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Background: The Taiwan Nursing Accreditation Council has proposed eight core professional nursing qualities including ethical literacy. Consequently, nursing ethics education is a required course for student nurses. These courses are intended to improve the ethical literacy. Moral sensitivity is the cornerstone of ethical literacy, and learning moral sensitivity is the initial step towards developing ethical literacy. Objectives: To explore the effect of nursing ethics educational interventions based on multiple teaching strategies on student nurses moral sensitivity. Based on the visual, auditory and kinaesthetic model, three strategies were developed for determining the programme components and corresponding learning styles. Research design: This was a quasi-experimental study. Participants: A total of 234 junior-college student nurses participated in this study. All participants were aged 18--19 years. Ethical considerations: The study protocol was approved by the institutional review boards of Kaohsiung Veterans General Hospital. Only the participants who signed an informed consent form took part in the study. The participants were permitted to withdraw from the study at any point if they wished to do so without affecting their academic score. Results: The scores of Modified Moral Sensitivity Questionnaire for Student Nurses were significantly improved after the intervention of integrating multiple teaching strategies (p ¼ .042). Significant relationships were observed between the satisfaction scores of two teaching strategies and moral sensitivity. The results indicated that using multiple teaching strategies is effective for promoting nursing ethics learning. Conclusion: This strategy was consistent with the student nurses' preferred learning style and was used to correct their erroneous ethical conceptions, assisting in developing their ethical knowledge. [ABSTRACT FROM AUTHOR]

Inconsistent results have been reported for the association between alcohol use and pancreatic cancer, particularly at low levels of alcohol consumption. Individuals genetically susceptible to the carcinogenic effect of alcohol might have higher pancreatic cancer risk after drinking alcohol. The current study investigated the association between alcohol use and pancreatic cancer with 419 pancreatic cancer cases and 963 controls recruited by a hospital-based case-control study in Taiwan. Gene-environment interaction between alcohol use and polymorphisms of two ethanol-metabolizing genes, ADH1B and ALDH2, on pancreatic risk was evaluated. Our results showed no significant association between alcohol drinking and an increased pancreatic cancer risk, even at high levels of alcohol consumption. Even among those genetically susceptible to the carcinogenic effect of alcohol (carriers of ADH1B*2/*2(fast activity) combined with ALDH2*1/*2(slow activity) or ALDH2*2/*2(almost non-functional)), no significant association between alcohol use and pancreatic cancer was observed. Overall, our results suggested that alcohol drinking is not a significant contributor to the occurrence of pancreatic cancer in Taiwan., (© 2021. The Author(s).)

Background: Due to differences in genetic background, it is unclear whether the genetic loci identified by the previous genome-wide association studies (GWAS) of pancreatic cancer also play significant roles in the development of pancreatic cancer among the Taiwanese population., Methods: This study aimed to validate the 25 pancreatic cancer GWAS-identified single nucleotide polymorphisms (SNPs) in a case-control study (278 cases and 658 controls) of pancreatic cancer conducted in Taiwan. Statistical analyses were conducted to determine the associations between the GWAS-identified SNPs and pancreatic cancer risk. Gene-environment interaction analysis was conducted to evaluate the interactions between SNPs and environmental factors on pancreatic cancer risk., Results: Among the 25 GWAS-identified SNPs, 7 (rs2816938 (~ 11 kb upstream of NR5A2), rs10094872 (~ 28 kb upstream of MYC), rs9581943 (200 bp upstream of PDX1) and 4 chromosome 13q22.1 SNPs: rs4885093, rs9573163, rs9543325, rs9573166) showed a statistically significant association with pancreatic cancer risk in the current study. Additional analyses showed two significant gene-environment interactions (between poor oral hygiene and NR5A2 rs2816938 and between obesity and PDX1 rs9581943) on the risk of pancreatic cancer., Conclusions: The current study confirmed the associations between 7 of the 25 GWAS-identified SNPs and pancreatic risk among the Taiwanese population. Furthermore, pancreatic cancer was jointly influenced by lifestyle and medical factors, genetic polymorphisms, and gene-environment interaction. Additional GWAS is needed to determine the genetic polymorphisms that are more relevant to the pancreatic cancer cases occurring in Taiwan.

Current treatment options for muscle injuries remain suboptimal and often result in delayed/incomplete recovery of damaged muscles. In this study, the effects of dextrose prolotherapy on inflammation and regeneration of skeletal muscles after a contusion injury were investigated. Mice were separated into five groups, including a normal control (NC), post-injury with no treatment (mass-drop injury, MDI), post-injury with 10% dextrose (MDI + 10% dextrose), post-injury with 20% dextrose (MDI + 20% dextrose), and post-injury with 30% dextrose (MDI + 30% dextrose). The gastrocnemius muscles of the mice were subjected to an MDI, and muscle samples were collected at 7 days post-injury. Results showed the serum creatine kinase (CK), blood urea nitrogen (BUN), creatinine (CREA), and low-density lipoprotein (LDH) of the MDI-alone group were significantly higher than those of the normal control group (p <0.05). However, levels of serum CK, BUN, CREA, and lactate dehydrogenase (LDH) significantly decreased with different concentrations of dextrose. In addition, dextrose suppressed the macrophage response (F4/80 protein decreased) and promoted muscle satellite cell regeneration (desmin protein increased). In conclusion, dextrose prolotherapy can effectively help repair muscles; therefore, it may be one of the methods for clinically treating muscle injuries., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.

Background: While diabetes is considered as a risk factor for colorectal cancer, there are few studies that address the association between glycemic statuses and different colon polyps, ranging from non-neoplastic polyps to advanced adenomatous polyps., Methods: A total of 6,348 participants, consisting of 3,777 men and 2,571 women, with a mean age of 50.5 years, were included for final analysis after excluding subjects with a past history of colorectal cancer, colon polyps/polypectomy, familial adenomatous polyposis, and colorectomy, or missing data. Diabetes and pre-diabetes were defined using the 2011 American Diabetes Association criteria. Subjects were classified into four groups: polyp-free, non-neoplastic polyps, non-advanced and advanced adenomatous polyps., Results: There were significant differences in the prevalence of diabetes and pre-diabetes among groups with different kinds of colon polyps. In addition, significant differences were also noted in age, total cholesterol, body mass index, triglyceride, high density lipoprotein-cholesterol, fasting plasma glucose, and the prevalence of male gender, hypertension, obesity, current smoking and alcohol drinking among groups. In the multinomial logistic regression analyses, diabetes was related to both non-advanced and advanced adenomatous polyps, while pre-diabetes was only related to non-advanced adenomatous polyps. In addition, age ≥65 years and male gender were associated with both non-advanced and advanced adenomatous polyps, while hypertension and current smoking were independently related to advanced and non-advanced adenomatous polyps, respectively., Conclusions: Diabetes, but not pre-diabetes, was associated with a higher risk of advanced adenomatous polyps. In addition, both diabetes and pre-diabetes were important correlates of non-advanced adenomatous polyps.