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315 results on '"Basson, Craig T."'

1. Constitutively Activating GNAS Somatic Mutation in Right Ventricular Outflow Tract Tachycardia.

Author

Ip, James E, Xu, Linna, Dai, Jie, Steegborn, Clemens, Jaffré, Fabrice, Evans, Todd, Cheung, Jim W, Basson, Craig T, Panaghie, Gianina, Krogh-Madsen, Trine, Abbott, Geoffrey W, and Lerman, Bruce B

Subjects
Myocardium, Heart Conduction System, Humans, Tachycardia, Ventricular, GTP-Binding Protein alpha Subunits, Gs, Chromogranins, DNA, Electrocardiography, Catheter Ablation, Biopsy, DNA Mutational Analysis, Mutation, Missense, Aged, Male, GTP-binding proteins, arrhythmia, mutation, signal transduction, tachycardia, ventricular, tachycardia, ventricular, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Medical Physiology, Cardiovascular System & Hematology
Abstract

[Figure: see text].

Published
2021

2. MAA868, a novel FXI antibody with a unique binding mode, shows durable effects on markers of anticoagulation in humans

Author

Koch, Alexander W., Schiering, Nikolaus, Melkko, Samu, Ewert, Stefan, Salter, Janeen, Zhang, Yiming, McCormack, Peter, Yu, Jianying, Huang, Xueming, Chiu, Yu-Hsin, Chen, Zhiping, Schleeger, Simone, Horny, Geraldine, DiPetrillo, Keith, Muller, Lionel, Hein, Andreas, Villard, Frederic, Scharenberg, Meike, Ramage, Paul, Hassiepen, Ulrich, Côté, Serge, DeGagne, Julie, Krantz, Carsten, Eder, Jörg, Stoll, Brian, Kulmatycki, Kenneth, Feldman, David L., Hoffmann, Peter, Basson, Craig T., Frost, Robert J.A., and Khder, Yasser

Published
2019
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4. Comparative PRKAR1A Genotype-Phenotype Analyses in Humans with Carney Complex and prkar1a Haploinsufficient Mice

Author

Veugelers, Mark, Wilkes, David, Burton, Kimberly, McDermott, Deborah A., Song, Yan, Goldstein, Marsha M., La Perle, Krista, Vaughan, Carl J., O'Hagan, Art, Bennett, Kenneth R., Meyer, Beat J., Legius, Eric, Karttunen, Mervi, Norio, Reijo, Kaariainen, Helena, Lavyne, Michael, Neau, Jean-Philippe, Richter, Gert, Kirali, Kaan, Farnsworth, Alan, Stapleton, Karen, Morelli, Peter, Takanashi, Yoshinori, Bamforth, John-Steven, Eitelberger, Franz, Noszian, Irene, Manfroi, Waldimiro, Powers, James, Mochizuki, Yoshihiko, Imai, Tsuneo, Driscoll, Deborah A., Goldmuntz, Elizabeth, Edelberg, Jay M., Collins, Amanda, Eccles, Diana, Irvine, Alan D., McKnight, G. Stanley, Basson, Craig T., and Taylor, Susan S.

Published
2004

5. Different TBX5 Interactions in Heart and Limb Defined by Holt-Oram Syndrome Mutations

Author

Basson, Craig T., Huang, Taosheng, Lin, Robert C., Bachinsky, David R., Weremowicz, Stanislawa, Vaglio, Alicia, Bruzzone, Rina, Quadrelli, Roberto, Lerone, Margherita, Romeo, Giovanni, Silengo, Margherita, Pereira, Alexandre, Krieger, Jose, Mesouita, Sonia F., Kamisago, Mitsuhiro, Morton, Cynthia C., Müller, Chistoph W., Seidman, J. G., and Seidman, Christine E.

