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Alexander W. Pastuszak
Researcher at University of Utah
Publications - 196
Citations - 3560
Alexander W. Pastuszak is an academic researcher from University of Utah. The author has contributed to research in topics: Infertility & Erectile dysfunction. The author has an hindex of 28, co-authored 190 publications receiving 2589 citations. Previous affiliations of Alexander W. Pastuszak include Baylor University & University of California, San Francisco.
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Journal ArticleDOI
The use of genomics, proteomics, and metabolomics in identifying biomarkers of male infertility.
TL;DR: This review focuses on the various methodologies used in the discovery of novel biomarkers along with their findings, and specific attention is paid to recent advances in the fields of genetics, proteomics, and metabolomics.
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Testosterone Replacement Therapy in Patients with Prostate Cancer After Radical Prostatectomy
Alexander W. Pastuszak,Amy M. Pearlman,Win Shun Lai,Guilherme Godoy,Kumaran Sathyamoorthy,Joceline S. Liu,Brian J. Miles,Larry I. Lipshultz,Mohit Khera +8 more
TL;DR: Testosterone therapy is effective and, while followed by an increase in prostate specific antigen, does not appear to increase cancer recurrence rates, even in men with high risk prostate cancer.
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Loss of Tolerance and Autoimmunity Affecting Multiple Organs in STAT5A/5B-Deficient Mice
Jonathan W. Snow,Ninan Abraham,Melissa C. Ma,Brian G. Herndier,Alexander W. Pastuszak,Mark A. Goldsmith +5 more
TL;DR: Data provide strong evidence for a requirement for STAT5 in the maintenance of tolerance in vivo, and it is hypothesized that the tolerizing role of STAT5A/5B was triggered via activation of the IL-2R.
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Intramolecular regulatory switch in ZAP-70 : analogy with receptor tyrosine kinases
TL;DR: Findings suggest that a general autoinhibitory mechanism employed by RTKs is also used by some cytoplasmic tyrosine kinases, including ZAP-70 and the related Syk kinase.
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Erythrocytosis Following Testosterone Therapy
TL;DR: Short-acting injectable testosterone is associated with greater risk of erythrocytosis compared with other formulations, and the mechanism of the pathophysiology and its role on thromboembolic events remain unclear, although some data support an increased risk of cardiovascular events resulting from testosterone-induced erythropoietinosis.