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Background In the past, the diagnosis of hourglass-like fascicular constriction(s) of the anterior interosseous nerve mostly depended on electrophysiological examination, by which the location could not be diagnosed. There are few studies on the evaluation of hourglass-like fascicular constriction(s) by ultrasonography. Purpose To evaluate the role of ultrasonography in the diagnosis of hourglass-like fascicular constriction(s) of the anterior interosseous nerve. Material and Methods A retrospective analysis of 12 patients with hourglass-like fascicular constriction(s) of the anterior interosseous nerve was carried out, and the characteristics of the high-frequency ultrasonographic images were summarized and compared with surgical exploration. Results The 12 cases of hourglass-like fascicular constriction(s) of the anterior interosseous nerve were all located in the median nerve of the distal upper arm, including nine cases of single hourglass-like fascicular constriction and three cases of multiple hourglass-like fascicular constrictions. High-frequency ultrasonography can accurately locate the hourglass-like fascicular constriction(s) of the anterior interosseous nerve and the extent of neuropathy. The ultrasonographic images of hourglass-like fascicular constriction(s) of the anterior interosseous nerve showed single or multiple hourglass-like change(s) in the median nerve of the distal upper arm. The nerve fascicles on both sides of the affected nerve with hourglass-like change thickened. Conclusions High-frequency ultrasonography could be a reliable, convenient, and non-invasive diagnostic imaging method for hourglass-like fascicular constriction(s) of the anterior interosseous nerve.

Objective and design: The age-associated increase of aseptic inflammation and necroptosis are closely related to the emergence of various age-associated diseases. Methods In this study, the role of HMGB1/TLR4-induced necroptosis in abdominal aortic aneurysm (AAA) formation was investigated. Firstly, the levels of sterile inflammatory mediators (HMGB1, TLR4) and necroptosis markers in the abdominal aorta of adult and old C57BL/6J mice were tested. We observed that sterile inflammatory mediators and necroptosis markers were greatly increased in old mice’s abdominal aorta. Then, using angiotensin II (Ang II)-induced AAA model of APOE−/− mice, the models were treated with RIP1 inhibitor Necrostatin-1 (Nec-1), TLR4 inhibitor TAK-242, respectively. Results We found that HMGB1, TLR4, and necroptosis markers were elevated with the development of AAA in APOE−/− mice. In addition, necroptosis inhibition by Nec-1 alleviated Ang II-induced AAA development, while the expressions of HMGB1/TLR4 declined. Notably, after blocking TLR4 by TAK-242, the expression of necroptosis markers decreased significantly, and the progression of AAA was also alleviated in APOE−/− mice. Conclusions Our results indicate that HMGB1/TLR4-mediated necroptosis enhances AAA development in Ang II-induced AAA model of APOE−/− mice and the possible therapeutic roles for TLR4 inhibition in AAA.