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1 ress led to increased anxiety phenotypes but did not exacerbate 5-HT1A knockdown-mediated anxiety lev
2 nterleukin-2 (IL-2) that was well tolerated, did not exacerbate alloimmunity, augmented Treg in vivo,
3 e results show that lack of SphK1 expression did not exacerbate angiotensin II (Ang II)-induced acute
4 n the presence of SP-resistant P. falciparum did not exacerbate any parasitologic, histologic, or cli
6 urprisingly, exposure to PS50G nanoparticles did not exacerbate but instead inhibited key features of
9 PP/IL-2 cotreatment during chronic infection did not exacerbate disease, and more importantly it coul
11 verall, allopurinol lowered urate levels but did not exacerbate dopaminergic neuron degeneration, fin
12 d no deleterious long-term repercussions and did not exacerbate EAE, but i) halted progression of dis
14 paired glucose tolerance in control mice but did not exacerbate glucose intolerance in G4KO mice.
16 r, were the observations that IL-7 treatment did not exacerbate graft-versus-host disease (GVHD) in r
18 uction following moderate IRI in WT mice but did not exacerbate injury or enhance IFN-gamma productio
22 3 weeks of the cold compared with those who did not exacerbate (P = 0.006, 0.01, 0.048, respectively
23 PTp-SP failed to inhibit parasite growth but did not exacerbate pathology among women infected with s
24 nted products, HMG-CoA reductase inhibitors, did not exacerbate pre-existing diseases, and actually h
25 ne expression, preceding influenza (21 days) did not exacerbate secondary Staphylococcus aureus infec
26 adult population, high folate concentrations did not exacerbate the biochemical abnormalities related
27 ely, in vivo neutralization of IL-7 or Bcl-2 did not exacerbate the contraction of 2W1S-specific CD4+
28 Interestingly, the lack of both A20 and CYLD did not exacerbate the developmental defects and hyperre
29 logic analyses showed that CBLB502 treatment did not exacerbate the moderate graft-versus-host diseas
31 defined limits of disease and, surprisingly, did not exacerbate the pathology of EAE on a sensitive h
33 ay 1, indicating that administration of L-NA did not exacerbate the severity of myocardial stunning 2
35 presence of circulating CA125 in a rat model did not exacerbate the toxicity of 3A5 drug conjugates.
36 oss of Dvl2 function in Vangl2(Lp/+) embryos did not exacerbate the Vangl2(Lp/+) neuronal migration p
37 niae infection in nonasthmatic cells, but it did not exacerbate these three parameters already activa
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