997 resultados para Inode-link reverse map
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This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
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This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
Resumo:
This document is the State Map of Iowa, both front and back of the year in the title. All maps were are in pdf format and can be used as a historical reference.
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OBJECTIVE: Chronic activation of the nuclear factor-kappaB (NF-kappaB) in white adipose tissue leads to increased production of pro-inflammatory cytokines, which are involved in the development of insulin resistance. It is presently unknown whether peroxisome proliferator-activated receptor (PPAR) beta/delta activation prevents inflammation in adipocytes. RESEARCH DESIGN AND METHODS AND RESULTS: First, we examined whether the PPARbeta/delta agonist GW501516 prevents lipopolysaccharide (LPS)-induced cytokine production in differentiated 3T3-L1 adipocytes. Treatment with GW501516 blocked LPS-induced IL-6 expression and secretion by adipocytes and the subsequent activation of the signal transducer and activator of transcription 3 (STAT3)-Suppressor of cytokine signaling 3 (SOCS3) pathway. This effect was associated with the capacity of GW501516 to impede LPS-induced NF-kappaB activation. Second, in in vivo studies, white adipose tissue from Zucker diabetic fatty (ZDF) rats, compared with that of lean rats, showed reduced PPARbeta/delta expression and PPAR DNA-binding activity, which was accompanied by enhanced IL-6 expression and NF-kappaB DNA-binding activity. Furthermore, IL-6 expression and NF-kappaB DNA-binding activity was higher in white adipose tissue from PPARbeta/delta-null mice than in wild-type mice. Because mitogen-activated protein kinase-extracellular signal-related kinase (ERK)1/2 (MEK1/2) is involved in LPS-induced NF-kappaB activation in adipocytes, we explored whether PPARbeta/delta prevented NF-kappaB activation by inhibiting this pathway. Interestingly, GW501516 prevented ERK1/2 phosphorylation by LPS. Furthermore, white adipose tissue from animal showing constitutively increased NF-kappaB activity, such as ZDF rats and PPARbeta/delta-null mice, also showed enhanced phospho-ERK1/2 levels. CONCLUSIONS: These findings indicate that activation of PPARbeta/delta inhibits enhanced cytokine production in adipocytes by preventing NF-kappaB activation via ERK1/2, an effect that may help prevent insulin resistance.
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Targeted Small Business News from the Iowa Department of Economic Development, Spring 2011, Volume 4, Number 2
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OBJECTIVE: In vivo differentiation of cardiac myocytes is associated with downregulation of the glucose transporter isoform GLUT1 and upregulation of the isoform GLUT4. Adult rat cardiomyocytes in primary culture undergo spontaneous dedifferentiation, followed by spreading and partial redifferentiation, which can be influenced by growth factors. We used this model to study the signaling mechanisms modifying the expression of GLUT4 in cardiac myocytes. RESULTS: Adult rat cardiomyocytes in primary culture exhibited spontaneous upregulation of GLUT1 and downregulation of GLUT4, suggesting resumption of a fetal program of GLUT gene expression. Treatment with IGF-1 and, to a minor extent, FGF-2 resulted in restored expression of GLUT4 protein and mRNA. Activation of p38 MAPK mediated the increased expression of GLUT4 in response to IGF-1. Transient transfection experiments in neonatal cardiac myocytes confirmed that p38 MAPK could activate the glut4 promoter. Electrophoretic mobility shift assay in adult rat cardiomyocytes and transient transfection experiments in neonatal cardiac myocytes indicated that MEF2 was the main transcription factor transducing the effect of p38 MAPK activation on the glut4 promoter. CONCLUSION: Spontaneous dedifferentiation of adult rat cardiomyocytes in vitro is associated with downregulation of GLUT4, which can be reversed by treatment with IGF-1. The effect of IGF-1 is mediated by the p38 MAPK/MEF2 axis, which is a strong inducer of GLUT4 expression.