Triceps aponeurosis and deltoid tuberosity as a landmarks for radial nerve dissection: a cadaveric study.

Background: The radial nerve, originating from the posterior cord of the brachial plexus, traverses the posterior humerus. Incidences of radial nerve injury have been noted following surgical interventions like fracture fixation and exploration in this area. There's a paucity of literature detailing soft tissue anatomical cues for radial nerve dissection. This study aimed to identify reliable soft tissue and bony landmarks (triceps aponeurosis and deltoid tuberosity) that can be of substantial importance in dissecting the radial nerve and reducing iatrogenic nerve injury utilizing the posterior approach. Methods: Thirty-two fresh-frozen cadaver specimens underwent dissection using a posterior triceps-splitting approach to expose the radial nerve. The distance between the apex of the triceps aponeurosis and the radial nerve was measured, alongside noting the radial nerve's position relative to the deltoid tuberosity. Results: Of the cadavers, 78% were female, and 22% were male, with a mean age of 76 (range: 62-85). The average distance between the aponeurosis apex and the radial nerve was 40.3 mm (range: 28-60). The radial nerve was consistently found in all specimens, situated posteriorly at the humerus's mid-axial level at the distal part of the deltoid tuberosity. Conclusion: The triceps aponeurosis and distal deltoid tuberosity serve as reliable and practical landmarks for dissecting and exploring the radial nerve during posterior humeral approaches. These landmarks prove especially valuable when fractures obscure conventional anatomical cues.

Expanded CUG Repeats Trigger Disease Phenotype and Expression Changes through the RNAi Machinery in C. elegans.

Myotonic dystrophy type 1 is an autosomal-dominant inherited disorder caused by the expansion of CTG repeats in the 3' untranslated region of the DMPK gene. The RNAs bearing these expanded repeats have a range of toxic effects. Here we provide evidence from a Caenorhabditis elegans myotonic dystrophy type 1 model that the RNA interference (RNAi) machinery plays a key role in causing RNA toxicity and disease phenotypes. We show that the expanded repeats systematically affect a range of endogenous genes bearing short non-pathogenic repeats and that this mechanism is dependent on the small RNA pathway. Conversely, by perturbating the RNA interference machinery, we reversed the RNA toxicity effect and reduced the disease pathogenesis. Our results unveil a role for RNA repeats as templates (based on sequence homology) for moderate but constant gene silencing. Such a silencing effect affects the cell steady state over time, with diverse impacts depending on tissue, developmental stage, and the type of repeat. Importantly, such a mechanism may be common among repeats and similar in human cells with different expanded repeat diseases.