LeMoyne–Owen College is a fully accredited, four-year private historically black college located in Memphis, Tennessee, affiliated with the United Church of Christ. It resulted from the 1968 merger of historically black colleges and other schools established by northern Protestant missions during and after the American Civil War to educate freedmen. Wikipedia.
Tremper-Wells B.,Cornell University |
Tremper-Wells B.,LeMoyne-Owen College |
Resnick R.J.,Cornell University |
Zheng X.,Cornell University |
And 2 more authors.
Genes to Cells | Year: 2010
Two isoforms of the transmembrane protein tyrosine phosphatase PTPα, which differ by nine amino acids in their extracellular regions, are expressed in a tissue-specific manner. Over-expression of the shorter isoform transforms rodent cells, and it has previously been reasonable to assume that this was a direct consequence of its dephosphorylation and activation of Src. Transformation by the longer wild-type isoform has not previously been studied. We tested the activities of both isoforms in NIH3T3 cells and found that, while both dephosphorylated and activated Src similarly, only the shorter isoform induced focus formation or anchorage-independent growth. Differences in phosphorylation of PTPα at its known regulatory sites, Grb2 binding to PTPα, phosphorylation level of focal adhesion kinase by PTPα, or overall localization were excluded as possible explanations for the differences in transforming activities. The results suggest that transformation by PTPα involves at least one function other than, or in addition to, its activation of Src and that this depends on PTPα's extracellular domain. Previous studies have suggested that PTPα might be a useful target in breast and colon cancer therapy, and the results presented here suggest that it may be advantageous to develop isoform-specific therapeutic reagents. © 2010 The Authors. Journal compilation © 2010 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd.
Khan N.R.,University of Tennessee Health Science Center |
Thompson C.J.,George Washington University |
Decuypere M.,University of Tennessee Health Science Center |
Angotti J.M.,University of Tennessee Health Science Center |
And 6 more authors.
Journal of Neurosurgery: Spine | Year: 2014
Object: Surgical site infection (SSI) is a serious and costly complication of spinal surgery. There have been several conflicting reports on the use of intrawound vancomycin powder in decreasing SSI in spine surgery. The purpose of this study is to answer the question: "Does intrawound vancomycin powder reduce the rate of SSIs in spine surgery?" Methods: A comprehensive search of multiple electronic databases and bibliographies was conducted to identify clinical studies that evaluated the rates of SSI with and without the use of intrawound vancomycin powder in spine surgery. Independent reviewers extracted data and graded the quality of each paper that met inclusion criteria. A random effects meta-analysis was then performed. Results: The search identified 9 retrospective cohort studies (Level III evidence) and 1 randomized controlled trial (Level II evidence). There were 2574 cases and 106 infections in the control group (4.1%) and 2518 cases and 33 infections (1.3%) in the treatment group, yielding a pooled absolute risk reduction and relative risk reduction of 2.8% and 68%, respectively. The meta-analysis revealed the use of vancomycin powder to be protective in preventing SSI (relative risk = 0.34, 95% confidence interval 0.17-0.66, p = 0.021). The number needed to treat to prevent 1 SSI was 36. A subgroup analysis found that patients who had implants had a reduced risk of SSI with vancomycin powder (p = 0.023), compared with those who had noninstrumented spinal operations (p = 0.226). Conclusions: This meta-analysis suggests that the use of vancomycin powder may be protective against SSI in open spinal surgery; however, the exact population in which it should be used is not clear. This benefit may be most appreciated in higher-risk populations or in facilities with a high baseline rate of infection. © AANS, 2014.
