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Moreover, findings from in vivo experimental models demonstrate reduced demyelination and loss of oligodendrocytes [ 76, 77] with quetiapine treatment, as well as faster return of myelin proteins [ 78].
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Both models demonstrated reduced adiposity but accompanied by severely impaired insulin signaling in adipose tissue (Bluher et al 2002; Xu et al 2002a).
Our DPD Morse model demonstrated reduced compressibility while preserving other fluid properties such as the fluid density and viscosity.
The in vivo model demonstrated reduced phosphorylation of TnT and TnI, suggesting that the integrated effect of altered troponin phosphorylation may be involved in the observed contractile response.
Our data identified an important difference in vascular response between acute endotoxaemia and a 5-day peritonitis model: the first 2 to 6 h of acute endotoxaemia models typically demonstrate reduced vasoconstriction in response to α1-adrenoceptor stimulation [10,16,33,46].
Animal models also demonstrate reduced pathological injury with HFOV, with less hyaline membrane formation, less alveolar leukocyte infiltration and less airway epithelial damage compared with CV [ 12- 14].
These models also demonstrate reduced levels of epineurial vessel superoxide and nitrotyrosine, suggesting that the relationship between oxidative stress and PARP may be bidirectional rather than unidirectional.
In animal models, exudate neutrophils demonstrate reduced chemotactic response [ 166].
Human infants who are small for gestational age demonstrate reduced body weight and brain weight, as do animal models.
Furthermore, studies using animal models have demonstrated reduced brain size and abnormal migration of neural cells in mice exposed to ethanol in utero (Godin et al. 2010; Parnell et al. 2009).
Moreover, evidence exists that GLP-1 receptors are expressed within cardiomyocytes and arterial walls, and rodent models have demonstrated reduced infarct size and improved left-ventricular-ejection function during coronary ischemia when treated with a GLP-1 RA. 8 No current studies have been published with major adverse cardiovascular events for dulaglutide.
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