Reimagining educational equity through strategic alliance partnerships in response to the USA STEM-M diversity gap.

Addressing the USA diversity gap in science, technology, engineering, mathematics and medicine (STEM-M) through strategic alliance partnerships (SAPs) is an innovative solution toward combating the educational inequalities presented in K-12 education for marginalized youth interested in STEM-M professions. We present a model that unites multiple stakeholder s committed to diversifying the workforce in STEM-M, through the implementation of a multi-year high school pipeline program designed to better achieve STEM-M equity, access and opportunity at the secondary school level. We developed a unique model based on an SAP in a large metropolitan area in the Midwest that joins an Academic Medical Center and a local Public High School. Our results involving 46 students over 8 years demonstrate 100% high school graduation rates; 97% college attendance with full or partial scholarship support, and early evidence of post-graduation aspirations in STEM-M careers. Our early progress calls for more rigorous study against standard educational practices. If our program is proven to be more effective, then potentially more strategic public-private partnerships to foster K-12 pipeline programs to better achieve equity through educational access, opportunities and resources should be developed and targeted for those marginalized youth that have been historically denied STEM-M opportunities. After 10 years of dedicated effort, we see evidence of potential benefits of this SAP to develop K-12 pipeline programs with similar aims of STEM-M diversification, particularly by way of more-equitable provision of educational opportunities to students belonging to minority racial and ethnic groups.

Absence of renal enlargement in fructose-fed proximal-tubule-select insulin receptor (IR), insulin-like-growth factor receptor (IGF1R) double knockout mice.

The major site of fructose metabolism in the kidney is the proximal tubule (PT). To test whether insulin and/or IGF1 signaling in the PT is involved in renal structural/functional responses to dietary fructose, we bred mice with dual knockout (KO) of the insulin receptor (IR) and the IGF1 receptor (IGF1R) in PT by Cre-lox recombination, using a γ-glutamyl transferase promoter. KO mice had slightly (~10%) reduced body and kidney weights, as well as, a reduction in mean protein-to-DNA ratio in kidney cortex suggesting smaller cell size. Under control diet, IR and IGF1R protein band densities were 30-50% (P < 0.05) lower than WT, and the relative difference was greater in male animals. Male, but not female KO, also had significantly reduced band densities for Akt (protein kinase B), phosphorylated AktT308 and IRY1162/1163 A high-fructose diet (1-month) led to a significant increase in kidney weight in WT males (12%), but not in KO males or in either genotype of female mice. Kidney enlargement in the WT males was accompanied by a small, insignificant fall in protein-to-DNA ratio, supporting hyperplasia rather than hypertrophy. Fructose feeding of male WT mice led to significantly higher sodium bicarbonate exchanger (NBCe1), sodium hydrogen exchanger (NHE3), sodium phosphate co-transporter (NaPi-2), and transforming growth factor-ß (TGF-ß) abundances, as compared to male KO, suggesting elevated transport capacity and an early feature of fibrosis may have accompanied the renal enlargement. Overall, IR and/or IGF1R appear to have a role in PT cell size and enlargement in response to high-fructose diet.