Southern University at New Orleans is a historically African American university located in New Orleans, Louisiana, United States. It is a member of the Southern University System. The University is a member-school of Thurgood Marshall College Fund. Wikipedia.
Quick Q.A.,Southern University at New Orleans |
Faison M.O.,Virginia State University
Experimental and Therapeutic Medicine | Year: 2012
The unfolded protein endoplasmic reticulum stress response has emerged as a cellular physiological target to invoke tumor cell killing due to its homeostatic and cytoprotective functions. In this study, thapsigargin and tunicamycin, two endoplasmic reticulum stress inducers, were investigated for their efficacy on glioblastomas. We demonstrate that clinically relevant concentrations of thapsigargin and tunicamycin eliminate the glioblastoma cell reproductive capacity as a consequence of cell death. The mode of glioblastoma-induced cell death was determined to be via apoptosis as supported by increased C/EBP homologous protein (CHOP) levels and caspase 3 activity, two proteins with established roles in endoplasmic reticulum stress-induced cell death. In conclusion, this study provides evidence that glioblastomas are responsive to endoplasmic reticulum stress induction as a cellular program to eradicate this tumor via programmed cell death. Source
McGowin C.L.,Louisiana State University Health Sciences Center |
Annan R.S.,Louisiana State University Health Sciences Center |
Quayle A.J.,Louisiana State University Health Sciences Center |
Greene S.J.,Louisiana State University Health Sciences Center |
And 5 more authors.
Infection and Immunity | Year: 2012
Infection with Mycoplasma genitalium has been associated with male and female urogenital disease syndromes, including urethritis, cervicitis, pelvic inflammatory disease (PID), and tubal factor infertility. Basic investigations of mucosal cytotoxicity, microbial persistence, and host immune responses are imperative to understanding these inflammatory urogenital syndromes, particularly in females, considering the potential severity of upper tract infections. Here, we report that M. genitalium can establish long-term infection of human endocervical epithelial cells that results in chronic inflammatory cytokine secretion and increased responsiveness to secondary Toll-like receptor (TLR) stimulation. Using a novel quantitative PCR assay, M. genitalium was shown to replicate from 0 to 80 days postinoculation (p.i.), during which at most time points the median ratio of M. genitalium organisms to host cells was≤10, indicating that low organism burdens are capable of eliciting chronic inflammation in endocervical epithelial cells. This observation is consistent with clinical findings in women. Persistently secreted cytokines predominately consisted of potent chemotactic and/or activating factors for phagocytes, including interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and macrophage inflammatory protein 1β (MIP-1β). Despite persistent cytokine elaboration, no host cell cytotoxicity was observed except with superphysiologic loads of M. genitalium, suggesting that persistent infection occurs with minimal direct damage to the epithelium. However, it is hypothesized that chronic chemokine secretion with leukocyte trafficking to the epithelium could lead to significant inflammatory sequelae. Therefore, persistent M. genitalium infection could have important consequences for acquisition and/or pathogenesis of other sexually transmitted infections (STIs) and perhaps explain the positive associations between this organism and human immunodeficiency virus (HIV) shedding. © 2012, American Society for Microbiology. Source
Hill J.M.,Louisiana State University Health Sciences Center |
Quenelle D.C.,University of Alabama at Birmingham |
Cardin R.D.,University of Cincinnati |
Vogel J.L.,National Institute of Allergy and Infectious Diseases |
And 11 more authors.
Science Translational Medicine | Year: 2014
Herpesviruses are highly prevalent and maintain lifelong latent reservoirs, thus posing challenges to the control of herpetic disease despite the availability of antiviral pharmaceuticals that target viral DNA replication. The initiation of herpes simplex virus infection and reactivation from latency is dependent on a transcriptional coactivator complex that contains two required histone demethylases, LSD1 (lysine-specific demethylase 1) and a member of the JMJD2 family (Jumonji C domain-containing protein 2). Inhibition of either of these enzymes results in heterochromatic suppression of the viral genome and blocks infection and reactivation in vitro. We demonstrate that viral infection can be epigenetically suppressed in three animal models of herpes simplex virus infection and disease. Treating animals with the monoamine oxidase inhibitor tranylcypromine to inhibit LSD1 suppressed viral lytic infection, subclinical shedding, and reactivation from latency in vivo. This phenotypic suppression was correlated with enhanced epigenetic suppression of the viral genome and suggests that, even during latency, the chromatin state of the virus is dynamic. Therefore, epi-pharmaceuticals may represent a promising approach to treat herpetic diseases. © 2014, American Association for the Advancement of Science. All rights reserved. Source
Marinov T.T.,Southern University at New Orleans |
Deng K.,University of Louisiana at Lafayette
Journal of Scientific Computing | Year: 2011
New schemes, based on the characteristics line method, for solving a hierarchical size-structured model with nonlinear growth, mortality and reproduction rate are developed. The idea of the schemes is not to follow the characteristics from the initial condition, but for each time-step to find the origins of the grid nodes at the previous time level. Numerical tests, including comparison with exact solutions for the new schemes, are elaborated. Numerical results that confirm the theoretical order of convergence of the new schemes are presented. © 2010 Springer Science+Business Media, LLC. Source
Agency: NSF | Branch: Standard Grant | Program: | Phase: UNGRAD RES MENTORING IN BIO | Award Amount: 173.98K | Year: 2010
An award has been made to the University of New Orleans (UNO) and Southern University New Orleans (SUNO) to establish an Undergraduate Research and Mentoring (URM) program. The program will provide two-year research experiences in biology to four cohorts of scholars, starting in the fall of 2010 and continuing through summer 2013. Each cohort consists of four students (three from UNO and one from SUNO) who will be trained in research in biological sciences. URM scholars will be able to select from a wide range of research projects including conservation genetics, ecology, phylogenetic systematics, physiological and evolutionary ecology, molecular physiology, molecular biology, microbiology, and biochemistry. URM scholars will participate in individual research experiences, a stepwise educational program, and tiered mentoring. The major goals of the project are (1) to provide a diversity of opportunities for research in biology, (2) to offer a range of different faculty role models that can be matched to meet student needs and interests, (3) to provide a structured program beginning with general training in research methods, followed by hands-on research ultimately culminating in the presentation of research results, and (4) to provided a tiered mentoring process. URM students will conduct independent research mentored by faculty, and will participate in enhancement activities such as seminars, a foundational course in Basic Research Tools, and weekly lab meetings. Students will be mentored in communication skills development and will present their research results in a departmental research symposium, and will be encouraged to present at national or regional scientific meetings. Participants will be selected based individual applications, interviews, and successful completion of one semester of freshman biology. A formative evaluation to monitor the effectiveness of project implementation, and a summative evaluation to assess the quality and impact of the project in reaching its program goals will be conducted. More information is available by linking through http://biology.uno.edu/or by contacting Wendy Schluchter (firstname.lastname@example.org) or Carla Penz (email@example.com).