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Functional experiment is an important part of training program of basic medical experiment technology in medical colleges, and a scientific laboratory management system is a prerequisite for ensuring the progress and training outcomes of the education. Based on the school-running concept of “small-scale elite education” in Peking Union Medical College, this paper expounds the progress of the construction of medical functional experiment teaching system in Peking Union Medical College from many aspects, such as the reform of medical functional experiment teaching, the construction of functional laboratory and so on, and puts forward some ideas for building of a qualified training laboratory, so as to provide reference for further deepening the reform of experimental teaching and supporting sustainable development of teaching laboratory of medical schools.

We aimed to explore the aberrant expression status of hsa-miR-141-3p and dual-specificity protein phosphatase 1 (DUSP1) and their relative mechanisms in uterine cervical carcinoma (UCC).Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was conducted to detect the expression of hsa-miR-141-3p. Immunohistochemical (IHC) staining was performed to examine the expression of DUSP1 in UCC. Gene chips and RNA-seq datasets were also obtained to assess the expression level. Integrated standardized mean difference (SMD) was calculated to evaluate the expression status of hsa-miR-141-3p in UCC tissues comprehensively. DUSP1-overexpression and hsa-miR-141-3p-inhibition HeLa cells were established, and CCK-8, transwell, wound healing, cell cycle, and apoptosis assays were implemented. The targets of hsa-miR-141-3p were obtained with online tools, and the combination of hsa-miR-141-3p and DUSP1 was validated via dual-luciferase reporter assay. Single-cell RNA-seq data were analyzed to explore hsa-miR-141-3p and DUSP1 in different cells. An integrated SMD of 1.41 (95% CI[0.45, 2.38], p = 0.0041) with 558 samples revealed the overexpression of hsa-miR-141-3p in UCC tissues. And the pooled SMD of -1.06 (95% CI[-1.45, -0.66], p < 0.0001) with 1,268 samples indicated the downregulation of DUSP1. Inhibition of hsa-miR-141-3p could upregulate DUSP1 expression and suppress invasiveness and metastasis of HeLa cells. Overexpression of DUSP1 could hamper proliferation, invasion, and migration and boost apoptosis and distribution of G1 phase. The dual-luciferase reporter assay validated the combination of hsa-miR-141-3p and DUSP1. Moreover, the targets of hsa-miR-141-3p were mainly enriched in the MAPK signaling pathway and activated in fibroblasts and endothelial cells. The current study illustrated the upregulation of hsa-miR-141-3p and the downregulation of DUSP1 in UCC tissues. Hsa-miR-141-3p could promote UCC progression by targeting DUSP1. [ABSTRACT FROM AUTHOR]

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Steroid 11β‐hydroxylase deficiency (11β‐OHD) is a rare autosomal recessive disorder caused by pathogenic variants of CYP11B1 gene. This study aimed to perform molecular analysis of a Chinese 11β‐OHD series and in vitro functional study of twenty CYP11B1 missense variants. Twelve Chinese patients with clinical diagnosis of 11β‐OHD were included in the study to analyze their molecular etiology. Genomic DNA of patients was extracted to be sequenced all coding exons and intronic flanking sequences of CYP11B1. Fourteen missense variants found in 12 patients mentioned above along with 6 missense variants previously reported by our team were evaluated functionally. Amino acid substitutions were analyzed with computational program to determine their effects on the three‐dimensional structure of CYP11B1 protein. Clinical characteristics and hormone levels at baseline of the 18 patients carrying 18 missense variants aforementioned were recorded to perform genotype–phenotype correlation. A total of 21 rare variants including 9 novel and 12 recurrent ones were identified in 12 patients, out of which 17 were missense, 2 were nonsense, 1 was a splice site variant, and 1 was a deletion–insertion variant. Results of in vitro functional study revealed that 3 out of 20 missense mutants (p.Leu3Pro, p.Gly267Ser, and p.Ala367Ser) had partial enzyme activity and the other 17 had little enzymatic activity. The impairment degree of enzymatic activity in vitro functional study was also reflected in the severity degree of interaction change between the wild‐type/mutant‐type amino acid and its adjacent amino acids in three‐dimensional model. In conclusion, the addition of 9 novel variants expands the spectrum of CYP11B1 pathogenic variants. Our results demonstrate that twenty CYP11B1 variants lead to impaired 11β‐hydroxylase activity in vitro. Visualizing these variants in the three‐dimensional model structure of CYP11B1 protein can provide a plausible explanation for the results measured in vitro. [ABSTRACT FROM AUTHOR]

During the pandemic of COVID-19, in order to respond to the call of the Ministry of Education that “teaching and learning are not stopped even though courses are stopped”, universities across the country have launched online teaching. Taking the “functional experiment” course in Beijing University of Traditional Chinese Medicine as an example, this course was carried out using online virtual experiment platform. On the basis of experimental teaching during the pandemic, teachers have collected experience and students' feedback. This paper summarizes the strengthens and weakness of this teaching method during the pandemic.

