Rewinding the Clock: Preparing the Next Generation of Radiology Residents for Oral Boards.

The replacement of the ABR in-person oral examination with the DR certifying examination affected approximately 15,000 radiologists, spanning from 2013 to 2027. This decision was motivated by better aligning with the timing of other American Board of Medical Specialty (ABMS) members, more closely reflecting real-world practice of radiology and narrowing training geared towards the trainee's subspecialty preference. However, in retrospect, this change may have subtracted from the quality and value of diagnostic radiology training as a whole with the de-emphasis on competence in general radiology, communication skills, and cognitive reasoning. In this paper, the authors lay out a blueprint necessary in order to rewind the clock of how diagnostic radiology programs can prepare their trainees for the new DR oral examination. Such a change will require substantial redactions affecting all designations, including radiology faculty, education teams, departmental leadership, academic institutions, ACGME, and ABR. The authors believe that implementing these modifications will not only effectively equip radiology candidates for the new DR oral examination but will also augment the significance of radiologists as indispensable members of multidisciplinary teams. The authors also outline the challenges that could emerge from these changes and speculate on the anticipated role of AI in future oral board examinations.

Superficial brachioulnar artery and its clinical significance.

The authors report a rare variation of the vasculature in the upper limbs of an 84-year-old male cadaver. A high bifurcation of the brachial artery occurred bilaterally at the proximal one-third of each arm. The radial arteries were larger than the ulnar arteries and gave origin to the common interosseous arteries. At the cubital fossa, the ulnar arteries traversed medial to the median nerves, continuing superficial to all forearm muscles except the palmaris longus tendon, characteristic of superficial brachioulnar arteries. The aforementioned variations have rarely been reported in previous literature and demonstrate important clinical significance in relation to accidental intra-arterial injections, errors in blood pressure readings, as well as orthopedic, plastic, and vascular surgeries of the upper limbs.

The inhibition of TDP-43 mitochondrial localization blocks its neuronal toxicity.

Genetic mutations in TAR DNA-binding protein 43 (TARDBP, also known as TDP-43) cause amyotrophic lateral sclerosis (ALS), and an increase in the presence of TDP-43 (encoded by TARDBP) in the cytoplasm is a prominent histopathological feature of degenerating neurons in various neurodegenerative diseases. However, the molecular mechanisms by which TDP-43 contributes to ALS pathophysiology remain elusive. Here we have found that TDP-43 accumulates in the mitochondria of neurons in subjects with ALS or frontotemporal dementia (FTD). Disease-associated mutations increase TDP-43 mitochondrial localization. In mitochondria, wild-type (WT) and mutant TDP-43 preferentially bind mitochondria-transcribed messenger RNAs (mRNAs) encoding respiratory complex I subunits ND3 and ND6, impair their expression and specifically cause complex I disassembly. The suppression of TDP-43 mitochondrial localization abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improves phenotypes of transgenic mutant TDP-43 mice. Thus, our studies link TDP-43 toxicity directly to mitochondrial bioenergetics and propose the targeting of TDP-43 mitochondrial localization as a promising therapeutic approach for neurodegeneration.