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This resistance might be mitigated by recent data indicating that hormone replacement therapy with estrogen alone does not increase the risk for breast cancer [ 37].
This hypothesis is also supported by recent data indicating that the vast majority of patients first reported trauma, then substance use, which again was followed by additional traumatic experiences, and further substance use [ 21].
This could possibly be explained by recent data indicating that Tregs harbor a dual role in cancer, suppressing anti-tumor immune response (inducible Treg) and suppressing inflammation which is known to promote carcinogenesis (natural Treg) [ 26, 27].
This hypothesis is supported by recent data indicating that PE is associated with decreased levels of α1-microglobulin (A1M), crucial for the removal of radicals and heme and furthermore, that treatment with A1M infusions can reduced PE symptoms in a large animal model [90,91].
The potential utility of dual SRC-ABL inhibitors to override imatinib resistance in CML is further supported by recent data indicating that imatinib resistance is associated with upregulated expression of the SRC kinase, Lyn (Donato et al. 2004; Wu et al. 2004).
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This is consistent with the recent data indicating that shuffling of P. furiosus genetic material is caused by mobile genetic elements [ 18, 19, 32, 33].
By contrast, recent data indicate that PRMT5 uses a distributive mechanism to catalyze the symmetric dimethylation of histone H4 and its N-terminal peptide fragment.
By contrast, more recent data indicate that the stability of the latent reservoir despite intensive therapy requires new strategies to eradicate HIV-1 from this reservoir (Gandhi et al. 2010; Sagot-Lerolle et al. 2008; Archin et al. 2010).
It is known that their generation can be modulated by MRFs, and as our recent data indicate also by HO-1.
However, the more recent data indicate that pore-formation by VacA is independent of the N-terminus.
Recent data indicate reduced cell death induction by MitoVES in the S68A variant, but the functional consequences of this mutation for CII activity have not been studied.
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by histomorphometric data indicating
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by economic data indicating
by qualitative data indicating
by epidemiological data indicating
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