic liver disease (CLD) is largely unknown. We studied the liver injury patterns of SARS-Cov-2 in CLD patients, with or without cirrhosis. Methods: Data was collected from 13 Asian countries on patients with CLD, known or newly diagnosed, with confirmed COVID-19. Result: Altogether, 228 patients [185 CLD without cirrhosis and 43 with cirrhosis] were enrolled, with comorbidities in nearly 80%. Metabolism associated fatty liver disease (113, 61%) and viral etiology (26, 60%) were common. In CLD without cirrhosis, diabetes [57.7% vs 39.7%, OR=2.1(1.1-3.7), p=0.01] and in cirrhotics, obesity, [64.3% vs. 17.2%, OR=8.1(1.9-38.8), p=0.002) predisposed more to liver injury than those without these. Forty three percent of CLD without cirrhosis presented as acute liver injury and 20% cirrhotics presented with either acute-on-chronic liver failure [5(11.6%)] or acute decompensation [4(9%)]. Liver related complications increased (p<0.05) with stage of liver disease; a Child-Turcotte Pugh score of 9 or more at presentation predicted high mortality [AUROC-0.94, HR=19.2(95CI 2.3-163.3), p<0.001, sensitivity 85.7% and specificity 94.4%). In decompensated cirrhotics, the liver injury was progressive in 57% patients, with 43% mortality. Rising bilirubin and AST/ALT ratio predicted mortality among cirrhosis. Conclusions: SARS-Cov-2 infection causes significant liver injury in CLD patients, decompensating one fifth of cirrhosis, and worsening the clinical status of the already decompensated. The CLD patients with diabetes and obesity are more vulnerable and should be closely monitored.