MRI detects tubulointerstitial changes in mouse models of radiation-induced nephropathy.

Purpose: We hypothesized that radiation-induced tubulointerstitial changes in the kidney can be assessed using MRI-based T relaxation time measurements.

Methods: We performed MRI, histology, and serum biochemistry in two mouse models of radiation nephropathy: one involving external beam radiotherapy and the other using internal irradiation with an α-particle-emitting actinium-225 radiolabeled antibody. We compared the mean T values of different renal compartments between control and external beam radiotherapy or α-particle-emitting actinium-225 radiolabeled antibody-treated groups and between the two radiation-treated groups using a Wilcoxon rank-sum test.

The proton resonance enhancement for CEST imaging and shift exchange (PRECISE) family of RF pulse shapes for CEST MRI.

Purpose: To optimize a 100 ms pulse for producing CEST MRI contrast and evaluate in mice.

Methods: A gradient ascent algorithm was employed to generate a family of 100 point, 100 ms pulses for use in CEST pulse trains (proton resonance enhancement for CEST imaging and shift exchange). Gradient ascent optimizations were performed for exchange rates = 500, 1500, 2500, 3500, and 4500 s; and labile proton offsets (Δω) = 9.

Insurance gaps at age-19 and age-26 health insurance eligibility thresholds by childhood-onset condition severity, Colorado 2014-2018.

Objective: To characterize health insurance gap patterns related to age-19 Medicaid and age-26 commercial age-eligibility cutoffs.

Study Setting And Design: This descriptive analysis spans 2014-2018, after Affordable Care Act implementation, but before COVID-19 emergency provisions. We defined insurance gaps as ≥3 consecutive months without observed enrollment, preceded and followed by ≥1 month of enrollment and stratified results by insurance source and clinical severity (e.

Exploring the therapeutic potential of modulating nonsense-mediated mRNA decay.

Discovered more than four decades ago, nonsense-mediated mRNA decay (NMD) plays a fundamental role in the regulation of gene expression and is a major contributor to numerous diseases. With advanced technologies, several novel approaches aim to directly circumvent the effects of disease-causing frameshift and nonsense mutations. Additional therapeutics aim to globally dampen the NMD pathway in diseases associated with pathway hyperactivation, one example being Fragile X Syndrome.