The purpose of this study was to establish whether functional near-infrared spectroscopy (fNIRS), an emerging brain-imaging technique based on optical principles, is suitable for studying the brain activity that underlies effortful listening. In an event-related fNIRS experiment, normally-hearing adults listened to sentences that were either clear or degraded (noise vocoded). These sentences were presented simultaneously with a non-speech distractor, and on each trial participants were instructed to attend either to the speech or to the distractor. The primary region of interest for the fNIRS measurements was the left inferior frontal gyrus (LIFG), a cortical region involved in higher-order language processing. The fNIRS results confirmed findings previously reported in the functional magnetic resonance imaging (fMRI) literature. Firstly, the LIFG exhibited an elevated response to degraded versus clear speech, but only when attention was directed towards the speech. This attention-dependent increase in frontal brain activation may be a neural marker for effortful listening. Secondly, during attentive listening to degraded speech, the haemodynamic response peaked significantly later in the LIFG than in superior temporal cortex, possibly reflecting the engagement of working memory to help reconstruct the meaning of degraded sentences. The homologous region in the right hemisphere may play an equivalent role to the LIFG in some left-handed individuals. In conclusion, fNIRS holds promise as a flexible tool to examine the neural signature of effortful listening.
Hepatocyte senescence is associated with liver fibrosis. However, the possibility of a direct, causal relation between hepatocyte senescence and hepatic stellate cell (HSC) activation was the subject of this study. Liver biopsy specimens obtained from 50 patients with non-alcoholic fatty liver disease and a spectrum of liver fibrosis stages were stained for p16, αSMA, and picrosirius red (PSR). Primary human HSCs were cultured in conditioned media derived from senescent or control HepG2 cells. Expression of inflammatory and fibrogenic genes in HSCs cultured in conditioned media were studied using RT-PCR. ELISAs were undertaken to measure factors known to activate HSCs in the conditioned media from senescent and control HepG2 cells and serum samples from healthy volunteers or patients with biopsy-proven cirrhosis. There was a strong association between proportion of senescent hepatocytes and hepatic stellate cell activation. Both proportion of hepatocyte senescence and hepatic stellate cell activation were closely associated with fibrosis stage. Inflammatory and fibrogenic genes were up-regulated significantly in HSCs cultured in conditioned media from senescent HepG2 cells compared with control HepG2 cells. PDGF levels were significantly higher in the conditioned media from senescent hepatocytes than control HepG2-conditioned media, and in serum samples from patients with cirrhosis than healthy volunteers. In conclusion, this ‘proof of concept’ study revealed activation of human HSCs by media from senescent HepG2 cells, indicating direct involvement of factors secreted by senescent hepatocytes in liver fibrosis.
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