Louisiana State University Health science Center Shreveport, also known as LSU Health Shreveport, is an academic center for medicine and medical research in Shreveport, North Louisiana, in the United States. It is part of the Louisiana State University System. The medical school opened in 1969. Among the founders were Joe E. Holoubek of Shreveport and Edgar Hull, who in 1931 had been one of the founders of the Medical Center of Louisiana at New Orleans. Wikipedia.
Huffnagle G.B.,University of Michigan |
Noverr M.C.,Louisiana State University Health Sciences Center
Trends in Microbiology | Year: 2013
The study of the fungal microbiota ('mycobiome') is a new and rapidly emerging field that lags behind our understanding of the bacterial microbiome. Every human has fungi as part of their microbiota, but the total number of fungal cells is orders of magnitude smaller than that of the bacterial microbiota. However, the impact of the mycobiome on human health is significant, especially as a reservoir for blooms of pathogenic microbes when the host is compromised and as a potential cofactor in inflammatory diseases and metabolic disorders. © 2013 Elsevier Ltd.
Diaz J.H.,Louisiana State University Health Sciences Center
Clinical Microbiology Reviews | Year: 2013
Paragonimiasis is a parasitic lung infection caused by lung flukes of the genus Paragonimus, with most cases reported from Asia and caused by P. westermani following consumption of raw or undercooked crustaceans. With the exception of imported P. westermani cases in immigrants, in travelers returning from areas of disease endemicity, and in clusters of acquired cases following consumption of imported Asian crabs, human paragonimiasis caused by native lung flukes is rarely described in the United States, which has only one indigenous species of lung fluke, Paragonimus kellicotti. Clinicians should inquire about the consumption of raw or undercooked freshwater crabs by immigrants, expatriates, and returning travelers, and the consumption of raw or undercooked crayfish in U.S. freshwater river systems where P. kellicotti is endemic when evaluating patients presenting with unexplained fever, cough, rales, hemoptysis, pleural effusions, and peripheral eosinophilia. Diagnostic evaluation by specific parasitological, radiological, serological, and molecular methods will be required in order to differentiate paragonimiasis from tuberculosis, which is not uncommon in recent Asian immigrants. All cases of imported and locally acquired paragonimiasis will require treatment with oral praziquantel to avoid any potential pulmonary and cerebral complications of paragonimiasis, some of which may require surgical interventions. © 2013, American Society for Microbiology. All Rights Reserved.
Wang G.,Louisiana State University Health Sciences Center
Immunological Reviews | Year: 2016
Phagocytes, such as neutrophils and macrophages, engulf microbes into phagosomes and launch chemical attacks to kill and degrade them. Such a critical innate immune function necessitates ion participation. Chloride, the most abundant anion in the human body, is an indispensable constituent of the myeloperoxidase (MPO)–H2O2–halide system that produces the potent microbicide hypochlorous acid (HOCl). It also serves as a balancing ion to set membrane potentials, optimize cytosolic and phagosomal pH, and regulate phagosomal enzymatic activities. Deficient supply of this anion to or defective attainment of this anion by phagocytes is linked to innate immune defects. However, how phagocytes acquire chloride from their residing environment especially when they are deployed to epithelium-lined lumens, and how chloride is intracellularly transported to phagosomes remain largely unknown. This review article will provide an overview of chloride protein carriers, potential mechanisms for phagocytic chloride preservation and acquisition, intracellular chloride supply to phagosomes for oxidant production, and methods to measure chloride levels in phagocytes and their phagosomes. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Weiss J.S.,Louisiana State University Health Sciences Center
Cornea | Year: 2015
