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Background Follow-up is a necessary step in the management of chronic disease patients. Cloud follow-up as a new form of follow-up may improve the quality of follow-up. However, there is currently a lack of patient-oriented evaluation tools for cloud follow-up service quality. Objective To develop a scale for evaluating the service experience of chronic disease patients in cloud follow-up and to examine its reliability and validity, in order to provide a tool for evaluating the quality of cloud follow-up services. Methods Guided by the service quality evaluation model, the scale was developed by using methods including literature review, semi-structured interview, expert consultation. During August to October 2022, a survey was conducted among chronic disease patients (n=480) discharged from a tertiary hospital and lived under the network of a community service center in Hangzhou, China. Item analysis and tests of reliability and validity were test on the developed scale. Results The developed scale for evaluating the service experience of chronic disease patients in cloud follow-up had 37 items distributed in 5 dimensions. Patients' perceptions and expectations to each item were evaluated simultaneously. The overall Cronbach's α coefficient of the developed scale was 0.962, with split-half reliability of 0.732 and test-retest reliability of 0.844. The content validity index of the scale was 0.980. The correlation coefficient between the scale and satisfaction scores was 0.754 (P

Background Hypertriglyceridemia has been increasingly valued as a risk factor for acute pancreatitis (AP) . However, the relationship between obesity and AP has not yet been confirmed, whether baseline triglyceride (TG) affects the risk of AP in non-obese people is still inconclusive. Objective To explore the association between baseline serum triglyceride (TG) and the risk of AP in a nonobese cohort from Kailuan Group. Methods A prospective cohort study was performed among in-service and retired workers of Kailuan Group (non-obese, without a history of AP, with complete TG information) who first attended the annual health screening for workers of the group as a benefit conducted between 2006 and 2007 or between 2008-2009. The cumulative incidence of AP across serum TG tertile groups: 〔Q1 group (TG≤0.96 mmol/L) , Q2 group (0.96 mmol/L

Abstract Background The 1555A > G mutation is the most common cause of aminoglycoside-induced and non-syndromic deafness. However, the variable clinical phenotype and incomplete penetrance of A1555G-induced hearing loss complicate our understanding of this mutation. Environmental factors, nuclear genes, mitochondrial haplotypes/variants and a possible threshold effect have been reported to may be involved in its manifestation. Methods Here, we performed a clinical, molecular, genetic and phylogenic analysis in a six-generation Chinese family. Results A clinical evaluation revealed that affected individuals without aminoglycoside exposure developed hearing loss extending gradually from 12000 Hz to 8000 Hz and then to 4000 Hz. Using pyrosequencing, we detected an identical homoplasmic 1555A > G mutation in all individuals except one. We did not find any correlation between the mutation load and the severity of hearing loss. T123N coexisted with the 1555A > G mutation in six affected subjects in our pedigree. Analysis of the complete mtDNA genome of this family revealed that this family belonged to haplotype B4C1C and exhibited high penetrance. Upon the inclusion of subjects that had been exposed to aminoglycosides, the penetrance of the hearing loss was 63.6%.; without exposure to aminoglycosides, it was 51.5%. This pedigree and another reported Chinese pedigree share the same haplotype (B4C1C) and lack functionally significant mitochondrial tRNA variants, but nevertheless they exhibit a different penetrance of hearing loss. Conclusions Our results imply that the factors responsible for the higher penetrance and variable expression of the deafness associated with the 1555A > G mutation in this pedigree may not be mtDNA haplotype/variants, but rather nuclear genes and/or aminoglycosides.