Neuroblastoma is one of the leading causes of cancer‑associated mortality worldwide, particularly in children, partially due to the absence of effective therapeutic targets and diagnostic biomarkers. Therefore, novel molecular targets are critical to the development of therapeutic approaches for neuroblastoma. In the present study, the functions of zinc transporter ZIP8 (Zip8), a member of the zinc transporting protein family, were investigated as novel molecular targets in neuroblastoma cancer cells. The proliferation rates of neuroblastoma cancer cells were significantly decreased when Zip8 was knocked down by lentiviral‑mediated RNA interference. Study of the molecular mechanism suggested that Zip8 modulated the expression of key genes involved in the nuclear factor‑κB signaling pathway. Furthermore, Zip8 depletion suppressed the migratory potential of neuroblastoma cancer cells by reducing the expression levels of matrix metalloproteinases. In conclusion, the results of the present study suggested that Zip8 was an important regulator of neuroblastoma cell proliferation and migration, indicating that Zip8 may be a potential anticancer therapeutic target and a promising diagnostic biomarker for human neuroblastoma.
To observe the effect of puerarin on learning and memory function and tau phosphorylation in APP/PS1 transgenic mice, drugs were administered to 3-month old APP/PS1 transgenic mice. Learning and memory function of mice were assessed by Morris water maze test 3 months after treatment. Animals were decapitated after behavioral test. The levels of Aβ were detected by ELISA, the expression of protein [tau, phosphorylated tau, GSK3β and p-GSK3β(Ser9)] were assessed by Western blot. Morris water maze test showed that the escape latency of APP/PS1 double transgenic mice was significantly longer than that of the normal control group, and the residence time of the original quadrant was significantly shorter. The escape latency of puerarin group was significantly shorter and the residence time of the original quadrant was prolonged compared with the model group. Compared with the normal control group, the levels of Aβ in the cortex of APP/PS1 transgenic mice were increased, the expression of phosphorylated tau was significantly increased, and the expression of phosphorylated GSK3β(Ser9) protein was decreased. Treatment with puerarin, the latency of APP/PS1 transgenic mice was significantly reduced, the level of Aβ was decreased, the expression of phosphorylated tau was significantly decreased, and the expression of phosphorylated GSK3β(Ser9) protein was increased. Puerarin improves the learning and memory impairment by reducing the formation of Aβ, activating the GSK3β signaling pathway, inhibiting the phosphorylation of tau in APP/PS1 double transgenic mice.
Phenolic molecules are a kind of toxic organic pollutants commonly discharged from industrial effluents. Catalytic ozonation holds great potential in removing phenolic pollutants and further improving the removal efficiency is still the research focus of this field. In this study, defect engineering was used to construct Bi 2 O 3 with rich oxygen vacancies (denoted as O v -Bi 2 O 3 ). O v -Bi 2 O 3 was found to exhibit efficient activity toward the removal of phenolic derivatives. Combined DFT calculations and experimental results suggest that oxygen vacancies play two important roles: (1) the exposed Bi sites induced by rich oxygen vacancies endow a special bridging O 3 adsorption, which is beneficial to improve the kinetics of O 3 decomposition; (2) O 2 produced during the O 3 decomposition process can be reutilized to generate 1 O 2 , which prolongs the utilization efficiency of O 3 . In addition, O v -Bi 2 O 3 was loaded onto carbon fiber, which also demonstrates efficient activity. This work provides an alternative way to design efficient catalysts toward removal of phenolic pollutants via ozone oxidation.
Background The global prevalence of autism spectrum disorder (ASD) is on the rise, and high levels of exposure to toxic heavy metals may be associated with this increase. Urine analysis is a noninvasive method for investigating the accumulation and excretion of heavy metals. The aim of this study was to identify ASD-associated urinary metal markers. Methods Overall, 70 children with ASD and 71 children with typical development (TD) were enrolled in this retrospective case—control study. In this metallomics investigation, inductively coupled plasma mass spectrometry was performed to obtain the urine profile of 27 metals. Results Children with ASD could be distinguished from children with TD based on the urine metal profile, with ASD children showing an increased urine metal Shannon diversity. A metallome-wide association analysis was used to identify seven ASD-related metals in urine, with cobalt, aluminum, selenium, and lithium significantly higher, and manganese, mercury, and titanium significantly lower in the urine of children with ASD than in children with TD. The least absolute shrinkage and selection operator (LASSO) machine learning method was used to rank the seven urine metals in terms of their effect on ASD. On the basis of these seven urine metals, we constructed a LASSO regression model for ASD classification and found an area under the receiver operating characteristic curve of 0.913. We also constructed a clinical prediction model for ASD based on the seven metals that were different in the urine of children with ASD and found that the model would be useful for the clinical prediction of ASD risk. Conclusions The study findings suggest that altered urine metal concentrations may be an important risk factor for ASD, and we recommend further exploration of the mechanisms and clinical treatment measures for such alterations.
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