PURPOSE:: To update the 2008 International Classification of Corneal Dystrophies (IC3D) incorporating new clinical, histopathologic, and genetic information.METHODS:: The IC3D reviewed worldwide peer-reviewed articles for new information on corneal dystrophies published between 2008 and 2014. Using this information, corneal dystrophy templates and anatomic classification were updated. New clinical, histopathologic, and confocal photographs were added.RESULTS:: On the basis of revisiting the cellular origin of corneal dystrophy, a modified anatomic classification is proposed consisting of (1) epithelial and subepithelial dystrophies, (2) epithelial–stromal TGFBI dystrophies, (3) stromal dystrophies, and (4) endothelial dystrophies. Most of the dystrophy templates are updated. The entity “Epithelial recurrent erosion dystrophies” actually includes a number of potentially distinct epithelial dystrophies (Franceschetti corneal dystrophy, Dystrophia Smolandiensis, and Dystrophia Helsinglandica) but must be differentiated from dystrophies such as TGFBI-induced dystrophies, which are also often associated with recurrent epithelial erosions. The chromosome locus of Thiel-Behnke corneal dystrophy is only located on 5q31. The entity previously designated as a variant of Thiel-Behnke corneal dystrophy on chromosome 10q24 may represent a novel corneal dystrophy. Congenital hereditary endothelial dystrophy (CHED, formerly CHED2) is most likely only an autosomal recessive disorder. The so-called autosomal dominant inherited CHED (formerly CHED1) is insufficiently distinct to continue to be considered a unique corneal dystrophy. On review of almost all of the published cases, the description appeared most similar to a type of posterior polymorphous corneal dystrophy linked to the same chromosome 20 locus (PPCD1). Confocal microscopy also has emerged as a helpful tool to reveal in vivo features of several corneal dystrophies that previously required histopathologic examination to definitively diagnose.CONCLUSIONS:: This revision of the IC3D classification includes an updated anatomic classification of corneal dystrophies more accurately classifying TGFBI dystrophies that affect multiple layers rather than are confined to one corneal layer. Typical histopathologic and confocal images have been added to the corneal dystrophy templates. © 2015 by Lippincott Williams & Wilkins.
Pandey U.B.,Louisiana State University Health Sciences Center |
Nichols C.D.,Louisiana State University Health Sciences Center
Pharmacological Reviews | Year: 2011
The common fruit fly, Drosophila melanogaster, is a well studied and highly tractable genetic model organism for understanding molecular mechanisms of human diseases. Many basic biological, physiological, and neurological properties are conserved between mammals and D. melanogaster, and nearly 75% of human disease-causing genes are believed to have a functional homolog in the fly. In the discovery process for therapeutics, traditional approaches employ high-throughput screening for small molecules that is based primarily on in vitro cell culture, enzymatic assays, or receptor binding assays. The majority of positive hits identified through these types of in vitro screens, unfortunately, are found to be ineffective and/or toxic in subsequent validation experiments in whole-animal models. New tools and platforms are needed in the discovery arena to overcome these limitations. The incorporation of D. melanogaster into the therapeutic discovery process holds tremendous promise for an enhanced rate of discovery of higher quality leads. D. melanogaster models of human diseases provide several unique features such as powerful genetics, highly conserved disease pathways, and very low comparative costs. The fly can effectively be used for low- to high-throughput drug screens as well as in target discovery. Here, we review the basic biology of the fly and discuss models of human diseases and opportunities for therapeutic discovery for central nervous system disorders, inflammatory disorders, cardiovascular disease, cancer, and diabetes. We also provide information and resources for those interested in pursuing fly models of human disease, as well as those interested in using D. melanogaster in the drug discovery process. © 2011 by The American Society for Pharmacology and Experimental Therapeutics.
