Exact(3)
This indicates that similar mechanisms of isoQC and CCL2 regulation are active in the diseased human brain and in the transgenic mouse model analyzed.
The brain region specific mislocalization of hyperphosphorylated tau to dendritic spines in the tauopathy mouse model analyzed here is supported by very similar findings in AD patients.
However, from the mouse model analyzed here, we expect that humans with a partial or complete loss of BK channel function suffer from ataxia (14), increased susceptibility of OHCs to noise trauma (17), and auditory processing disorder.
Similar(57)
However, it remains possible that Notch signaling may play some role in cholangiocyte differentiation, since none of the three mouse models analyzed (Hes1-null mice, Jag1dDSL/+ Notch2del1/+ mice, and Notch2-cko mice) are likely to be entirely deficient in Notch signaling when the cholangiocyte-hepatocyte cell fate decision is made.
In addition, these results indicates that transcripts modulated by bexarotene in the MMTV-ErbB2 mammary gland share almost all the common features among the transgenic mouse models analyzed.
We show here a study on the pathogenesis and the physiopathology of the meningoencephalomyelitis by ROCV in a mouse experimental model, analyzing aspects of the histopathology including inflammatory response and cytokine production, looking for the virus, and also for messenger RNA (mRNA) of cytokines in nervous tissues.
In order to better define the role of the IL-6 cytokines in the gp130 knockout mouse model, we analyzed gp130 dependent gene expression in isolated hepatocytes using a whole transcriptome approach.
We established a heterotopic transplantation mouse model and analyzed lymph node metastasis by quantitative real-time RT-PCR.
Results for the Hu-PBL SCID mouse model were analyzed with a two sided Fisher's exact test.
In this study the effect of the Raf kinase inhibitor BAY 43-9006 and of the MEK inhibitor CI-1040 (PD184352) on a Raf dependent lung tumor mouse model was analyzed in detail.
In this study, we investigated the therapeutic potential of HM90822B, originally synthesized to inhibit IAP activity, on NSCLC cells and in a xenograft mouse model and analyzed the cellular effects of the drug to elucidate its mechanism of action.
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