To explain how to ensure and improve the quality of the clinical practice teaching for the clinical institutes,we expatiate on the practical experience in the hospital from enhancing the practice teaching management,improving the teaching consciousness,meliorating the teaching environment and reforming the method.

Objective To evaluate the needs of performing a standardized communication skill training program for residents according to the differences in history taking mode of residents with different degrees and before and after the standardized training in Shanghai Changhai Hospital in 2010.Methods History taking modes of 81 residents in 2010 before and after the standardized training in Shanghai Changhai hospital were categorized.History taking modes were classified into:no effectiveness mode,traditional mode,disease-sickness mode and Calgary-Cambridge Guide mode.Distribution differences of history taking mode of residents with different medical degrees were analyzed by Fisher exact probability method (α =0.05).Distribution differences of history taking mode of residents before and after standardized training were analyzed by Pearson x2 test (α =0.05).Results 19.8％ residents took no effectiveness mode,53.0％ took traditional mode and 27.2％ used disease-sickness mode.There were significant differences in history taking modes among residents with different medical degrees (P =0.008).After training,history taking modes of residents were significantly changed (P=0.001),only 1.2％ residents used no effectiveness mode,59.3％ used traditional mode and 34.6％ used disease-sickness mode.But residents using the Calgary-Cambridge mode were not increased.Conclusions There are significant differences in history taking modes among residents with different medical degrees.History taking mode of residents changed after standardized training.But some of the residents still use non-optimal history taking modes; therefore a standardized communication skill training program might be needed in the future.

Objective: To analyze the hotspots of known pathogenic disease-causing variants of glucose-6-phosphate dehydrogenase (G6PD) and the phenotype spectrum of neonatal patients with known pathogenic disease-causing variants of G6PD. Methods: The known pathogenic disease-causing variants of G6PD were collected from Human Gene Mutation Database. Screening was performed for these variants among the 7 966 cases (2 357 neonatal, 5 609 non-neonatal) in the database of sequencing at Molecular Diagnosis Center, Children's Hospital of Fudan University. All these samples were from patients suspected with genetic disorder. The database contained Whole Exon Sequencing data and Clinical Exon Sequencing data. We screened out the patients with known pathogenic disease-causing variants of G6PD, analyzed the hotspot of G6PD and the phenotype spectrum of neonatal patients with known pathogenic disease-causing variants of G6PD. Results: (1) Among the next generation sequencing data of the 7 966 samples, 86 samples (1.1%) were detected as positive for the known pathogenic disease-causing variants of G6PD (positive samples set). In the positive sample set, 51 patients (33 males, 18 females) were newborn babies. Forty-three patients (26 males, 17 females) had the enzyme activity data of G6PD. (2) Among the 86 samples, Arg463His, Arg459Leu, Leu342Phe, Val291Met were the leading 4 disease-causing variants found in 72 samples (84%). (3) Male neonatal patients with the same variants had the statistically significant differences in enzyme activity: among 13 patients with Arg463His, enzyme activity of 9 patients was ranked as grade Ⅲ, 1 case ranked as Ⅳ, 3 cases had no activity data;among 10 patients with Arg459Leu, enzyme activity of 4 patients was ranked as Ⅱ, 4 cases ranked as Ⅲ, 2 cases had no activity data;among 2 patients with His32Arg, enzyme activity of one patient was ranked as Ⅱ, another was Ⅲ. Male neonatal patients with the same mutation and enzyme activity also had the statistically significant differences in phenotype spectrum: among 9 patients with Arg463His and level Ⅲ enzyme activity, 6 presented hyperbilirubinemia, 2 met the criteria for exchange transfusion therapy, 2 showed hemolysis;among 4 patients with Arg459Leu and level Ⅱ enzyme activity, 3 presented hyperbilirubinemia;among 4 patients with Arg459Leu and level Ⅲ enzyme activity, 2 presented hyperbilirubinemia, 1 met the standard of exchange transfusion therapy;among 3 patients with Val291Met and level Ⅲ enzyme activity, 1 presented hyperbilirubinemia. Conclusions Arg463His, Arg459Leu, Leu342Phe, Val291Met were the hotspots variants for the G6PD. Patients with the same G6PD variants and sex present different phenotype, patients with the same G6PD variants, sex and enzyme activity also present different phenotype .

