Medical Morphology Training Using the Xuexi Tong Platform During the COVID-19 Pandemic: Development and Validation of a Web-Based Teaching Approach.

BACKGROUND: Histology and Embryology and Pathology are two important basic medical morphology courses for studying human histological structures under healthy and pathological conditions, respectively. There is a natural succession between the two courses. At the beginning of 2020, the COVID-19 pandemic suddenly swept the world. During this unusual period, to ensure that medical students would understand and master basic medical knowledge and to lay a solid foundation for future medical bridge courses and professional courses, a web-based medical morphology teaching team, mainly including teachers of courses in Histology and Embryology and Pathology, was established. OBJECTIVE: This study aimed to explore a new teaching mode of Histology and Embryology and Pathology courses during the COVID-19 pandemic and to illustrate its feasibility and acceptability. METHODS: From March to July 2020, our team selected clinical medicine undergraduate students who started their studies in 2018 and 2019 as recipients of web-based teaching. Meanwhile, nursing undergraduate students who started their studies in 2019 and 2020 were selected for traditional offline teaching as the control group. For the web-based teaching, our team used the Xuexi Tong platform as the major platform to realize a new "seven-in-one" teaching method (ie, videos, materials, chapter tests, interactions, homework, live broadcasts, and case analysis/discussion). This new teaching mode involved diverse web-based teaching methods and contents, including flipped classroom, screen-to-screen experimental teaching, a drawing competition, and a writing activity on the theme of "What I Know About COVID-19." When the teaching was about to end, a questionnaire was administered to obtain feedback regarding the teaching performance. In the meantime, the final written pathology examination results of the web-based teaching and traditional offline teaching groups were compared to examine the mastery of knowledge of the students. RESULTS: Using the Xuexi Tong platform as the major platform to conduct "seven-in-one" teaching is feasible and acceptable. With regard to the teaching performance of this new web-based teaching mode, students demonstrated a high degree of satisfaction, and the questionnaire showed that 71.3% or more of the students in different groups reported a greater degree of satisfaction or being very satisfied. In fact, more students achieved high scores (90-100) in the web-based learning group than in the offline learning control group (P=.02). Especially, the number of students with objective scores >60 in the web-based learning group was greater than that in the offline learning control group (P=.045). CONCLUSIONS: This study showed that the web-based teaching mode was not inferior to the traditional offline teaching mode for medical morphology courses, proving the feasibility and acceptability of web-based teaching during the COVID-19 pandemic. Our findings lay a solid theoretical foundation for follow-up studies of medical students.

MicroRNA-331 inhibits development of gastric cancer through targeting musashi1.

BACKGROUND: The molecular mechanisms involved in microRNAs (miRNAs) have been extensively investigated in gastric cancer (GC). However, how miR-331 regulates GC pathogenesis remains unknown. AIM: To illuminate the effect of miR-331 on cell metastasis and tumor growth in GC. METHODS: The qRT-PCR, CCK8, Transwell, cell adhesion, Western blot, luciferase reporter and xenograft tumor formation assays were applied to explore the regulatory mechanism of miR-331 in GC. RESULTS: Downregulation of miR-331 associated with poor prognosis was detected in GC. Functionally, miR-331 suppressed cell proliferation, metastasis and tumor growth in GC. Further, miR-331 was verified to directly target musashi1 (MSI1). In addition, miR-331 inversely regulated MSI1 expression in GC tissues. Furthermore, upregulation of MSI1 weakened the inhibitory effect of miR-331 in GC. CONCLUSION: miR-331 inhibited development of GC through targeting MSI1, which may be used as an indicator for the prediction and prognosis of GC.

Inhibited CD47 gene affects the clearance of acute myelogenous leukemia stem cells.

OBJECTIVE: To investigate the effect of targeted inhibition of CD47 gene expression on stem cell clearance in acute myeloid leukemia. METHODS: After the lentiviral CD47-siRNA was transfected into acute myelogenous leukemia stem cells (LSCs), the proliferative status of acute myelogenous LSCs was detected by cell counting kit-8, and the apoptosis of stem cells of acute myeloid leukemia was detected by annexin/propidium iodide flow assays. The expression of Bcl-2, Bcl-xl, MCL-1, PIK3p110ß, and interleukin (IL)-3 in acute myeloid LSCs was detected by Western blot analysis and the activity of protein phosphatase 2A (PP2A) and the protein content of CD96 and CD90 were measured by enzyme-linked immunosorbent assay kits. RESULTS: After transfection of the lentivirus CD47-siRNA into acute myeloid LSCs, compared with the empty vector transfection group (control group), the cell viability of the CD47-siRNA transfection group was decreased, and the apoptosis rate was increased. Furthermore, the antiapoptotic protein Bcl-2, Bcl-xl, and MCL-1 and the content of IL-3 protein, CD96, and CD90 was decreased, whereas the activity of PIK3p110ß and PP2A protein was increased. CONCLUSION: Targeted inhibition of CD47 could inhibit the proliferation of myeloid LSCs, promote apoptosis, mobilize the cells into the cell cycle, and reduce the high expression of immune proteins on the cell surface, therefore providing a theoretical basis for the elimination and eradication of LSCs.

