Development and validation of the coronary heart disease scale under the system of quality of life instruments for chronic diseases QLICD-CHD: combinations of classical test theory and Generalizability Theory.

BACKGROUND: Quality of life (QOL) for patients with coronary heart disease (CHD) is now concerned worldwide with the specific instruments being seldom and no one developed by the modular approach. OBJECTIVES: This paper is aimed to develop the CHD scale of the system of Quality of Life Instruments for Chronic Diseases (QLICD-CHD) by the modular approach and validate it by both classical test theory and Generalizability Theory. METHODS: The QLICD-CHD was developed based on programmed decision procedures with multiple nominal and focus group discussions, in-depth interview, pre-testing and quantitative statistical procedures. 146 inpatients with CHD were used to provide the data measuring QOL three times before and after treatments. The psychometric properties of the scale were evaluated with respect to validity, reliability and responsiveness employing correlation analysis, factor analyses, multi-trait scaling analysis, t-tests and also G studies and D studies of Genralizability Theory analysis. RESULTS: Multi-trait scaling analysis, correlation and factor analyses confirmed good construct validity and criterion-related validity when using SF-36 as a criterion. The internal consistency α and test-retest reliability coefficients (Pearson r and Intra-class correlations ICC) for the overall instrument and all domains were higher than 0.70 and 0.80 respectively; The overall and all domains except for social domain had statistically significant changes after treatments with moderate effect size SRM (standardized response mea) ranging from 0.32 to 0.67. G-coefficients and index of dependability (Ф coefficients) confirmed the reliability of the scale further with more exact variance components. CONCLUSIONS: The QLICD-CHD has good validity, reliability, and moderate responsiveness and some highlights, and can be used as the quality of life instrument for patients with CHD. However, in order to obtain better reliability, the numbers of items for social domain should be increased or the items' quality, not quantity, should be improved.

Diagnostic Value of Color Doppler Flow Imaging Combined with Serum CRP, PCT, and IL-6 Levels for Neonatal Pneumonia.

Objective: To evaluate the diagnostic value of combined detection of color Doppler flow imaging (CDFI) and serum C-reactive protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6) levels for neonatal pneumonia. Methods: In this prospective study, 30 newborns with pneumonia and 30 healthy newborns in our hospital from January 2019 to January 2020 were recruited. The healthy newborns were assigned to the control group, and the newborns with pneumonia were assigned to the experimental group. All subjects underwent CDFI and measurement of the levels of serum CRP, PCT, and IL-6. The serum indices and imaging results of the two groups were analyzed, and the specificity and sensitivity of different detection methods in the diagnosis of neonatal pneumonia were calculated and analyzed. Results: The levels of serum CRP, PCT, and IL-6 in the experimental group were significantly higher than those in the control group (P < 0.001). Combined detection had a larger detection area, higher sensitivity, and a superior overall detection outcome than single detection (P < 0.05). The diagnostic results of combined detection and clinical diagnosis in 30 newborns with pneumonia were similar (P > 0.05). Conclusion: The combined detection of CDFI and serum CRP, PCT, and IL-6 levels in the diagnosis of neonatal pneumonia shows a promising diagnostic outcome, so it is worthy of clinical application.

Ferroptosis mediated DSS-induced ulcerative colitis associated with Nrf2/HO-1 signaling pathway.

Ulcerative colitis (UC) is an inflammatory disease characterized by an uncontrolled inflammatory response. Previous study showed that the immunological impairment elicted the alteration of inflammatory mediators, and ferroptosis was implicated with the lethal accumulation of reactive oxygen species (ROS). Therefore, this study aimed to investigate the role of ferroptosis in dextran sulfate sodium (DSS)-induced UC. The animal model was established and the molecular markers of ferroptosis were detected by using western blot. The results suggested that the expression of COX2 and ACSL4 was increased dramatically, while the level of GPX4 and FTH1 was deceased in 3% DSS group compared with Control group (P < 0.05). Meanwhile, the body weight and colon length were significantly increased, and the inflammation indexes and MDA levels were reduced in 3% DSS+ ferrostatin-1 group, 3% DSS+ liproxstatin-1 group and 3% DSS+ deferprone group compared to 3% DSS group (P < 0.05). Additionally, the mRNA and protein level of COX2 and ACSL4 were obviously upregulated, but the GPX4 and FTH1 expression were downregulated in 3% DSS group (P < 0.05); however, the expression level of COX2, ACSL4, GPX4 and FTH1 was revered after ferrostatin-1, liproxstatin-1 (Lip-1) or deferprone (DFP) administration. The immunohistochemical assay showed that the staining intensity of COX2 was decreased and the staining intensity of GPX4 was increased in 3% DSS+ Ferr-1 group compared with 3% DSS group (P < 0.05). Moreover, the nuclear factor erythoid 2-related 2 (Nrf2) and HO-1 expression were lower in 3% DSS+ Ferr-1 group than 3% DSS group (P < 0.05). These data revealed that suppressing ferroptosis could effectively ameliorate DSS-induced UC involved in blocking Nrf2/HO-1 signaling pathway.

LncRNA-ENST00000446135 is a novel biomarker of cadmium toxicity in 16HBE cells, rats, and Cd-exposed workers and regulates DNA damage and repair.

Cadmium (Cd) and its compounds are well-known human carcinogens, but the mechanisms underlying the carcinogenesis are not well understood. This study aimed to investigate whether long noncoding RNA (LncRNA)-ENST00000446135 could serve as a novel biomarker of Cd toxicity in cells, animals, and Cd-exposed workers and regulate DNA damage and repair. LncRNA-ENST00000446135 expression increased gradually in cadmium chloride-transformed 16HBE cells. Small interfering RNA-mediated knockdown of LncRNA-ENST00000446135 inhibited the growth of DNA-damaged cells and decreased the expressions of DNA damage-related genes (ATM, ATR, and ATRIP), whereas increased the expressions of DNA repair-related genes (DDB1, DDB2, OGG1, ERCC1, MSH2, XRCC1, and BARD1). Chromatin immunoprecipitation-sequencing showed that MSH2 is a direct transcriptional target of lncRNA-ENST00000446135. Cadmium increased lncRNA-ENST00000446135 expression in the lung of Cd-exposed rats in a dose-dependent manner. A significant positive correlation was observed between blood ENST00000446135 expression and urinary/blood Cd concentrations, and there were significant correlations of LncRNA-ENST00000446135 expression with the DNA damage cell and the expressions of target genes in the lung of Cd-exposed rats and the blood of Cd-exposed workers and significantly correlated with liver and renal function in Cd-exposed workers. These results indicate that the expression of LncRNA-ENST00000446135 is upregulated and may serve as a signature for DNA damage and repair related to the epigenetic mechanisms underlying the cadmium toxicity and become a novel biomarker of cadmium toxicity.