Bir S.C.,Louisiana State University Health Sciences Center
Diabetes | Year: 2014
Nitrite anion has been demonstrated to be a prodrug of nitric oxide (NO) with positive effects on tissue ischemia/reperfusion injury, cytoprotection, and vasodilation. However, effects of nitrite anion therapy for ischemic tissue vascular remodeling during diabetes remain unknown. We examined whether sodium nitrite therapy altered ischemic revascularization in BKS-Lepr(db/db) mice subjected to permanent unilateral femoral artery ligation. Sodium nitrite therapy completely restored ischemic hind limb blood flow compared with nitrate or PBS therapy. Importantly, delayed nitrite therapy 5 days after ischemia restored ischemic limb blood flow in aged diabetic mice. Restoration of blood flow was associated with increases in ischemic tissue angiogenesis activity and cell proliferation. Moreover, nitrite but not nitrate therapy significantly prevented ischemia-mediated tissue necrosis in aged mice. Nitrite therapy significantly increased ischemic tissue vascular endothelial growth factor (VEGF) protein expression that was essential for nitrite-mediated reperfusion of ischemic hind limbs. Nitrite significantly increased ischemic tissue NO bioavailability along with concomitant reduction of superoxide formation. Lastly, nitrite treatment also significantly stimulated hypoxic endothelial cell proliferation and migration in the presence of high glucose in an NO/VEGF-dependent manner. These results demonstrate that nitrite therapy effectively stimulates ischemic tissue vascular remodeling in the setting of metabolic dysfunction that may be clinically useful.
Agency: NSF | Branch: Standard Grant | Program: | Phase: RSCH EXPER FOR UNDERGRAD SITES | Award Amount: 332.68K | Year: 2014
This REU Site award to the Louisiana State University Health Sciences Center in New Orleans, LA will support the training of 10 students for 10 weeks during the summers of 2014-16. Training will focus on research fields including genetics, microbiology, biochemistry, neurosciences, physiology, and pharmacology. Sample projects include: the study of proteins involved in DNA repair, cell cycle, and signal transduction; the regulation of transcription factors through phosphorylation; and the analysis of the platelet-activating factor (PAF) signaling in interneuronal rearrangements. The program will provide students with one-on-one mentoring on hypothesis development, experimental design, research methods, and scientific presentation skills. Students will learn how research is conducted and many will present the results of their work at scientific conferences. Interactive workshops will include topics such as resume writing for graduate school applications, responsible conduct in research, and discussions of career pathways with faculty members from the LSUHSC Basic Sciences Departments and Centers.
Students will be selected for participation based on academic record, research interest, and plans for a career in scientific research. Students attending Historically Black Colleges and Universities and from schools with limited research opportunities are encouraged to apply. The program is targeting undergraduates from diverse social and educational backgrounds, especially from the New Orleans area. REU program alumni will be recruited to volunteer at partnering K-12 New Orleans schools during the academic year where they will explain biology and genetics to science classes and serve as role models to younger generations of potential scientists.
Assessment of the program is by qualitative and quantitative participant surveys, mentor evaluations, and by the BIO/REU common assessment tool. Students are required to be tracked after the program and must respond to an automatic email sent via the NSF reporting system. More information is available by visiting http://www.medschool.lsuhsc.edu/genetics/reu.aspx or by contacting the PI (Dr. Fern Tsien at firstname.lastname@example.org).
Agency: NSF | Branch: Standard Grant | Program: | Phase: ORGANIZATION | Award Amount: 395.00K | Year: 2015
Brain neurons can sense the activity level of neuron networks. If the activity levels are too low or too high, the neurons can adjust the communication level between the neurons. The way that this is accomplished is not completely understood. In previous work, the researcher found one interesting way that involves a protein called protein phosphatase-1 (PP1) that is regulated by another protein called inhibitor-2 (I-2). In this project, the researcher will investigate the role of these two proteins in regulating neuron communications. This work will lay the foundation for future studies in animals to understand how the brain adapts to visual experience or deprivation. Adaptation to environmental light is important for daily life, so these studies will have broad impact on understanding vision in other animals, including humans. The project will provide opportunities for a postdoctoral fellow, undergraduate, and high school students, including underrepresented minorities and women, to be trained in research in this EPSCoR state.
