Application of flipped classroom teaching mode supported by 3D printing model in embryology experiment teaching / 解剖学报

Objective To explore the teaching effect of flipped classroom teaching mode supported by the 3D printing model in the embryology experiment. Methods Totally 76 students from class 2016 were randomly divided into two groups: the experimental group previewed the embryo 3D models before class and taught other students in class, while the control group did not preview the embryo 3D models before class. An embryo knowledge test and a questionnaire survey were carried out before and after the experimental class to compare the differences of knowledge mastery and self-evaluation between the two groups. Results In the aspect of self-evaluation, the self-evaluation of the experimental group students in explaining the causes and explaining the process of development was significantly improved after the lecture (P<0.05), while the self-evaluation of the control group students in identifying the structure, understanding knowledge, telling the causes and explaining the process of development was significantly improved (P< 0.05). In terms of knowledge test scores, the scores of students in the experimental group and the control group after teaching were higher than those before teaching (P < 0.05). The improvement of the knowledge test in the control group was significantly higher than that in the experimental group (P<0.05). The experiment group' s grades of knowledge test were significantly higher than the control group in the second experiment. 70.27% of the students thought that they were still lack of knowledge in the introspection of the causes of wrong answers. The misunderstanding of English nouns (15.54%), psychological factors (5.41%) and other factors (8.78%) also caused the students to lose points in the knowledge tests. Conclusion The combination of the 3D printing model and the flipped classroom teaching mode can effectively improve the teaching effect, which should be paid attention to in the reform of embryology experimental teaching.

Mutation screening and functional analysis of low density lipoprotein receptor in a familial hypercholesterolemia family / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To screen the mutations of the low density lipoprotein receptor (LDLR) gene in a familial hypercholesterolemia (FH) family, and analyze the LDL-uptaking function of LDLR on lymphocytes of patients.</p><p><b>METHODS</b>Genomic DNA was extracted from four affected members in a Chinese FH family. The presence of apoB100 gene R3500Q mutation which results in familial defective apolipoprotein B100 (FDB) was excluded first. Fragments of the LDLR gene were amplified by touch-down polymerase chain reaction (Touch-down PCR) and analyzed by single-strand conformational polymorphism (SSCP). The suspect fragments of the LDLR gene were cloned and sequenced. Furthermore, the lymphocytes bounded with fluorescent-labeled LDL (DiI-LDL) were measured by fluorescence flow cytometry.</p><p><b>RESULTS</b>A nonsense mutation was identified in exon 10 of LDLR gene. This mutation gave rise to a premature stop codon (W462X), resulting in the absence of most of the LDLR domains. It was detected in all the affected members of the FH family. The ratios of functional LDLR in lymphocytes from patients and normal controls were 63.7% and 77.3% respectively. As a result, the activity of the functional LDLR in patients was just 82.4% of that in the normal controls.</p><p><b>CONCLUSION</b>It is possible that the W462X mutation of LDLR gene is the main cause for the disease in this family.</p>

Quantitative analysis of a panel of gene expression in prostate cancer--with emphasis on NPY expression analysis / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

<p><b>OBJECTIVE</b>To investigate molecular alterations associating with prostate carcinoma progression and potentially provide information toward more accurate prognosis/diagnosis.</p><p><b>METHODS</b>A set of laser captured microdissected (LCM) specimens from 300 prostate cancer (PCa) patients undergoing radical prostatectomy (RP) were defined. Ten patients representing "aggressive" PCa, and 10 representing "non-aggressive" PCa were selected based on prostate-specific antigen (PSA) recurrence, Gleason score, pathological stage and tumor cell differentiation, with matched patient age and race between the two groups. Normal and neoplastic prostate epithelial cells were collected with LCM from frozen tissue slides obtained from the RP specimens. The expressions of a panel of genes, including NPY, PTEN, AR, AMACR, DD3, and GSTP1, were measured by quantitative real-time RT-PCR (TaqMan), and correlation was analyzed with clinicopathological features.</p><p><b>RESULTS</b>The expressions of AMACR and DD3 were consistently up-regulated in cancer cells compared to benign prostate epithelial cells in all PCa patients, whereas GSTP1 expression was down regulated in each patient. NPY, PTEN and AR exhibited a striking difference in their expression patterns between aggressive and non-aggressive PCas (P=0.0203, 0.0284, and 0.0378, respectively, Wilcoxon rank sum test). The lower expression of NPY showed association with "aggressive" PCas based on a larger PCa patient cohort analysis (P=0.0037, univariate generalized linear model (GLM) analysis).</p><p><b>CONCLUSION</b>Despite widely noted heterogeneous nature of PCa, gene expression alterations of AMACR, DD3, and GSTP1 in LCM-derived PCa epithelial cells suggest for common underlying mechanisms in the initiation of PCa. Lower NPY expression level is significantly associated with more aggressive clinical behavior of PCa; PTEN and AR may have potential in defining PCa with aggressive clinical behavior. Studies along these lines have potential to define PCa-associated gene expression alterations and likely co-regulation of genes/pathways critical in the biology of PCa onset/progression.</p>