The STEM Interest Attrition tool utilizes a cohort of nearly 100,000 students selected from the myCollegeOptions program.
To measure growth and proliferation we utilized a cohort of 3 4 or 9 10 months old A53T α-Syn+/+ and age-matched control mice (males and females, separated).
We utilized a cohort of HIV+ individuals who are considered HIV+ slow-progressors as defined by viral loads of less than 50,000 copies/ml in the absence of antiviral therapy that have been well characterized in respect to their HIV-specific immune responses.
We have utilized a cohort of genotyped healthy subjects to better understand how these genetic variants contribute to the failure of B-cell tolerance seen in SLE.
It is important to note that while this study utilized a cohort of patients enrolled in a multicenter, high-dose therapy trial, our primary study question was not related to high-dose therapy.
To extend our findings, we utilized a cohort of patients from the Nurses Health Studyy (NHS) with ER/PR data recorded in the medical record and assessed on tissue microarrays (n = 2,011).
For this study, we utilized a cohort of 88 untreated primary human neuroblastoma samples and examined the prognostic values for ELK1, CDK4, CREB1, MMP2, AURKβ, FRA, MYB, JUND, BIRC5, AKT2, SELE, TNFα, NOS3, ESR1, KRTAP1-1, MMP3, NF2, CXCR4, ADAMTS1, CD54, EGFR, and AKT1 expression.
Replication will not be possible utilizing a larger cohort of patients as it simply does not exist.
Utilizing an independent cohort of patients (cohort 3), we screened for cancer-related signaling proteins altered in PRDX1 positive tumors.
