Sandblasting increases the microtensile bond strength between resin and sclerotic dentin in noncarious cervical lesions.

PURPOSE: To evaluate the effect of sandblasting on the microtensile strength between sclerotic dentin and resin composite. METHODS: 32 premolars with noncarious cervical lesions (NCCLs) were collected, and the teeth were randomly assigned to the control group (C group) and the sandblasted group (S group). Teeth in the S group were sandblasted with 110 µm Al2O3 particles at a pressure of 75 psi, while those in the C group received no further treatment. The characteristics of the tooth surface were observed by scanning electron microscopy (SEM), and the relative area of open dentin tubules (OTs) was calculated by IPP6.0 software. Surface roughness (Ra) was also assessed. The noncarious cervical lesions of all teeth were restored with a resin composite and subsequently sectioned into sticks to measure the microtensile bond strength (µTBS). RESULTS: The mean ± SD µTBS (in MPa) of the sandblasted group was 17.9 ± 0.69 and 14.23 ± 0.44 in the control group (P< 0.05). The relative area of OTs at the gingival wall of the sandblasted group was 69.74 ± 5.23%, and 47.24 ± 7.67% in the control group (P< 0.05). The average surface roughness (µm) was 1.01 ± 0.05 in the sandblasted group and 0.16 ± 0.03 in the control group. Sandblasting could increase the bond strength of sclerotic dentin and resin restorations. CLINICAL SIGNIFICANCE: After sandblasting, the microtensile strength of sclerotic dentin on the surface of noncarious cervical lesions increased, prolonging the resin adhesion longevity. Sandblasting could also alleviate the pain of patients during the treatment process and achieve a minimally invasive treatment.

FUS Selectively Facilitates circRNAs Packing into Small Extracellular Vesicles within Hypoxia Neuron.

Small extracellular vesicles (sEVs) contain abundant circular RNAs (circRNAs) and are involved in cellular processes, particularly hypoxia. However, the process that packaging of circRNAs into neuronal sEVs under hypoxia is unclear. This study revealed the spatial mechanism of the Fused in Sarcoma protein (FUS) that facilitates the loading of functional circRNAs into sEVs in hypoxia neurons. It is found that FUS translocated from the nucleus to the cytoplasm and is more enriched in hypoxic neuronal sEVs than in normal sEVs. Cytoplasmic FUS formed aggregates with the sEVs marker protein CD63 in cytoplasmic stress granules (SGs) under hypoxic stress. Meanwhile, cytoplasmic FUS recruited of functional cytoplasmic circRNAs to SGs. Upon relief of hypoxic stress and degradation of SGs, cytoplasmic FUS is transported with those circRNAs from SGs to sEVs. Validation of FUS knockout dramatically reduced the recruitment of circRNAs from SGs and led to low circRNA loading in sEVs, which is also confirmed by the accumulation of circRNAs in the cytoplasm. Furthermore, it is showed that the FUS Zf_RanBP domain regulates the transport of circRNAs to sEVs by interacting with hypoxic circRNAs in SGs. Overall, these findings have revealed a FUS-mediated transport mechanism of hypoxia-related cytoplasmic circRNAs loaded into sEVs under hypoxic conditions.