Objective To discuss the diagnosis and surgical management of multilocular cystic renal cell carcinoma ( MCRCC) and to evaluate the gene function of the mutation of von Hippel-Lindau ( VHL) gene in MCRCC. Methods Seve...Objective To discuss the diagnosis and surgical management of multilocular cystic renal cell carcinoma ( MCRCC) and to evaluate the gene function of the mutation of von Hippel-Lindau ( VHL) gene in MCRCC. Methods Seventeen MCRCC cases ( 11 men and展开更多
Background: Flight and cabin crew are known to be at increased risk for atherosclerotic cardiovascular disease (ASCVD). However, ASCVD risks have not yet been compared in flight and cabin crew in low resource settings...Background: Flight and cabin crew are known to be at increased risk for atherosclerotic cardiovascular disease (ASCVD). However, ASCVD risks have not yet been compared in flight and cabin crew in low resource settings like sub-Saharan Africa. Objectives: To assess absolute ASCVD risk estimate and its clinical correlates among flight and cabin crew. Methods: From June 1st 2015 to December 30th 2015, 379 consecutive aviation navigants (Flight crew: 62.5%, pilots: 46.2%, women: 29.6%, Caucasians 23.2%) were enrolled in a cross-sectional survey of ASCVD risk estimate using the Framingham tools. They underwent a physical examination for either initial or renewal medical certificate Class 1 or 2 including blood chemistry, ECG, and echocardiogram as per International Civil Aviation Organization (ICAO) and Civil Aviation Authority (CAA-DRC) medical regulations. We modeled the risk of moderate and high ASCVD estimate in a stepwise logistic regression. Results: Low, moderate and high ASCVD risk estimates were observed respectively in 248 (65.4%), 64 (16.9%), and 67 (17.7%) navigants. Moderate and high ASCVD risk estimates predominated among flight than cabin crew (23.6% vs. 5.6%;p 0.0001 and 28.3% vs. null;p 0.001), low ASCVD risk estimate among cabin than flight crew (94.4% vs. 48.1%;p ≤ 0.001). Low ASCVD risk?estimates.展开更多
Triple-negative breast cancer(TNBC)is currently the worst prognostic subtype of breast cancer,and there is no effective treatment other than chemotherapy.Processing of precursors 1(POP1)is the most substantially up-re...Triple-negative breast cancer(TNBC)is currently the worst prognostic subtype of breast cancer,and there is no effective treatment other than chemotherapy.Processing of precursors 1(POP1)is the most substantially up-regulated RNA-binding protein(RBP)in TNBC.However,the role of POP1 in TNBC remains clarified.A series of molecular biological experiments in vitro and invivo and clinical correlation analyses were conducted to clarify the biological function and regulatory mechanism of POP1 in TNBC.Here,we identified that POP1 is significantly up-regulated in TNBC and associated with poor prognosis.We further demonstrate that POP1 promotes the cell cycle and proliferation of TNBC in vitro and vivo.Mechanistically,POP1 directly binds to the coding sequence(CDS)region of CDKN1AmRNA and degrades it.The degradation process depends on the N6-methyladenosine(m6A)modification at the 497th site of CDKN1A and the recognition of this modification by YTH N6-methyladenosine RNA binding protein 2(YTHDF2).Moreover,the m6A inhibitor STM2457 potently impaired the proliferation of POP1-overexpressed TNBC cells and improved the sensitivity to paclitaxel.In summary,our findings reveal the pivotal role of POP1in promoting TNBC proliferation by degrading the mRNA of CDKN1A and that inhibition of m6A with STM2457 is a promising therapeutic strategy for TNBC.展开更多
文摘Objective To discuss the diagnosis and surgical management of multilocular cystic renal cell carcinoma ( MCRCC) and to evaluate the gene function of the mutation of von Hippel-Lindau ( VHL) gene in MCRCC. Methods Seventeen MCRCC cases ( 11 men and
文摘Background: Flight and cabin crew are known to be at increased risk for atherosclerotic cardiovascular disease (ASCVD). However, ASCVD risks have not yet been compared in flight and cabin crew in low resource settings like sub-Saharan Africa. Objectives: To assess absolute ASCVD risk estimate and its clinical correlates among flight and cabin crew. Methods: From June 1st 2015 to December 30th 2015, 379 consecutive aviation navigants (Flight crew: 62.5%, pilots: 46.2%, women: 29.6%, Caucasians 23.2%) were enrolled in a cross-sectional survey of ASCVD risk estimate using the Framingham tools. They underwent a physical examination for either initial or renewal medical certificate Class 1 or 2 including blood chemistry, ECG, and echocardiogram as per International Civil Aviation Organization (ICAO) and Civil Aviation Authority (CAA-DRC) medical regulations. We modeled the risk of moderate and high ASCVD estimate in a stepwise logistic regression. Results: Low, moderate and high ASCVD risk estimates were observed respectively in 248 (65.4%), 64 (16.9%), and 67 (17.7%) navigants. Moderate and high ASCVD risk estimates predominated among flight than cabin crew (23.6% vs. 5.6%;p 0.0001 and 28.3% vs. null;p 0.001), low ASCVD risk estimate among cabin than flight crew (94.4% vs. 48.1%;p ≤ 0.001). Low ASCVD risk?estimates.
基金supported by the National Natural Science Foundation of China(no.82273399,H.T.).
文摘Triple-negative breast cancer(TNBC)is currently the worst prognostic subtype of breast cancer,and there is no effective treatment other than chemotherapy.Processing of precursors 1(POP1)is the most substantially up-regulated RNA-binding protein(RBP)in TNBC.However,the role of POP1 in TNBC remains clarified.A series of molecular biological experiments in vitro and invivo and clinical correlation analyses were conducted to clarify the biological function and regulatory mechanism of POP1 in TNBC.Here,we identified that POP1 is significantly up-regulated in TNBC and associated with poor prognosis.We further demonstrate that POP1 promotes the cell cycle and proliferation of TNBC in vitro and vivo.Mechanistically,POP1 directly binds to the coding sequence(CDS)region of CDKN1AmRNA and degrades it.The degradation process depends on the N6-methyladenosine(m6A)modification at the 497th site of CDKN1A and the recognition of this modification by YTH N6-methyladenosine RNA binding protein 2(YTHDF2).Moreover,the m6A inhibitor STM2457 potently impaired the proliferation of POP1-overexpressed TNBC cells and improved the sensitivity to paclitaxel.In summary,our findings reveal the pivotal role of POP1in promoting TNBC proliferation by degrading the mRNA of CDKN1A and that inhibition of m6A with STM2457 is a promising therapeutic strategy for TNBC.