Studies will focus on the function of an abundant enzyme, protein phosphatase-1 (PP1), and its regulator, inhibitor-2 (I-2), in bi-directional synaptic scaling. The study will also determine how I-2 regulates PP1 function in the dephosphorylation of serine 295 (Ser295) on postsynaptic density protein 95 kilo Dalton (PSD95), a molecule critical for synapse architecture and neuronal communication. The impact of I-2 regulation by myosin light chain kinases (MLCK) via I-2 phosphorylation at serine 43 (Ser43) will be determined in the context of both PP1 function on PSD95 dephosphorylation at Ser295 and synaptic scaling. Using primary rat cortical neurons as a model system, the PI will apply bicuculline to enhance neuronal activity or tetrodotoxin (TTX) to decrease neuronal activity. I-2 will be knocked-down (KD) by expression of I-2 short hairpin RNA fragment RNA (ShRNA), and its effect on PSD95 phosphorylation at Ser295 will be examined by western blotting. The effect of I-2 KD on synaptic transmission will be examined by electrophysiological recording. The identity of the MLCK isoform responsible for I-2 phosphorylation at Ser43 will be determined by examining the effect of ShRNAs of various MLCK isoforms on I-2pS43 by western blotting. MLCK isoform effects on bi-directional synaptic scaling will be determined using electrophysiological recordings of neurons expressing the corresponding ShRNA.
Agency: NSF | Branch: Standard Grant | Program: | Phase: I-Corps | Award Amount: 50.00K | Year: 2017
The broader impact/commercial potential of this I-Corps project is to improve diagnostic tests for gastrointestinal disease and to reduce healthcare costs. Digestive diseases constitute a worldwide burden on health care. Moreover, the incidence of inflammatory bowel diseases has increased in children and in adults. Current diagnostic tools, such as biopsy, are not usually available to initiate patient treatment or management; nor is it a favorable method for repeat sampling needed in such chronic conditions. Thus, lack of tools to molecularly identify disease has restricted the ability to manage gastrointestinal inflammation in both pediatric and adult patients. A molecular diagnosis can translate to better care for the patient and financial advantage for payers.
This I-Corps project will examine the potential product-market fit of diagnostic biomarkers for gastrointestinal tract disorders. Accurate, rapid, and inexpensive diagnostics can make personalized management of inflammatory bowel disease accessible. A prototype of a simple and accurate diagnostic medical device for a common and devastating bowel disease in preterm infants has been developed. Customer interviews will provide an in-depth understanding and prioritization of their needs and requirements. They also will trigger an iterative evolution of the team?s business model and product design. Beyond the economic benefit of improved clinical management of patients, technology use in clinical labs, veterinary labs, and pharmaceutical development markets can be evaluated.
Agency: NSF | Branch: Standard Grant | Program: | Phase: Campus Cyberinfrastrc (CC-NIE) | Award Amount: 499.64K | Year: 2017
This CC* Networking Infrastructure project at LSU Health Sciences Center New Orleans (LSUHSC-NO) is constructing a high-speed science network to connect LSUHSC-NOs research areas to facilitate unimpeded movement of large data sets and to provide a pathway to national and global high-performance computing resources. The project enables researchers, scientists, and students to exchange and store large data sets, to expand their opportunities for remote collaboration, and to facilitate leadership in research and education within multiple disciplines of Science at LSUHSC-NO: Anatomy, Biochemistry, Cell Biology, Genetics, Hematology, Immunology, Microbiology, Molecular Biology, Oncology, Ophthalmology, Parasitology, Pathology, Pharmacology, and Physiology. This project has broader implications for the scientific community including the next generation of researchers and scientists. Whether it is a high school student pondering ones future by participating in a summer research program or internship, a budding student enrolled in curricula at LSUHSC-NO, or a collaborative researcher somewhere in cyberspace, this project is key to the future of research at LSUHSC-NO and this project unlocks the door to many exciting discoveries.
This project consists of three objectives: (i) Upgrade the distribution and access layer networking infrastructure to provide 10Gbps and/or 1Gbps ports in the research areas; (ii) Re-architect the campus network to support large data flows by designing and building a Science DMZ; and (iii) Connect to LSUHSC-NOs regional optical exchanges Science DMZ via 20Gbps connections.