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The efficacy of nintedanib at improving lung function has also been shown in a recent IPF mouse model, indicating that it not only reduces fibrosis but also significantly enhances the pulmonary microvasculature [15].
Collectively, we demonstrated that miR-17~92 miR-17~92d tumor progresuppressednhibitumortumor angiogenesis in a genetically engineered mouse model, indicating the progression cellular context-dependent pro- and anti-cancer effects of miR-17~92.
Inhibiting ATM also prolonged survival of the allograft mouse model, indicating that targeting the DNA damage response pathways alone or in combination with other chemotherapeutic agents may be beneficial in patients with AML.
In conclusion, this study demonstrates that cis-urocanic acid is effective in reducing the severity of colitis in a chemically-induced mouse model, indicating that pathways induced by ultraviolet radiation to the skin can influence distal sites of inflammation.
However, the tumor recovers, and growth accelerates rapidly in the mouse model, indicating that, in fact, vorinostat is unlikely to be of clinical benefit to the patient.
Moreover, miR-188 is capable of inhibiting tumor initiation and progression in xenograft mouse model, indicating that miR-188 may have anti-cancer potential in human nasopharyngeal cancer.
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Similarly, in vivo evaluations in KP mouse model indicated successful CD44/EGFR-targeted delivery.
These studies with a mouse model indicate that PAF-AH is not a major secondary target of OP pesticide poisoning.
Preclinical assessment of p52−/p36− GAP in a humanized mouse model indicated an early and severe liver stage growth defect.
In conclusion, the mouse model indicated retarded disease progression upon cessation or switching to pMRTP which alone had no adverse effects.
Open wound healing tests with a mouse model indicate that the catechol-chitosan film suppresses the bacterial population at the wound site, induces less inflammation and promotes wound healing.
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