MicroRNA-146a expression inhibits the proliferation and promotes the apoptosis of bronchial smooth muscle cells in asthma by directly targeting the epidermal growth factor receptor.

The present study aimed to determine the expression of microRNA-146a (miR-146a) in the plasma of children with asthma, and to investigate the effect of miR-146a on the proliferation and apoptosis of bronchial smooth muscle cells (BSMCs). Reverse transcription-quantitative polymerase chain reaction was used to determine the expression levels of miR-146a mimics and its inhibitor. A Cell Counting kit-8 assay was performed to examine the proliferation of BSMCs. Caspase-3/7 activity was determined using a Caspase-Glo 3/7 kit. To measure the expression levels of proteins associated with apoptosis, western blotting was performed. The target gene of miR-146a was identified using a dual-luciferase reporter assay. The plasma levels of miR-146a in children with asthma were significantly higher compared with those in healthy children. Enhanced miR-146a expression inhibited the proliferation of BSMCs. BSMC apoptosis was promoted by miR-146a. The mechanism underlying the miR-146a-induced promotion of BSMC apoptosis may be its direct targeting of epidermal growth factor receptor (EGFR), which affects downstream signaling pathways. In conclusion, miR-146a expression in asthma inhibits the proliferation and promotes the apoptosis of BSMCs by direct targeting of EGFR.

[Establishment of a Model of Infection by Enterovirus 71 in ICR Mice].

We aimed to study infections in neonatal ICR mice of different ages infected with Enterovirus 71(EV-A71)through three routes of infection, and to explore the dynamic distribution and infection mechanism of EV-A71 in vivo.Three-,5-and 9-day-old neonatal ICR mice were infected with an EV-A71 strain isolated from a child with severe hand, foot and mouth disease through intramuscular(IM), intraperitoneal (IP)and intracerebral (IC)injection, respectively. Consequently, blood, brain, hind-limb muscle, heart, and intestines of mice were collected at regular intervals. Changes in viral load in organs were measured using real-time polymerase chain reaction. Hematoxylin and eosin staining and immunohistochemical (IHC)analyses were undertaken to detect pathogenic and pathologic changes in infected mice.Five-day-old neonatal mice infected with EV-A71 through IM,IP or IC routes had obvious neurologic symptoms and a high mortality rate. Symptoms were alleviated slightly with increasing age of mice upon injection. However, the pathogenicity associated with IM and IP injections was more severe than that of IC injection. Also, the mortality rates of IM and IP injections were significantly higher than that of IC injection. Compared with the control group, the mean body weight(in g)of 3-day-old neonatal mice at 6days post-infection(dpi)injected by IM,IP and IC routes decreased by 1.54(31.43%),1.31(15.06%)and 2.52(44.28%),respectively. Similarly, the mean body weight(in g)of 5-day-old neonatal mice at 6dpi injected by IM and IP decreased by 0.605(8.95%),0.886(15.51%),whereas that of mice injected by IC increased by 0.904(14.70%).The body weight of all infection groups was significantly lower than that of the control group(P<0.05).All 3-day-old neonatal mice infected with EV-A71 through IM,IP and IC routes died at 9dpi.Survival rates of 5-day-old neonatal mice infected through IM,IP and IC routes at 9dpi and14 dpi were 42.8%,25%,and 87.5%,and 0%,0%,and 25%,respectively.Those of 9-day-old neonatal mice at 14 dpi were 70%,69.23% and 100%,respectively.Pathologic and IHC examination showed that EV-A71 had a strong preference for infecting nervous systems and skeletal muscle, and could also lead to: viremia; necrosis of brain neurons and skeletal muscle; myocardial interstitial edema; inflammatory response of multiple organs. These data suggest that 5-day-old ICR neonatal mice injected through IM or IP routes can establish an ideal model of infection by EV-A71 in mice.