The relationship between miRNA-210 and SCN1B in fetal rats with hypoxic-ischemic brain injury.

Hypoxic-ischemic brain injury contributes to major neurodevelopmental disorders and is one of the leading causes of seizures, which substantially results in neurodevelopmental impairments with long-lasting outcomes and is one of the main causes of death in neonates. We aimed to investigate the correlation between miRNA-210 and SCN1B, a voltage-gated sodium channel gene, in brain tissue of fetal rats with hypoxic-ischemic brain injury. We found that after 10 min of hypoxia-ischemia, all reperfusion groups showed different degrees of damage. The degree of the injury increased in all the groups after 30 min of hypoxia-ischemia. Those changes include changes in the pericellular lumen, capillaries in the cortex, erythrocytes, enlarged pericellular lumen, the enlarged pericapillary lumen in the cortex, edema around glial cells, enlarged gap to form multiple necrotic foci, deformation of neurons, and loss of cell structure. The expression levels of HIF-1α, miRNA-210, and HIF-1α mRNA were higher in the hypoxic-ischemic groups than that in the control groups, among which the expression levels in the severe group were higher than that in mild group. SCN1B is down-regulated in both the mild and severe groups, and the lowest level was found at 30 min after hypoxia in both groups. MiRNA-210 plays a role in the development of hypoxic-ischemic encephalopathy (HIE) by regulating the expression changes of SCN1B. The brain tissue of fetal rats in the hypoxic-ischemic animal model showed pathological changes of brain injury.

Influence of Monocalcium Phosphate on the Properties of Bioactive Magnesium Phosphate Bone Cement for Bone Regeneration.

Bone defects occurring for various reasons can lead to deformities and dysfunctions of the human body. Considering the need for clinical applications, it is essential for bone regeneration to exploit a scaffold with bioactive bone cement. In this study, we fabricated bioactive magnesium phosphate bone cement (BMPC) at room temperature; then, it was set at to °C and 100% humidity for 2 h. The process was as follows: Simulating a clinical environment, magnesium oxide (MgO) was formed by calcining basic magnesium carbonate (Mg2(OH)2CO3). MgO, potassium dihydrogen phosphate (KH2PO4) and carboxymethyl chitosan (C20H37N3O14, CMC) were mixed to form magnesium phosphate bone cement (MPC); then, monocalcium phosphate (Ca(H2PO4)2) was added to neutralize the alkaline product after MPC hydration to fabricate bioactive magnesium phosphate bone cement (BMPC). The influence of the doped content of Ca(H2PO4)2 on the properties of bone cement was discussed. The results showed that Ca(H2PO4)2 and CMC can adjust the setting time of bone cement to between 8 and 25 min. The compressive strength increased first and then decreased. After 48 h without additional pressure, the compressive strength reached the maximum value, which was about 38.6 MPa. Ca(H2PO4)2 and CMC can play a synergistic role in regulating the properties of BMPC. The BMPC was degradable in the simulated body fluid (SBF). The results of the cytotoxicity experiment and laser confocal microscopy experiment indicated that BMPC fabricated at room temperature had better biocompatibility and degradability, which was more consistent with clinical operation requirements. BMPC is a promising orthopedic material and is suitable for repairing bone defects.