ObjectivesThe study aims to investigate the state anxiety of parents of special needs children during the 2019 coronavirus disease (COVID-19) epidemic and the influence of parental stress, social support, and other related variables on the anxiety of parents.MethodsBespoke questionnaires of children’s and parent’s mental and behavioral problems during the epidemic were used in the study. We also used the State Anxiety Inventory (S-AI), the Parenting Stress Index—Short Form-15 (PSI-SF-15), the NEO Five-Factor Inventory (NEO-FFI), and the Multidimensional Scale of Perceived Social Support (MSPSS). The data used in the study were pooled from an online survey of parents of special needs children and analyzed by one-way analysis of variance (ANOVA) and multiple linear regression.ResultsOverall, 1,451 individuals were included, of which 402 were fathers (27.71%) and 1,049 were mothers (72.29%). ANOVA results showed that educational background, family monthly income, and type of their child’s disability made parents’ state anxiety significantly different. The results of multiple linear regression showed that during the epidemic, social support negatively predicted parents’ state anxiety (B = −0.15, p < 0.001), whereas parenting stress (B = 0.07, p = 0.001) and parental mental and behavioral problems (B = 0.37, p < 0.001) positively predicted parents’ state anxiety.ConclusionsDuring the outbreak of COVID-19, parents of special needs children suffered mental and behavioral problems, together with parenting stress and social support, which influenced their state anxiety. These findings can be used to develop relevant psychological interventions to improve the mental health of vulnerable groups during a pandemic like COVID-19.

Numerous studies have reported the association of long non-coding RNAs (lncRNAs) in cancers, yet the function of lncRNA high expressed in hepatocellular carcinoma (HEIH) in esophageal carcinoma (EC) has seldom been explored. Here, we aimed to explore the mechanism of HEIH on EC via microRNA-185 (miR-185)/kallikrein-related peptidase 5 (KLK5) modulation. Cancer and non-tumoral tissues were collected, in which HEIH, miR-185 and KLK5 expression were detected, as well as their correlations. Also, the relation between the prognosis of EC patients and HEIH/miR-185/KLK5 expression was clarified. EC cells (KYSE-30 and TE-1) were screened for subsequent gain- and loss-of-function assays and their biological functions were further monitored. Tumor volume and weight in EC mice were also measured. Results from this study indicated that HEIH and KLK5 were elevated and miR-185 was declined in EC. The positive correlation was seen in HEIH and KLK5 expression, while the negative correlation was observed in HEIH or KLK5 and miR-185 expression. High HEIH and KLK5 indicated worse prognosis and high miR-185 suggested better prognosis of EC patients. Depleting HEIH or restoring miR-185 suppressed the malignant phenotypes of EC cells, and delayed tumor growth in EC mice. HEIH was found to bind with miR-185 to regulate KLK5 expression. Overexpressing KLK5 alone promoted EC cell progression while up-regulating miR-185 reversed such effects on EC cells. Collectively, we reveal that HEIH depletion dampens EC progression by upregulating miR-185 and downregulating KLK5, which provides novel treatments for EC.

27‐Hydroxycholesterol (27‐HC) has been implicated in the pathological process of estrogen receptor positive breast cancer. However, the role of 27‐HC in lung adenocarcinoma is still unclear. Because bone metastasis is a main reason for the high mortality of lung adenocarcinoma, this study aimed to investigate the effect of 27‐HC on osteoclastogenesis in lung adenocarcinoma microenvironment. The results showed that the conditioned media (CM) from lung adenocarcinoma cells cocultured with macrophages promoted osteoclast differentiation, which was enhanced by 27‐HC. Further investigation showed that CM inhibited miR‐139 expression and promoted c‐Fos expression. Luciferase reporter assay identified c‐Fos as a direct target of miR‐139. CM also induced the expression and nuclear translocation of NFATc1 and STAT3 phosphorylation, which was enlarged by 27‐HC but was attenuated by miR‐139. Coimmunoprecipitation assay demonstrated that 27‐HC increased the interaction between NFATc1 and phosphorylated STAT3, which was restricted by miR‐139. Chromatin immunoprecipitation assay showed that pSTAT3 could bind to the promoter of c‐Fos, c‐Fos could bind to the promoter of NFATc1, and both pSTAT3 and NFATc1 could bind to the promoter of Oscar, which were enlarged by 27‐HC but were blocked by miR‐139. Knockdown of c‐Fos mimicked the effect of miR‐139. These results suggested that CM, especially containing 27‐HC, promoted osteoclastogenesis by inhibiting miR‐139 expression and activating the STAT3/c‐Fos/NFATc1 pathway.

Dietary cholesterol has been implicated to promote lung cancer. Lung adenocarcinoma (LAC) is a main type of lung cancer, whereas the functional mechanism of cholesterol in LAC remained largely unknown. In the present study, we evidenced that cholesterol promoted cell proliferation and invasion of LAC in vitro as well as LAC metastasis in vivo. Cyp27A1 knockdown reduced the cholesterol-induced LAC cells proliferation and invasion. In contrast, Cyp7B1 knockdown enhanced the effect of cholesterol on LAC cells proliferation and invasion. Furthermore, Cyp27A1 deficiency remarkably reduced high cholesterol-induced LAC metastasis in vivo. Mechanism investigation demonstrated that exposure of LAC cells to 27-hydroxycholesterol induced the phosphorylation of AKT and NFκB p65, and promoted the expression of peptidylprolyl isomerase B (PPIB), especially in the coculture with THP1-derived macrophage. Meanwhile, 27-hydroxycholesterol induced the secretion of FGF2 and IL-6, which contributed to the expression of snail and vimentin. Luciferase report assay and ChIP assay confirmed that NFκB p65 controlled the transcription of PPIB. Inhibiting NFκB p65 activation reduced PPIB expression. PPIB inhibition reduced 27-hydroxycholesterol-induced expression of snail and vimentin. These results indicated that 27-hydroxycholesterol linked high cholesterol and LAC metastasis by regulating NFκB/PPIB axis and the secretion of FGF2 and IL-6.