Jpen Parenter Enter
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Jpen Parenter Enter · Sep 2006
Glutamine attenuation of cell death and inducible nitric oxide synthase expression following inflammatory cytokine-induced injury is dependent on heat shock factor-1 expression.
Glutamine (GLN) has been shown to improve outcome after experimental and clinical models of critical illness. Enhanced expression of heat shock protein (HSP) has been hypothesized to be responsible for this protection. The heat shock response has been shown to inhibit inducible nitric oxide synthase (iNOS) gene expression and nitric oxide (NO) production. This study tested the hypothesis that GLN-mediated activation of the HSP pathway is responsible for improved survival and attenuation of iNOS expression after an inflammatory cytokine-induced injury. ⋯ This is the first demonstration that GLN-mediated cellular protection after inflammatory cytokine injury is due to HSF-1 expression and cellular capacity to activate an HSP response.
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Jpen Parenter Enter · Sep 2006
Glutamine-mediated attenuation of cellular metabolic dysfunction and cell death after injury is dependent on heat shock factor-1 expression.
Cellular metabolic dysfunction is associated with occurrence of multiple-organ failure after critical illness. Glutamine (GLN) attenuates cellular metabolic dysfunction in critical illness models. The mechanism of this protection is unclear. We previously demonstrated that GLN's benefit in critical illness might be due to enhanced heat shock protein (HSP) expression. We hypothesize that GLN's attenuation of cellular metabolic dysfunction is dependent on presence of heat shock factor-1 (HSF-1). ⋯ GLN treatment attenuated cellular metabolic dysfunction and improved cell membrane recovery only in HSF-1+/+ cells. Cellular injury, as measured by lactate release and cell survival assay, was improved by GLN treatment in HSF-1+/+ cells alone. Thus, GLN's beneficial effect on cellular metabolic dysfunction and cell survival appears to be dependent on HSF-1 expression.
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Jpen Parenter Enter · Sep 2006
Interleukin-7 dose-dependently restores parenteral nutrition-induced gut-associated lymphoid tissue cell loss but does not improve intestinal immunoglobulin a levels.
Without enteral nutrition, the mass and function of gut-associated lymphoid tissue (GALT), a center of systemic mucosal immunity, are reduced. Therefore, new therapeutic methods, designed to preserve mucosal immunity during parenteral nutrition (PN), are needed. Our recent study revealed that exogenous interleukin-7 (IL-7; 1 microg/kg twice a day) restores the GALT cell mass lost during intravenous (IV) PN but does not improve secretory immunoglobulin A (IgA) levels. Herein, we studied the IL-7 dose response to determine the optimal IL-7 dose for recovery of GALT mass and function during IV PN. We hypothesized that a high dose of IL-7 would increase intestinal IgA levels, as well as GALT cell numbers. ⋯ Exogenous IL-7 dose-dependently reverses PN-induced GALT cell loss, with no major changes in small intestinal IgA levels. IL-7 treatment during PN appears to have beneficial effects on gut immunity, but other therapeutic methods are needed to restore secretory IgA levels.
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Jpen Parenter Enter · Jul 2006
The incidence and impact of dextrose dose on hyperglycemia from parenteral nutrition (PN) exposure in hematopoietic stem cell transplant (HSCT) recipients.
Short-term, transient hyperglycemia is associated with adverse outcomes in acutely ill populations. Because parenteral nutrition (PN) is dextrose based, we hypothesized that exposure to PN would be associated with hyperglycemia and that greater levels of dextrose infusion would be associated with higher glucose concentrations. Our objective was to examine the temporality, incidence, and dose response from dextrose load upon hyperglycemia using several serum glucose cut points in PN vs non-PN HSCT recipients. ⋯ The broad use of PN at levels within current clinical guidelines in HSCT adults was associated with profound hyperglycemia; however, greater dextrose dose, within the narrow levels administered in this cohort, was not associated with higher glucose concentrations.
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Jpen Parenter Enter · Jul 2006
Olive oil-based lipid emulsion's neutral effects on neutrophil functions and leukocyte-endothelial cell interactions.
Infection remains a drawback of parenteral nutrition (PN), probably related, among other factors, to immunosuppressive effects of its lipid component. Newer preparations may have lesser immunosuppressive impact. This study examines the effects of an olive oil-based lipid emulsion (long-chain triacylglycerols-monounsaturated fatty acids [LCT-MUFA]; ClinOleic) on various functions of human neutrophils in vitro and on rat leukocyte-endothelial cell interactions in vivo compared with LCT (Intralipid) and 50% LCT-50% medium-chain triacylglycerols (MCT; Lipofundin) mixture. ⋯ LCT-MUFA showed lower in vitro and in vivo impact on neutrophil function compared with LCT and LCT-MCT.