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| 1 | Opioid-induced respiratory depression is associated with increased tidal volume variability显示文摘 | Bouillon T Bruhn J Roepcke H | 2003 | Eur J Anaesthesiol2003，20，2： | 1 |
| 2 | Spectral Entropy and Bispectral Index as Measures of the Electroencephalographic Effects of Sevoflurane显示文摘 | Richard Klaus Ellerkmann Vidal-Markus Liermann Thorsten Michael Alves Ingobert Wenningmann Sascha Kreuer Wolfram Wilhelm Heiko Roepcke Andreas Hoeft J?rgen Bruhn | 2004 | Anesthesiology2004，，6： | 1 |
| 3 | Sex-specific pathways in early cardiac response to pressure overload in mice显示文摘Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF), which are associated with sex differences in cardiac morphology and function. We aimed to identify genes that may cause HF-related sex differences. We used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks, but with sex differences in hypertrophy 6 and 9 weeks after TAC. Cardiac gene expression was analyzed 2 weeks after surgery. Deregulated genes were classified into functional gene ontology(GO) categories and used for pathway analysis. Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin, ANP, BNP, CTGF). Thirty-five genes controlling mitochondrial function(PGC-1, cytochrome oxidase, carnitine palmitoyl transferase, acyl-Co A dehydrogenase, pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC. Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3, matrix metalloproteinase 2, TIMP2, and TGFβ2, all about twofold) after TAC. We confirmed 87% of the gene expression by real-time polymerase chain reaction. By GO classification, female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis. Promoter studies confirmed the upregulation of PGC-1 by E2. Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO. These differences could contribute to subsequent sex differences in cardiac function and Hf. | Henning Witt Carola Schubert Juliane Jaekel Daniela Fliegner Adam Penkalla Klaus Tiemann Joerg Stypmann Stefan Roepcke Sebastian Brokat Shokoufeh Mahmoodzadeh Eva Brozova Mercy M.Davidson Patricia Ruiz Noppinger Christian Grohé Vera Regitz-Zagrosek | 2015 | 世界最新医学信息文摘2015，15，A0： | 1 |
| 4 | Spectral entropy and bispectral index as measures of the electroencephalographic effects of propofol显示文摘 | Ellerkmann R K Soehle M Alves T M Liermann V M Wen ningmann I Roepcke H | 2006 | Anesth Analg2006，102，： | 1 |
| 5 | Opioid-induced respira-tory depression is associated with increased tidal volume vari-a-bility显示文摘 | Bouillon T Bruhn J Roepcke H | | 0，，02： | 1 |
| 6 | WlF1 ,a component of the Wnt pathway,is downregulated in prostate, breast, lung, and bladder cancer 显示文摘 | Wissmann C Wild P J Kaiser S Roepcke S Stoehr R Woenckhaus M | 2003 | J Pathol2003，201，： | 1 |
| 7 | Characteristic differences between the promoters of intron-containing and intronless ribosomal protein genes in yeast显示文摘 | Zhang J Vingron M Roepcke S | 2008 | BMC Res Notes2008，1，： | 1 |
| 8 | Com-parative3′UTR analysis allows identification of regu-latory clusters that drive Eph/ephrin expression in cancer cell lines显示文摘 | WINTER J ROEPCKE S KRAUSE S | 2008 | PLoS One2008，3，7： | 1 |
| 9 | Sex-specific pathways in early cardiac response to pressure overload in mice显示文摘Pressure overload(PO)first causes cardiac hypertrophy and then heart failure(HF),which are associated with sex differences in cardiac morphology and function.We aimed to identify genes that may cause HF-related sex differences.We used a transverse aortic constriction(TAC)mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks,but with sex differences in hypertrophy 6 and 9 weeks after TAC.Cardiac gene expression was analyzed 2 weeks after surgery.Deregulated genes were classified into functional gene ontology(GO)categories and used for pathway analysis.Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin,ANP,BNP,CTGF).Thirty-five genes controlling mitochondrial function(PGC-1,cytochrome oxidase,carnitine palmitoyl transferase,acyl-CoA dehydrogenase,pyruvate dehydrogenase kinase)had lower expression in males compared to females after TAC.Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3,matrix metalloproteinase 2,TIMP2,and TGFβ2,all about twofold)after TAC.We confirmed 87%of the gene expression by real-time polymerase chain reaction.By GO classification,female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis.Promoter studies confirmed the upregulation of PGC-1 by E2.Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO.These differences could contribute to subsequent sex differences in cardiac function and HF. | Henning Witt Carola Schubert Juliane Jaekel Daniela Fliegner Adam Penkalla Klaus Tiemann Joerg Stypmann Stefan Roepcke Sebastian Brokat Shokoufeh Mahmoodzadeh Eva Brozova Mercy M.Davidson Patricia Ruiz Noppinger Christian Grohé Vera Regitz-Zagrosek | 2016 | 世界最新医学信息文摘2016，16，2： | 0 |