PubMed | University of Calgary, The Claremont Colleges, Valdosta State University, Northern Arizona University and LeMoyne-Owen College
Type: | Journal: The Journal of experimental biology | Year: 2016
Titin has long been known to contribute to muscle passive tension. Recently, it was also demonstrated that titin-based stiffness increases upon Ca
Zimmer J.C.,LeMoyne-Owen College |
Arsal R.E.,Clemson University |
Al-Marzouq M.,Kuwait University |
Grover V.,Clemson University
Information and Management | Year: 2010
Organizations rely on customer information to design new products and offer new services. However, people should not share their personal information online. We produced and tested a model of information disclosure. While prior work focused on the effects of trust and its relationship to risk in determining intent to disclose information, we assumed that information relevance was a critical antecedent to disclosure and that both relevance and trust could alleviate perceptions of risk associated with disclosure, thereby increasing peoples' intentions to disclose information. We tested our model using 264 subjects in an experimental setting. The results showed the importance of relevance on intentions to disclose information - allowing us to draw implications for practice about voluntary information disclosure in online settings. © 2009 Elsevier B.V. All rights reserved.
Talukder J.R.,LeMoyne-Owen College |
Boyd B.,LeMoyne-Owen College |
Griffin A.,LeMoyne-Owen College |
Jaima A.,LeMoyne-Owen College |
Rajendran V.M.,West Virginia University
Canadian Journal of Physiology and Pharmacology | Year: 2013
Glutamine (Gln), a preferred fuel source for enterocytes, is critical for intestinal epithelial cell integrity and barrier function. Chronic enteritis inhibits apical Na+-Gln cotransport. It is not known whether inflammatory cytokines that are secreted during inflammation inhibit Na+-Gln cotransport. Thus, this study aimed to examine whether TNF-α would affect apical Na+-Gln cotransport in intestinal epithelial cells. In this study, the presence of Na+-Gln cotransport was established by measuring Gln uptake in 10 days postconfluent IEC-6 cells grown on transwell plates. Cation, amino acid specificity, and siRNA transfection studies established that Na+-Gln cotransport is mediated via B0AT1. Immunoblotting and immunofluorescence studies established the apical membrane localization of B0AT1 in IEC-6 cells. Tumour necrosis factor _ (TNF-α) inhibited Na+-Gln cotransport in a concentration- and time-dependent manner with an inhibitory concentration of 1.53 nmol·L-1. Quantitative real-time PCR and Western blot analyses indicated that TNF-α did not alter B0AT1-specific transcripts or protein expression level. Kinetic studies revealed that TNF-α inhibited Na+-Gln cotransport by reducing the affinity of the cotransporters for Gln, and this effect was antagonized by genistein. Thus, we conclude that the TNF-α inhibition of Na+-Gln cotransport occurs at the posttranslational level, and that the IEC-6 cell line is an excellent system to study the role of cytokines in Na+-Gln cotransport.
Mendonca D.,Rensselaer Polytechnic Institute |
Brooks J.D.,Rensselaer Polytechnic Institute |
Grabowski M.,Rensselaer Polytechnic Institute |
Grabowski M.,LeMoyne-Owen College
IEEE Transactions on Human-Machine Systems | Year: 2014
This paper considers how changes in team composition (such as the number and rate of turnover of team members) are linked to team performance, as assessed in terms of efficiency, effectiveness, and equality (i.e., distribution of effort). Study data are taken from a large-scale, postdisaster debris removal operation in the USA, collected through existing transaction-level data logging systems. The data enable a detailed (and objective) examination of team performance, thus overcoming many shortcomings of retrospective methods such as questionnaires. The results show that the increased turnover diminishes performance along all dimensions, while an increased team size contributes to effectiveness but reduces equality. Implications of this study for theory and future empirical work are both discussed. © 2013 IEEE.
