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Institution

University of Texas Health Science Center at Houston

EducationHouston, Texas, United States
About: University of Texas Health Science Center at Houston is a education organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 27309 authors who have published 42520 publications receiving 2151596 citations. The organization is also known as: UTHealth & The UT Health Science Center at Houston.


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Journal ArticleDOI
TL;DR: The improved accuracy of the new formula was proven by performing IOL power calculations on 2,000 eyes from 12 surgeons and comparing the results to seven other currently used formulas.
Abstract: A three-part system that determines the correct power for an intraocular lens (IOL) to achieve a desired postoperative refraction is presented. The three components are (1) data screening criteria to identify improbable axial length and keratometry measurements, (2) a new IOL calculation formula that exceeds the current accuracy of other formulas for short, medium, and long eyes, and (3) a personalized "surgeon factor" that adjusts for any consistent bias in the surgeon's results, from any source, based on a reverse solution of the new formula; the reverse solution uses the postoperative stabilized refraction, the dioptric power of the implanted IOL, and the preoperative corneal and axial length measurements to calculate the personalized surgeon factor. The improved accuracy of the new formula was proven by performing IOL power calculations on 2,000 eyes from 12 surgeons and comparing the results to seven other currently used formulas.

729 citations

Journal ArticleDOI
Lianne Schmaal1, Derrek P. Hibar2, Philipp G. Sämann3, Geoffrey B. Hall4, Bernhard T. Baune5, Neda Jahanshad2, Joshua W. Cheung2, T.G.M. van Erp6, Daniel Bos7, M. A. Ikram7, Meike W. Vernooij7, Wiro J. Niessen7, Wiro J. Niessen8, Henning Tiemeier9, Henning Tiemeier7, A. Hofman7, Katharina Wittfeld10, Hans-Jörgen Grabe10, Hans-Jörgen Grabe11, Deborah Janowitz11, Robin Bülow11, M Selonke11, Henry Völzke11, Dominik Grotegerd12, Udo Dannlowski13, Udo Dannlowski12, Volker Arolt12, Nils Opel12, Walter Heindel12, Harald Kugel12, D. Hoehn3, Michael Czisch3, Baptiste Couvy-Duchesne14, Baptiste Couvy-Duchesne15, Miguel E. Rentería15, Lachlan T. Strike14, Margaret J. Wright14, Natalie T. Mills15, Natalie T. Mills14, G.I. de Zubicaray16, Katie L. McMahon14, Sarah E. Medland15, Nicholas G. Martin15, Nathan A. Gillespie17, Roberto Goya-Maldonado18, Oliver Gruber19, Bernd Krämer19, Sean N. Hatton20, Jim Lagopoulos20, Ian B. Hickie20, Thomas Frodl21, Thomas Frodl22, Angela Carballedo21, Eva-Maria Frey23, L. S. van Velzen1, B.W.J.H. Penninx1, M-J van Tol24, N.J. van der Wee25, Christopher G. Davey26, Ben J. Harrison26, Benson Mwangi27, Bo Cao27, Jair C. Soares27, Ilya M. Veer28, Henrik Walter28, D. Schoepf29, Bartosz Zurowski30, Carsten Konrad13, Elisabeth Schramm31, Claus Normann31, Knut Schnell19, Matthew D. Sacchet32, Ian H. Gotlib32, Glenda MacQueen33, Beata R. Godlewska34, Thomas Nickson35, Andrew M. McIntosh35, Andrew M. McIntosh36, Martina Papmeyer37, Martina Papmeyer35, Heather C. Whalley35, Jeremy Hall38, Jeremy Hall35, J.E. Sussmann35, Meng Li39, Martin Walter39, Martin Walter40, Lyubomir I. Aftanas, Ivan Brack, Nikolay A. Bokhan41, Nikolay A. Bokhan42, Nikolay A. Bokhan43, Paul M. Thompson2, Dick J. Veltman1 
TL;DR: In this article, the authors present the largest ever worldwide study by the ENIGMA (Enhancing Neuro Imaging Genetics through Meta-Analysis) Major Depressive Disorder Working Group on cortical structural alterations in MDD.
Abstract: The neuro-anatomical substrates of major depressive disorder (MDD) are still not well understood, despite many neuroimaging studies over the past few decades. Here we present the largest ever worldwide study by the ENIGMA (Enhancing Neuro Imaging Genetics through Meta-Analysis) Major Depressive Disorder Working Group on cortical structural alterations in MDD. Structural T1-weighted brain magnetic resonance imaging (MRI) scans from 2148 MDD patients and 7957 healthy controls were analysed with harmonized protocols at 20 sites around the world. To detect consistent effects of MDD and its modulators on cortical thickness and surface area estimates derived from MRI, statistical effects from sites were meta-analysed separately for adults and adolescents. Adults with MDD had thinner cortical gray matter than controls in the orbitofrontal cortex (OFC), anterior and posterior cingulate, insula and temporal lobes (Cohen's d effect sizes: -0.10 to -0.14). These effects were most pronounced in first episode and adult-onset patients (>21 years). Compared to matched controls, adolescents with MDD had lower total surface area (but no differences in cortical thickness) and regional reductions in frontal regions (medial OFC and superior frontal gyrus) and primary and higher-order visual, somatosensory and motor areas (d: -0.26 to -0.57). The strongest effects were found in recurrent adolescent patients. This highly powered global effort to identify consistent brain abnormalities showed widespread cortical alterations in MDD patients as compared to controls and suggests that MDD may impact brain structure in a highly dynamic way, with different patterns of alterations at different stages of life.