Published
1999

8. TET2-Driven Clonal Hematopoiesis and Response to Canakinumab

Author

Svensson, Eric C., primary, Madar, Aviv, additional, Campbell, Catarina D., additional, He, Yunsheng, additional, Sultan, Marc, additional, Healey, Margaret L., additional, Xu, Huilei, additional, D’Aco, Katie, additional, Fernandez, Anita, additional, Wache-Mainier, Clarisse, additional, Libby, Peter, additional, Ridker, Paul M., additional, Beste, Michael T., additional, and Basson, Craig T., additional

Published
2022
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10. The National Registry of Genetically Triggered Thoracic Aortic Aneurysms and Cardiovascular Conditions (GenTAC): Results from phase I and scientific opportunities in phase II

Author

Kroner, Barbara L., Tolunay, H. Eser, Basson, Craig T., Pyeritz, Reed E., Holmes, Kathryn W., Maslen, Cheryl L., Milewicz, Dianna M., LeMaire, Scott A., Hendershot, Tabitha, Desvigne-Nickens, Patrice, Devereux, Richard B., Dietz, Harry C., Song, Howard K., Ringer, Danny, Mitchell, Megan, Weinsaft, Jonathan W., Ravekes, William, Menashe, Victor, and Eagle, Kim A.

Published
2011
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12. Surgical Treatment of Patients Enrolled in the National Registry of Genetically Triggered Thoracic Aortic Conditions

Author

Song, Howard K., Bavaria, Joseph E., Kindem, Mark W., Holmes, Kathryn W., Milewicz, Dianna M., Maslen, Cheryl L., Pyeritz, Reed E., Basson, Craig T., Eagle, Kim, Tolunay, H. Eser, Kroner, Barbara L., Dietz, Hal, Menashe, Victor, Devereux, Richard B., Desvigne-Nickens, Patrice, Ravekes, William, Weinsaft, Jonathan W., Brambilla, Donald, Stylianou, Mario P., Hendershot, Tabitha, Mitchell, Megan S., and LeMaire, Scott A.

Published
2009
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13. Licogliflozin versus placebo in women with polycystic ovary syndrome: A randomized, double‐blind, phase 2 trial

Author

Tan, Susanne, primary, Ignatenko, Stanislav, additional, Wagner, Frank, additional, Dokras, Anuja, additional, Seufert, Jochen, additional, Zwanziger, Denise, additional, Dunschen, Karin, additional, Zakaria, Marjorie, additional, Huseinovic, Neda, additional, Basson, Craig T., additional, Mahling, Ping, additional, Fuhrer, Dagmar, additional, and Hinder, Markus, additional

Published
2021
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15. BOS172738, a highly potent and selective RET inhibitor, for the treatment of RET-altered tumors including RET-fusion+ NSCLC and RET-mutant MTC: Phase 1 study results.

Author

Schoffski, Patrick, primary, Cho, Byoung Chul, additional, Italiano, Antoine, additional, Loong, Herbert H. F., additional, Massard, Christophe, additional, Medina Rodriguez, Laura, additional, Shih, Jin-Yuan, additional, Subbiah, Vivek, additional, Verlingue, Loic, additional, Andreas, Karen, additional, Basson, Craig T., additional, Clawson, Alicia, additional, Ho, Peter T.C., additional, Knight, Shelley, additional, Scheuber, Anita, additional, and Keegan, Mitchell, additional

Published
2021
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17. Mutant desmocollin-2 causes arrhythmogenic right ventricular cardiomyopathy

Author

Heuser, Arnd, Plovie, Eva R., Ellinor, Patrick T., Grossmann, Katja S., Shin, Jordan T., Wichter, Thomas, Basson, Craig T., Sasse-Klaassen, Sabine, Thierfelder, Ludwig, MacRae, Calum A., and Gerull, Brenda

Subjects
Cardiomyopathy -- Genetic aspects, Heart diseases -- Genetic aspects, Introns -- Research, Gene mutations -- Research, Desmosomes -- Structure, Desmosomes -- Research, Biological sciences
Abstract

Many unrelated patients with the disorder for mutation in human desmosomal cadherin desmocollin-2 (DSC2) are investigated. The results have identified DSC2 mutations as a cause of arrhythmogenic right ventricular cardiomyopathy (ARVC) in humans and have shown that physiologic levels of DSC2 are crucial for normal cardiac desmosome formation, early cardiac morphogenesis and cardiac function.

