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Background Lung adenocarcinoma (LAC) is the most prominent histological subtype of non‐small cell lung cancer (NSCLC) with a high rate of mortality and metastasis. Accumulating evidence has shown that long non‐coding RNAs (lncRNAs) play malfunctioning roles in the development of human tumors. Hence, this study aimed to determine the biological function of LINC00511 in LAC and to provide a novel diagnostic and therapeutic target for it. Methods LINC00511 expression in LAC tissues and cell lines (H1299 and A549) were detected by real time‐polymerase chain reaction (RT‐qPCR). Cell counting kit‐8 (CCK‐8) assay was employed to analyze cell proliferative ability. Cell metastasis change was measured using transwell assay. Moreover, we revealed a novel target gene of LINC00511 and elucidated the underlying competitive endogenous RNA regulatory mechanism in LAC cells. Results Data from our study demonstrated that LINC00511 expression was increased in LAC tissues and cells in comparison to their corresponding controls. Moreover, overexpression of LINC00511 indicated the poor prognosis of LAC patients. Overexpression of LINC00511 promoted proliferation, invasion and migration capacities of LAC cells. Moreover, LINC00511 promoted LAC progression via serving as a sponge of miR‐625‐5p and regulating PKM2 expression. Conclusions The present study showed that LINC00511 was involved in LAC progression by targeting miR‐625‐5p/PKM2, indicating that LINC00511/miR‐625‐5p/PKM2 may function as promising therapeutic targets for LAC.

In the early 2000s, emerging SARS‐CoV‐2, which is highly pathogenic, posed a great threat to public health. During COVID‐19, epigenetic regulation is deemed to be an important part of the pathophysiology and illness severity. Using the Illumina Infinium Methylation EPIC BeadChip (850 K), we investigated genome‐wide differences in DNA methylation between healthy subjects and COVID‐19 patients with different disease severities. We conducted a combined analysis and selected 35 “marker” genes that could indicate a SARS‐CoV‐2 infection, including 12 ( ATHL1 , CHN2 , CHST15 , CPLX2 , CRHR2 , DCAKD , GNAI2 , HECW1 , HYAL1 , MIR510 , PDE11A , and SMG6 ) situated in the promoter region. The functions and pathways of differentially methylated genes were enriched in biological processes, signal transduction, and the immune system. In the “Severe versus Mild” group, differentially methylated genes, after eliminating duplicates, were used for PPI analyses. The four hub genes ( GNG7 , GNAS , PRKCZ , and PRKAG2 ) that had the highest degree of nodes were identified and among them, GNG7 and GNAS genes expressions were also downregulated in the severe group in sequencing results. Above all, the results suggest that GNG7 and GNAS may play a non‐ignorable role in the progression of COVID‐19. In conclusion, the identified key genes and related pathways in the current study can be used to study the molecular mechanisms of COVID‐19 and may provide possibilities for specific treatments.

Aim. To explore the potential relationship between NLR and micronutrient deficiency in patients with severe COVID-19 infection. Methods. Sixteen patients were categorized into the mild group (mild COVID-19) and severe group (severe COVID-19) based on the guideline of the management of COVID-19. The lactate dehydrogenase (LDH); superoxide dismutase (SOD), the inflammatory markers (neutrophil lymphocyte ratio (NLR)), erythrocyte sedimentation rate (ESR), c-reactive protein (CRP), selenium (Se), iron (Fe), zinc (Zn), nickel (Ni), copper (Cu), chromium (Cr), cadmium (Cd), arsenic (As), and manganese (Mn) were measured in the blood. Results. Compared to the mild group, the NLR ( P < 0.05 ) and the level of Se ( P < 0.01 ), Fe ( P < 0.05 ), and Zn ( P < 0.05 ) were significantly decreased in the severe group. The level of Se, Fe, and Zn was significantly correlated to NLR levels. Furthermore, close positive correlation was found between NLR and severity of COVID-19. Conclusion. The micronutrient deficiency in the blood is associated with NLR in the severity of COVID-19 patients.

Acute and chronic respiratory diseases are associated with abnormal coagulation regulation and fibrolysis. However, the detailed mechanism by which coagulation regulation and fibrolysis affect the occurrence and development of lung diseases remain to be elucidated. Protease activated receptor-1 (PAR-1), a major high-affinity thrombin receptor, and nuclear factor kappa B (NF-κB), a transcription factor, are involved in cell survival, differentiation, and proliferation. We have investigated the potential mechanism of thrombin-induced fibroblast proliferation and roles of PAR-1 and NF-κB signalling in this process. The effect of thrombin on proliferation of human pulmonary fibroblasts (HPF) was assessed by 5-bromo-2-deoxyuridine (BrdU) incorporation assay. The expression of PAR1 and NF-κB subunit p65 protein was detected by Western blot. Nuclear translocation of p65 was examined by laser scanning confocal microscopy. We show that thrombin significantly increased proliferation of HPF as determined by induction of BrdU-positive incorporation ratio. Induced PAR1 protein expression was also seen in HPF cells treated with thrombin. However, thrombin had no significant effect on expression and translocation of NF-κB p65 in HPF cells. The results indicate that, by increasing protein expression and interacting with PAR1, thrombin promotes HPF proliferation. NF-κB signalling appears to play no role in this process.