361) amplitudes and latencies) and behavioral [response times (RTs), error rates] indices |
362) rn in the comparison, resulting in faster response times for patterns that have fewe |
363) as been shown to influence same-different response times in a specific way, which ha |
364) molecular features that modify biological response, which can facilitate identificat |
365) P-induced changes in TJs and inflammatory response, which serve to protect against B |
366) nd long-lasting increases of the HPC-mPFC response, which shares the common expressi |
367) recording auditory nerve brainstem evoked response (ABR) thresholds to stimulation b |
368) Auditory brainstem-evoked response (ABR) was performed before and af |
369) s and DSBs), and activation of DNA Damage Response (DDR) pathway. |
370) d cells) can communicate their DNA damage response (DDR) status to cells that have n |
371) The unfolded protein response (UPR) is an essential pathway for |
372) major ER chaperones and unfolded protein response (UPR) pathway genes are measured |
373) l was to characterize differences in cell response after exposure to active beam sca |
374) No change was observed in blood glucose response after glucose ingestion after tra |
375) issect out which components of the innate response are helpful or harmful. |
376) ion of chromatin remodelers in DNA damage response are largely unknown. |
377) nly relies on the strategic adjustment of response boundaries but involves variation |
378) e fits revealed the canonical decrease of response boundaries with increasing time p |
379) lays in morphogen-based Turing models and response delays for cell-based Turing mode |
380) e dynamics of pigment cells is subject to response delays implicit in the cell cycle |
381) cumulative urine CTX-I showed clear dose-response effects at/over 24 h for SRT, wi |
382) The time-related and dose-response effects of ethanol on rectal temp |
383) ine-rich protein 1 (PELP1) to an estrogen response element in the CTSD distal promot |
384) ivate the TrkB promoter via a putative RA response element within the TrkB promoter. |
385) ion, and cell counting), pro-inflammatory response evaluation (ELISA for GM-CSF, IL- |
386) This consensus paper has used the human response evaluation criteria in solid tumo |
387) ive stress and pro-inflammatory cytokines response following acute myocardial infarc |
388) uable tools for studying the inflammatory response following myocardial infarction b |
389) insensitive to nonelastic response from incompressibility, but that |
390) ation strength required to evoke a muscle response from the primary motor cortex (M1 |
391) tressors that induce a systemic genotoxic response including a widely studied tumor |
392) Physiological responses, including potentiated startle, |
393) ed across these stations and expressed in response latency and magnitude were classi |
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