This report presented the endemic status of schistosomiasis in the People's Republic of China at a national level in 2020, and analyzed the data collected from the national schistosomiasis prevention and control system and national schistosomiasis surveillance sites. Among the 12 provinces (municipality and autonomous region) endemic for schistosomiasis in China, Shanghai Municipality, Zhejiang Province, Fujian Province, Guangdong Province and Guangxi Zhuang Autonomous Region continued to consolidate the achievements of schistosomiasis elimination, and Sichuan and Jiangsu provinces maintained the criteria of transmission interruption, while Yunnan, Hubei, Anhui, Jiangxi and Hunan provinces maintained the criteria of transmission control by the end of 2020. A total of 450 counties (cites, districts) were found to be endemic for schistosomiasis in China, with 28 376 endemic villages covering 71 370 400 people at risk of infections. Among the 450 endemic counties (cities, districts), 74.89% (337/450), 21.87% (98 was achieved as scheduled; however, the endemic situation of schistosomiasis rebounded in local areas. Precision schistosomiasis control and intensified monitoring of the endemic situation and transmission risk of schistosomiasis are required to be performed to facilitate the progress towards elimination of schistosomiasis steadily.Frailty is a syndrome involving increased vulnerability that usually develops from age-related decline in physiological reserves and function in multiple organ systems, resulting in an impaired ability to respond to acute changes in health conditions. It is imperative that healthcare providers who work with older adults in primary care and community settings understand how to assess frailty and can identify appropriate interventions. This article reports the results of a rapid review that examined how frailty is assessed in community-dwelling older adults and what interventions are used to address frailty in this population. Long non-coding RNAs (lncRNAs) are involved in the development of many cancers, including colorectal cancer (CRC). FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) is a key lncRNA in the regulation of CRC progression, but its potential molecular mechanisms need to be further explored. To investigate the mechanism of lncRNA FEZF1-AS1 in the progression of CRC. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure FEZF1-AS1 and miR-363-3p expression. Cell proliferation, migration and invasion were analyzed using Cell Counting Kit-8 (CCK-8) and transwell assays. Protein expression of epithelial-mesenchymal transformation (EMT)-related markers and paired-related homeobox 1 (PRRX1) were determined using western blot analysis. The interactions among FEZF1-AS1, miR-363-3p and PRRX1 were verified with dual-luciferase reporter assay. YAP-TEAD Inhibitor 1 in vivo A xenograft model was constructed in vivo to confirm the role of FEZF1-AS1 in CRC tumor growth. We demonstrated that FEZF1-AS1 expression was upregulated in CRC, and its silencing reduced CRC cell proliferation, migration, invasion, and EMT. MiR-363-3p could be inhibited by FEZF1-AS1, which inhibitor could reverse the suppressive effect of FEZF1-AS1 silencing on CRC progression. Paired-related homeobox 1 could be targeted by miR-363-3p, and the inhibitory effect of FEZF1-AS1 knockdown on CRC progression could also be eliminated by PRRX1 overexpression. Furthermore, interference of FEZF1-AS1 reduced the tumor growth of CRC in vivo. Our data demonstrate that FEZF1-AS1 regulated PRRX1 expression to promote CRC progression via inhibition of miR-363-3p.Our data demonstrate that FEZF1-AS1 regulated PRRX1 expression to promote CRC progression via inhibition of miR-363-3p.The paper summarizes the current knowledge about the influence of SARS-CoV-2 on the thyroid gland and benign thyroid diseases, with emphasis on the situation in Poland. Based on the latest scientific literature published up to May 1, 2021 and the PubMed, Google Scholar, EMBASE and Web of Science database searches, keywords related to SARS-CoV-2 and its impact on the thyroid gland and benign thyroid diseases were searched. COVID-19-related thyroid disorders include non-thyroid syndrome, hypothyroidism and thyrotoxicosis. The authors paid special attention to the treatment of thyroid disease during the pandemic. The emphasis was on radioiodine therapy, which is of high clinical value due to the lower risk of neutropenia or agranulocytosis. It is currently unknown whether COVID-19 may lead to de novo thyroid dysfunction or if it can aggravate an existing thyroid disease. Patients with uncontrolled thyrotoxicosis are in a risk group for complications (e.g., cytokine storm) from any infection (especially from SARS-CoV-2 infection). Moreover, this group of patients should receive more extensive care, bearing in mind the neutropenia from taking antithyroid drugs, which may mask the symptoms of COVID-19. Induction of acquired drug resistance occurs frequently with cisplatin-based therapy for non-small cell lung cancer (NSCLC). As recent studies have demonstrated that deregulation of microRNAs (miRNAs) is associated with drug resistance in cancers, correcting the deregulation of miRNAs represents a promising strategy to reverse acquired resistance in NSCLC. This study investigated the functional role of miR-15b in cisplatin resistance in NSCLC. Cisplatin-resistant PC9 and A549 NSCLC cell lines (PC9-R and A549-R) were established through long-term exposure to cisplatin. Differences in miR-15b expression between cisplatin-resistant NSCLC cell lines and their parental cell lines were identified through quantitative real-time polymerase chain reaction (qRT-PCR). The effect of anti-miR-15b on the sensitivity of PC9-R and A549-R to cisplatin-induced cytotoxicity was evaluated using Cell Counting Kit-8 (CCK-8) assays. Regulation of GSK-3β by miR-15b was confirmed with luciferase reporter assays. Cell apoptosis and mitochondrial membrane potential (MMP) were measured using flow cytometry analysis. In PC9-R and A549-R cells, miR-15b was significantly overexpressed. However, knockdown of miR-15b clearly reduced cisplatin resistance in PC9-R and A549-R cells. Researching the mechanism, we proved that GSK-3β was the target of miR-15b. Knockdown of miR-15b significantly increased the expression GSK-3β and thus promoted the degradation of MCL-1, which is a key anti-apoptosis protein. As a result, anti-miR-15b expanded the cisplatin-induced apoptosis in cisplatin-resistant NSCLC cells. Knockdown of miR-15b partially reversed cisplatin resistance in NSCLC cells through the GSK-3β/MCL-1 pathway.Knockdown of miR-15b partially reversed cisplatin resistance in NSCLC cells through the GSK-3β/MCL-1 pathway.