Sonocatalytic nanoagents (SCNs), a kind of sonosensitizers, could catalyze oxygen to generate abundant reactive oxygen species (ROS) under stimulations of noninvasive and deep-penetrating ultrasound (US), which is commonly used for sonodynamic therapy (SDT) of tumors such as malignant melanoma. However, poor bioavailability of most SCNs and fast quenching of extracellular-generating ROS from SDT limit further applications of SCNs in the SDT of tumors. Herein, we synthesized a new kind of TiO 2 -based SCN functionalized with the malignant melanoma cell membrane (B16F10M) and programmed cell death-ligand 1 antibody (aPD-L1) for homology and immune checkpoint dual-targeted and enhanced sonodynamic tumor therapy. Under US irradiation, the synthesized SCN can catalytically generate a large amount of 1 O 2 .In vitro experiments validate that functionalized SCNs exhibit precise targeting effects, high tumor cell uptake, and intracellular sonocatalytic killing of the B16F10 cells by a large amount of localized ROS. Utilizing the melanoma animal model, the functionalized SCN displays visible long-term retention in the tumor area, which assists the homology and immune checkpoint synergistically dual-targeted and enhanced in vivo SDT of the tumor. We suggest that this highly bioavailable and dual-functionalized SCN may provide a promising strategy and nanoplatform for enhancing sonodynamic tumor therapies.
Background: Achilles tendinopathy is a frequent sports injury, and extracorporeal shock wave therapy (ESWT) has been proposed as a treatment. Purpose: To compare outcomes between ESWT and other nonsurgical intervention (including sham shock wave therapy) in Achilles tendinopathy patients. Study Design: Systematic review; Level of evidence, 2. Methods: We included 5 randomized controlled trials and 3 case-control studies published between 2005 and 2018. We analyzed pain scores and other outcomes that were reported in more than 3 of the 8 studies. Results: ESWT was associated with significantly better scores than comparison therapy on the visual analog scale for pain ( P < .01), American Orthopaedic Foot & Ankle Society scale ( P = .01), Likert scale for satisfaction ( P = .03), Roles and Maudsley scale ( P < .01), Victorian Institute of Sports Assessment–Achilles questionnaire ( P < .01), and numerical rating scale ( P = .02). The 2 patient groups did not differ significantly in tenderness ( P = .34) or pain threshold ( P = .24). Subgroup analysis showed that ESWT led to better VAS pain scores than comparison treatments at both low-energy level (0.06-0.11 mJ/mm2) and medium-energy level (0.12-0.25 mJ/mm2) and at both shorter (<6 months) and longer (≥6 months) follow-up. Conclusion: ESWT improves pain and functional outcomes in patients with Achilles tendinopathy. Further research is needed to determine the optimal energy level.
As an electrophilic nitroalkene fatty acid, nitro-oleic acid (OA-NO2) exerts multiple biological effects that contribute to anti-inflammation, anti-oxidative stress, and antiapoptosis. However, little is known about the role of OA-NO2 in peritoneal fibrosis. Thus, in the present study, we examined the effects of OA-NO2 on the high glucose (HG)-induced epithelial-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs) and evaluated the morphological and immunohistochemical changes in a rat model of peritoneal dialysis-related peritoneal fibrosis. In in vitro experiments, we found that HG reduced the expression level of E-cadherin and increased Snail, N-cadherin, and α-smooth muscle actin expression levels in HPMCs. The above-mentioned changes were attenuated by pretreatment with OA-NO2. Additionally, OA-NO2 also inhibited HG-induced activation of the transforming growth factor-β1/Smad signaling pathway and NF-κB signaling pathway. Meanwhile, OA-NO2 inhibited HG-induced phosphorylation of Erk and JNK. The results from the in vivo experiments showed that OA-NO2 notably relieved peritoneal fibrosis by decreasing the thickness of the peritoneum; it also inhibited expression of transforming growth factor-β1, α-smooth muscle actin, N-cadherin, and vimentin and enhanced expression of E-cadherin in the peritoneum. Collectively, these results suggest that OA-NO2 inhibits the HG-induced epithelial-mesenchymal transition in HPMCs and attenuates peritoneal dialysis-related peritoneal fibrosis.
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