Jennifer Bonheur - Academia.edu (original) (raw)
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Papers by Jennifer Bonheur
World Journal of Gastroenterology, 2007
To elucidate the preferences of gastroenterologists at our institution and compare them to those ... more To elucidate the preferences of gastroenterologists at our institution and compare them to those of obstetricians when making decisions in the pregnant patient, including which type of bowel preparations to use for fl exible sigmoidoscopy or colonoscopy, as well as which laxatives can be used safely.
Inflammatory Bowel Diseases, 2008
Molecular and Chemical Neuropathology, 1993
As an in vitro model of CNS excitatory amino acid (EAA) injury, rat cortical neuronal cultures we... more As an in vitro model of CNS excitatory amino acid (EAA) injury, rat cortical neuronal cultures were challenged with glutamate (0.5 or 10 mM) and the levels of released lactate dehydrogenase (LDH) were monitored at 1 h, 1, 2, and 7 d. LDH release is correlated with levels of plasma membrane damage. GM1 has been shown to be continuously distributed on the outer surface of CNS cellular membranes. By staining for the distribution of endogenous GM1 ganglioside using cholera toxin/antitoxin immunohistochemistry, we were able to assess morphologically cellular plasma membrane integrity after damage. We used these two measures (LDH and GM1 localization) to study the neuroprotective effects of exogenous GM1 ganglioside to further elucidate its mechanism. Cortical cultures derived from 15-d rat fetuses were subjected to the glutamate challenge for 30 min. Parallel cultures were either pre- or post-treated with 80 microM of GM1. Exposure to 10 mM glutamate caused a highly significant increase in LDH release at 1-48 h. Pretreatment with GM1 reduced the release, whereas posttreatment reduced the LDH release even more. Plasma membrane changes observed by the GM1 immunohistochemistry reflected the LDH release data. All cultures treated with GM1 evidenced substantial structural integrity (continuous staining of GM1 along perikarya and processes) as compared to untreated cultures. These data support our hypothesis that GM1 treatment (pre- and post-) reduces plasma membrane damage.
World Journal of Gastroenterology, 2007
To elucidate the preferences of gastroenterologists at our institution and compare them to those ... more To elucidate the preferences of gastroenterologists at our institution and compare them to those of obstetricians when making decisions in the pregnant patient, including which type of bowel preparations to use for fl exible sigmoidoscopy or colonoscopy, as well as which laxatives can be used safely.
Inflammatory Bowel Diseases, 2008
Molecular and Chemical Neuropathology, 1993
As an in vitro model of CNS excitatory amino acid (EAA) injury, rat cortical neuronal cultures we... more As an in vitro model of CNS excitatory amino acid (EAA) injury, rat cortical neuronal cultures were challenged with glutamate (0.5 or 10 mM) and the levels of released lactate dehydrogenase (LDH) were monitored at 1 h, 1, 2, and 7 d. LDH release is correlated with levels of plasma membrane damage. GM1 has been shown to be continuously distributed on the outer surface of CNS cellular membranes. By staining for the distribution of endogenous GM1 ganglioside using cholera toxin/antitoxin immunohistochemistry, we were able to assess morphologically cellular plasma membrane integrity after damage. We used these two measures (LDH and GM1 localization) to study the neuroprotective effects of exogenous GM1 ganglioside to further elucidate its mechanism. Cortical cultures derived from 15-d rat fetuses were subjected to the glutamate challenge for 30 min. Parallel cultures were either pre- or post-treated with 80 microM of GM1. Exposure to 10 mM glutamate caused a highly significant increase in LDH release at 1-48 h. Pretreatment with GM1 reduced the release, whereas posttreatment reduced the LDH release even more. Plasma membrane changes observed by the GM1 immunohistochemistry reflected the LDH release data. All cultures treated with GM1 evidenced substantial structural integrity (continuous staining of GM1 along perikarya and processes) as compared to untreated cultures. These data support our hypothesis that GM1 treatment (pre- and post-) reduces plasma membrane damage.