Scientific Writing Join this club
Director: Sunita Seemanapalli (sseema1@lsu.edu)
Focus: Writing skills related to Research Papers and Grantmanship
Description: The goal of this Journal club is to develop our skills in writing research papers and grants.
Schedules:
2009-06-04 09:00:00 UTC: Influenza virus-details - organized by Sunita Seemanapalli
Influenza virus details
Disgussion
Summary: Influenza virus.
Influenza virus DisgussionSummary: Summary by Anu and Sona
Influenza virus-Summary DisgussionSummary: Summary by Anu and Sona
2009-05-25 19:47:00 UTC: Swine flu 2009 - organized by Piyanate Sunyakumthorn
2009-05-25 01:41:00 UTC: Swine flu-assingment - organized by Sunita Seemanapalli
Swine influenza
Disgussion
Summary: Swine Influenza
2009-04-24 09:00:00 UTC: Scientific Writing-Booklet - organized by Sunita Seemanapalli
Scientific Writing -Booklet
Disgussion
Summary: Scientific Writing -Booklet Compiled by Marc E. Tischler, Ph.D. Dept of Biochemistry and Biophysics-Univ. of Arizona Table of Contents: General Guidelines Using an Outline to prepare your paper Word Usage in Scientific Writing Gramar Active versus Passive Voice in Writing Writing the Introduction Writing the Methods Writing the Results and Discussion Preparing the Reference Section Answers to Active-Passive Exercise Sources for Further Information
2009-03-28 09:00:00 UTC: Activation of TLR-9 Induces IL-8 Secretion through - organized by Gayathriy Balamayooran
paper with shorter introduction
Disgussion
Summary: Bacterial DNA containing unmethylated CpG motifs is emerging as an important regulator of functions of human neutrophil granulocytes (polymorphonuclear leukocytes (PMN)). These motifs are recognized by TLR-9. Recent studies indicate that peroxynitrite (ONOO) may function as an intracellular signal for the production of IL-8, one of the key regulators of leukocyte trafficking in inflammation. In this study we investigated whether bacterial DNA (CpG-DNA) could induce ONOO signaling in human PMN. Human whole blood, isolated PMN (purity, >95%), and high purity (>99%) PMN respond to CpG-DNA, but not to calf thymus DNA, with secretion of IL-8 and, to a lesser extent, IL-6 and TNF. Methylation of cytosines in CpG-DNA resulted in a complete loss of activity. The endosomal acidification inhibitors, bafilomycin A and chloroquine, inhibited CpG-DNA-induced cytokine release from PMN. CpG-DNA-induced IL-8 mRNA expression and release was also blocked by the NO synthase inhibitor N-nitro-L-arginine methyl ester. CpG-DNA evoked concomitant increases in intracellular superoxide and NO levels, leading to enhanced ONOO formation and, consequently, nuclear accumulation of c-Fos and NF-B. Pharmacological inhibition of NF-B activation attenuated 75% of CpG-DNA-evoked IL-8 release. These results identify ONOO-dependent activation of NF-B and c-Fos as an important mechanism that mediates PMN responses, including IL-8 gene expression and release, to bacterial DNA and unmethylated CpG motifs in particular. Enhanced ONOO formation represents a mechanism by which bacterial DNA may contribute to prolongation and amplification of the inflammatory response.
2009-03-06 09:00:00 UTC: Summary of comments on a Research Article - organized by Sunita Seemanapalli
Non-Opsonic Phagocytosis of Legionella pneumophila by Macrophages is mediated by Phosphatidylinositol 3-kinase
Disgussion
Summary: Non-Opsonic Phagocytosis of Legionella pneumophila by Macrophages Is Mediated by Phosphatidylinositol 3-Kinase Souvenir D. Tachado¤a, Mustapha M. Samrakandi¤b, Jeffrey D. Cirillo* Department of Microbial and Molecular Pathogenesis, Texas A&M Health Science Center, College Station, Texas, United States of America. 2008 PLoS ONE 3(10): e3324.doi:10.1371/journal.pone.0003324 Background: Legionella pneumophila, is an intracellular pathogen that causes Legionnaires’ disease in humans, a potentially lethal pneumonia. L. pneumophila has the ability to enter and replicate in the host and is essential for pathogenesis. Methodology/Principal Findings: Phagocytosis was measured by cell invasion assays. Construction of PI3K mutant by PCR cloning and expression of dominant negative mutant was detected byWestern blot. PI3K activity was measured by 32P labeling and detection of phospholipids products by thin layer chromatography. Infection of macrophages with virulent L. pneumophila stimulated the formation of phosphatidylinositol 3-phosphate (PIP3), a phosphorylated lipid product of PI3K whereas two structurally distinct phosphatidylinositol 3 kinase (PI3K) inhibitors, wortmannin and LY294002, reduced L. pneumophila entry into macrophages in a dose-dependent fashion. Furthermore, PI3K activation led to Akt stimulation, a serine/threonine kinase, which was also inhibited by wortmannin and LY294002. In contrast, PI3K and protein kinase B (PKB/Akt) activities were lower in macrophages infected with an avirulent bacterial strain. Only virulent L. pneumophila increased lipid kinase activity present in immunoprecipitates of the p85a subunit of class I PI3K and tyrosine phosphorylated proteins. In addition, macrophages expressing a specific dominant negative mutant of PI3K reduced L. pneumophila entry into these cells. Conclusion/Significance: Entry of L. pneumophila is mediated by PI3K/Akt signaling pathway. These results suggest an important role for PI3K and Akt in the L. pneumophila infection process. They point to possible novel strategies for undermining L. pneumophila host uptake and reducing pathogenesis of Legionnaires’ disease.
PI3K/Ark pathway DisgussionSummary: The PI3K/Akt signal transduction cascade has been investigated extensively for its roles in oncogenic transformation. Initial studies implicated both PI3K and Akt in prevention of apoptosis. However, more recent evidence has also associated this pathway with regulation of cell cycle progression. Uncovering the signaling network spanning from extracellular environment to the nucleus should illuminate biochemical events contributing to malignant transformation.
Club members: Send an invitation
Sunita Seemanapalli : sseema1@lsu.edu
Qilong Xu : qxu@vetmed.lsu.edu
Yihe Ge : geyihe@lsu.edu
Kohila Mahadevan : kmahad1@tigers.lsu.edu
balamayooran theivanthiran : mayoorant@yahoo.com
Gayathriy Balamayooran : gmahad1@tigers.lsu.edu.com
david marthiue : shawn.shliu@gmail.com
Piyanate Sunyakumthorn : psunyaku@tigers.lsu.edu
Moara Martins : mmartins@vetmed.lsu.edu
poonam dadhwal : pdadhw1@tigers.lsu.edu
Rahul Sharma : rsharm4@lsu.edu
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