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New Orleans, LA, United States

Tulane University of Louisiana is a private, nonsectarian research university located in New Orleans, Louisiana, United States. Founded as a public medical college in 1834, the school grew into a comprehensive university in 1847 and was eventually privatized under the endowments of Paul Tulane and Josephine Louise Newcomb in 1884. Tulane is a member of the Association of American Universities. Wikipedia.


Daniel J.M.,Tulane University
Hormones and Behavior | Year: 2013

This article is part of a Special Issue "Hormones & Neurotrauma".Estrogens have been shown to be protective agents against neurodegeneration and associated cognitive decline in aging females. However, clinical data have been equivocal as to the benefits to the brain and cognition of estrogen therapy in postmenopausal women. One factor that is proposed to be critical in determining the efficacy of hormone therapy is the timing of its initiation. The critical period or window of opportunity hypothesis proposes that following long-term ovarian hormone deprivation, the brain and cognition become insensitive to exogenously administered estrogens. In contrast, if estrogens are administered during a critical period near the time of cessation of ovarian function, they will exert beneficial effects. The focus of the current review is the examination of evidence from rodent models investigating the critical period hypothesis. A growing body of experimental data indicates that beneficial effects of 17β-estradiol (estradiol) on cognition and on cholinergic function and hippocampal plasticity, both of which have been linked to the ability of estradiol to exert beneficial effects on cognition, are attenuated if estradiol is administered following a period of long-term ovarian hormone deprivation. Further, emerging data implicate loss of estrogen receptor alpha (ERα) in the brain resulting from long-term hormone deprivation as a basis for the existence of the critical period. A unifying model is proposed by which the presence or absence of estrogens during a critical period following the cessation of ovarian function permanently alters the system resulting in decreased or increased risk, respectively, of neurodegeneration and cognitive decline. © 2012 Elsevier Inc. Source


Jazwinski S.M.,Tulane University
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2013

Mitochondria are responsible for generating adenosine triphosphate (ATP) and metabolic intermediates for biosynthesis. These dual functions require the activity of the electron transport chain in the mitochondrial inner membrane. The performance of these electron carriers is imperfect, resulting in release of damaging reactive oxygen species. Thus, continued mitochondrial activity requires maintenance. There are numerous means by which this quality control is ensured. Autophagy and selective mitophagy are among them. However, the cell inevitably must compensate for declining quality control by activating a variety of adaptations that entail the signaling of the presence of mitochondrial dysfunction to the nucleus. The best known of these is the retrograde response. This signaling pathway is triggered by the loss of mitochondrial membrane potential, which engages a series of signal transduction proteins, and it culminates in the induction of a broad array of nuclear target genes. One of the hallmarks of the retrograde response is its capacity to extend the replicative life span of the cell. The retrograde signaling pathway interacts with several other signaling pathways, such as target of rapamycin (TOR) and ceramide signaling. All of these pathways respond to stress, including metabolic stress. The retrograde response is also linked to both autophagy and mitophagy at the gene and protein activation levels. Another quality control mechanism involves age-asymmetry in the segregation of dysfunctional mitochondria. One of the processes that impinge on this age-asymmetry is related to biogenesis of the organelle. Altogether, it is apparent that mitochondrial quality control constitutes a complex network of processes, whose full understanding will require a systems approach. This article is part of a Special Issue entitled: Protein Import and Quality Control in Mitochondria and Plastids. © 2012 Elsevier B.V. Source