Athenikos S.J.,Drexel University |
Han H.,LeMoyne-Owen College
Computer Methods and Programs in Biomedicine | Year: 2010
Objectives: In this survey, we reviewed the current state of the art in biomedical QA (Question Answering), within a broader framework of semantic knowledge-based QA approaches, and projected directions for the future research development in this critical area of intersection between Artificial Intelligence, Information Retrieval, and Biomedical Informatics. Materials and methods: We devised a conceptual framework within which to categorize current QA approaches. In particular, we used " semantic knowledge-based QA" as a category under which to subsume QA techniques and approaches, both corpus-based and knowledge base (KB)-based, that utilize semantic knowledge-informed techniques in the QA process, and we further classified those approaches into three subcategories: (1) semantics-based, (2) inference-based, and (3) logic-based. Based on the framework, we first conducted a survey of open-domain or non-biomedical-domain QA approaches that belong to each of the three subcategories. We then conducted an in-depth review of biomedical QA, by first noting the characteristics of, and resources available for, biomedical QA and then reviewing medical QA approaches and biological QA approaches, in turn. The research articles reviewed in this paper were found and selected through online searches. Results: Our review suggested the following tasks ahead for the future research development in this area: (1) Construction of domain-specific typology and taxonomy of questions (biological QA), (2) Development of more sophisticated techniques for natural language (NL) question analysis and classification, (3) Development of effective methods for answer generation from potentially conflicting evidences, (4) More extensive and integrated utilization of semantic knowledge throughout the QA process, and (5) Incorporation of logic and reasoning mechanisms for answer inference. Conclusion: Corresponding to the growth of biomedical information, there is a growing need for QA systems that can help users better utilize the ever-accumulating information. Continued research toward development of more sophisticated techniques for processing NL text, for utilizing semantic knowledge, and for incorporating logic and reasoning mechanisms, will lead to more useful QA systems. © 2009 Elsevier Ireland Ltd.
Singh S.,Marshall University |
Arthur S.,Marshall University |
Talukder J.,LeMoyne-Owen College |
Palaniappan B.,Marshall University |
And 2 more authors.
BMC Gastroenterology | Year: 2015
Background: In the chronically inflamed rabbit small intestine, brush border membrane (BBM) Na-glutamine co-transport is inhibited in villus cells (mediated by B0AT1), while it is stimulated in crypt cells (mediated by SN2/SNAT5). How mast cells, known to be enhanced in the chronically inflamed intestine, may regulate B0AT1 in villus and SN2/SNAT5 in crypt cell is unknown. Thus, the aim of the present study is to determine the regulation of B0AT1 and SN2/SNAT5 by mast cells during chronic enteritis. Methods: Chronic intestinal inflammation was induced in male rabbits with intra-gastric inoculation of Eimeria magna oocytes. Rabbits with chronic inflammation were treated with ketotifen (10mg/day) or saline (Placebo) for 2days. Villus and crypts cells were isolated from the rabbit intestine using the Ca++ chelation technique. Na/K-ATPase activity was measured as Pi from cellular homogenate. BBM vesicles (BBMV) were prepared from villus and crypt cells and uptake studies were performed using rapid filtration technique with 3H-Glutamine. Western blot analyses were done using B0AT1 and SN2 specific antibodies. Results: In villus cells, Na-glutamine co-transport inhibition observed during inflammation was completely reversed by ketotifen, a mast cell stabilizer. In contrast, in crypt cells, Na-glutamine co-transport stimulation was reversed to normal levels by ketotifen. Kinetic studies demonstrated that ketotifen reversed the inhibition of B0AT1 in villus cells by restoring co-transporter numbers in the BBM, whereas the stimulation of SN2/SNAT5 in crypts cells was reversed secondary to restoration of affinity of the co-transporter. Western blot analysis showed that ketotifen restored immune-reactive levels of B0AT1 in villus cells, while SN2/SNAT5 levels from crypts cell remained unchanged. Conclusion: In the present study we demonstrate that mast cells likely function as a common upstream immune pathway regulator of the Na-dependent glutamine co-transporters, B0AT1 in villus cells and SN2 in crypts cells that are uniquely altered in the chronically inflamed small intestine. © Singh et al.; licensee BioMed Central.
