Accelerated diffusion-weighted imaging of the prostate using deep learning image reconstruction: A retrospective comparison with standard diffusion-weighted imaging.

PURPOSE: Routine multiparametric MRI of the prostate reduces overtreatment and increases sensitivity in the diagnosis of the most common solid cancer in men. However, the capacity of MRI systems is limited. Here we investigate the ability of deep learning image reconstruction to accelerate time consuming diffusion-weighted imaging (DWI) acquisition while maintaining diagnostic image quality. METHOD: In this retrospective study, raw data of DWI sequences of consecutive patients undergoing MRI of the prostate at a tertiary care hospital in Germany were reconstructed using standard and deep learning reconstruction. To simulate a shortening of acquisition times by 39 %, one instead of two and six instead of ten averages were used in the reconstruction of b = 0 and 1000 s/mm2 images, respectively. Image quality was assessed by three radiologists and objective image quality metrics. RESULTS: After the application of exclusion criteria, 35 out of 147 patients examined between September 2022 and January 2023 were included in this study. The radiologists perceived less image noise on deep learning reconstructed images at b = 0 s/mm2 images and ADC maps with good inter-reader agreement. Signal-to-noise ratios were similar overall with discretely reduced values in the transitional zone after deep learning reconstruction. CONCLUSIONS: An acquisition time reduction of 39 % without loss in image quality is feasible in DWI of the prostate when using deep learning image reconstruction.

[Diagnostic delaying factors in hepatic alveolar echinococcosis]. / Diagnoseverzögernde Faktoren bei hepatischer alveolärer Echinokokkose.

PURPOSE: The purpose of this study was to analyze the diagnostic workflow of patients with alveolar echinococcosis (AE) and to identify possible diagnosis-delaying factors. METHODS: The number and type of diagnostic procedures of patients diagnosed with alveolar echinococcosis were investigated. The disease history was recorded on the basis of questionnaires, the available findings, and data supplements from the hospital information system (SAP). Statistical analyses were performed using SAS version 9.4 and Microsoft Excel version 16.43. The study population of the cross-sectional study included n = 109 patients with confirmed alveolar echinococcosis. RESULTS: The definitive diagnosis of alveolar echinococcosis of the liver was made at 26.5 ± 65.0 (mean ± standard deviation) months (min - max: 0 - 344, median = 3). The majority of patients were diagnosed because of incidental imaging findings of the liver (n = 74/109 (67.9%)). A total of n = 56/74 (75.7%) of all incidental findings were diagnosed in an outpatient setting, while n = 15/74 (20.3%) of cases were diagnosed during inpatient hospitalization. On average, 1.1 ± 1.2 (0-11, median = 1) ionizing imaging modalities were used for each patient. Contrast-enhanced sonography was received by 0.3 ± 0.5 (0-2, median = 0) patients. Almost all patients (n = 104/109 (95.4%) had at least one suspected hepatic or extrahepatic malignancy at some time. Exclusion of suspected malignancy occurred at a mean of 4.1 ± 16.5 months (0 -133.8, median = 1). CONCLUSIONS: The diagnostic clarification process of AE patients is lengthy and stressful. The psychological burden of a questionable malignant diagnosis is considerable. Early use of contrast-enhanced sonography and, if necessary, puncture of unclear hepatic masses helps to shorten the difficult diagnostic process.

Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway.

Developmental neuron death plays a pivotal role in refining organization and wiring during neocortex formation. Aberrant regulation of this process results in neurodevelopmental disorders including impaired learning and memory. Underlying molecular pathways are incompletely determined. Loss of Bcl11a in cortical projection neurons induces pronounced cell death in upper-layer cortical projection neurons during postnatal corticogenesis. We use this genetic model to explore genetic mechanisms by which developmental neuron death is controlled. Unexpectedly, we find Bcl6, previously shown to be involved in the transition of cortical neurons from progenitor to postmitotic differentiation state to provide a major checkpoint regulating neuron survival during late cortical development. We show that Bcl11a is a direct transcriptional regulator of Bcl6. Deletion of Bcl6 exerts death of cortical projection neurons. In turn, reintroduction of Bcl6 into Bcl11a mutants prevents induction of cell death in these neurons. Together, our data identify a novel Bcl11a/Bcl6-dependent molecular pathway in regulation of developmental cell death during corticogenesis.