Abstract：Structural variation (SV) is a fundamental genetic cause for cancer, with demonstrated correlation to disease progression and treatment response. Traditional sequencing method cannot provide full genomic landscape especially large-scale and complex structural variation. To overcome these limitations, we adopted a combined sequencing approaches, including optical mapping, single molecular sequencing and short reads shotgun sequencing, to evaluate the SV in thyroid cancer. Different numbers, length and types of structural variation, with genes affected by SV were scrutinized. Integrating these results could showed comprehensive scenario for thyroid cancer in a genomic view. We demonstrate that integrated approaches could provide a powerful tool for capturing a higher level of genomic SV, creating new interpretation of sequencing data of particular relevance to human cancer.

Objective: Since the outbreak of COVID-19, wearing masks and frequent hand washing have become common phenomena. The purpose of this study was to explore the impact of such lifestyle changes on adenoid hypertrophy in children in Beijing. Methods: Baidu Index platform was used to search with adenoid hypertrophy as the keyword, and the search volume of terms from 2017 to 2021 was recorded weekly. Meanwhile, the visits to adenoid hypertrophy in the otolaryngology department of Children’s Hospital, Capital Institute of Pediatrics in the same period were collected and compared, and analyzed. Results: (1) Baidu index indicated that the following group of adenoid hypertrophy was mainly parents of childbearing age, and female parents paid more attention;  (2) From 2017 to 2019, the online attention and outpatient visits to adenoid hypertrophy increased year by year. After the COVID-19 outbreak, the increasing trend declined and stagnated. Conclusions: After the outbreak of COVID-19, epidemic prevention policies (wearing masks, hand hygiene, reducing movement of people, etc.) have a certain inhibitory effect on adenoid hypertrophy.  Keywords: adenoid hypertrophy, COVID-19, Baidu Index platform, masks, hand hygiene Key points: Adenoid hypertrophy may be associated with recurrent respiratory infections in childhood. After the onset of COVID-19, China enacted many epidemic prevention policies. Wearing masks and hand hygiene may reduce the incidence of respiratory infections. Web data provides insight into the real needs of the population. After the onset of COVID, there was a stagnation in network attention and outpatient visit rates for adenoid hypertrophy.

Background and Purpose：As important components of lung tissue, endothelial cells (ECs) are associated with many lung diseases. The role of ECs dysfunction in idiopathic pulmonary fibrosis (IPF) and how to improve alveolar capillary barrier (ACB) to treat IPF is incompletely understood. Therefore we investigated the involvment of endothelial Sphingosine-1-phosphate receptor 1 (S1pr1) in PF and therapeutic effect of selective S1pr1 agonist IMMH002. Experimental approach：Databases of IPF patients and individuals without fibrosis were mined by Seurat. We generated an endothelial-conditional S1pr1 knockout (S1pr1+/−) mice and we also examined a bleomycin-induced model of pulmonary fibrosis (PF). We performed qRT-PCR,Western blot, Immunofluorescence staining and EC permeability experiments. Key results：Expression of S1pr1 in ECs was reduced markedly in IPF patients. Mice with endothelial-specific S1pr1 deficiency exhibited severer inflammation and fibrosis upon challenge with bleomycin. Significant accumulation of alpha-smooth muscle actin (α-SMA) was observed near vessels after S1pr1 deficiency, which indicated a potential connection between ACB injury and fibrosis. S1pr1 activation by a selective agonist IMMH002 could ameliorate PF by improving tight junctions in ECs and protects the ACB. Conclusion and Implications: Our results suggest that S1pr1 plays a significant role in ACB and it could be a potential target for IPF. Activation of S1pr1 with IMMH002 elicits a potent therapeutic effect in bleomycin-induced fibrosis by increasing tight junctions in endothelial cells and protecting the integrity of ACB therefore improve survial rate and lung function.