PubMed | LeMoyne-Owen College
Type: Journal Article | Journal: Canadian journal of physiology and pharmacology | Year: 2014
Various immunoinflammatory cytokines are produced during chronic intestinal inflammation, which inhibits Na(+)-glucose cotransport (SGLT1) in villus cells. Lactoferrin (Lf), abundantly present in colostrum, is a multifunctional glycoprotein that is absorbed by receptor-mediated transcytosis in humans and animals and has been shown to exert anti-inflammatory effects. Therefore, this study aimed to examine whether Lf would prevent PGE2 effect on SGLT1 for glucose absorption in enterocytes. Intestinal epithelial cells (IEC-6) were grown on transwell plates, treated with phlorizin, PGE2, AH6809, and Lf, and 3-O-methyl d-glucopyranose (OMG) uptake was measured in 10 days postconfluent. Na(+)-dependent OMG uptake, phlorizin, and immunoblotting studies established the activity and apical membrane localization of SGLT1 in IEC-6 cells. PGE2 inhibited SGLT1 in a concentration- and time-dependent manner with an inhibitory constant (Ki) of 50.0 nmol/L and that was antagonized by prostanoid receptor inhibitor, AH6809. PGE2 did not alter Na(+)/K(+)-ATPase activity. In contrast, quantitative real-time polymerase chain reaction and Western blot analyses revealed that SGLT1-specific transcripts and protein expression level were decreased 3-fold by PGE2. Furthermore, PGE2 treatment increased intracellular cyclic adenosine monophosphate (cAMP) and Ca(2+) concentrations and decreased SGLT1 expression on the apical membrane, and these effects were ameliorated by Lf. Therefore, we conclude that Lf ameliorates the PGE2 inhibition of SGLT1 most likely via the Ca(2+)- and cAMP-signaling pathways.
PubMed | Boston University, Marshall University and LeMoyne-Owen College
Type: | Journal: BMC gastroenterology | Year: 2015
In the chronically inflamed rabbit small intestine, brush border membrane (BBM) Na-glutamine co-transport is inhibited in villus cells (mediated by B0AT1), while it is stimulated in crypt cells (mediated by SN2/SNAT5). How mast cells, known to be enhanced in the chronically inflamed intestine, may regulate B0AT1 in villus and SN2/SNAT5 in crypt cell is unknown. Thus, the aim of the present study is to determine the regulation of B0AT1 and SN2/SNAT5 by mast cells during chronic enteritis.Chronic intestinal inflammation was induced in male rabbits with intra-gastric inoculation of Eimeria magna oocytes. Rabbits with chronic inflammation were treated with ketotifen (10 mg/day) or saline (Placebo) for 2 days. Villus and crypts cells were isolated from the rabbit intestine using the Ca++ chelation technique. Na/K-ATPase activity was measured as Pi from cellular homogenate. BBM vesicles (BBMV) were prepared from villus and crypt cells and uptake studies were performed using rapid filtration technique with (3)H-Glutamine. Western blot analyses were done using B0AT1 and SN2 specific antibodies.In villus cells, Na-glutamine co-transport inhibition observed during inflammation was completely reversed by ketotifen, a mast cell stabilizer. In contrast, in crypt cells, Na-glutamine co-transport stimulation was reversed to normal levels by ketotifen. Kinetic studies demonstrated that ketotifen reversed the inhibition of B0AT1 in villus cells by restoring co-transporter numbers in the BBM, whereas the stimulation of SN2/SNAT5 in crypts cells was reversed secondary to restoration of affinity of the co-transporter. Western blot analysis showed that ketotifen restored immune-reactive levels of B0AT1 in villus cells, while SN2/SNAT5 levels from crypts cell remained unchanged.In the present study we demonstrate that mast cells likely function as a common upstream immune pathway regulator of the Na-dependent glutamine co-transporters, B0AT1 in villus cells and SN2 in crypts cells that are uniquely altered in the chronically inflamed small intestine.