Example of coloration measurement taken in ImageJ for <i>M</i>. <i>mercenaria</i> specimen w48 at the conclusion of the 20.5-week experiment. by Teagan McMahon (20108036)

Data_Sheet_1_Decreased water temperature enhance Piscine orthoreovirus genotype 3 replication and severe heart pathology in experimentally infected rainbow trout.pdf by Juliane Sørensen (14596838)

Table_5_Effectiveness and tolerability of different therapies in preventive treatment of MOG-IgG-associated disorder: A network meta-analysis.docx by Xiaofei Wang (135107)

“…AZA, MMF, OC and RTX showed a trend to decrease ARR, but those results did not reach significant differences. …”

PCAIs inhibit NCI-H23 cell line viability. by Matthew D. Gregory (19929096)

“…Polyisoprenylated Cysteinyl amide Inhibitors (PCAIs) constitute a group of potential cancer therapy agents that we designed to specifically disrupt and suppress hyperactive G-protein signaling, such as that caused by mutated RAS proteins. …”

PCAIs disrupt actin filaments in NCI-H23 cells. by Matthew D. Gregory (19929096)

“…Polyisoprenylated Cysteinyl amide Inhibitors (PCAIs) constitute a group of potential cancer therapy agents that we designed to specifically disrupt and suppress hyperactive G-protein signaling, such as that caused by mutated RAS proteins. …”

PCAIs suppress 3D NCI-H23 cell invasion. by Matthew D. Gregory (19929096)

“…Polyisoprenylated Cysteinyl amide Inhibitors (PCAIs) constitute a group of potential cancer therapy agents that we designed to specifically disrupt and suppress hyperactive G-protein signaling, such as that caused by mutated RAS proteins. …”

PCAIs suppress NCI-H23 cancer cell migration. by Matthew D. Gregory (19929096)

“…Polyisoprenylated Cysteinyl amide Inhibitors (PCAIs) constitute a group of potential cancer therapy agents that we designed to specifically disrupt and suppress hyperactive G-protein signaling, such as that caused by mutated RAS proteins. …”

PCAIs induce apoptosis in NCI-H23 cells. by Matthew D. Gregory (19929096)

“…Polyisoprenylated Cysteinyl amide Inhibitors (PCAIs) constitute a group of potential cancer therapy agents that we designed to specifically disrupt and suppress hyperactive G-protein signaling, such as that caused by mutated RAS proteins. …”

Maternal and infant characteristics of the study population at 6 months. by Michelle A. E. Jansen (740955)

MLN4924-resistant K562 (R-K562_MLN) leukemia cells show decreased sensitivity to MLN4924, but not all chemotherapeutics. by G. Wei Xu (545673)

Impact of TLR5 knockout on specific taxa in the fecal microbiota of mice and differences in comparing two colonies (TLR5KO1 and TLR5KO2) bred in different laboratories. by Wei Zhang (405)

“…<p>Heat map showing statistically significant changes (p<0.05) on different fecal taxa. Red shows a significant increase, blue signifies a significant decrease, and black shows not found. …”

Changes in classification of COPD diagnosis timing by look back period (LBP) among the baseline population with 5-year Medicare fee-for -service continuous enrollment (CE). by Eman Metwally (19928829)

Juvenile demyelination impairs the maturation of PV interneurons in the PFC. by Sara Hijazi (21656615)

“…Representative traces of voltage responses following +450 pA current injection. Scale bar: 100 ms, 10 mV. …”

Image1_RETRACTED: miR-16 and Fluoxetine Both Reverse Autophagic and Apoptotic Change in Chronic Unpredictable Mild Stress Model Rats.tif by Yang Yang (45629)

“…Expression levels of miR-16 and BDNF in the hippocampus were examined with RT-PCR, and it was found that increased 5-HT2a receptor expression induced by CUMS can be decreased by miR-16 and Fluoxetine administration. …”

Incubation in Normal Saline (NS) or Plasma-Lyte (PL) rendered acidic leads to decreased endothelial dependent relaxation in intact naïve porcine saphenous veins (PSV). by Joyce Cheung-Flynn (344249)

All data points from Fig 2. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 8. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 3. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 1. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 4. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”