Prevention of post-operative nausea and vomiting with honey as a pre-operative oral carbohydrate : a randomised controlled pilot trial

Background: Post-operative nausea and vomiting (PONV) is the second-most common post-operative complication. Prolonged pre-operative fasting is common in Australia despite guidelines recommending reduced fasting to improve patient outcomes, such as PONV. Commercially prepared preoperative oral carbohydrate (OC) drinks may be used to reduce fasting time. In this study commercial products were replaced with honey, an inexpensive and common food item. Design: Partially blinded, four parallel arms randomised controlled non-inferiority trial compared pre-operative OC loading with overnight fasting. Methods: Adult elective laparoscopic cholecystectomy and thyroidectomy patients having two or more risk factors for PONV were allocated into intervention and control groups by simple randomisation. The intervention group ingested 60g of honey in 100 ml of water at least two hours before surgery as pre-operative OC loading to reduce PONV. Participants and assessors to the group assignment were blinded to the study outcomes. Early PONV (0–6 hours) was measured with Rhodes index of nausea, vomiting and retching (R-INVR) and a numeric rating scale (NRS). Results: The four groups (N = 142) were control and intervention groups of thyroidectomy patients (n = 72: C = 37, I = 35), and control and intervention groups of laparoscopic cholecystectomy patients (n = 70: C = 37, I = 33) and had similar distributions of variables. The estimated effect size was 140 with a 95 percent confidence interval. The PONV incidence (Pearson χ2 = 4.54; df = 1; p = 0.03) and severity were significantly lower in the laparoscopic cholecystectomy intervention group (R-INVR: Mann–Whitney U = 446.5; p = 0.01; NRS: Mann–Whitney U = 444.5; p = 0.01) and results were not conclusive in the thyroidectomy group (NRS: Mann–Whitney U = 629.5; p = 0.95; R-INVR: Mann–Whitney U = 629.5; p = 0.76). Conclusion: Honey could be recommended as an inexpensive pre-operative OC to reduce PONV in adult patients receiving general anaesthesia

Is Metaverse in education a blessing or a curse: a combined content and bibliometric analysis

The Metaverse has been the centre of attraction for educationists for quite some time. This field got renewed interest with the announcement of social media giant Facebook as it rebranding and positioning it as Meta. While several studies conducted literature reviews to summarize the findings related to the Metaverse in general, no study to the best of our knowledge focused on systematically summarizing the finding related to the Metaverse in education. To cover this gap, this study conducts a systematic literature review of the Metaverse in education. It then applies both content and bibliometric analysis to reveal the research trends, focus, and limitations of this research topic. The obtained findings reveal the research gap in lifelogging applications in educational Metaverse. The findings also show that the design of Metaverse in education has evolved over generations, where generation Z is more targeted with artificial intelligence technologies compared to generation X or Y. In terms of learning scenarios, there have been very few studies focusing on mobile learning, hybrid learning, and micro learning. Additionally, no study focused on using the Metaverse in education for students with disabilities. The findings of this study provide a roadmap of future research directions to be taken into consideration and investigated to enhance the adoption of the Metaverse in education worldwide, as well as to enhance the learning and teaching experiences in the Metaverse

Glutamine depletion by crisantaspase hinders the growth of human hepatocellular carcinoma xenografts

Background: A subset of human hepatocellular carcinomas (HCC) exhibit mutations of β-catenin gene CTNNB1 and overexpress Glutamine synthetase (GS). The CTNNB1-mutated HCC cell line HepG2 is sensitive to glutamine starvation induced in vitro with the antileukemic drug Crisantaspase and the GS inhibitor methionine-L-sulfoximine (MSO). Methods: Immunodeficient mice with subcutaneous xenografts of the CTNNB1-mutated HCC cell lines HepG2 and HC-AFW1 were treated with Crisantaspase and/or MSO, and tumour growth was monitored. At the end of treatment, tumour weight and histology were assessed. Serum and tissue amino acids were determined by HPLC. Gene and protein expression were estimated with RT-PCR and western blot and GS activity with a colorimetric method. mTOR activity was evaluated from the phosphorylation of p70S6K1. Results: Crisantaspase and MSO depleted serum glutamine, lowered glutamine in liver and tumour tissue, and inhibited liver GS activity. HepG2 tumour growth was significantly reduced by either Crisantaspase or MSO, and completely suppressed by the combined treatment. The combined treatment was also effective against xenografts of the HC-AFW1 cell line, which is Crisantaspase resistant in vitro. Conclusions: The combination of Crisantaspase and MSO reduces glutamine supply to CTNNB1-mutated HCC xenografts and hinders their growth

Metabolomic profiles of hepatocellular carcinoma in a European prospective cohort

Background: Hepatocellular carcinoma (HCC), the most prevalent form of liver cancer, is difficult to diagnose and has limited treatment options with a low survival rate. Aside from a few key risk factors, such as hepatitis, high alcohol consumption, smoking, obesity, and diabetes, there is incomplete etiologic understanding of the disease and little progress in identification of early risk biomarkers. Methods: To address these aspects, an untargeted nuclear magnetic resonance metabolomic approach was applied to pre-diagnostic serum samples obtained from first incident, primary HCC cases (n = 114) and matched controls (n = 222) identified from amongst the participants of a large European prospective cohort. Results: A metabolic pattern associated with HCC risk comprised of perturbations in fatty acid oxidation and amino acid, lipid, and carbohydrate metabolism was observed. Sixteen metabolites of either endogenous or exogenous origin were found to be significantly associated with HCC risk. The influence of hepatitis infection and potential liver damage was assessed, and further analyses were made to distinguish patterns of early or later diagnosis. Conclusion: Our results show clear metabolic alterations from early stages of HCC development with application for better etiologic understanding, prevention, and early detection of this increasingly common cancer.This work was supported by the French National Cancer Institute (L’Institut National du Cancer; INCA; grant number 2009-139; PI: M. Jenab). AF received financial support (BDI fellowship) from the Centre National de la Recherche Scientifique (CNRS) and Bruker Biospin. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l’Education Nationale, and Institut National de la Santé et de la Recherche Médicale (INSERM) (France); Deutsche Krebshilfe, Deutsches Krebsforschungszentrum (DKFZ), and Federal Ministry of Education and Research (Germany); Hellenic Health Foundation (Greece); Italian Association for Research on Cancer (AIRC), National Research Council, Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy, and AIRE-ONLUS Ragusa, AVIS Ragusa, Sicilian Government (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), and Statistics Netherlands (the Netherlands); European Research Council (ERC; grant number ERC-2009-AdG 232997) and Nordforsk, and Nordic Center of Excellence Programme on Food, Nutrition and Health (Norway); Health Research Fund (FIS), Regional Governments of Andalucía, Asturias, Basque Country, Murcia (No. 6236) and Navarra, and ISCIII RETIC (RD06/0020) (Spain); Swedish Cancer Society, Swedish Scientific Council, and Regional Government of Skåne and Västerbotten (Sweden); Cancer Research UK, Medical Research Council, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, and Wellcome Trust (UK)

Muscle GCMS data

<p>GCMS data</p