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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

Highly active and durable Pd-based electrocatalysts for ethanol oxidation reaction (EOR) play a crucial role in the commercialization of direct ethanol fuel cells (DEFCs). However, the poisonous intermediates (especially adsorbed CO species (COad)) formed during the EOR process can easily adsorb and block the active sites on Pd electrodes, which in turn limits the catalytic efficiency. Hence, we present a series of Pd-based composites with a strong coupling interface consisting of Pd nanosheets and amorphous Bi(OH)3 species. The incorporation of Bi(OH)3 can induce an electron-rich state adjacent to the Pd sites and effectively separate the Pd ensemble, leading to excellent CO tolerance. The optimal Pd-Bi(OH)3 NSs catalyst manifests a mass activity of 2.2 A·mgPd−1, which is 5.7 and 2.0 times higher than that of Pd NSs and commercial Pd/C catalyst, respectively. Further CO-stripping experiments and CO-DRIFTS tests confirm the excellent CO tolerance on Pd-Bi(OH)3 NSs electrode, leading to the enhanced EOR durability. [ABSTRACT FROM AUTHOR]

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.

Endostatin has previously been demonstrated to efficiently inhibit the angiogenesis and growth of endothelial cells. However, the role of endostatin in the tumor microenvironment remains to be elucidated. To investigate the antitumor effect of endostatin in lung cancer, the present study was designed to explore the alterations of microvessel density in Lewis lung cancer models and the expression of vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-17, interferon (IFN)-γ and hypoxia inducible factor (HIF)-1α, following endostatin therapy. It was demonstrated that the growth and angiogenesis of tumors were markedly suppressed by treatment with endostatin, compared with control group. The microvessel density in mice treated with endostatin was significantly inhibited in a dose-dependent manner. The expression levels of VEGF, IL-6 and IL-17 in tumors were decreased, however IFN-γ and HIF-1α expression levels were increased, following treatment with endostatin. In addition, the proportion of myeloid derived suppressor cells and tumor associated macrophages (TAMs; M2 type) were significantly decreased, whereas those of mature dendritic cells and TAMs (M1 type) were increased, and cluster of differentiation (CD)8+ T cells were recruited to infiltrate the tumors following treatment with endostatin. In addition, the expression levels of IL-6, IL-10, tumor growth factor-β and IL-17 in tumor tissue were potently decreased with endostatin therapy. These results indicated that endostatin efficiently inhibited tumor angiogenesis and reversed the immunosuppressive microenvironment associated with the presence of tumors. [ABSTRACT FROM AUTHOR]