INT7127
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The increase in sPLA2-IIA expression in AD hippocampus, but not in AD cerebellum, is in agreement with the neuropathological observations that reactive astrocytes are increasingly associated with pathology in hippocampus and cortex, whereas diffuse amyloid deposits and limited astrocyte activation are found in cerebellum [3,42]. | |||||||||||||||
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Increased plasma levels of sPLA2-IIA predicted recurrent coronary events, mainly revascularization procedures, independently of other established risk factors (Kugiyama et al 2000). | |||||||||||||||
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Moreover, HDL- and ApoA-I-catabolism as well as HDL-cholesteryl ester tissue uptake were significantly enhanced under conditions of sPLA2-IIA overexpression even in the absence of inflammatory preconditions (Tietge et al 2000). | |||||||||||||||
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This stimulation resulted in enhanced sPLA2-IIA protein expression and sPLA2-IIA activity. | |||||||||||||||
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This stimulation resulted in enhanced sPLA2-IIA protein expression and sPLA2-IIA activity. | |||||||||||||||
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The cDNA encoding the human PLA2 was subcloned into an expression vector and subsequently transfected into Chinese hamster ovary (CHO) cells. | |||||||||||||||
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RT-PCR indicated very low sPLA2-IIA mRNA expression in control and IFN? | |||||||||||||||
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Using a new approach with SBTI as an internal standard, we showed that part of the major tear protein components increased in tears of AC patients and further demonstrated that the sPLA2-IIa expression is increased in the AC patients. | |||||||||||||||
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Our finding of increased sPLA2-IIa expression in SAC and PAC patients is in agreement with the study by Chen et al., which demonstrated that sPLA2-IIa is an inflammatory mediator when the ocular surface is compromised [21]. | |||||||||||||||
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This stimulation resulted in enhanced sPLA2-IIA protein expression and sPLA2-IIA activity. | |||||||||||||||
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This stimulation resulted in enhanced sPLA2-IIA protein expression and sPLA2-IIA activity. | |||||||||||||||
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In this report, we provide data demonstrating up-regulation of sPLA2-IIA mRNA and protein expression in reactive astrocytes in AD brains as compared to age-matched non-demented (ND) control brains. | |||||||||||||||
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However, studies with rat models of brain injury have demonstrated an increase in sPLA2-IIA expression associated with different forms of neuronal insults, including cerebral ischemia [34,35] as well as other types of neuronal injuries [36,37]. | |||||||||||||||
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This study demonstrates for the first time an increase in protein expression of sPLA2-IIA in GFAP-positive astrocytes in AD brains as compared to ND brains. | |||||||||||||||
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Moreover, increased plasma levels of sPLA2 in stable patients undergoing percutaneous coronary angioplasty (PCI) also provide independent prognostic information over other classic cardiovascular risk factors and clinical covariables (Liu et al 2003). | |||||||||||||||
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However, the contribution of PLA2G2A to sporadic CRC predisposition cannot be excluded, and it has been suggested that the increase in PLA2G2A expression could cause the accumulation of arachidonic acid, a molecule likely to have pro-apoptotic properties [41]. | |||||||||||||||
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A hypothesis for the protective role of variant c.435+230T might therefore be its enhancement of PLA2G2A expression. | |||||||||||||||
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