Search

Background: Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole-induced SCAR remains unclear., Objective: We aimed to investigate the genetic predisposition of co-trimoxazole-induced SCAR., Methods: We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole-induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia., Results: The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole-induced SCAR (P = 8.2 × 10 -9 ; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole-related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole-induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10 -21 ; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10 -5 ; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole-induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10 -23 ; OR = 40.1)., Conclusion: This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole-induced SCAR in Asians., (Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Information on the association between long-term exposure to PM 2.5 and gastrointestinal cancer mortality is scarce., Objectives: This study investigated the association between long-term exposure to PM 2.5 and deaths from gastrointestinal cancer and its subtypes in adults in Taiwan., Methods: A total of 385,650 Taiwanese adults (≥18 years old) jointed a standard medical examination program between 2001 and 2014 and were followed up until 2016. Their vital data were obtained from the National Death Registry maintained by the Ministry of Health and Welfare in Taiwan. We estimated the ambient PM 2.5 concentration at individual's address utilising a satellite-based spatiotemporal model at a resolution of 1 km 2 . Cox proportional hazard regression model was used to investigate the associations between ambient PM 2.5 and deaths from gastrointestinal, stomach, colorectal and liver cancers., Results: We found that each 10 µg/m 3 increase in PM 2.5 was associated with an increased hazard risk (HR) of 1.09 (95% confidence interval (CI): 1.03-1.16) and 1.13 (95%CI: 1.02-1.24) in deaths from gastrointestinal and liver cancers, respectively. The association between PM 2.5 and death from colorectal cancer was marginally statistically significant [HR: 1.13 (95%CI: 1.00-1.26)]. We did not find significant associations between PM 2.5 and mortality from stomach cancer., Conclusions: Long-term exposure to ambient PM 2.5 was associated with an increased risk of deaths from gastrointestinal cancers, liver cancer and also potentially colorectal cancer. Air pollution control strategies are necessary to reduce the burden of gastrointestinal cancer., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Antrodia cinnamomea, a polyporus mushroom of Taiwan, has long been used as a remedy for cancer, hypertension, and hangover, with an annual market of over $100 million (US) in Taiwan. We obtained a 32.15-Mb genome draft containing 9,254 genes. Genome ontology enrichment and pathway analyses shed light on sexual development and the biosynthesis of sesquiterpenoids, triterpenoids, ergostanes, antroquinonol, and antrocamphin. We identified genes differentially expressed between mycelium and fruiting body and 242 proteins in the mevalonate pathway, terpenoid pathways, cytochrome P450s, and polyketide synthases, which may contribute to the production of medicinal secondary metabolites. Genes of secondary metabolite biosynthetic pathways showed expression enrichment for tissue-specific compounds, including 14-α-demethylase (CYP51F1) in fruiting body for converting lanostane to ergostane triterpenoids, coenzymes Q (COQ) for antroquinonol biosynthesis in mycelium, and polyketide synthase for antrocamphin biosynthesis in fruiting body. Our data will be useful for developing a strategy to increase the production of useful metabolites.

The purpose of this article was to investigate the issues related to nursing students' clinical practicum when severe contagious diseases occur. Based on the concept that patient-benefit must come first, the authors suggested that nursing students should remain on duty even if there were an outbreak of a severe contagious disease. The authors also discussed relevant issues in terms of professional roles and the safety of the learning environment. The problems identified and the proposed strategies for solving them are outlined in this article. There is no single strategy applicable to all conditions, however. Finally, the authors urge schools and hospitals to develop effective communications and close cooperation and to remain well informed about severe contagious diseases.