Deep Learning Segmentation of the Nucleus Basalis of Meynert on 3T MRI.

BACKGROUND AND PURPOSE: The nucleus basalis of Meynert is a key subcortical structure that is important in arousal and cognition and has been explored as a deep brain stimulation target but is difficult to study due to its small size, variability among patients, and lack of contrast on 3T MR imaging. Thus, our goal was to establish and evaluate a deep learning network for automatic, accurate, and patient-specific segmentations with 3T MR imaging. MATERIALS AND METHODS: Patient-specific segmentations can be produced manually; however, the nucleus basalis of Meynert is difficult to accurately segment on 3T MR imaging, with 7T being preferred. Thus, paired 3T and 7T MR imaging data sets of 21 healthy subjects were obtained. A test data set of 6 subjects was completely withheld. The nucleus was expertly segmented on 7T, providing accurate labels for the paired 3T MR imaging. An external data set of 14 patients with temporal lobe epilepsy was used to test the model on brains with neurologic disorders. A 3D-Unet convolutional neural network was constructed, and a 5-fold cross-validation was performed. RESULTS: The novel segmentation model demonstrated significantly improved Dice coefficients over the standard probabilistic atlas for both healthy subjects (mean, 0.68 [SD, 0.10] versus 0.45 [SD, 0.11], P = .002, t test) and patients (0.64 [SD, 0.10] versus 0.37 [SD, 0.22], P < .001). Additionally, the model demonstrated significantly decreased centroid distance in patients (1.18 [SD, 0.43] mm, 3.09 [SD, 2.56] mm, P = .007). CONCLUSIONS: We developed the first model, to our knowledge, for automatic and accurate patient-specific segmentation of the nucleus basalis of Meynert. This model may enable further study into the nucleus, impacting new treatments such as deep brain stimulation.

Effects of heat-induced damage on the radial component of thermal diffusivity of bovine aorta.

The extent of the change in thermal diffusivity of soft tissues due to heat-induced damage is not well known. Reported here are the results of using the flash method to measure the through-the-wall component of thermal diffusivity of bovine aorta before and after the tissue has undergone two hours of heating at 75 degrees C. The measurements indicate a 10.1 percent increase in the thermal diffusivity of the tissue post-heating. While this change may not result in a significant change in the tissue temperature profile, further study is needed to quantify the thermal diffusivity in other coordinate directions, as well as the mechanisms by which this change in properties occurs.

Measurement of thermal diffusivity of bovine aorta subject to finite deformation.

The flash thermal diffusivity measurement technique is applied to tissue for the first time. Making use of its minimal contact with the specimen, the flash technique is extended to allow for well-defined, biaxial, finite strain. As an example application, the radial component of thermal diffusivity of bovine descending aorta is measured in vitro as a function of equibiaxial stretch, at room temperature. Data analysis is accomplished using a Marquardt algorithm coupled with a finite difference solution of the thermal diffusion equation. Extension of this method to measure simultaneously three orthogonal components of diffusivity, at different levels of temperature, is discussed.

Effects of hypoxia and severity of diabetes on Na,K-ATPase activity and arachidonoyl-containing glycerophospholipid molecular species in nerve from streptozotocin diabetic rats.

The pathogenesis of experimental diabetic neuropathy is associated with the development of endoneurial hypoxia. Exposure of normal rats to hypoxic conditions has previously been shown to reduce nerve conduction velocity. To study the biochemical effects of hypoxia further, streptozotocin-induced diabetic and age-matched nondiabetic rats were maintained in air containing 10% oxygen for nine weeks. As compared to nondiabetic rats kept in room air, sciatic nerve Na,K-ATPase activity was decreased 38% in nondiabetic, hypoxic rats and tended to be lower in diabetic animals maintained in a normoxic environment. However, the enzyme activity was unchanged in diabetic, hypoxic rats, suggesting the existence of an undefined compensatory interaction between these two conditions. Arachidonoyl-containing molecular species (ACMS) of phosphatidylcholine and phosphatidylethanolamine were substantially depleted in nerves from diabetic rats. Hypoxia alone also caused a lesser depletion of some but not all of these ACMS. However, the two conditions together did not produce a further decrease, consistent with the concept that the same mechanism is responsible for loss of ACMS in hypoxia and diabetes. To examine the effects of severity of diabetes on these parameters, groups of rats were injected with either 50 mg/kg or 100 mg/kg streptozotocin. The latter group was maintained by administration of minimal insulin doses and the experiment was terminated after 3 weeks. Serum glucose in rats that received the high dose of drug averaged 12% higher than in the low dose group. As compared to nondiabetic rats, Na,K-ATPase activity was reduced 32-36%, but there was no difference in activity between the two diabetic groups. However, there was a greater loss of ACMS in the more severely hyperglycemic rats. In rats that received comparable streptozotocin doses, measurement of ACMS depletion after 3, 9 and 32 weeks of diabetes revealed the loss is progressive with time. Thus, glycerophospholipid ACMS is a sensitive index of the severity and duration of experimental diabetic neuropathy.