Institution
University of Alabama at Birmingham
Education•Birmingham, Alabama, United States•
About: University of Alabama at Birmingham is a education organization based out in Birmingham, Alabama, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 38523 authors who have published 86775 publications receiving 3930642 citations. The organization is also known as: UAB & The University of Alabama at Birmingham.
Topics: Population, Poison control, Transplantation, Health care, Immune system
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TL;DR: In this article, the authors examined the relationship between circulating levels of total adiponectin and the relative distribution of multimeric forms with key features of the metabolic syndrome and concluded that it is HMW quantity, not total or HMW-to-total adiponiectin ratio, that was primarily responsible for these relationships.
Abstract: Adiponectin circulates in human plasma mainly as a 180-kDa low molecular weight (LMW) hexamer and a high molecular weight (HMW) multimer of approximately 360 kDa. We comprehensively examined the relationships between circulating levels of total adiponectin, adiponectin multimers, and the relative distribution (i.e., ratio) of multimeric forms with key features of the metabolic syndrome. Total adiponectin (r = 0.45), HMW (r = 0.47), LMW (r = 0.31), and HMW-to-total adiponectin ratio (r = 0.29) were significantly correlated with insulin-stimulated glucose disposal rate. Similarly, total (r = -0.30), HMW (r = -0.38), and HMW-to-total adiponectin ratio (r = -0.34) were correlated with central fat distribution but not with total fat mass or BMI. Regarding energy metabolism, although there were no effects on resting metabolic rate, total (r = 0.41) and HMW (r = 0.44) were associated with increasing rates of fat oxidation. HMW-to-total adiponectin ratio increased as a function of total adiponectin, and it was HMW quantity (not total or HMW-to-total adiponectin ratio or LMW) that was primarily responsible for all of these relationships. Impact on nuclear magnetic resonance lipoprotein subclasses was assessed. HMW and total adiponectin were correlated with decreases in large VLDL (r = -0.44 and -0.41); decreases in small LDL (r = -0.41 and -0.36) and increases in large LDL (r = 0.36 and 0.30) particle concentrations accompanied by increased LDL particle size (r = 0.47 and 0.39); and increases in large HDL (r = 0.45 and 0.37) and HDL particle size (r = 0.53 and 0.47). Most of these correlations persisted after adjustment for metabolic covariables. In conclusion, first, serum adiponectin is associated with increased insulin sensitivity, reduced abdominal fat, and high basal lipid oxidation; however, it is HMW quantity, not total or HMW-to-total adiponectin ratio, that is primarily responsible for these relationships. Second, reduced quantities of HMW independently recapitulate the lipoprotein subclass profile associated with insulin resistance after correcting for glucose disposal rate and BMI. Finally, HMW adiponectin is an important factor in explaining the metabolic syndrome.
480 citations
TL;DR: The presence of the estrogen receptor is not required for the isoflavones to inhibit tumor cell growth (MDA-468 vs MCF-7 cells), and the effects of genistein and biochanin A are not attenuated by overexpression of the multi-drug resistance gene product.
479 citations
Scott & White Hospital1, University of Connecticut2, University of Pittsburgh3, University of Oklahoma Health Sciences Center4, Emory University5, University of Southern California6, University of Alabama at Birmingham7, University of California, San Francisco8, Mayo Clinic9, University of Pennsylvania10, Medical College of Wisconsin11, Icahn School of Medicine at Mount Sinai12, University of California, San Diego13, University Hospitals of Cleveland14, Harvard University15, Henry Ford Hospital16, National Institutes of Health17, Northwestern University18, American Academy of Dermatology19
TL;DR: The treatment of psoriasis with biologic agents will be reviewed, emphasizing treatment recommendations and the role of the dermatologist in monitoring and educating patients regarding benefits as well as associated risks.
Abstract: Psoriasis is a chronic, inflammatory multisystem disease that affects up to 3.2% of the US population. This guideline addresses important clinical questions that arise in psoriasis management and care, providing recommendations based on the available evidence. The treatment of psoriasis with biologic agents will be reviewed, emphasizing treatment recommendations and the role of the dermatologist in monitoring and educating patients regarding benefits as well as associated risks.
479 citations
TL;DR: It is demonstrated that overexpression of LRRK2 enhances alpha-synuclein-mediated cytotoxicity and inhibition of L RRK2 expression is suggested as a potential therapeutic option for ameliorating alpha- synucleIn-induced neurodegeneration.
479 citations
University of Pennsylvania1, Autonomous University of Barcelona2, Mayo Clinic3, University of Manchester4, Erasmus University Rotterdam5, VU University Amsterdam6, Indiana University – Purdue University Indianapolis7, University of Siena8, National Institutes of Health9, Neuroscience Research Australia10, University of Cambridge11, University of Michigan12, Oregon Health & Science University13, Northwestern University14, King's College London15, University of Texas at Dallas16, University of Texas Southwestern Medical Center17, University of Barcelona18, University of Zurich19, Ludwig Maximilian University of Munich20, Duke University21, University of California, San Francisco22, Veterans Health Administration23, Boston University24, Emory University25, University College London26, University of British Columbia27, University of Pittsburgh28, University of Virginia29, Flanders Institute for Biotechnology30, University of Antwerp31, Columbia University32, Johns Hopkins University33, University of Sydney34, University of New South Wales35, University of Washington36, University of Sheffield37, Washington University in St. Louis38, Alfred Hospital39, University of California, Davis40, Harvard University41, Icahn School of Medicine at Mount Sinai42, Rush University Medical Center43, University of Arizona44, University of California, Los Angeles45, University of Southern California46, University of Eastern Finland47, Uppsala University48, Pierre-and-Marie-Curie University49, University of California, San Diego50, University of California, Irvine51, University of Toronto52, University of Alabama at Birmingham53, University of Würzburg54, Karolinska Institutet55
TL;DR: It is found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM 106B, which implicate variants in TMEM106B as a strong risk factor for FTLD, suggesting an underlying pathogenic mechanism.
Abstract: Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 x 10(-11); odds ratio, minor allele (C) 0.61, 95% CI 0.53-0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 x 10(-4)). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.
479 citations
Authors
Showing all 38940 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Rudolf Jaenisch | 206 | 606 | 178436 |
| Joel Schwartz | 183 | 1149 | 109985 |
| Tadamitsu Kishimoto | 181 | 1067 | 130860 |
| Jasvinder A. Singh | 176 | 2382 | 223370 |
| Gregg L. Semenza | 168 | 502 | 130316 |
| David R. Jacobs | 165 | 1262 | 113892 |
| Hua Zhang | 163 | 1503 | 116769 |
| David R. Holmes | 161 | 1624 | 114187 |
| David Cella | 156 | 1258 | 106402 |
| Elaine S. Jaffe | 156 | 828 | 112412 |
| Michael A. Matthay | 151 | 998 | 98687 |
| Lawrence Corey | 146 | 773 | 78105 |
| Barton F. Haynes | 144 | 911 | 79014 |
| Douglas D. Richman | 142 | 633 | 82806 |
| Kjell Fuxe | 142 | 1479 | 89846 |