Anbalagan M.,Tulane University
Nuclear receptor signaling | Year: 2012

Nuclear receptors (NR) impact a myriad of physiological processes including homeostasis, reproduction, development, and metabolism. NRs are regulated by post-translational modifications (PTM) that markedly impact receptor function. Recent studies have identified NR PTMs that are involved in the onset and progression of human diseases, including cancer. The majority of evidence linking NR PTMs with disease has been demonstrated for phosphorylation, acetylation and sumoylation of androgen receptor (AR), estrogen receptor α (ERα), glucocorticoid receptor (GR) and peroxisome proliferator activated receptor γ (PPARγ). Phosphorylation of AR has been associated with hormone refractory prostate cancer and decreased disease-specific survival. AR acetylation and sumoylation increased growth of prostate cancer tumor models. AR phosphorylation reduced the toxicity of the expanded polyglutamine AR in Kennedy's Disease as a consequence of reduced ligand binding. A comprehensive evaluation of ERα phosphorylation in breast cancer revealed several sites associated with better clinical outcome to tamoxifen therapy, whereas other phosphorylation sites were associated with poorer clinical outcome. ERα acetylation and sumoylation may also have predictive value for breast cancer. GR phosphorylation and acetylation impact GR responsiveness to glucocorticoids that are used as anti-inflammatory drugs. PPARγ phosphorylation can regulate the balance between growth and differentiation in adipose tissue that is linked to obesity and insulin resistance. Sumoylation of PPARγ is linked to repression of inflammatory genes important in patients with inflammatory diseases. NR PTMs provide an additional measure of NR function that can be used as both biomarkers of disease progression, and predictive markers for patient response to NR-directed treatments. Source


Navar L.G.,Tulane University
Current Opinion in Nephrology and Hypertension | Year: 2014

PURPOSE OF REVIEW: The purpose of this review is to provide an update on the current knowledge regarding the role of the intrarenal rennin-angiotensin system (RAS) in the regulation of glomerular function including glomerular dynamics and filtration rate, glomerular permeability and structural alterations during chronic increases in intrarenal angiotensin (Ang) II. RECENT FINDINGS: Recent studies have continued to delineate the complex interactions among the various RAS components that participate in regulating glomerular function. Although Ang II acting on AT1 receptors remains as the predominant influence on glomerular dynamics, some of these effects are indirectly mediated by Ang II modulating the sensitivity of the macula densa tubuloglomerular feedback mechanism as well as the more recently described feedback mechanism from the connecting tubule. Interestingly, the actions of Ang II on these systems cause opposite effects on glomerular function demonstrating the complexities associated with the influences of Ang II on glomerular function. When chronically elevated, Ang II also stimulates and/or interacts with other factors, including reactive oxygen species, cytokines and growth factors and other hormones or paracrine agents, to elicit structural alterations. SUMMARY: Recent studies have provided further evidence for the presence of many components of the RAS in glomerular structures, which supports the importance of locally produced angiotensin peptides to regulate glomerular haemodynamics, filtration rate and macromolecular permeability and contribute to fibrosis and glomerular injury when inappropriately augmented. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source


Veazey R.S.,Tulane University
Current Opinion in HIV and AIDS | Year: 2013

PURPOSE OF REVIEW: Early studies have cast doubt on the utility of animal models for predicting success or failure of HIV-prevention strategies, but results of multiple human phase 3 microbicide trials, and interrogations into the discrepancies between human and animal model trials, indicate that animal models were, and are, predictive of safety and efficacy of microbicide candidates. RECENT FINDINGS: Recent studies have shown that topically applied vaginal gels, and oral prophylaxis using single or combination antiretrovirals are indeed effective in preventing sexual HIV transmission in humans, and all of these successes were predicted in animal models. Further, prior discrepancies between animal and human results are finally being deciphered as inadequacies in study design in the model, or quite often, noncompliance in human trials, the latter being increasingly recognized as a major problem in human microbicide trials. SUMMARY: Successful microbicide studies in humans have validated results in animal models, and several ongoing studies are further investigating questions of tissue distribution, duration of efficacy, and continued safety with repeated application of these, and other promising microbicide candidates in both murine and nonhuman primate models. Now that we finally have positive correlations with prevention strategies and protection from HIV transmission, we can retrospectively validate animal models for their ability to predict these results, and more importantly, prospectively use these models to select and advance even safer, more effective, and importantly, more durable microbicide candidates into human trials. © 2013 Wolters Kluwer Health | Lippincott Williams &Wilkins. Source

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