Sentence examples for vitro models show from inspiring English sources
Both in vivo and in vitro models show the benefit of delivering, for example, platelet released growth factors (i.e., PDGF-AB) into a wound area [ 19].
In vitro models show that TNF-α potentiates the direct functional inactivation and destruction of β-cells by other cytokines such as interleukin-1β and interferon-γ (7– 11).
Data from animal and in vitro models show that flavonoids, including flavanols, can interact with the neuronal intracellular signaling pathways mediating neurodegeneration and neuroinflammation and with the cellular and molecular architecture of the brain responsible for memory, learning, and cognitive function (10, 12).
Taken together, these results appear to be inconsistent with in vitro models showing a role for Nod2 in inducing inflammatory responses to B. burgdorferi and instead suggest that Nod2 may have a role in reducing inflammation.
In vitro models showed a cytotoxic and wound healing delay in a mouse model.
All three in vitro models showed similar effects on ERK/Akt signaling, cell proliferation, cell metabolism and apoptosis.
This is supported by in vitro models showing that overexpression of wild-type or mutant α-synuclein increases the vulnerability for ER stress through various mechanisms [ 17, 100].
This study will test the in vitro models showing that growth factor targeted therapy, such as trastuzumab, can restore endocrine sensitivity.
We tested whether gene expression level differed between the alleles of the polymorphism because previously reported data from in vitro models shows that growth inhibitory signalling activity is low for the type I receptor coded by the TGFBR1*6A allele [ 5].
This confirms previous findings in in vitro models showing the importance of protein synthesis for stabilization of both weakening (e.g., long-term depression) and strengthening (e.g., long-term potentiation) of synapses and demonstrates the requirement for mTOR during sleep in both processes.
This approach is based on observations that in vitro models showing high sensitivity to PARP inhibitors often have BRCA and PTEN deficiencies [ 7, 8], copy number variations involving BRCA1 and PARP1 [ 32], and/or hypermethylation of the promoter regions of genes BRCA1 and FANCF [ 20].