Abstract Background Hepatocellular carcinoma (HCC) remains one of the most common malignant neoplasms. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) plays a key role in the lipid remodelling and is correlated with various neoplasms. Nonetheless, the biological functions and molecular mechanisms of LPCAT1 underlying HCC remain obscure. Methods In the present study, we investigated the role of LPCAT1 in the progression of HCC. In-house RT-qPCR, tissue microarrays, and immunohistochemistry were performed to detect the expression levels and the clinical value of LPCAT1 in HCC. External datasets were downloaded to confirm the results. Proliferation, migration, invasiveness, cell cycle, and apoptosis assays were conducted to reveal the biological effects LPCAT1 has on SMMC-7721 and Huh7 cells. HCC differentially expressed genes and LPCAT1 co-expressed genes were identified to explore the molecular mechanisms underlying HCC progression. Results LPCAT1 showed upregulated expression in 3715 HCC specimens as opposed to 3105 non-tumour specimens. Additionally, LPCAT1 might be an independent prognostic factor for HCC. LPCAT1-knockout hampered cellular proliferation, migration, and metastasis in SMMC-7721 and Huh7 cells. More importantly, the cell cycle and chemical carcinogenesis were the two most enriched signalling pathways. Conclusions The present study demonstrated that increased LPCAT1 correlated with poor prognosis in HCC patients and fuelled HCC progression by promoting cellular growth, migration, and metastasis.

X-Linked recessive chondrodysplasia punctata (CDPX1) is a rare skeletal dysplasia characterized by stippled epiphyses, brachytelephalangy, and nasomaxillary hypoplasia. CDPX1 is caused by function loss of arylsulfatase E (ARSE, also known as ARSL). Pathogenic mutations in ARSE are responsible for CDPX1 in newborns or adults; however, studies have not fully explored prenatal cases. In the current study, a novel missense mutation (c.265A > G) in ARSE was identified in a fetus with short limbs using whole-exome sequencing (WES). Bioinformatic analysis showed that the variant was pathogenic, and RT-qPCR, Western blot, and enzymatic assays were performed to further explore pathogenicity of the variant. The findings showed that the variant decreased transcription and protein expression levels and led to loss of enzymatic activity of the protein. The novel mutation c.265A > G in ARSE was thus the genetic cause for the phenotype presented by the fetus. The current study presents a prenatal case in Chinese population using functional analysis of ARSE, which helps the family to predict recurrence risks for future pregnancies and provides more information for understanding this rare condition. The findings show that WES is a feasible method for prenatal diagnosis of fetuses with CDPX1.

