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4.
EClinicalMedicine ; 23: 100383, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32637891

RESUMO

BACKGROUND: Appendectomy is one of the most common surgical procedures; however, the possible long-term consequences have not been fully explored. The appendix has been associated with microflora of the gut and immune functions. However, literature examining the relationship between prior appendectomy and the risk of irritable bowel syndrome (IBS) is lacking. The aim of this study was to evaluate the risk of irritable bowel syndrome for patients who underwent appendectomy by using a nationwide longitudinal population-based cohort. METHODS: Data from this study was collected from Taiwan's National Health Insurance Research Database (NHIRD), a population-based database. We identified 12,760 patients who underwent appendectomy between January 1, 2000 and December 31, 2012. A total of 9236 patients who had appendectomy (case group) were randomly matched with 9236 patients who had not undergone appendectomy (control group) in a ratio of 1:1 by means of propensity scores. The hazard ratio (HR) of IBS was calculated by multiple Cox regression. Furthermore, sensitivity test and stratified analysis were performed. FINDINGS: The incidence rate of IBS was 51.30 per 10,000 person-years in patients having appendectomy, more than the 35.28 per 10,000 person-years in patients not having appendectomy. Patients who underwent appendectomy had 1.46-fold risk of IBS compared to patients not having appendectomy (HR, 1.46; 95% CI, 1.24-1.72). Stratified analysis revealed that the higher HR of 1.55 (95% CI, 1.18-2.04) in patients <40 years old, and particularly within the first 5 years follow-up period of undergoing appendectomy. In addition, patients diagnosed with fibromyalgia had a greater risk of suffering IBS after appendectomy (HR, 1.41; 95% CI, 1.04-1.92). INTERPRETATION: Patients with appendectomy have a higher incidental risk of IBS than the control population. The risk is higher for patients under 40 years old and those who received appendectomy within 5 years. Physicians could take this into consideration for treatment plans of patients who have underwent this surgery. Further research on the pathogenesis of this association is required. FUNDING: This work was supported by grants from the Ministry of Health and Welfare, Taiwan (MOHW108-TDU-B-212-133004), China Medical University Hospital, Academia Sinica Stroke Biosignature Project (BM10701010021), MOST Clinical Trial Consortium for Stroke (MOST 108-2321-B-039-003-), Tseng-Lien Lin Foundation, Taichung, Taiwan, and Katsuzo and Kiyo Aoshima Memorial Funds, Japan.

5.
Toxins (Basel) ; 11(5)2019 05 08.
Artigo em Inglês | MEDLINE | ID: mdl-31072027

RESUMO

Aflatoxins are carcinogenic secondary metabolites of fungi that contaminate many staple crops and foods. Aflatoxin contamination is a worldwide problem, especially in developing countries, posing health hazards, e.g., causing aflatoxicosis and hepatocellular carcinoma, and even death. Biological solutions for aflatoxin detoxification are environmentally friendly and a cheaper alternative than chemical methods. The aims of the current study were to investigate: (1) the ability of MSMEG_5998, an aflatoxin-degrading F420H2-dependent reductase from Mycobacterium smegmatis, to degrade aflatoxin B1 (AFB1) and reduce AFB1-caused damage in HepG2 cell culture model; and (2) whether a thioredoxin (Trx) linkage of MSMEG_5998 enhanced the enzyme activity. We show that Trx-linked MSMEG_5998 degraded 63% AFB1 and native MSMEG_5998 degraded 31% after 4 h at 22 °C, indicating that the Trx-linked enzyme had a better AFB1-degrading ability. In a HepG2 cell culture model, Trx-linked MSMEG_5998 reduced DNA damage and p53-mediated apoptosis caused by AFB1 to a greater extent than the native enzyme. These findings suggest that Trx-linked MSMEG_5998 could potentially be developed to protect the liver from AFB1 damage, or as a candidate protein to reduce AFB1-related toxicity in animals.


Assuntos
Aflatoxinas/toxicidade , Mycobacterium smegmatis/enzimologia , Oxirredutases/farmacologia , Substâncias Protetoras/farmacologia , Apoptose/efeitos dos fármacos , Dano ao DNA , Estabilidade Enzimática , Células Hep G2 , Humanos , Proteínas Recombinantes/farmacologia
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