Objective: To explore the gender related differences of clinical symptoms and triggering factors in patients with acute myocardial infarction (AMI) in China.
Methods: A population of 14 854 AMI patients with CAMI registration from 2013-01 to 2014-03 were studied, which included 10999 (74.0%) male and 3855 (26.0%) female. The gender related differences of clinical symptoms and triggering factors were analyzed in the population.
Results: The chest pain and severe sweating were the most common symptoms of AMI patient, there were 66.4%of patients with persistent chest pain and 63.7%of patients with severe sweating. Male patients were more with chest pain (67.8%vs 62.4%) and severe sweating (65.8%vs 58.0%) than female, while female patients were more with radiating pain (36.0%vs 31.0%) and nausea/vomiting (35.6%vs 25.0%) than male, all P<0.05. There were 19.4%of patients having clear cause of AMI, and physical stress was the most frequent trigger (48.5%) for AMI. Male patients usually had clear cause than female (20.9%vs 15.1%), especially because of physical stress (49.5%vs 44.5%) and excessive recent unhealthy lifestyles (15.4%vs 8.8%), all P<0.05.
Conclusion: Chest pain and severe sweating were the most common clinical symptoms for AMI patients in China, about 1/5 of them had triggering factors and it was more in male patients.

Objective To investigate the current status of acute stress disorder in ICU survivors after transferring and analyze the influencing factors. Methods A total of 73 ICU survivors who underwent ICU therapy for more than 48 hours and were transferred from ICU during hospitalization from May 2016 to August 2016 in the department of general surgery and the department of vascular surgery in our hospital were analyzed for ASD. And the influencing factors of ASD were analyzed. Results The positive rate of acute stress disorder (ASD)was 39. 7％ in surgical ICU patients within 1 week after transferred out of the ICU. Logistic regression revealed that the high age and low Barthel index were risk factors of ASD after surgical ICU patients were transferred from the ICU. Conclusion The incidence of ASD in surgical ICU survivors is as high as 39. 7％, which is related to the age and the level of daily living ability of the patients when transferred out of ICU.

Purpose: There is no optimal prognostic model for T-cell lymphoblastic lymphoma (T-LBL). Here, we discussed the predictive value of total metabolic tumor volume (TMTV) and total lesion glycolysis (TLG) measured on 18F-fluorodeoxyglucose positron emission tomography–computed tomography (PET-CT) in T-LBL. Materials and Methods: Thirty-seven treatment naïve T-LBL patients with PET-CT scans were enrolled. TMTV was obtained using the 41% maximum standardized uptake value (SUVmax) threshold method, and TLG was measured as metabolic tumor volume multiplied by the mean SUV. Progression-free survival (PFS) and overall survival (OS) were analyzed by Kaplan-Meier curves and compared by the log-rank test. Results: The optimal cutoff values for SUVmax, TMTV, and TLG were 12.7, 302 cm3, and 890, respectively. A high SUVmax, TMTV, and TLG indicated a shorten PFS and OS. On multivariable analysis, TMTV ≥ 302 cm3, and central nervous system (CNS) involvement predicted inferior PFS, while high SUVmax, TLG and CNS involvement were associated with worse OS. Subsequently, we generated a risk model comprising high SUVmax, TMTV or TLG and CNS involvement, which stratified the population into three risk groups, which had significantly different median PFS of not reached, 14 months, and 7 months for low-risk group, mediate-risk group, and high-risk group, respectively (p < 0.001). Median OS were not reached, 27 months, and 13 months, respectively (p < 0.001). Conclusion Baseline SUVmax, TMTV, and TLG measured on PET-CT are strong predictors of worse outcome in T-LBL. A risk model integrating these three parameters with CNS involvement identifies patients at high risk of disease progression.