Published
2006

18. Mutation of perinatal myosin heavy chain associated with a carney complex variant

Author

Veugelers, Mark, Bressan, Michael, McDermott, Deborah A., Chaudron, Jean-Marie, Weremowicz, Stanislawa, Zunamon, Alan, Destree Anne, Basson, Craig T., Morton, Cynthia C., Mabry, C. Charlton, and Lefaivre, Jean-Francois

Subjects
Arthrogryposis -- Evaluation, Myosin -- Genetic aspects, Myosin -- Research, Genetic research
Abstract

The R6740 mutation of the MYH8 gene encoding perinatal myosin heavy chain causes a variant form of the carney complex associated with distal arthrogryposis, which includes typical spotty pigmentation of the skin, familial cardiac and cutaneous myxoma, and endocrinopathy. Novel roles for perinatal myosin in both the development of skeletal muscle and cardiac tumorigenesis are demonstrated.

Published
2004

20. A 27-year-old woman with two intracardiac masses and a history of endocrinopathy

Author

Basson, Craig T. and Aretz, H. Thomas

Subjects
Thoracic cancer -- Case studies
Abstract

A 27-year-old woman who began having episodes of fainting was found to have a heart tumor called a cardiac myxoma. She also had a history of Cushing's disease and freckles. She was diagnosed with a medical syndrome called Carney complex.

Published
2002

21. A molecular basis for Wolff-Parkinson-White syndrome

Author

Basson, Craig T.

Subjects
Wolff-Parkinson-White syndrome -- Genetic aspects, Gene mutations -- Health aspects
Abstract

A mutation in the gene for the gamma2 regulatory subunit of AMP-activated protein kinase has been linked to a heart arrhythmia called Wolff-Parkinson-White syndrome. The arrhythmia is caused by an abnormal electrical pathway between the upper and lower parts of the heart.

Published
2001

23. LLF580, an FGF21 Analog, Reduces Triglycerides and Hepatic Fat in Obese Adults With Modest Hypertriglyceridemia.

Author

Rader, Daniel J., Maratos-Flier, Eleftheria, Nguyen, Amanda, Doug Hom, Ferriere, Michael, Yifang Li, Kompa, Jill, Martic, Miljen, Hinder, Markus, Basson, Craig T., Yowe, David, Diener, John, and Goldfine, Allison B.

Subjects
ASPARTATE aminotransferase, NON-alcoholic fatty liver disease, HDL cholesterol, FIBROBLAST growth factors, LDL cholesterol, HEPATIC fibrosis
Abstract

Purpose: To evaluate the safety and potential efficacy of LLF580, a genetically engineered variant of human fibroblast growth factor-21, for triglyceride lowering, weight loss, and hepatic fat reduction. Methods: A multicenter, double-blind, parallel design trial in obese, mildly hypertriglyceridemic adults randomized (1:1) to LLF580 300 mg or placebo subcutaneously every 4 weeks for 3 doses. Results: Of 64 randomized study participants, 61 (mean ± SD: age 45 ± 11 years, 49% male, 80/15/5% Caucasian/African American/other, body mass index 36.1 ± 3.8 kg/m2) received LLF580 (n = 30) or placebo (n = 31) at 7 research sites in the United States. LLF580 lowered serum triglycerides by 54% (least square mean placebo adjusted change from baseline), total cholesterol 7%, low-density lipoprotein cholesterol 12%, and increased high-density lipoprotein cholesterol 36% compared with placebo (all P < 0.001) over 12 weeks. Substantial reduction of liver fat of 52% over placebo (P < 0.001) was also demonstrated in the setting of improved liver function tests including alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, the composite enhanced liver fibrosis score, and N-terminal type III collagen propeptide (all P < 0.05). Insulin and C-peptide levels and insulin resistance by homeostatic model assessment for insulin resistance were all lower, and adiponectin higher with LLF580 treatment compared with placebo, whereas fasting glucose and glycated hemoglobin were unchanged. Reductions in biomarkers of bone formation without differences in markers of bone resorption were observed. LLF580 was generally safe and well tolerated, except for higher incidence of generally mild to moderate gastrointestinal adverse effects. Conclusions: In obese, mildly hypertriglyceridemic adults, LLF580 was generally safe and demonstrated beneficial effects on serum lipids, liver fat, and biomarkers of liver injury, suggesting it may be effective for treatment of select metabolic disorders including hypertriglyceridemia and nonalcoholic fatty liver disease. Assessments of longer term safety and efficacy are warranted. [ABSTRACT FROM AUTHOR]

