In a previous report, we have shown that fructose-mediated apoA-I modification results in severe loss of several beneficial functions of apoA-I and HDL, producing pro-atherogenic and proaging molecules (Park et al., 2010a).
Sample text:```Previous studies revealed that acylcarnitines were elevated early after APAP treatment and that their elevation was indicative of mitochondrial damage and dysfunction.(15,19) In the present study these observations were confirmed, as palmitoylcarnitine was elevated by toxic doses of APAP and maintained at normal levels (compared with untreated controls) by Wy-14,643 pretreatment.```
Sample intent: result
Sample text:```Intriguingly, using MPRs-deficient MEF cells, mouse and human CLN5 have been shown to reach lysosomes in an MPRindependent manner [12].```
Sample intent: background



Sample text:```Our results on working memory performance are similar to those of earlier studies (e.g. Archbold et al., 2009; Cosentino et al., 2008; Naegele et al., 2006) in showing impaired working memory in the OSA group.```
Sample intent: result



Sample text:```Induction of C1qa in the CNS promotes synapse elimination and synaptic dysfunction during development, neurodegenerative diseases such as glaucoma and AD, and aging [29,30,31,32,74].```
Sample intent: method



Sample text:```The inter-relationships between K1, K1O and anticoagulants in dogs and humans have been previously investigated [25, 26].```
Sample intent: background



Sample text:```Other studies suggest that altering affinity to FcRn might alter the bioavailability of mAbs (Deng et al., 2010; Deng et al., 2012), and SC bioavailability appears lower in FcRn-deficient mice as compared to wild type animals (Wang et al., 2008).```
Sample intent: method
Sample text:```Unlabeled DNA substrates containing consensus 12-RSS, 23-RSS, Hox11 or non-specific DNA sequences (DAR81/82) were prepared from oligonucleotides described previously [11,24].```
Sample intent: background



Sample text:```Our results confi rm previous studies that reached the same conclusion (Boushey et al 1994; Vermeulen et al 2000; Till et al 2005; Marcucci et al 2005).```
Sample intent: result



Sample text:```In line with our results, several previous studies demonstrated the anti-proliferative effect of PPARs agonists in several cell types [11-15].```
Sample intent: result



Sample text:```Because previous studies indicated that hexapeptides bind the junction core (29, 32), we tested two junctions, one with an AT-rich core and the other with a GC-rich core (Fig.```
Sample intent: result



Sample text:```Induction of C1qa in the CNS promotes synapse elimination and synaptic dysfunction during development, neurodegenerative diseases such as glaucoma and AD, and aging [29,30,31,32,74].```
Sample intent: method



Sample text:```They demonstrated by in vitro and ex vivo studies that ATP1A1 mutants showed loss of pump activity and strongly reduced affinity for potassium, causing inappropriate depolarization of the cells (Beuschlein et al. 2013).```
Sample intent: method



Sample text:```Similarly, a synergistic effect of sequence differences at the resistin locus on obesity and risk of type II diabetes has been observed (Ma et al, 2002).```
Sample intent: method



Sample text:```For experiments measuring the effect of Sch-28080 and ouabain on pHi recovery in ICs, only basolateral Cl removal was used to differentiate IC types (15, 17).```
Sample intent: background



Sample text:```Other studies suggest that altering affinity to FcRn might alter the bioavailability of mAbs (Deng et al., 2010; Deng et al., 2012), and SC bioavailability appears lower in FcRn-deficient mice as compared to wild type animals (Wang et al., 2008).```
Sample intent: method



Sample text:```Intriguingly, using MPRs-deficient MEF cells, mouse and human CLN5 have been shown to reach lysosomes in an MPRindependent manner [12].```
Sample intent: background