Purpose: There is no optimal prognostic model for T-cell lymphoblastic lymphoma (T-LBL). Here, we discussed the predictive value of total metabolic tumor volume (TMTV) and total lesion glycolysis (TLG) measured on 18F-fluorodeoxyglucose positron emission tomography–computed tomography (PET-CT) in T-LBL. Materials and Methods: Thirty-seven treatment naïve T-LBL patients with PET-CT scans were enrolled. TMTV was obtained using the 41% maximum standardized uptake value (SUVmax) threshold method, and TLG was measured as metabolic tumor volume multiplied by the mean SUV. Progression-free survival (PFS) and overall survival (OS) were analyzed by Kaplan-Meier curves and compared by the log-rank test. Results: The optimal cutoff values for SUVmax, TMTV, and TLG were 12.7, 302 cm3, and 890, respectively. A high SUVmax, TMTV, and TLG indicated a shorten PFS and OS. On multivariable analysis, TMTV ≥ 302 cm3, and central nervous system (CNS) involvement predicted inferior PFS, while high SUVmax, TLG and CNS involvement were associated with worse OS. Subsequently, we generated a risk model comprising high SUVmax, TMTV or TLG and CNS involvement, which stratified the population into three risk groups, which had significantly different median PFS of not reached, 14 months, and 7 months for low-risk group, mediate-risk group, and high-risk group, respectively (p < 0.001). Median OS were not reached, 27 months, and 13 months, respectively (p < 0.001). Conclusion Baseline SUVmax, TMTV, and TLG measured on PET-CT are strong predictors of worse outcome in T-LBL. A risk model integrating these three parameters with CNS involvement identifies patients at high risk of disease progression.

Objective To investigate the regulatory effects of LINC00467 on proliferation and metastasis of lung adenocarcinoma cells and the involvement of autophagy in its regulatory mechanism.Methods LINC00467 expression levels in lung adenocarcinoma tissues and their correlation with the patients'survival outcomes were analyzed using data from TCGA database.LINC00467 expression was also examined using qRT-PCR in human bronchial epithelial cells 16HBE and lung adenocarcinoma cell lines A549 and H1299.In A549 and H1299 cells transfected with a short hairpin RNA targeting LINC00467(shLINC00467),the effects of 3-methyladenine(3-MA,an autophagy inhibitor)and BML-275(an AMPK inhibitor)treatment on cell proliferation,migration,and expressions of LC3 and the AMPK/mTOR pathway proteins were tested using colony formation assay,wound-healing and Transwell assays,immunofluorescence staining and Western blotting.GSEA enrichment analysis was conducted to analyze the correlation between LINC00467 and the autophagy pathway.Results The expression level of LINC00467 was significantly higher in lung adenocarcinoma tissues than in the adjacent tissues(P<0.001)and increased progressively with the clinical stage(P<0.05),and its high expression was associated with a poor overall survival(P=0.049)and a high first progression rate(P=0.026)of the patients.LINC00467 expression was also significantly higher in A549 and H1299 cells than in 16HBE cells.In A549 and H1299 cells,LINC00467 knockdown significantly decreased colony-forming,migration and invasion abilities of the cells,lowered p-mTOR/mTOR and p62 expressions,and increased p-AMPK/AMPK expressions and LC3Ⅱ/Ⅰ ratio,and these effects were strongly attenuated by application of either 3-MA or BML-275.GSEA analysis suggested an inhibitory effect on LINC00467 on the autophagy pathway(|NES|>1,P<0.05,FDR<0.25).Conclusion High expressions of LINC00467 promote proliferation and metastasis of lung adenocarcinoma cells possibly by inhibiting cell autophagy mediated by the AMPK/mTOR signaling pathway.