Published
2022
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25. CONTRIBUTORS

Author

Ackerman, Michael J., primary, Ashikaga, Hiroshi, additional, Baldini, Antonio, additional, Basson, Craig T., additional, Ben-Yehuda, Ori, additional, Brown, Joan Heller, additional, Brown, Roger W., additional, Campbell, Kevin P., additional, Chen, Ju, additional, and Chien, Kenneth R., additional

Published
2004
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27. 10.1177_1358863X19859072_supplementary_material – Supplemental material for A randomized, placebo-controlled trial of canakinumab in patients with peripheral artery disease

Author

Russell, Kerry S, Yates, Denise P, Kramer, Christopher M, Feller, Andrea, Mahling, Ping, Colin, Laurence, Clough, Timothy, Tianke Wang, LaPerna, Lucy, Alpa Patel, Lawall, Holger, Shennak, Mustafa M, Fulmer, James, Nikol, Sigrid, Smith, William B, Müller, Oliver J, Ratchford, Elizabeth V, and Basson, Craig T

Subjects
FOS: Clinical medicine, Cardiology, 110323 Surgery
Abstract

Supplemental material, 10.1177_1358863X19859072_supplementary_material for A randomized, placebo-controlled trial of canakinumab in patients with peripheral artery disease by Kerry S Russell, Denise P Yates, Christopher M Kramer, Andrea Feller, Ping Mahling, Laurence Colin, Timothy Clough, Tianke Wang, Lucy LaPerna, Alpa Patel, Holger Lawall, Mustafa M Shennak, James Fulmer, Sigrid Nikol, William B Smith, Oliver J Müller, Elizabeth V Ratchford and Craig T Basson in Vascular Medicine

Published
2019
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37. The clinical and genetic spectrum of the Holt-Oram syndrome (heart-hand syndrome)

Author

Basson, Craig T., Cowley, Glenn S., Solomon, Scott D., Weissman, Barbara, Poznanski, Andrew K., Traill, Thomas A., Seidman, J.G., and Seidman, Christine E.

Subjects
Congenital heart disease -- Genetic aspects, Chromosome abnormalities -- Physiological aspects, Extremities, Upper -- Abnormalities, Osteal manifestations of general diseases -- Genetic aspects
Abstract

Holt-Oram syndrome may be caused by mutations in a gene on chromosome 12q2. Holt-Oram syndrome is an inherited disorder characterized by skeletal deformities and heart defects. Researchers performed clinical and genetic-linkage studies on two large, unrelated families with the syndrome. In Family A, 26 of 49 members were affected and 18 surviving members were evaluated. All affected members of Family A had skeletal abnormalities and cardiovascular disease. Eleven had heart conduction diseases. In Family B, 18 of 31 affected members were still alive for examination. All affected family members had skeletal abnormalities and had severe skeletal deformities more frequently than affected members of Family A. In contrast, Family B had less severe and less frequent cardiovascular disease than Family A and only one member had a heart conduction disease. Genetic analysis revealed a linkage of the syndrome to mutations on chromosome 12.

Published
1994

41. A randomized, placebo-controlled trial of canakinumab in patients with peripheral artery disease

Author

Russell, Kerry S, primary, Yates, Denise P, additional, Kramer, Christopher M, additional, Feller, Andrea, additional, Mahling, Ping, additional, Colin, Laurence, additional, Clough, Timothy, additional, Wang, Tianke, additional, LaPerna, Lucy, additional, Patel, Alpa, additional, Lawall, Holger, additional, Shennak, Mustafa M, additional, Fulmer, James, additional, Nikol, Sigrid, additional, Smith, William B, additional, Müller, Oliver J, additional, Ratchford, Elizabeth V, additional, and Basson, Craig T, additional

Published
2019
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45. Abstract 11: Effects of Canakinumab in Patients With Peripheral Artery Disease

