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Leverage Digital Receives Prestigious Distinction from the University of South Florida Alumni Association as Top 25 Fastest Growing Company Leverage Digital has been recognized again for its growth by the University of South Florida Alumni Association. For the second straight year, the Tampa-based digital marketing agency was inducted into the top 25 of the USF Fast 56 by USF System President Judy Genshaft and USF Alumni Association Board of Directors Chair Jim Harvey. The 2017 USF Fast 56 honors the fifty-six fastest growing companies led by a USF alumnus. This year, Leverage Digital moved up two spots to rank 12th on the list after ranking 14th in 2016. “We’re proud to recognize Leverage Digital as one of the 56 fastest growing USF Bull-led businesses in the world,” said USF Alumni Association Executive Director Bill McCausland. “It’s a tremendous honor to be recognized again by the University of South Florida as one of the fastest growing alumni-led companies. I greatly value the time that I spent at USF, and owe Leverage Digital’s success in large part to the education received, relationships built, and activities participated in while attending USF,” said Jay Taylor, Founder and Managing Director at Leverage Digital. Mr. Taylor received both a bachelor’s degree in 2004 and a master’s degree in 2008 from USF. The 2017 USF Fast 56 was revealed in a ceremony on Friday, April 28, at the Marshall Student Center Ballroom and Oval Theater at the USF Tampa campus. The winning organizations are required to have been in business for at least three years, have revenues of $250,000 or more for the most recent 12-month period, and be owned or led by a University of South Florida alumnus. The 2017 USF Fast 56 companies were ranked by percentage of cumulative annual growth in revenue, as documented by Cherry Bekaert, a public accounting firm based in Tampa. Fifty-six USF alumni-owned or led businesses were selected as recipients, in recognition of the year USF was founded, 1956. Of the 56 winners, the top 25 companies received special recognition during the awards ceremony. ABOUT LEVERAGE DIGITAL Leverage Digital is an award-winning digital marketing agency that partners with brands to successfully engage their audiences and achieve measurable results. The agency is a Certified Google Partner, and its work has garnered numerous industry accolades over the years, receiving honors from the International Davey Awards, Hermes Awards, W3 Awards, and Communicator Awards to name a few. In 2016, Leverage Digital was named the 14th fastest growing company owned or led by a University of South Florida alumnus. For more information, please visit http://www.leveragedigital.com/. ABOUT THE USF FAST 56 AWARDS The Fast 56 identifies, recognizes, and celebrates the world’s fastest growing USF Bull-owned or Bull-led businesses. The awards celebrate their success while also providing a forum for passing lessons to the next generation of Bull entrepreneurs. For more information, please visit http://www.usfalumni.org/.


Kacanek D.,Harvard University | Kacanek D.,Center for Biostatistics in Research | Angelidou K.,Center for Biostatistics in Research | Williams P.L.,Harvard University | And 60 more authors.
AIDS | Year: 2015

Objectives: The relationship of specific psychiatric conditions to adherence has not been examined in longitudinal studies of youth with perinatal HIV infection (PHIV). We examined associations between psychiatric conditions and antiretroviral nonadherence over 2 years. Design: Longitudinal study in 294 PHIV youth, 6'17 years old, in the United States and Puerto Rico. Methods: We annually assessed three nonadherence outcomes: missed above 5% of doses in the past 3 days, missed a dose within the past month, and unsuppressed viral load (>400 copies/ml). We fit multivariable logistic models for nonadherence using Generalized Estimating Equations, and evaluated associations of psychiatric conditions (attention deficit hyperactivity disorder, disruptive behavior, depression, anxiety) at entry with incident nonadherence using multivariable logistic regression. Results: Nonadherence prevalence at study entry was 14% (3-day recall), 32% (past month nonadherence), and 38% (unsuppressed viral load), remaining similar over time. At entry, 38% met symptom cut-off criteria for at least one psychiatric condition. Greater odds of 3-day recall nonadherence were observed at week 96 for those with depression [adjusted odds ratio (aOR) 4.14, 95% confidence interval (CI) 1.11'15.42] or disruptive behavior (aOR 3.36, 95% CI 1.02'11.10], but not at entry. Those with vs. without attention deficit hyperactivity disorder had elevated odds of unsuppressed viral load at weeks 48 (aOR 2.46, 95% CI 1.27'4.78) and 96 (aOR 2.35, 95% CI 1.01'5.45), but not at entry. Among 232 youth adherent at entry, 16% reported incident 3-day recall nonadherence. Disruptive behavior conditions at entry were associated with incident 3- day recall nonadherence (aOR 3.01, 95% CI 1.24'7.31). Conclusion: In PHIV youth, comprehensive adherence interventions that address psychiatric conditions throughout the transition to adult care are needed. © 2015 Wolters Kluwer Health, Inc. All rights reserved.


