Study on education of professional degree postgraduates in department of breast surgery with precision medicine mode / 中华医学教育探索杂志

We integrate the precision medicine into the training process of breast surgery postgraduates. Besides the traditional training, we emphasize the idea of precision medicine and provide precision medicine lessons. We also carry out multidisciplinary precision-medicine teaching ward-rounds, and take use of AI system to assist clinical decision making, so as to stimulate the subjective initiative of the postgraduates, and strengthen the training of clinical practical capabilities. Our experience has showed that applying the precision medicine mode to the training of breast surgery postgraduates is more conducive to strengthening their clinical capabilities and overall quality.

SP13786 Inhibits the Migration and Invasion of Lung Adenocarcinoma Cell A549 by Supressing Stat3-EMT via CAFs Exosomes / 中国肺癌杂志

BACKGROUND@#Fibroblast activation protein (FAP) is one of the surface markers of cancer-associated fibroblasts (CAFs) and is closely related to the malignant characterization of CAFs. SP13786 is a specific micromolecule inhibitor of FAP and this study is to investigate the effects and mechanism of SP13786 on the migration and invasion of A549 cells through regulating exosomes of CAFs.@*METHODS@#CAFs and paracancerous fibroblasts (PTFs) were isolated and subcultured from freshly resected lung adenocarcinoma tissues and paracancerous normal tissues separately. MTT assay was used to detect the proliferation of CAFs incubated by different concentrations of SP13786; PTFs-exo, CAFs-exo and CAFs+SP13786-exo were extracted by polymer precipitation method. The A549 cells were divided into Ctrl group, PTFs group, CAFs group and SP13786 group and each group was incubated with DMEM, PTFs-exo, CAFs-exo and CAFs+SP13786-exo separately. Laser confocal microscope was used to observe the endocytoses of exosomes by A549 cells. The expression of alpha-smooth muscle actin (α-SMA) and FAP in PTFs and CAFs and the expression of E-cadherin, N-cadherin, Slug, Stat3 and P-Stat3 in A549 cells were detected by immunofluorescence, immunohistochemistry and Western blot. The migration and invasion ability of A549 cells were detected by cell scratch and transwell methods.@*RESULTS@#α-SMA and FAP were expressed much higher in CAFs than that in PTFs which indicate that CAFs and PTFs were successfully obtained from lung adenocarcinoma and paracancerous tissues (P0.05). Finally, WP1066 (a specific inhibitor of Stat3) was used to comfirm whether SP13786 could influence EMT of A549 cells by inhibiting Stat3 phosphorylation via CAFs-Exo. The results showed that when the phosphorylation of Stat3 in CAFs group was inhibited by WP1066, SP13786 could not influence the P-Stat3 expression and EMT of A549 cells anymore (P>0.05).@*CONCLUSIONS@#As a specific micromolecule inhibitor of FAP, SP13786 indirectly inhibits the migration and invasion of A549 cells by affecting exosomes of CAFs. The possible mechanism is to inhibit the phosphorylation of Stat3 and thus affect the EMT of A549 cells.

Overexpression of Tumor Protein p53-regulated Apoptosis-inducing Protein 1 Regulates Proliferation and Apoptosis of Breast Cancer Cells through the PI3K/Akt Pathway / 한국유방암학회지

PURPOSE: Tumor protein p53-regulated apoptosis-inducing protein 1 (TP53AIP1) functions in various cancers. We studied the effect and molecular mechanism of TP53AIP1 in breast cancer. METHODS: The degree of correlation between TP53AIP1 expression and overall survival in patients with breast cancer was obtained from the online The Cancer Genome Atlas database. Six of the TP53AIP1 levels in the tumor and adjacent non-tumor tissues randomly selected from 38 breast cancer patients were determined. Transgenic technology was used to enhance the expression of TP53AIP1 in breast cancer cell lines, MDA-MB-415 and MDA-MB-468, and to observe the effects of gene overexpression on the proliferation, cell cycle, and apoptosis of breast cancer cells. The molecular mechanism of association between cell cycle- and apoptosis-related factors and the phosphoinositide 3-kinases/protein kinase B (PI3K/Akt) pathway was also studied. RESULTS: The messenger RNA and protein expression levels of TP53AIP1 in cancer tissues were significantly lower than those in the control group. TP53AIP1 overexpression inhibits cell viability. The mechanism of TP53AIP1 inhibition of proliferation and growth of breast cancer cells includes cell cycle arrest, apoptosis promotion (p < 0.01), promotion of the expression of cleaved-caspase-3 (p < 0.01), cleaved-caspase-9 (p < 0.01), B cell lymphoma/leukemia-2 (Bcl-2)-associated X protein, and p53 (p < 0.01), and the inhibition of Bcl-2, Ki67, and PI3K/Akt pathways (p < 0.01). CONCLUSION: TP53AIP1 may be a novel tumor suppressor gene in breast cancer and can potentially be used as an effective target gene for the treatment of breast cancer.

