Precision assessment of bowel motion quantification using 3D cine-MRI for radiotherapy

Objective. The bowel is an important organ at risk for toxicity during pelvic and abdominal radiotherapy. Identifying regions of high and low bowel motion with MRI during radiotherapy may help to understand the development of bowel toxicity, but the acquisition time of MRI is rather long. The aim of this study is to retrospectively evaluate the precision of bowel motion quantification and to estimate the minimum MRI acquisition time. Approach. We included 22 gynaecologic cancer patients receiving definitive radiotherapy with curative intent. The 10 min pre-treatment 3D cine-MRI scan consisted of 160 dynamics with an acquisition time of 3.7 s per volume. Deformable registration of consecutive images generated 159 deformation vector fields (DVFs). We defined two motion metrics, the 50th percentile vector lengths (VL50) of the complete set of DVFs was used to measure median bowel motion. The 95th percentile vector lengths (VL95) was used to quantify high motion of the bowel. The precision of these metrics was assessed by calculating their variation (interquartile range) in three different time frames, defined as subsets of 40, 80, and 120 consecutive images, corresponding to acquisition times of 2.5, 5.0, and 7.5 min, respectively. Main results. For the full 10 min scan, the minimum motion per frame of 50% of the bowel volume (M50%) ranged from 0.6-3.5 mm for the VL50 motion metric and 2.3-9.0 mm for the VL95 motion metric, across all patients. At 7.5 min scan time, the variation in M50% was less than 0.5 mm in 100% (VL50) and 95% (VL95) of the subsets. A scan time of 5.0 and 2.5 min achieved a variation within 0.5 mm in 95.2%/81% and 85.7%/57.1% of the subsets, respectively. Significance. Our 3D cine-MRI technique quantifies bowel loop motion with 95%-100% confidence with a precision of 0.5 mm variation or less, using a 7.5 min scan time.</p

Anomalous spin-splitting of two-dimensional electrons in an AlAs Quantum Well

We measure the effective Lande g-factor of high-mobility two-dimensional electrons in a modulation-doped AlAs quantum well by tilting the sample in a magnetic field and monitoring the evolution of the magnetoresistance oscillations. The data reveal that |g| = 9.0, which is much enhanced with respect to the reported bulk value of 1.9. Surprisingly, in a large range of magnetic field and Landau level fillings, the value of the enhanced g-factor appears to be constant.Comment: 4 pages, 3 figure

Apparent Metallic Behavior at B = 0 of a two-dimensional electron system in AlAs

We report the observation of metallic-like behavior at low temperatures and zero magnetic field in two dimensional (2D) electrons in an AlAs quantum well. At high densities the resistance of the sample decreases with decreasing temperature, but as the density is reduced the behavior changes to insulating, with the resistance increasing as the temperature is decreased. The effect is similar to that observed in 2D electrons in Si-MOSFETs, and in 2D holes in SiGe and GaAs, and points to the generality of this phenomenon

The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model

Background: Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease worldwide and remains without effective cure. Increasing evidence is supporting the mitochondrial cascade hypothesis, proposing that loss of mitochondrial fitness and subsequent ROS and ATP imbalance are important contributors to AD pathophysiology. Methods: Here, we tested the effects of SUL-138, a small hibernation-derived molecule that supports mitochondrial bioenergetics via complex I/IV activation, on molecular, physiological, behavioral, and pathological outcomes in APP/PS1 and wildtype mice. Results: SUL-138 treatment rescued long-term potentiation and hippocampal memory impairments and decreased beta-amyloid plaque load in APP/PS1 mice. This was paralleled by a partial rescue of dysregulated protein expression in APP/PS1 mice as assessed by mass spectrometry-based proteomics. In-depth analysis of protein expression revealed a prominent effect of SUL-138 in APP/PS1 mice on mitochondrial protein expression. SUL-138 increased the levels of proteins involved in fatty acid metabolism in both wildtype and APP/PS1 mice. Additionally, in APP/PS1 mice only, SUL-138 increased the levels of proteins involved in glycolysis and amino acid metabolism pathways, indicating that SUL-138 rescues mitochondrial impairments that are typically observed in AD. Conclusion: Our study demonstrates a SUL-138-induced shift in metabolic input towards the electron transport chain in synaptic mitochondria, coinciding with increased synaptic plasticity and memory. In conclusion, targeting mitochondrial bioenergetics might provide a promising new way to treat cognitive impairments in AD and reduce disease progression