Paredes D.,USF Tampa | Paredes D.,Laboratory of Molecular Biology | Acosta S.,USF Tampa | Gemma C.,USF Tampa | Bickford P.C.,USF Tampa
Aging and Disease | Year: 2010

Tumor necrosis factor alpha (TNF-α) is a multifunctional proinflammatory cytokine, which is a critical inflammatory mediator involved in aging and neurodegenerative diseases of aging. Previous work has shown that diets enriched with antioxidants reduce levels of the cytokine TNF-α and improve classical eyeblink conditioning performance. Therefore we tested the hypothesis that the proinflamatory cytokine TNF-α may be a critical factor that modulates classical conditioning behavior. If increased levels of endogenous cerebellar TNF-α negatively affect performance on the eyeblink conditioning task in aged rats, then exogenous administration of TNF-α in young rats should result in an impaired acquisition and/or retention of eyeblink conditioning memory. On the other hand, the reduction or blockage of the age-related increase in cerebellar TNF-α levels in aged rats should result in an improvement in memory. Young (3 month old) F344 rats were pretreated with an intracerebellar injection of recombinant rat (rr)TNF-α or denatured (rr)TNF-α prior to eyeblink conditioning coupled to microdialysis. The results showed that young rats treated with rrTNF-α have a decreased rate of learning compared to the control group. Norepinephrine which has been shown to play a critical role in cerebellar learning tasks presented a shift on training day one of young rats resembling that observed in aged rats. In a second experiment aged (22 month old) F344 rats were pretreated with intracerebellar microinjection of anti-rat TNF-α three times a week for 4 weeks prior to eyeblink conditioning training couple to microdialysis. Aged rats showed a better performance in the conditioned responses when compared to controls. The release of norepinephrine in this group reached basal levels sooner than the control group but not as early as the young rats. The results of these experiments demonstrate a critical correlation between TNF-α and the rate of learning and the pattern of NE release during eyeblink conditioning.


PubMed | Laboratory of Molecular Biology, USF Tampa, USF Health Byrd Alzheimers Institute and Current Inc.
Type: Journal Article | Journal: American journal of neurodegenerative disease | Year: 2016

Transcription factors are involved to varying extents in the health and survival of neurons in the brain and a better understanding of their roles with respect to the pathogenesis of Alzheimers disease (AD) could lead to the development of additional treatment strategies. Sp1 is a transcription factor that responds to inflammatory signals occurring in the AD brain. It is known to regulate genes with demonstrated importance in AD, and we have previously found it upregulated in the AD brain and in brains of transgenic AD model mice. To better understand the role of Sp1 in AD, we tested whether we could affect memory function (measured with a battery of behavioral tests discriminating different aspects of cognitive function) in a transgenic model of AD by pharmaceutical modulation of Sp1. We found that inhibition of Sp1 function in transgenic AD model mice increased memory deficits, while there were no changes in sensorimotor or anxiety tests. A42 and A40 peptide levels were significantly higher in the treated mice, indicating that Sp1 elevation in AD could be a functionally protective response. Circulating levels of CXCL1 (KC) decreased following treatment with mithramycin, while a battery of other cytokines, including IL-1, IL-6, INF- and MCP-1, were unchanged. Gene expression levels for several genes important to neuronal health were determined by qRT-PCR, and none of these appeared to change at the transcriptional level.


Gemma C.,USF Tampa | Bachstetter A.D.,USF Tampa | Bachstetter A.D.,University of Kentucky | Bickford P.C.,USF Tampa
Aging and Disease | Year: 2010

Age-related changes in innate immune function and glial-neuronal communication are early and critical events in brain aging and neurodegenerative disease, and lead to a chronic increase in oxidative stress and inflammation, which initiates neuronal dysfunction and reduced synaptic plasticity, and ultimately disruption in learning and memory in the aged brain. Several lines of evidence suggest a correlation between adult neurogenesis and learning. It has been proposed that a decline in hippocampal neurogenesis contributes to a physiologic decline in brain function. Recently, new and important insights relating to the production of new neurons affecting hippocampal-dependent memory ability have been provided. A multitude of factors have been shown to regulate the production of new neurons in the adult hippocampus, many of which change as a result of aging. Yet, the potential importance of neurogenesis in some affective and cognitive behaviors, as well as endogenous tissue repair mechanisms, makes further investigation of neurogenic regulators warranted. We have recent evidence that key regulators of communication between neurons and microglia are disrupted in the aged brain and may be one of the factors that precedes and initiates the observed increase in chronic inflammatory state. In this review the role of dysfunction in these neuronal-glial communication regulators underlying age-related impairments in cognition and hippocampal neurogenesis will be discussed. An understanding of these mechanisms will lead to the development of preventive or protective therapies.

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