Delayed tendon healing after injury in tetranectin-deficient mice

Hanaka, Megumi; Iba, Kousuke; Hayakawa, Hikaru; Kiyomoto, Kenta; Ibe, Koji; Teramoto, Atsushi; Emori, Makoto; Yamashita, Toshihiko

doi:10.1016/j.jos.2020.12.011

Cited by 1 publication

(1 citation statement)

References 27 publications

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“…Moreover, the level of IL-6 had no significant statistical difference between t-ES of 0.3 mA and 2D ES of 0.175 mA, which means that 2D ES achieved the same effect of t-ES but with a 41.7% lower stimulation current. To gain a comprehensive analysis of inflammation after tendon injury, TNF-α, IL-10 and IL-1β were also tested 45 – 47 . The result showed that the level of TNF-α was not a good indicator because there is no significant difference between sham and non-ES group.…”

Section: Resultsmentioning

confidence: 99%

Neuromorphic electro-stimulation based on atomically thin semiconductor for damage-free inflammation inhibition

Bao,

Wang,

Liu

et al. 2024

Nat Commun

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Inflammation, caused by accumulation of inflammatory cytokines from immunocytes, is prevalent in a variety of diseases. Electro-stimulation emerges as a promising candidate for inflammatory inhibition. Although electroacupuncture is free from surgical injury, it faces the challenges of imprecise pathways/current spikes, and insufficiently defined mechanisms, while non-optimal pathway or spike would require high current amplitude, which makes electro-stimulation usually accompanied by damage and complications. Here, we propose a neuromorphic electro-stimulation based on atomically thin semiconductor floating-gate memory interdigital circuit. Direct stimulation is achieved by wrapping sympathetic chain with flexible electrodes and floating-gate memory are programmable to fire bionic spikes, thus minimizing nerve damage. A substantial decrease (73.5%) in inflammatory cytokine IL-6 occurred, which also enabled better efficacy than commercial stimulator at record-low currents with damage-free to sympathetic neurons. Additionally, using transgenic mice, the anti-inflammation effect is determined by β2 adrenergic signaling from myeloid cell lineage (monocytes/macrophages and granulocytes).

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Section: Resultsmentioning

confidence: 99%