728 citations

Journal ArticleDOI
28 Apr 2006-Science
TL;DR: It is found that BoNT/A enters neurons by binding to the synaptic vesicle protein SV2 (isoforms A, B, and C), and SV2 acts as the protein receptor for Bo NT/A.
Abstract: How the widely used botulinum neurotoxin A (BoNT/A) recognizes and enters neurons is poorly understood. We found that BoNT/A enters neurons by binding to the synaptic vesicle protein SV2 (isoforms A, B, and C). Fragments of SV2 that harbor the toxin interaction domain inhibited BoNT/A from binding to neurons. BoNT/A binding to SV2A and SV2B knockout hippocampal neurons was abolished and was restored by expressing SV2A, SV2B, or SV2C. Reduction of SV2 expression in PC12 and Neuro-2a cells also inhibited entry of BoNT/A, which could be restored by expressing SV2 isoforms. Finally, mice that lacked an SV2 isoform (SV2B) displayed reduced sensitivity to BoNT/A. Thus, SV2 acts as the protein receptor for BoNT/A.

728 citations

Journal ArticleDOI
TL;DR: In this article, the largest genetic association study of blood pressure traits (systolic, diastolic and pulse pressure) to date in over 1 million people of European ancestry was conducted.
Abstract: High blood pressure is a highly heritable and modifiable risk factor for cardiovascular disease We report the largest genetic association study of blood pressure traits (systolic, diastolic and pulse pressure) to date in over 1 million people of European ancestry We identify 535 novel blood pressure loci that not only offer new biological insights into blood pressure regulation but also highlight shared genetic architecture between blood pressure and lifestyle exposures Our findings identify new biological pathways for blood pressure regulation with potential for improved cardiovascular disease prevention in the future

728 citations

Journal ArticleDOI
TL;DR: In this paper, the association between self-reported endometriosis and risk of ovarian cancer was found to be a risk factor for epithelial ovarian cancer; however, whether this risk extends to all invasive histological subtypes or borderline tumours is not clear.
Abstract: Summary Background Endometriosis is a risk factor for epithelial ovarian cancer; however, whether this risk extends to all invasive histological subtypes or borderline tumours is not clear. We undertook an international collaborative study to assess the association between endometriosis and histological subtypes of ovarian cancer. Methods Data from 13 ovarian cancer case–control studies, which were part of the Ovarian Cancer Association Consortium, were pooled and logistic regression analyses were undertaken to assess the association between self-reported endometriosis and risk of ovarian cancer. Analyses of invasive cases were done with respect to histological subtypes, grade, and stage, and analyses of borderline tumours by histological subtype. Age, ethnic origin, study site, parity, and duration of oral contraceptive use were included in all analytical models. Findings 13 226 controls and 7911 women with invasive ovarian cancer were included in this analysis. 818 and 738, respectively, reported a history of endometriosis. 1907 women with borderline ovarian cancer were also included in the analysis, and 168 of these reported a history of endometriosis. Self-reported endometriosis was associated with a significantly increased risk of clear-cell (136 [20·2%] of 674 cases vs 818 [6·2%] of 13 226 controls, odds ratio 3·05, 95% CI 2·43–3·84, p Interpretation Clinicians should be aware of the increased risk of specific subtypes of ovarian cancer in women with endometriosis. Future efforts should focus on understanding the mechanisms that might lead to malignant transformation of endometriosis so as to help identify subsets of women at increased risk of ovarian cancer. Funding Ovarian Cancer Research Fund, National Institutes of Health, California Cancer Research Program, California Department of Health Services, Lon V Smith Foundation, European Community's Seventh Framework Programme, German Federal Ministry of Education and Research of Germany, Programme of Clinical Biomedical Research, German Cancer Research Centre, Eve Appeal, Oak Foundation, UK National Institute of Health Research, National Health and Medical Research Council of Australia, US Army Medical Research and Materiel Command, Cancer Council Tasmania, Cancer Foundation of Western Australia, Mermaid 1, Danish Cancer Society, and Roswell Park Alliance Foundation.

726 citations


Authors

Showing all 27450 results

NameH-indexPapersCitations
Paul M. Ridker2331242245097
Eugene Braunwald2301711264576
Eric N. Olson206814144586
Hagop M. Kantarjian2043708210208
André G. Uitterlinden1991229156747
Gordon B. Mills1871273186451
Eric Boerwinkle1831321170971
Bruce M. Psaty1811205138244
Aaron R. Folsom1811118134044
Daniel R. Weinberger177879128450
Bharat B. Aggarwal175706116213
Richard A. Gibbs172889249708
Russel J. Reiter1691646121010
James F. Sallis169825144836
Steven N. Blair165879132929
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202342
2022231
20213,048
20202,807
20192,467
20182,224