Human and rat islets cultured in high glucose for 1 week exhibit b-cell dysfunction and apoptosis, but an associated increase in mitochondrial oxidative stress was only documented in rat islets (Duprez et al., 2012; Brun et al., 2015).
Sample text:```LG/J and SM/J mice have been shown to differ in their response to a high-fat diet for traits involved in various metabolic syndrome domains [23,24].```
Sample intent: method
Sample text:```Group 3: mice were anesthetized in a Plexiglas chamber with 3% isoflurane in air for 25 min (after the desired concentration was reached) twice daily, as described previously (12); 0.```
Sample intent: background



Sample text:```These results are in line with morphological abnormalities in a rabbit model of pneumococcal meningitis [8, 47], in neonatal and adult rat models [7, 51] and in human autopsy cases [20].```
Sample intent: result



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:```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:```Although the time-constants of the learning window used in this study were much shorter than those reported for hippocampal neurons by Bi and Poo [27] (viz.```
Sample intent: background
Sample text:```LG/J and SM/J mice have been shown to differ in their response to a high-fat diet for traits involved in various metabolic syndrome domains [23,24].```
Sample intent: method



Sample text:```Two days after transfection, cells were harvested and D2 activity was measured in lysates using HPLC, as described previously (20).```
Sample intent: background



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:```Endothelial cell cultures and capillary tubeswere generated as previously described (5, 11).```
Sample intent: background



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:```due to mitochondrial dysfunction caused by age-related mitochondrial DNA mutations, deletions 151 (10, 21) and damage (25, 59).```
Sample intent: method



Sample text:```Our results show that after 4 h of thiotepa treatment, the level of expression of anti-apoptotic Bcl-2 was not changed; this confirms the results of a previous study [25].```
Sample intent: result



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:```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