Fundamental studies in stroke on ADC changes and their relationship with simultaneous astrocyte swelling and neuronal shrinking to explain such changes in terms of cellular alterations were conducted in collaboration with Marc Fisher, Kai-Feng Liu and the late Julio Garcia [ 126– 126].
An attempt to reproduce this histological alteration was conducted in rats for the first time by Frautschy and colleagues in 1992 by injecting purified amyloid plaques extracted from human AD brains into the cortex and hippocampus of adult rats [ 30].
Patients were unaware as to which group they were in, as the dose alteration or no change was conducted by telemetry with the screen not visible to the patient.
To avoid the biasing effect of multiple outcomes within the same study, all meta-analyses on the main outcome of interest (i.e. the prevalence of data fabrication, falsification and alteration) were conducted using only one outcome per study.
To identify MDS-specific genome alterations, whole-genome sequencing was conducted on MonoMAC, MDS and BM-MSCs (Fig. 1).
To test whether the reduced invasion and cell viability induced by cryoablated tumor extracts were companied with the alterations in MAPKs pathways, Western blot was conducted to detect the phosphorylation levels of P38, ERK1/2, and JNK in GL261 glioma cells.
The present study was conducted to examine alterations of the intrinsic hepatic innervation at several time points following PH in rats, using the neuronal markers PGP9.5 and GAP-43.
This study was conducted to evaluate molecular alterations in the urethras of mice with experimentally induced SUI.
The trial was conducted with no major alterations to the initial protocol.
In addition, an analysis was conducted to examine probes whose signal alteration was significantly associated with muscle atrophy.
