232) Attribution of the immune response and consequent clinical outcomes |
233) Treatment response and disease-specific prognosis we |
234) r companies and determined that induction response and drug-drug risk assessment det |
235) se the most recent data regarding vaccine response and efficacy in this setting, par |
236) ology (electronic referral, coordination, response and feedback), processes (effecti |
237) re affected included the unfolded protein response and immune/defense responses. |
238) nd several enzymes associated with immune response and metabolism. |
239) APP/PS1 mice, including the immune system response and neurotransmission, represent |
240) of less intensive therapy to consolidate response and prevent relapses. |
241) shows an excellent sensing response, fast response and recovery time along with acce |
242) r refractory cancers harboring DNA damage response and repair alterations, including |
243) es of infection or injury is a key immune response and requires the breaching of end |
244) g miRNAs may be useful as markers of drug response and resistance in the guidance of |
245) ance between the efficiency of the immune response and the magnitude of viral load. |
246) V-2 by reducing the mucosal innate immune response and the proliferation of airway b |
247) ssociated with common human disease, drug response and various phenotypic traits. |
248) primary outcomes were efficacy (treatment response) and acceptability (all-cause dis |
249) dysfunction, a dysregulated inflammatory response, and cellular metabolic reprogram |
250) i-proliferative signaling, the DNA damage response, and cytoskeletal remodeling. |
251) ower autonomic tone, reduced baroreceptor response, and greater vascular function ar |
252) d treatment adherence also influence drug response, and may confound the relationshi |
253) s in the SLC22 family on disease and drug response, and summary of recent studies de |
254) ding of the mechanisms of adaptive immune response of B cells in the process of CHB |
255) The mechanical response of C-fibers appeared to increase |
256) 1 (SREBP1) degradation in conferring the response of EGFR mutant NSCLC cells to osi |
257) SREBP1 degradation and its impact on the response of EGFR mutant NSCLC cells to osi |
258) understanding the biology underlying the response of EGFR mutant non-small cell lun |
259) ely, Mincle can regulate the inflammatory response of KCs, which is necessary for th |
260) ellular processes that could modulate the response of TMX. |
261) e clinical manifestations and therapeutic response of asthma. |
262) Here, we studied the acute response of astrocytes and microglia to a |
263) (TG2) plays a key role in regulating the response of astrocytes to insults. |
264) lular signaling derived from the averaged response of entire neuronal populations ma |
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