An anxious, ambitious, down-on-his-luck postdoctoral researcher suddenly obtains results that look too good to be true — the virus he's injected into cancer-riddled mice appears to be melting away their tumors — and his girlfriend, another postdoc in the same lab, comes to suspect he's fudged his results.
Immune suppression, at least in newborn mice, appears to reflect a purposeful shift in the balance of immune cells.
Increased local elaboration of plasmin in the PAI-1−/− mice appears to have decreased extravascular fibrin deposition, which may have impaired containment of the infection within the pleural space.
Disease progression in VMD2-IL-10 transgenic mice appears to develop in two stages.
The osteopetrosis seen in S1PL−/− mice appears to be the result of dysfunctional osteoclasts.
Thus, the intrinsic excitability of striatal neurons in old A53T-SNCA overexpressing mice appears to be unchanged.
Consistent with this, the DA phenotype we observed in dcc +/− mice appears to be specific to the mPFC circuit.
Hence, activation of Stat3 within the ACF epithelium of TLR2−/− mice appears to promote a rise in NFkB driven pro-cancer TH17 inflammatory pathway while suppressing TH1 immunity.
The duration of protection conferred by vaccination with BCG in mice appears to be limited to the time that BCG persists in vivo [35].
At first glance the absence of ventricular enlargement in GD17 mice appears to shifts the specificity of this exposure away from schizophrenia at least.
The major side of effect of 4-1BB antibodyantreatmenteatment, at least in mice, appears to be an as yet poorly mechanistically defined inflammatory liver toxicity [10].