Objective:To investigate the effect of LRRK2G2019S mutation on activation of microglia after iron deprivation and its mechanism.Methods:(1) Microglia were differentiated from human induced pluripotent stem cells (IPSC) with the help of hematopoietic progenitor cells (HPC) and identified by immunofluorescent staining, and α-synuclein (α-syn) A53T mutant protein was obtained by protein purification technology. (2) Microglia were divided into control group, α-syn group, α-syn+ deferoxamine (DFO) group; phosphate buffer solution (PBS), 1 μmol/L purified α-syn A53T mutant protein, 1 μmol/L purified α-syn A53T mutant protein+30 mmol/L DFO were given respectively for 24 h. Fe 2+ concentration was detected by colorimetry, Rab35 protein expression was detected by Western blotting, intracellular reactive oxygen species (ROS) level was detected by flow cytometry, and interleukin-6 ( IL-6), tumor necrosis factor-α ( TNF-α) and transforming growth factor-β ( TGF-β) mRNA expressions were detected by real time-PCR (RT-PCR); microglia culture supernatant (MCS) in the 3 groups were transfered to SH-SY5Y cells, and SH-SY5Y cell apoptosis was detected by flow cytometry. (3) Bidirectional DNA sequencing was used to detect leucine rich repeat kinase 2 ( LRRK2) gene mutations in microglia treated with 1 μmol/L purified α-syn A53T mutant protein. Microglia were divided into control group, α-syn group and α-syn+GSK3357679A group, and treated with corresponding drugs for 24 h, respectively (LRRK2 inhibitor GSK3357679A concentration: 10 nmol/L), and LRRK2 protein expression was detected by Western blotting; microglia were divided into control group, α-syn group, α-syn+GSK3357679A, and α-syn+GSK3357679A+DFO group, and treated with corresponding drugs for 24 h, Rab35 protein expression was detected by Western blotting, intracellular ROS level was detected by flow cytometry, and IL-6, TNF-α and TGF-β mRNA expressions were detected by RT-PCR. (4) Microglia were divided into control group, α-syn group, α-syn+rapamycin (RAPA) group, and treated with corresponding drugs for 24 h (concentration of autophagy inducer RAPA: 50 nmol/L); protein expressions of Rab35, P62 and microtubule-associated protein light chain 3 II (LC3II) were detected by Western blotting; intracellular ROS level was detected by flow cytometry, and IL-6, TNF-α and TGF-β mRNA expressions were detected by RT-PCR. (5) Microglia were divided into control group, α-syn group, and α-syn+Rab35 group, and treated with corresponding drugs for 24 h (concentration of Rab35 overexpressed plasmids: 1 μg/mL); Rab35, P62, and LC3II protein expressions were detected by Western blotting; ROS level was detected by flow cytometry, and IL-6, TNF-α and TGF-β mRNA expressions were detected by RT-PCR. Results:(1) Immunofluorescent staining showed negative neuronal nuclei (NeuN) expression and positive ionized calcium-binding adapter molecule 1 (Iba1) expression in microglia, and high LRRK2 expression; PcDNA3.1-SNCA-A53T expression plasmid was constructed and α-syn A53T mutant protein was purified. (2) The Fe 2+ concentration in α-syn group was significantly higher than that in control group, and the Fe 2+ concentration in α-syn+DFO group was significantly lower than that in α-syn group ( P<0.05); the Rab35 protein and TGF-β mRNA expressions in control group, α-syn group and α-syn+DFO group were decreased successively, while the IL-6 and TNF-α mRNA expressions were increased successively, with significant differences ( P<0.05); ROS level and SH-SY5Y cell apoptosis rate in control group, α-syn group, α-syn+DFO group were increased successively. (3) Bidirectional DNA sequencing showed that the LRRK2G2019S mutation in microglia was the most obvious after α-syn A53T mutant protein stimulation; compared with the control group, the α-syn group had significantly increased LRRK2 protein expression, while the α-syn+GSK3357679A group had significantly decreased LRRK2 protein expression compared with α-syn group ( P<0.05); compared with the control group, the α-syn group had significantly decreased Rab35 protein and TGF-β mRNA expressions, and statistically increased IL-6 and TNF-α mRNA expressions ( P<0.05); compared with α-syn group, the α-syn+GSK3357679A group had significantly increased Rab35 protein and TGF-β mRNA expressions, and statistically decreased IL-6 and TNF-α mRNA expressions ( P<0.05); compared with α-syn+GSK3357679A group, α-syn+GSK3357679A+DFO group had significantly increased IL-6 and TNF-α mRNA expressions, and significantly decreased Rab35 protein and TGF-β mRNA expressions ( P<0.05). The α-syn group had higher ROS level than the control group, the α-syn+GSK3357679A group had lower ROS level than the α-syn group, and the α-syn+GSK3357679A+DFO group had higher ROS level than the α-syn+GSK3357679A group. (4) Compared with the control group, the α-syn group had significantly decreased Rab35 and LC3II protein, and TGF-β mRNA expressions, and significantly increased P62 protein, IL-6 and TNF-α mRNA expressions ( P<0.05); compared with α-syn group, the α-syn+RAPA group had significantly increased Rab35 and LC3II protein, and TGF-β mRNA expressions, and significantly decreased P62 protein, and IL-6 and TNF-α mRNA expressions ( P<0.05); the α-syn group had higher ROS level than the control group and α-syn+RAPA group. (5) Compared with the control group, the α-syn group had significantly decreased Rab35 and LC3II protein, and TGF-β mRNA expressions, and statistically increased P62 protein, and IL-6 and TNF-α mRNA expressions ( P<0.05); compared with the α-syn group, the α-syn+Rab35 group had significantly increased Rab35 and LC3II protein, and TGF-β mRNA expressions, and significantly decreased P62 protein, and IL-6 and TNF-α mRNA expressions ( P<0.05). The α-syn group had higher ROS level than the control group and α-syn+Rab35 group. Conclusion:LRRK2G2019S can induce neuroinflammation by inhibiting Rab35-related autophagy under iron deprivation, and Rab35 is expected to be a key factor in intervening neuroinflammation.