| 10 | Sex-specific pathways in early cardiac response to pressure overload in mice显示文摘Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF), which are associated with sex differences in cardiac morphology and function. We aimed to identify genes that may cause HF-related sex differences. We used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks, but with sex differences in hypertrophy 6 and 9 weeks after TAC. Cardiac gene expression was analyzed 2 weeks after surgery. Deregulated genes were classified into functional gene ontology(GO) categories and used for pathway analysis. Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin, ANP, BNP, CTGF). Thirty-five genes controlling mitochondrial function(PGC-1, cytochrome oxidase, carnitine palmitoyl transferase, acyl-CoA dehydrogenase, pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC. Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3, matrix metalloproteinase 2, TIMP2, and TGFβ2, all about twofold) after TAC. We confirmed 87% of the gene expression by real-time polymerase chain reaction. By GO classification, female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis. Promoter studies confirmed the upregulation of PGC-1 by E2. Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO. These differences could contribute to subsequent sex differences in cardiac function and HF. | Henning Witt Carola Schubert Juliane Jaekel Daniela Fliegner Adam Penkalla Klaus Tiemann Joerg Stypmann Stefan Roepcke Sebastian Brokat Shokoufeh Mahmoodzadeh Eva Brozova Mercy M.Davidson Patricia Ruiz Noppinger Christian Grohé Vera Regitz-Zagrosek | 2015 | 世界最新医学信息文摘2015，15，99： | 0 |
| 11 | Sex-specific pathways in early cardiac response to pressure overload in mice显示文摘Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF), which are associated with sex differences in cardiac morphology and function. We aimed to identify genes that may cause HF-related sex differences. We used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks, but with sex differences in hypertrophy 6 and 9 weeks after TAC. Cardiac gene expression was analyzed 2 weeks after surgery. Deregulated genes were classified into functional gene ontology(GO) categories and used for pathway analysis. Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin, ANP, BNP, CTGF). Thirty-five genes controlling mitochondrial function(PGC-1, cytochrome oxidase, carnitine palmitoyl transferase, acyl-Co A dehydrogenase, pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC. Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3, matrix metalloproteinase 2, TIMP2, and TGFβ2, all about twofold) after TAC. We confirmed 87% of the gene expression by real-time polymerase chain reaction. By GO classification, female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis. Promoter studies confirmed the upregulation of PGC-1 by E2. Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO. These differences could contribute to subsequent sex differences in cardiac function and Hf. | Henning Witt Carola Schubert Juliane Jaekel Daniela Fliegner Adam Penkalla Klaus Tiemann Joerg Stypmann Stefan Roepcke Sebastian Brokat Shokoufeh Mahmoodzadeh Eva Brozova Mercy M.Davidson Patricia Ruiz Noppinger Christian Grohé Vera Regitz-Zagrosek | 2015 | 世界最新医学信息文摘2015，15，90： | 0 |
| 12 | Sex-specific pathways in early cardiac response to pressure overload in mice显示文摘Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF),which are associated with sex differences in cardiac morphology and function.We aimed to identify genes that may cause HF-related sex differences.We used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks,but with sex differences in hypertrophy 6 and 9 weeks after TAC.Cardiac gene expression was analyzed 2 weeks after surgery.Deregulated genes were classified into functional gene ontology(GO) categories and used for pathway analysis.Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin,ANP,BNP,CTGF).Thirty-five genes controlling mitochondrial function(PGC-1,cytochrome oxidase,carnitine palmitoyl transferase,acyl-CoA dehydrogenase,pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC.Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3,matrix metalloproteinase 2,TIMP2,and TGFβ2,all about twofold) after TAC.We confirmed 87% of the gene expression by real-time polymerase chain reaction.By GO classification,female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis.Promoter studies confirmed the upregulation of PGC-1 by E2.Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO.These differences could contribute to subsequent sex differences in cardiac function and HF. | Henning Witt Carola Schubert Juliane Jaekel Daniela Fliegner Adam Penkalla Klaus Tiemann Joerg Stypmann Stefan Roepcke Sebastian Brokat Shokoufeh Mahmoodzadeh Eva Brozova Mercy M.Davidson Patricia Ruiz Noppmger Christian Grohe Vera Regitz-Zagrosek | 2016 | 世界最新医学信息文摘2016，16，4： | 0 |
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