Additional file 1: of Periosteal progenitors contribute to load-induced bone formation in adult mice and require primary cilia to sense mechanical stimulation

Figure S1. Mice lacking OCPs lack load-induced osteoblast differentiation at the periosteal surface. H&E stains of tissue sections from control (left) and experimental animals (right). Control animals exhibited differentiating osteoblasts at the periosteal surface (left, black box). These differentiating osteoblasts were not observed in animals with ablated OCPs (right) or the nonloaded contralateral limbs of both groups (data not shown). Micrographs were collected at 20X magnification. (TIF 7918 kb

Acoustic triggered nanobomb for US imaging guided sonodynamic therapy and activating antitumor immunity

We fabricated an ultrasound activated ‘nanobomb’ as a noninvasive and targeted physical therapeutic strategy for sonodynamic therapy and priming cancer immunotherapy. This ‘nanobomb’ was rationally designed via the encapsulation of indocyanine green (ICG) and perfluoropentane (PFP) into cRGD peptide-functionalized nano-liposome. The resulting Lip-ICG-PFP-cRGD nanoparticle linked with cRGD peptide could actively targeted ID8 and TC-1 cells and elicits ROS-mediated apoptosis after triggered by low-intensity focused ultrasound (LIFU). Moreover, the phase change of PFP (from droplets to microbubbles) under LIFU irradiation can produce a large number of microbubbles, which act as intra-tumoral bomber and can detonate explode tumor cells by acoustic cavitation effect. Instant necrosis of tumor cells further induces the release of biologically active damage-associated molecular patterns (DAMPs) to facilitate antitumor immunity. More important, the ‘nanobomb’ in combination with anti-PD-1checkpoint blockade therapy can significantly improve the antitumor efficacy in a subcutaneous model. In addition, the liposomes may also be used as an imaging probe for ultrasound (US) imaging after being irradiated with LIFU. In summary, the US imaging-guided, LIFU activated ROS production and explosion ‘nanobomb’ might significantly improve the antitumor efficacy and overcome drug resistance through combination of SDT and immunotherapy, we believe that this is a promising approach for targeted therapy of solid tumor including ovarian cancer. This ‘nanobomb’ was rationally designed via the encapsulation of ICG and PFP into cRGD peptide-functionalized nano-liposome. The US imaging-guided, LIFU activated ROS production and explosion ‘nanobomb’ can significantly improve anti-cancer efficacy and overcome drug resistance through combination of SDT and immunotherapy.</p

Additional file 2 of Identification of characteristic genes and construction of regulatory network in gallbladder carcinoma

Additional file 2: Table S1. Total differentially expressed miRNAs in GBC and normal tissues

Additional file 3 of Identification of characteristic genes and construction of regulatory network in gallbladder carcinoma

Additional file 3: Table S2. The 131 GBC-related DE-miRNAs

Additional file 4 of Identification of characteristic genes and construction of regulatory network in gallbladder carcinoma

Additional file 4: Table S3.The miRNA enrichment analysis results of dysregulated miRNAs

Additional file 8 of Identification of characteristic genes and construction of regulatory network in gallbladder carcinoma

Additional file 8: Table S7. Five molecular functions entries analysis of ceRNA regulatory network

Additional file 9 of Identification of characteristic genes and construction of regulatory network in gallbladder carcinoma

Additional file 9: Table S8. One KEGG pathway analysis of ceRNA regulatory network

Additional file 1 of Identification of characteristic genes and construction of regulatory network in gallbladder carcinoma

Additional file 1: Figure S1. Heatmap plot for the enriched pathways by miEAA

Environmentally Relevant Concentrations of the Flame Retardant Tris(2-butoxyethyl) Phosphate Accelerate <i>Caenorhabditis elegans</i> Senescence

Amid growing concerns surrounding the longevity of individuals, the acceleration of aging by pollutants has garnered significant attention. Tris­(2-butoxyethyl) phosphate (TBOEP), a widely used organophosphorus flame retardant (OPFR), has been frequently detected in the environment; however, its impact on organism life spans remains unclear. This study investigated the effects of TBOEP on the life span of Caenorhabditis elegans at environmentally relevant concentrations of 0, 50, 500, and 5000 ng/L. TBOEP exposure reduced motility and shortened the life span of C. elegans in a dose-dependent manner, with the most significant effects observed at 5000 ng/L. Transcriptomics and metabolomics revealed that 5000 ng/L TBOEP significantly disrupted longevity regulation in C. elegans. This was mainly attributed to the abnormal regulation of genes encoding the heat shock proteins, lipase, and stearoyl-CoA desaturase as well as the increased l-arginine content in C. elegans. Concurrently, exposure to 5000 ng/L TBOEP significantly upregulated the microRNAs in the lethal-7 family, thereby accelerating C. elegans senescence. Overall, this study provides important insights into the effects of TBOEP on C. elegans senescence and could inform further studies assessing the environmental health risks of OPFRs

Environmentally Relevant Concentrations of the Flame Retardant Tris(2-butoxyethyl) Phosphate Accelerate <i>Caenorhabditis elegans</i> Senescence

Amid growing concerns surrounding the longevity of individuals, the acceleration of aging by pollutants has garnered significant attention. Tris­(2-butoxyethyl) phosphate (TBOEP), a widely used organophosphorus flame retardant (OPFR), has been frequently detected in the environment; however, its impact on organism life spans remains unclear. This study investigated the effects of TBOEP on the life span of Caenorhabditis elegans at environmentally relevant concentrations of 0, 50, 500, and 5000 ng/L. TBOEP exposure reduced motility and shortened the life span of C. elegans in a dose-dependent manner, with the most significant effects observed at 5000 ng/L. Transcriptomics and metabolomics revealed that 5000 ng/L TBOEP significantly disrupted longevity regulation in C. elegans. This was mainly attributed to the abnormal regulation of genes encoding the heat shock proteins, lipase, and stearoyl-CoA desaturase as well as the increased l-arginine content in C. elegans. Concurrently, exposure to 5000 ng/L TBOEP significantly upregulated the microRNAs in the lethal-7 family, thereby accelerating C. elegans senescence. Overall, this study provides important insights into the effects of TBOEP on C. elegans senescence and could inform further studies assessing the environmental health risks of OPFRs