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Articles 1 - 5 of 5
Full-Text Articles in Life Sciences
The Effects Of Lipopolysaccharide-Induced Neuroinflammation On Learning And Forgetting In Juvenile Rats, Michele Barry
The Effects Of Lipopolysaccharide-Induced Neuroinflammation On Learning And Forgetting In Juvenile Rats, Michele Barry
Seton Hall University Dissertations and Theses (ETDs)
The inability to remember events experienced very early in life is referred to as Infantile Amnesia (IA) and has been observed in both humans and animals. Over the years interest in the phenomenon waned, but has recently increased with the discovery of new neurobiological methods to study brain function (e.g., Callaghan, Li & Richardson, 2014). The neurobiological mechanism behind IA has yet to be determined, but several innovative theories have been developed with these new research methods. The neurogenesis hypothesis theorizes that increased neurogenesis during early development disrupts previously established memories. The hippocampus, an area that mediates both the memory …
Mechanisms Involved In Enhanced Protection Against Gram Negative Bacterium Francisella Tularensis Utilizing An Fcr Targeted Vaccine Platform, Zulfia Babadjanova
Mechanisms Involved In Enhanced Protection Against Gram Negative Bacterium Francisella Tularensis Utilizing An Fcr Targeted Vaccine Platform, Zulfia Babadjanova
Seton Hall University Dissertations and Theses (ETDs)
Francisella tularensis is a gram-negative intracellular bacterium and the etiologic factor of a potentially fatal disease tularemia. Due to its high infectivity the Centers for Disease Control and Prevention has designated F. tularensis as a Category A biological agent. Nevertheless, the pathogenesis of F. tularensis is not fully understood and research has failed to develop an effective vaccine. Production of pro-inflammatory cytokines by innate immune cells at the early stages of bacterial infection is important for host protection against the pathogen. Many intracellular bacteria, including F. tularensis, utilize the anti-inflammatory cytokine IL-10, to evade the host immune response. It is …
Lps-Induced Production Of Inflammatory Mediators In The Liver Of Postnatal Animals, Valerie P. Le Rouzic
Lps-Induced Production Of Inflammatory Mediators In The Liver Of Postnatal Animals, Valerie P. Le Rouzic
Seton Hall University Dissertations and Theses (ETDs)
Lipopolysaccharide (LPS) is the primary component of the outer membrane of Gram-negative bacteria and is responsible for the majority of inflammatory effects of infections from Gram-negative bacteria. To gain better understanding of the effects that postnatal age has on the inflammatory response, pups were randomly assigned to be treated with 250 µg/kg of LPS or saline at postnatal day (P) 1, P21, and P70. Two hours post stimulation, the pups were sacrificed and their livers were harvested for total RN A extraction. Relative mRNA levels of inflammatory genes and �-actin were determined using RT-PCR analysis with appropriate rat sense and …
Modulation Of Lps-Induced Activation Of Hepatic Map Kinases, Oliver Surriga
Modulation Of Lps-Induced Activation Of Hepatic Map Kinases, Oliver Surriga
Seton Hall University Dissertations and Theses (ETDs)
Lipopolysaccharide (LPS) is a potent inflammagen that has been found to be primarily responsible for many symptoms caused by gram-negative bacterial infections. The LPS-initiated signal transduction pathways involve several terminal kinases, mainly p42/44 mitogen-activated protein kinase (MAPK), p38 MAPK and c-Jun N-terminal kinase (JNK), ultimately leading to increased expression of genes encoding such inflammatory cytokines as interleukin (IL )-1 �. IL-6 and tumor necrosis factors (TNF)-u. In this study, the effects of age on LPS-induced activation of MAPKs in the liver of rats were examined. Results show that the basal level of phosphorylated p42/44 MAPK was increased in postnatal day …
Lipopolysaccharide Induced Septicemia In Chronic Morphine Treated Rats, Frank Ocasio
Lipopolysaccharide Induced Septicemia In Chronic Morphine Treated Rats, Frank Ocasio
Seton Hall University Dissertations and Theses (ETDs)
Opiate-addicts have been known to show increased susceptibility to bacterial infection. Lipopolysaccharide (LPS), which is a cell wall component in gram-negative bacterial, is a potent stimulator of inflammation. We investigated how treatment with morphine alters LPS-induced inflammatory responses in the rat. Chronic morphine exposure alone elevated serum endotoxin levels. Animals treated with morphine and LPS (250 µglkg) developed hypothermia, decreased mean arterial pressure (MAP), increased plasma thrombin anti-thrombin III (TAT) complex, and approximately 67% exhibited progressive intramicrovascular coagulation. Morphine also enhanced LPS induced leukocyte endothelial adhesion (LEA), suppressed leukocyte flux and corticosterone production, and elevated interleukin- I�, tumor necrotic factor-a, …