Contaminated food through dietary intake has become the main potential risk impacts on human health. This study investigated concentrations of rare earth elements (REEs) in soil, vegetables, human hair and blood, and assessed human health risk through vegetables consumption in the vicinity of a large-scale mining area located in Hetian Town of Changting County, Fujian Province, Southeast China. The results of the study included the following mean concentrations for total and bio-available REEs of 242.92 ± 68.98 (135.85-327.56)μg g(-1) and 118.59 ± 38.49 (57.89-158.96)μg g(-1) dry weight (dw) in agricultural soil, respectively, and total REEs of 3.58 ± 5.28 (0.07-64.42)μg g(-1) dw in vegetable samples. Concentrations of total REEs in blood and hair collected from the local residents ranged from 424.76 to 1274.80 μg L(-1) with an average of 689.74 ± 254.25 μg L(-1) and from 0.06 to 1.59 μg g(-1) with an average of 0.48 ± 0.59 μg g(-1) of the study, respectively. In addition, a significant correlation was observed between REEs in blood and corresponding soil samples (R(2)=0.6556, p<0.05), however there was no correlation between REEs in hair and corresponding soils (p>0.05). Mean concentrations of REEs of 2.85 (0.59-10.24)μg L(-1) in well water from the local households was 53-fold than that in the drinking water of Fuzhou city (0.054 μg L(-1)). The health risk assessment indicated that vegetable consumption would not result in exceeding the safe values of estimate daily intake (EDI) REEs (100-110 μg kg(-1)d(-1)) for adults and children, but attention should be paid to monitoring human beings health in such rare earth mining areas due to long-term exposure to high dose REEs from food consumptions.

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This retrospective study aimed to evaluate the effectiveness and safety of 3 surgical procedures for Spontaneous Supratentorial Intracerebral Hemorrhage (SICH).A total of 63 patients with SICH were randomized into 3 groups. Group A (n = 21) underwent craniotomy surgery, group B (n = 22) underwent burr hole, urokinase infusion and catheter drainage, and group C (n = 20) underwent neuroendoscopic surgery. The hematoma evacuation rate of the operation was analyzed by 3D Slice software and the average surgery time, visualization during operation, decompressive effect, mortality, Glasgow Coma Scale (GCS) improvement, complications include rebleeding, pneumonia, intracranial infection were also compared among 3 groups.All procedures were successfully completed and the hematoma evacuation rate was significant differences among 3 groups which were 79.8%, 43.1%, 89.3% respectively (P < .01), and group C was the highest group. Group B was smallest traumatic one and shared the shortest operation time, but for the lack of hemostasis, it also the highest rebleeding group (P = .03). Although there were different in complications, but there was no significant in pneumonia, intracranial infection, GCS improvement and mortality rate.All these 3 methods had its own advantages and shortcomings, and every approach had its indications for SICH. Although for neuroendoscopic technical's minimal invasive, direct vision, effectively hematoma evacuation rate, and the relatively optimistic result, it might be a more promising approach for SICH.

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The gasdermin (GSDM) family act as executioners during pyroptosis. However, its expression and biological role in glioma remain to be determined. This study carried out gene expression from six public datasets. Westerns blots and immunohistochemistry (IHC) staining were employed to examine GSDM expression in glioma in an in-house cohort. Kaplan–Meier and Cox regression analyses were performed to evaluate the prognostic role of GSDMs in glioma. Association between gene expression and immune infiltration was assessed by IHC and immunofluorescence (IF) staining of tissue sections. TMZ-induced pyroptosis was assessed by observation of morphological changes, WB and ELISA detection. Only GSDMD expression was upregulated in glioma compared with nontumor brain tissues both in the public datasets and in-house cohort. High GSDMD expression was significantly associated with WHO grade IV, IDH 1/2 wild-type and mesenchymal subtypes. Besides, high GSDMD expression was associated with shorter overall survival and could be used as an independent risk factor for poor outcomes in LGG and GBM. GO enrichment analysis and IHC validation revealed that GSDMD expression might participate in regulating macrophage infiltration and polarization. TMZ treatment induced the pyroptosis in GBM cells and GSDMD expression increased with after treating with TMZ in a time-dependent manner. Moreover, knocking down GSDMD obviously decreased IL-1β expression and reduced TMZ-induced pyroptosis in in vitro. GSDMD was a novel prognostic biomarker, as well as TMZ-treatment response marker in glioma.

Malignant glioma remains the most frequent form of primary brain tumors all over the world. The gliomagenesis is characterized by various molecular processes such as neoplastic transformation, dysregulation of the cell cycle, and angiogenesis. Among these biomolecular events, the existence of inflammation and oxidative stress pathways in the development of glioma has been reported. PTPN2 is associated with several inflammatory disorders. However, the biological role of PTPN2 in inflammation responses and oxidative stress pathways involved in glioma remains poorly known. Here, we focused on its function in glioma development. Here, we observed that PTPN2 was significantly increased in glioma especially in a grade‐dependent manner. Meanwhile, interferon‐γ and tumor necrosis factor‐α, which have been identified as crucial inflammation cytokines, were able to trigger PTPN2 expression in a dose‐dependent course in T98G cells. Then, we found that PTPN2 was oxidated and inactivated by H2O2. Meanwhile, H2O2 induced glioma cell colony formation capacity and increased ki‐67 expression confirmed by flow cytometry assay. Finally, T98G cells were transfected with PTPN2 shRNA and it was shown that knockdown of PTPN2 obviously inhibited T98G cell colony formation and induced cell apoptosis. In summary, our findings indicated that PTPN2 could be induced by inflammatory response and oxidative stress and its deficiency depressed glioma cell growth.