Author

Russell, Kerry S, primary, Yates, Denise, additional, Feller, Andrea, additional, Wang, Tianke, additional, Chen, Ping, additional, Clough, Timothy, additional, Colin, Laurence, additional, LaPerna, Lucy, additional, Shennak, Mustafa M, additional, Lawall, Holger, additional, Nikol, Sigrid, additional, Smith, William, additional, Forst, Thomas, additional, Mueller, Oliver J, additional, Hoekstra, John, additional, Piatek, Marek, additional, Ratchford, Elizabeth V, additional, Kramer, Christopher M, additional, and Basson, Craig T, additional

Published
2017
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46. Aortic Dissection in Patients With Genetically Mediated Aneurysms: Incidence and Predictors in the GenTAC Registry

Author

Weinsaft, Jonathan W., Devereux, Richard B., Preiss, Liliana R., Feher, Attila, Roman, Mary J., Basson, Craig T., Geevarghese, Alexi, Ravekes, William, Dietz, Harry C., Holmes, Kathryn, Habashi, Jennifer, Pyeritz, Reed E., Bavaria, Joseph, Milewski, Karianna, LeMaire, Scott A., Morris, Shaine, Milewicz, Dianna M., Prakash, Siddharth, Maslen, Cheryl, Song, Howard K., Silberbach, G. Michael, Shohet, Ralph V., McDonnell, Nazli, Hendershot, Tabitha, Eagle, Kim A., and Asch, Federico M.

Subjects
Adult, Male, Loeys-Dietz Syndrome, Aortic Aneurysm, Thoracic, Incidence, Heart Valve Diseases, Turner Syndrome, Aorta, Thoracic, Organ Size, Middle Aged, Article, United States, Aortic Aneurysm, Marfan Syndrome, Aortic Dissection, Blood Vessel Prosthesis Implantation, Bicuspid Aortic Valve Disease, Aortic Valve, Commentary, Humans, Ehlers-Danlos Syndrome, Female, Aorta, Abdominal, Registries, Aorta
Abstract

Aortic dissection (AoD) is a serious complication of thoracic aortic aneurysm (TAA). Relative risk for AoD in relation to TAA etiology, incidence, and pattern after prophylactic TAA surgery are poorly understood.This study sought to determine the incidence, pattern, and relative risk for AoD among patients with genetically associated TAA.The population included adult GenTAC participants without AoD at baseline. Standardized core laboratory tests classified TAA etiology and measured aortic size. Follow-up was performed for AoD.Bicuspid aortic valve (BAV) (39%) and Marfan syndrome (MFS) (22%) were the leading diagnoses in the studied GenTAC participants (n = 1,991). AoD occurred in 1.6% over 3.6 ± 2.0 years; 61% of AoD occurred in patients with MFS. Cumulative AoD incidence was 6-fold higher among patients with MFS (4.5%) versus others (0.7%; p 0.001). MFS event rates were similarly elevated versus those in patients with BAV (0.3%; p 0.001). AoD originated in the distal arch or descending aorta in 71%; 52% of affected patients, including 68% with MFS, had previously undergone aortic grafting. In patients with proximal aortic surgery, distal aortic size (descending thoracic, abdominal aorta) was larger among patients with AoD versus those without AoD (both p 0.05), whereas the ascending aorta size was similar. Conversely, in patients without previous surgery, aortic root size was greater in patients with subsequent AoD (p 0.05), whereas distal aortic segments were of similar size. MFS (odds ratio: 7.42; 95% confidence interval: 3.43 to 16.82; p 0.001) and maximal aortic size (1.86 per cm; 95% confidence interval: 1.26 to 2.67; p = 0.001) were independently associated with AoD. Only 4 of 31 (13%) patients with AoD had pre-dissection images that fulfilled size criteria for prophylactic TAA surgery at a subsequent AoD site.Among patients with genetically associated TAA, MFS augments risk for AoD even after TAA grafting. Although increased aortic size is a risk factor for subsequent AoD, events typically occur below established thresholds for prophylactic TAA repair.