Objective To investigate the regulatory effects of LINC00467 on proliferation and metastasis of lung adenocarcinoma cells and the involvement of autophagy in its regulatory mechanism.Methods LINC00467 expression levels in lung adenocarcinoma tissues and their correlation with the patients'survival outcomes were analyzed using data from TCGA database.LINC00467 expression was also examined using qRT-PCR in human bronchial epithelial cells 16HBE and lung adenocarcinoma cell lines A549 and H1299.In A549 and H1299 cells transfected with a short hairpin RNA targeting LINC00467(shLINC00467),the effects of 3-methyladenine(3-MA,an autophagy inhibitor)and BML-275(an AMPK inhibitor)treatment on cell proliferation,migration,and expressions of LC3 and the AMPK/mTOR pathway proteins were tested using colony formation assay,wound-healing and Transwell assays,immunofluorescence staining and Western blotting.GSEA enrichment analysis was conducted to analyze the correlation between LINC00467 and the autophagy pathway.Results The expression level of LINC00467 was significantly higher in lung adenocarcinoma tissues than in the adjacent tissues(P<0.001)and increased progressively with the clinical stage(P<0.05),and its high expression was associated with a poor overall survival(P=0.049)and a high first progression rate(P=0.026)of the patients.LINC00467 expression was also significantly higher in A549 and H1299 cells than in 16HBE cells.In A549 and H1299 cells,LINC00467 knockdown significantly decreased colony-forming,migration and invasion abilities of the cells,lowered p-mTOR/mTOR and p62 expressions,and increased p-AMPK/AMPK expressions and LC3Ⅱ/Ⅰ ratio,and these effects were strongly attenuated by application of either 3-MA or BML-275.GSEA analysis suggested an inhibitory effect on LINC00467 on the autophagy pathway(|NES|>1,P<0.05,FDR<0.25).Conclusion High expressions of LINC00467 promote proliferation and metastasis of lung adenocarcinoma cells possibly by inhibiting cell autophagy mediated by the AMPK/mTOR signaling pathway.