Background Nomophobia or phobia of no mobile phone is the fear of being without a mobile phone or being unable to contact others via a mobile phone. It is a newly emerging psychiatric disorder among mobile phone users. Objective There are no psychometric scales available in China for examining nomophobia, although China has become the largest mobile phone handset consumer market in the world. Therefore, this study aimed to translate the original English version of a psychometric scale into Chinese and further examine its reliability and validity among Chinese college students. Methods The original version of the Nomophobia Questionnaire (NMP-Q) was first translated into Chinese using the backward and forward translation procedure. An exploratory factor analysis (a principal component analysis plus varimax rotation) and a confirmatory factor analysis (CFA) were performed to examine the underlying factor structure of the translated questionnaire. The internal consistency reliability of the scale was determined by computing the Cronbach alpha coefficient, the test-retest reliability, and the corrected item-total correlation. A multivariate regression analysis was used for examining associations between nomophobia and independent variables among the college students. Results A total of 2000 participants were included in the study. Their ages ranged from 16 to 25 years, with 51.95% (1039/2000) being male participants. The Chinese version of NMP-Q retained 18 items. The eigenvalues, total variance explained, and scree plot jointly support a 4-factor structure of the translated questionnaire. The CFA reached the adaptive standard, and the discriminant validity of the scale was good. The Cronbach alpha coefficient of this scale was .925, and the Cronbach alpha coefficients of the subscales were .882, .843, .895, and .818. The test-retest reliability was 0.947. Corrected item-total correlation ranged from 0.539 to 0.663. The significant predictors for each of the dimensions of nomophobia and total score of the questionnaire were the average number of hours spent on a mobile phone daily and gender. Conclusions The Chinese version of the NMP-Q exhibited satisfactory psychometric properties.

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The aims of the current study were to investigate the influence of insufficient radiofrequency ablation (RFA) on the cell proliferation of the human hepatocellular carcinoma (HCC) cells, SMMC7721, and to elucidate the underlying mechanism. SMMC7721 cells were subjected to a 47°C treatment regimen to simulate insufficient RFA, in the presence or absence of KN93 [a specific inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaMKII)], PD98059 [a specific inhibitor of extracellular signal-regulated kinase (ERK)], or axitinib (a specific inhibitor of vascular endothelial growth factor (VEGF) receptor]. Cell proliferation was determined using a thiazolyl terazolium assay (MTT). The levels of CaMKII, phospho-CaMKII, ERK, phospho-ERK and VEGF were observed by western blot analysis. The results demonstrated that the 47°C treatment regimen: i) Triggered upregulation of VEGF expression in the SMMC7721 cells, which was reduced by CaMKII or ERK inhibition; ii) induced ERK activation was prevented by KN93; and iii) promoted SMMC7721 cell proliferation, which was greatly inhibited by axitinib, KN93 and PD98059. In conclusion, the results indicated that insufficient RFA promotes SMMC7721 cell proliferation by activating CaMKII/ERK-dependent VEGF overexpression.

Cardiac fibrosis is considered an important pathological mechanism in the progression of cardiac remodeling and heart failure. Astragaloside IV (AsIV) is a major active ingredient in Astragalus membranaceus. In a preliminary experiment, it was demonstrated that this naturally occurring substance exhibited cardioprotective effects via preventing cardiomyocyte hypertrophy and apoptosis. The present study aimed to investigate the effects of AsIV on β‑adrenergic receptor (β‑AR)‑mediated cardiac fibrosis, and the associated mechanism. Cell Counting Kit‑8 (CCK‑8) assay was used to examine the proliferation of rat cardiac fibroblast (CF) cultures. Collagen I secretion was detected by ELISA. Dihydroethidium was used to determine intracellular ROS levels. Western blotting was used to examine the expression level of total and phosphorylated mitogen‑activated protein kinases (MAPKs). In the present study, the effects of AsIV on β‑adrenergic receptor (β‑AR) ‑mediated cardiac fibrosis were investigated, and the associated mechanism was revealed. Isoprenaline (ISO) is a selective β‑AR agonist, and treatment with AsIV significantly inhibited (ISO)‑triggered cardiac fibroblast proliferation and type I collagen synthesis. In addition, ISO resulted in a significant elevation of reactive oxygen species (ROS) levels and phosphorylation of the three profibrotic MAPKs, namely extracellular signal‑regulated kinase, p38MAPK and c‑Jun N‑terminal kinase. AsIV effectively reversed the aforementioned ISO‑induced alterations. In addition, N‑acetylcysteine, a typical ROS scavenger, mimicked the inhibitory effects of AsIV on MAPK activation. The present study demonstrated that AsIV may inhibit ISO‑induced cardiac fibrosis by suppressing ROS‑mediated MAPK activation.