X-Linked recessive chondrodysplasia punctata (CDPX1) is a rare skeletal dysplasia characterized by stippled epiphyses, brachytelephalangy, and nasomaxillary hypoplasia. CDPX1 is caused by function loss of arylsulfatase E (ARSE, also known as ARSL). Pathogenic mutations in ARSE are responsible for CDPX1 in newborns or adults; however, studies have not fully explored prenatal cases. In the current study, a novel missense mutation (c.265A > G) in ARSE was identified in a fetus with short limbs using whole-exome sequencing (WES). Bioinformatic analysis showed that the variant was pathogenic, and RT-qPCR, Western blot, and enzymatic assays were performed to further explore pathogenicity of the variant. The findings showed that the variant decreased transcription and protein expression levels and led to loss of enzymatic activity of the protein. The novel mutation c.265A > G in ARSE was thus the genetic cause for the phenotype presented by the fetus. The current study presents a prenatal case in Chinese population using functional analysis of ARSE , which helps the family to predict recurrence risks for future pregnancies and provides more information for understanding this rare condition. The findings show that WES is a feasible method for prenatal diagnosis of fetuses with CDPX1. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) remains one of the most common malignant neoplasms. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) plays a key role in the lipid remodelling and is correlated with various neoplasms. Nonetheless, the biological functions and molecular mechanisms of LPCAT1 underlying HCC remain obscure. Methods: In the present study, we investigated the role of LPCAT1 in the progression of HCC. In-house RT-qPCR, tissue microarrays, and immunohistochemistry were performed to detect the expression levels and the clinical value of LPCAT1 in HCC. External datasets were downloaded to confirm the results. Proliferation, migration, invasiveness, cell cycle, and apoptosis assays were conducted to reveal the biological effects LPCAT1 has on SMMC-7721 and Huh7 cells. HCC differentially expressed genes and LPCAT1 co-expressed genes were identified to explore the molecular mechanisms underlying HCC progression. Results: LPCAT1 showed upregulated expression in 3715 HCC specimens as opposed to 3105 non-tumour specimens. Additionally, LPCAT1 might be an independent prognostic factor for HCC. LPCAT1-knockout hampered cellular proliferation, migration, and metastasis in SMMC-7721 and Huh7 cells. More importantly, the cell cycle and chemical carcinogenesis were the two most enriched signalling pathways. Conclusions: The present study demonstrated that increased LPCAT1 correlated with poor prognosis in HCC patients and fuelled HCC progression by promoting cellular growth, migration, and metastasis. [ABSTRACT FROM AUTHOR]

Abstract Background Recent studies demonstrated that long non-coding RNAs (lncRNAs) could be intricately implicated in cancer-related molecular networks, and related to cancer occurrence, development and prognosis. However, clinicopathological and molecular features for these cancer-related lncRNAs, which are very important in bridging lncRNA basic research with clinical research, fail to well settle to integration. Results After manually reviewing more than 2500 published literature, we collected the cancer-related lncRNAs with the experimental proof of functions. By integrating from literature and public databases, we constructed CRlncRNA, a database of cancer-related lncRNAs. The current version of CRlncRNA embodied 355 entries of cancer-related lncRNAs, covering 1072 cancer-lncRNA associations regarding to 76 types of cancer, and 1238 interactions with different RNAs and proteins. We further annotated clinicopathological features of these lncRNAs, such as the clinical stages and the cancer hallmarks. We also provided tools for data browsing, searching and download, as well as online BLAST, genome browser and gene network visualization service. Conclusions CRlncRNA is a manually curated database for retrieving clinicopathological and molecular features of cancer-related lncRNAs supported by highly reliable evidences. CRlncRNA aims to provide a bridge from lncRNA basic research to clinical research. The lncRNA dataset collected by CRlncRNA can be used as a golden standard dataset for the prospective experimental and in-silico studies of cancer-related lncRNAs. CRlncRNA is freely available for all users at http://crlnc.xtbg.ac.cn.

The reform of teaching mode should be closely combined with the cultivation of students' ability. A functional experimental teaching system with the core of ability training has been gradually established. Experiment center constantly improves the teaching methods and establishes the formative assessment system and textbook teaching system. Taking the functional experiment teaching contents of five-year undergraduate medical students as the basic framework, a diversified teaching mode is established for students of different majors and levels by using various teaching methods. Thus we creates the pyramid model of talent cultivation: practice → the comprehensive quality → the cultivation process of innovative spirit. The teaching reform is closely combined with talent cultivation. The system has played a good role in improving medical hand operation ability, problem solving and problem analysis ability, innovation ability, independent learning ability. [ABSTRACT FROM AUTHOR]

In order to establish a sound course assessment system for Functional Experiment， the experimental operation skills examination is listed as the assessment content， and the effects of experimental operation skills examination in improving the teaching quality of Functional Experiment is discussed. Methods A total of 180 students from 6 experimental classes of clinical major from KunmingMedical University grade 2015 were randomly assigned to the experimental operation test class and the unattended class. The teaching effects are compared between the experimental operation results and the final closed- book examresults. Results The scores of experimental operations in the experimental operation class were significantly higher than those in the unattended class （P < 0.01）， and there was no statistically significant difference in the closed- book exam scors of the final test. （P > 0.05） . Conclusion The experimental operation skills examination improves the students' experimental operation ability and evaluates the students' learning effects in a real and comprehensive way. [ABSTRACT FROM AUTHOR]

