Background: The precise etiology of carpal tunnel syndrome (CTS) remains unclear. One of the accepted factors for CTS is the restriction of the median nerve. Previous reports using ultrasound had only observed and measured the movement of parts of the median nerve. In this study, we aimed to elucidate the difference in the movement of the entire median nerve in patients with CTS (before and after surgery) and healthy volunteers using a new measurement method. Methods: We expressed the amount of movement of the entire nerve by a new method creating the motion area of the median nerve (MAMn) from an ultrasonographic video image on the computer. We compared the MAMn, the real MAMn (RMMn) (the value obtained by subtracting the nerve cross-sectional area from the MAMn), and mobile ratio (MR) (the value obtained from dividing the MAMn by the nerve cross-sectional area) between six wrists of six cases of CTS (before and at an average of 3.5 months after surgery) and six wrists of six healthy volunteers. Results: During passive wrist flexion, the average MAMn, RMMn, and MR of healthy cases were 23.1 mm2, 16.4 mm2, and 3.52, respectively. The average MAMn, RMMn, and MR of cases of CTS were respectively 11.8 mm2, 5.4 mm2, and 1.86 preoperatively; and 16.2 mm2, 7.3 mm2, and 1.87, postoperatively. The MAMn, RMMn, and MR decreased more significantly in patients with CTS than in healthy volunteers (p < 0.01). The MAMn and RMMn increased postoperatively (p < 0.05), but the MR remained low. Conclusions: The new measurement method revealed that the mobility of the entire median nerve was significantly restricted in cases of CTS compared to healthy participants. However, after surgery, nerve restriction was not restored despite improvements in symptoms, suggesting that decreases in nerve mobility contribute to CTS but are not a direct cause of symptoms.
Background: Amyloidosis treatment has advanced rapidly along with the discovery of drugs to prevent amyloid deposition. Therefore, it is vital to detect amyloidosis at an early stage. Wild-type transthyretin, which can cause carpal tunnel syndrome, may also cause finger tenosynovitis. However, the correlation between wild-type transthyretin amyloid and finger tenosynovitis is unclear. Here, we investigated pathological and clinical findings for 20 patients with finger tenosynovitis who underwent operation at our hospital to determine the frequency of transthyretin amyloid deposition in idiopathic finger tenosynovitis. Methods: To check for the presence of amyloid deposition, all specimens (tendon synovium tissue or flexor tendon sheath) resected during the operation were stained by the direct fast scarlet method. Amyloid-positive specimens were evaluated by immunohistochemical staining using an anti-transthyretin antibody. Patient characteristics were evaluated with respect to amyloid presence. Results: Thirteen (65%) of 20 finger tenosynovitis cases had amyloid deposition. Nine (69.2%) of the 13 amyloid-positive cases exhibited extensive transthyretin staining and were considered to have transthyretin amyloid. Amyloid deposition was more frequent in men. The mean number of fingers with tenosynovitis was significantly higher in amyloid-positive cases (3.8 fingers) than in amyloid-negative cases (2.0 fingers). Conclusions: Men with multiple finger tenosynovitis tended to have transthyretin amyloid deposition. Our results support that multiple finger tenosynovitis may serve as an initial indication of evaluation for transthyretin amyloidosis.
Case:
Axillary nerve rupture without shoulder joint fracture or dislocation in contact sports is very rare. To date, there has been no detailed report on such cases. We present 2 rare cases of axillary nerve rupture in contact sports who were successfully treated with free nerve grafting.
Conclusion:
In contact sports, the deltoid muscle is sometimes paralyzed temporarily after a collision. However, similar to our cases, the axillary nerve can be lacerated without fracture or dislocation. It is necessary to watch the course of paralysis carefully and consider nerve reconstruction if it does not recover.
<p>Supplementary Fig. 7 shows the transcriptional regulation of Wnt10a by clock gene products. Supplementary Fig. 8 shows the down-regulation of Wnt10a in Aldh3a1::Luc-expressing 4T1 cells. Supplementary Fig. 9 Unedited full blots of Supplementary Fig. 8. Supplementary Fig. 10 shows the comparison of mRNA levels of Aldh3a1, Clock, Bnal1 and Rev-erbα between ALDH-positive and negative 4T1 cells which was isolated from 4T1 tumor implanted in BALB/c female mice, and influence of overexpression of Aldh3a1 on the temporal expression of clock genes.</p>
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