Listeria monocytogenes meningitis in a child:a case report / 临床儿科杂志

Objective The clinical characteristics and treatment outcomes of Listeria monocytogenes (LM) meningitis were reviewed. Methods The clinical data of a case of LM meningitis were retrospectively analyzed and a literature review was performed. Results The child initially presenting with fever, headache and vomit was treated with amoxicillin/clavulanic acid and ceftriaxone and the treatment effect was obvious. Cerebrospinal fluid and blood cultures were LM positive. In 17 related arti-cles, a total of 24 children with LM meningitis were reviewed. Among them, 4 patients died and 10 had hydrocephalus. The treatment with either ampicillin alone or in combination with aminoglycoside was effective. Conclusions LM meningitis was rare in immunocompetent children, but has high rates of mortality and sequelae.

Clinical analysis of 28 cases of non benign neonatal arrhythmias / 临床儿科杂志

Objective To discuss the etiology, clinical features and prognosis of non benign neonatal arrhythmias. Method Clinical data of 27 cases of non benign neonatal arrhythmias diagnosed from January 2005 to January 2010 were retrospectively analyzed. Results Among 27 neonats, there were 15 male and 12 female. Fourteen cases were early neonatal and 13 were late neonatal. Gestational age was less than 32 weeks in 6 cases, and more than 32 weeks in 21 cases. In 19 cases with tachyarrhythmia, 14 cases were induced by respiratory infection. The causes of 8 newborns with bradycardia arrhythmia were congenital heart disease (3 cases), electrolyte disturbance (2 cases), severe asphyxia with sepsis (2 cases), and severe asphyxia (1 case). The onset age and gestational age were lower in cases with bradycardia arrhythma that those in cases with tachyarrhythmia (P<0.005). The cure rate and effective rate of tachyarrhythmia was 89.5%and 100%, of bradycardia arrhythmia was 0%and 12.5%, respectively, and the differences were signiifcant (P<0.005). Conclusion Clinical characteristics, pathogenesis and prognosis were different between tachyarrhythmia and bradycardia arrhythmia in neonates.

Construction of lentivirus RNAi vector pLenti6/V5-DEST-IP_3R1 and identification of its silencing effects / 解放军医学杂志

Objective To construct lentiviral expression vector of rat IP3R1 gene,and identify its silencing effect by using PC12 cell lines. Methods Oligo DNA sequences of 4 pairs of miRNA,named as miRNA1,miRNA2,miRNA3 and miRNA4,were designed according to IP3R1 gene sequence (GenBank:NM_001007235). The single strand of oligo DNA was annealed to form double strand DNA,and then connected with the empty plasmid pcDNA TM 6.2-GW/EmGFP-miR. By using gateway technology,the expression vector pcDNA TM 6.2-GW/EmGFP-miR-IP3R1 was linked into lentiviral destination vector pLenti6/V5-DEST to form the lentiviral expression vector pLenti6/V5-DEST-IP3R1,then it was transformed into infectious lentiviral particles and to infect PC12 cell lines. Silencing effect of gene IP3R1 was detected by Real-time PCR and Western blot. Results The sequence of expression vector pcDNA TM 6.2-GW/EmGFP-miR-IP3R1 was proved correct using sequencing method. After the transfection of letivirus vector pLenti6/V5-DEST-IP3R1 into PC12 cell lines,the IP3R1 mRNA and protein level were down-regulated 48h later,of which miRNA2 and miRNA3 sequence showed the best silencing effect,and the expression of IP3R1 in the blank control and negative control showed no significant changes. Conclusions Lentiviral expression vector pLenti6/V5-DEST-IP3R1 was constructed successfully. pLenti6/V5-DEST-IP3R1 may render the IP3R1 expression in PC12 cell lines down-regulated,and it provides a foundation for studying the function of calcium release channel IP3R1.