Deoxidizing slag in making low-carbon steel in 100-ton arc furnaces

Kostromin, I. Ya.; Lavrov, A. S.; Lyalin, E. S.; Sitnikov, A. T.; Shapovalov, A. P.

doi:10.1007/bf00737950

Cited by 1 publication

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“…Reports of age-related changes in cAMP levels in human tissue are sparse and those in rodent brain are somewhat conflicting, but some general trends emerge (Figure 2B). In humans and rodents, basal cAMP levels were decreased in aged vs. young adult white blood cells [29–32]). cAMP levels were also reduced in serum from aged vs. young adult rodents, [33], but remained unchanged in aged human cerebral microvessels [34,35].…”

Section: Alterations In Cyclic Nucleotide Signaling Associated Witmentioning

confidence: 99%

Cyclic nucleotide signaling changes associated with normal aging and age-related diseases of the brain

Kelly

2018

Cellular Signalling

127

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Deficits in brain function that are associated with aging and age-related diseases benefit very little from currently available therapies, suggesting a better understanding of the underlying molecular mechanisms is needed to develop improved drugs. Here, we review the literature to test the hypothesis that a break down in cyclic nucleotide signaling at the level of synthesis, execution, and/or degradation may contribute to these deficits. A number of findings have been reported in both the human and animal model literature that point to brain region-specific changes in Galphas (a.k.a. Gαs or Gsα), adenylyl cyclase, 3',5'-adenosine monophosphate (cAMP) levels, protein kinase A (PKA), cAMP response element binding protein (CREB), exchange protein activated by cAMP (Epac), hyperpolarization-activated cyclic nucleotide-gated ion channels (HCNs), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), soluble and particulate guanylyl cyclase, 3',5'-guanosine monophosphate (cGMP), protein kinase G (PKG) and phosphodiesterases (PDEs). Among the most reproducible findings are 1) elevated circulating ANP and BNP levels being associated with cognitive dysfunction or dementia independent of cardiovascular effects, 2) reduced basal and/or NMDA-stimulated cGMP levels in brain with aging or Alzheimer's disease (AD), 3) reduced adenylyl cyclase activity in hippocampus and specific cortical regions with aging or AD, 4) reduced expression/activity of PKA in temporal cortex and hippocampus with AD, 5) reduced phosphorylation of CREB in hippocampus with aging or AD, 6) reduced expression/activity of the PDE4 family in brain with aging, 7) reduced expression of PDE10A in the striatum with Huntington's disease (HD) or Parkinson's disease, and 8) beneficial effects of select PDE inhibitors, particularly PDE10 inhibitors in HD models and PDE4 and PDE5 inhibitors in aging and AD models. Although these findings generally point to a reduction in cyclic nucleotide signaling being associated with aging and age-related diseases, there are exceptions. In particular, there is evidence for increased cAMP signaling specifically in aged prefrontal cortex, AD cerebral vessels, and PD hippocampus. Thus, if cyclic nucleotide signaling is going to be targeted effectively for therapeutic gain, it will have to be manipulated in a brain region-specific manner.

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