Published
2015

47. Arterial Effects of Canakinumab in Patients With Atherosclerosis and Type 2 Diabetes or Glucose Intolerance

Author

Choudhury, Robin P., primary, Birks, Jacqueline S., additional, Mani, Venkatesh, additional, Biasiolli, Luca, additional, Robson, Matthew D., additional, L'Allier, Philippe L., additional, Gingras, Marc-Alexandre, additional, Alie, Nadia, additional, McLaughlin, Mary Ann, additional, Basson, Craig T., additional, Schecter, Alison D., additional, Svensson, Eric C., additional, Zhang, Yiming, additional, Yates, Denise, additional, Tardif, Jean-Claude, additional, and Fayad, Zahi A., additional

Published
2016
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48. Aortic Dissection in Patients With Genetically Mediated Aneurysms

Author

Weinsaft, Jonathan W., primary, Devereux, Richard B., additional, Preiss, Liliana R., additional, Feher, Attila, additional, Roman, Mary J., additional, Basson, Craig T., additional, Geevarghese, Alexi, additional, Ravekes, William, additional, Dietz, Harry C., additional, Holmes, Kathryn, additional, Habashi, Jennifer, additional, Pyeritz, Reed E., additional, Bavaria, Joseph, additional, Milewski, Karianna, additional, LeMaire, Scott A., additional, Morris, Shaine, additional, Milewicz, Dianna M., additional, Prakash, Siddharth, additional, Maslen, Cheryl, additional, Song, Howard K., additional, Silberbach, G. Michael, additional, Shohet, Ralph V., additional, McDonnell, Nazli, additional, Hendershot, Tabitha, additional, Eagle, Kim A., additional, and Asch, Federico M., additional

Published
2016
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50. TGFbRIIb Mutations Trigger Aortic Aneurysm Pathogenesis by Altering TGFb2 Signal Transduction

Author

Bee, Katharine J., Wilkes, David C., Devereux, Richard B., Basson, Craig T., and Hatcher, Cathy J.

Subjects
Adult, Male, DNA Mutational Analysis, Molecular Sequence Data, Protein Serine-Threonine Kinases, Article, Cohort Studies, Transforming Growth Factor beta1, Transforming Growth Factor beta2, Young Adult, Humans, Genetic Predisposition to Disease, RNA, Messenger, Aged, Aged, 80 and over, Aortic Aneurysm, Thoracic, Base Sequence, Myosin Heavy Chains, Receptor, Transforming Growth Factor-beta Type II, Fibroblasts, Middle Aged, Pedigree, Gene Expression Regulation, Mutation, Female, Receptors, Transforming Growth Factor beta, Signal Transduction
Abstract

Thoracic aortic aneurysm (TAA) is a common progressive disorder involving gradual dilation of the ascending and/or descending thoracic aorta that eventually leads to dissection or rupture. Nonsydromic TAA can occur as a genetically triggered, familial disorder that is usually transmitted in a monogenic autosomal dominant fashion and is known as familial TAA. Genetic analyses of families affected with TAA have identified several chromosomal loci, and further mapping of familial TAA genes has highlighted disease-causing mutations in at least 4 genes: myosin heavy chain 11 (MYH11), α-smooth muscle actin (ACTA2), and transforming growth factor β receptors I and II (TGFβRI and TGFβRII).We evaluated 100 probands to determine the mutation frequency in MYH11, ACTA2, TGFβRI, and TGFβRII in an unbiased population of individuals with genetically mediated TAA. In this study, 9% of patients had a mutation in one of the genes analyzed, 3% of patients had mutations in ACTA2, 3% in MYH11, 1% in TGFβRII, and no mutations were found in TGFβRI. Additionally, we identified mutations in a 75 base pair alternatively spliced TGFβRII exon, exon 1a that produces the TGFβRIIb isoform and accounted for 2% of patients with mutations. Our in vitro analyses indicate that the TGFβRIIb activating mutations alter receptor function on TGFβ2 signaling.We propose that TGFβRIIb expression is a regulatory mechanism for TGFβ2 signal transduction. Dysregulation of the TGFβ2 signaling pathway, as a consequence of TGFβRIIb mutations, results in aortic aneurysm pathogenesis.

Published
2012

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