This paper analyzes the nature and characteristics of medical function experiment, designs the structure and the modules of the standardized experimental virtual platform, and builds the standardized operation virtual platform on medical function by using 3ds Max and Unity 3D engine. The virtual platform includes virtual training module, virtual examination module and interaction module. The platform brings the animal welfare into the standardized training and assessment to cultivate students "virtue spirits, to enhance the respect for life, and to help medical students for achieving moral self perfection. The platform serves the standardized training in undergraduates "experiment and postgraduates" scientific research. It has a short, clear theme, relatively independent features, and also can be applied to carry out micro class and the fragmentation of learning. The platform is an important complement to our national virtual simulation center. [ABSTRACT FROM AUTHOR]

The present study examines the functional and binding affinities of the aporphine alkaloid, (+)-boldine, at different α1- and α2-adrenoceptor subtypes, namely, α1A (rat vas deferens and kidney) and its L-like state (rabbit spleen), α1B (guinea pig spleen, mouse spleen and rabbit aorta), α1D (rat aorta and pulmonary artery), at possible subtypes of prejunctional α2-adrenoceptors in rat and rabbit vas deferens and rat atrium, α2D in guinea pig ileum, cloned human α1-adrenoceptor subtypes A, B and D and α2-adrenoceptor subtypes A, B and C as well as rat α2D-adrenoceptors. Additionally, we investigated its Ca2+ channel antagonism in vascular and cardiac preparations. (+)-Boldine had higher affinity at α1-adrenoceptor subtype A (pA2=7.46, pKi=7.21) compared with its L-like state (pA2=5.63) or subtype B (pA2=5.98– 6.12, pKi=5.79) and subtype D (pA2=6.18–6.37, pKi=6.09). Its affinities at α2-adrenoceptors in rat and rabbit vas deferens and rat atrium (pA2=6.02, 6.36, 6.06, respectively) were identical, but lower at guinea pig ileum α2D-adrenoceptors (pA2=4.38). (+)-Boldine displayed nearly undistinguishable affinity at cloned human α2-adrenoceptor subtypes A, B and C (pKi=6.26, 5.79 and 6.35, respectively), whereas its affinity at rat α2D-adrenoceptors was low (pKi=4.70). In perfused rat kidney, (+)-boldine inhibited K+-evoked vasoconstriction at doses 70-fold higher than diltiazem. In guinea pig Langendorff heart, (+)-boldine (10−5–2×10−4 M) was equieffective in increasing coronary flow and in depressing cardiac force, while lower concentrations already depressed heart rate. In papillary muscles from guinea pig, (+)-boldine (10−6–10−5 M) mainly prolonged the duration of action potential at levels >30% of repolarization. These data reveal that (+)-boldine, except for its moderate selectivity (15 to 25-fold) for α1A-adrenoceptors, does not discriminate between the α1-adrenoceptor subtypes B and D and α2-adrenoceptor subtypes A, B and C, at which the drug consistently displays micromolar affinity. In vascular and cardiac preparations, (+)-boldine, although being at least 50-fold weaker than diltiazem, shows Ca2+ channel antagonistic properties but no specificity for coronary dilatation relative to cardiodepression. [Copyright &y& Elsevier]

Background: Recent studies demonstrated that long non-coding RNAs (lncRNAs) could be intricately implicated in cancer-related molecular networks, and related to cancer occurrence, development and prognosis. However, clinicopathological and molecular features for these cancer-related lncRNAs, which are very important in bridging lncRNA basic research with clinical research, fail to well settle to integration. Results: After manually reviewing more than 2500 published literature, we collected the cancer-related lncRNAs with the experimental proof of functions. By integrating from literature and public databases, we constructed CRlncRNA, a database of cancer-related lncRNAs. The current version of CRlncRNA embodied 355 entries of cancer-related lncRNAs, covering 1072 cancer-lncRNA associations regarding to 76 types of cancer, and 1238 interactions with different RNAs and proteins. We further annotated clinicopathological features of these lncRNAs, such as the clinical stages and the cancer hallmarks. We also provided tools for data browsing, searching and download, as well as online BLAST, genome browser and gene network visualization service. Conclusions: CRlncRNA is a manually curated database for retrieving clinicopathological and molecular features of cancer-related lncRNAs supported by highly reliable evidences. CRlncRNA aims to provide a bridge from lncRNA basic research to clinical research. The lncRNA dataset collected by CRlncRNA can be used as a golden standard dataset for the prospective experimental and in-silico studies of cancer-related lncRNAs. CRlncRNA is freely available for all users at http://crlnc.xtbg.ac.cn. [ABSTRACT FROM AUTHOR]