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Background: Single‐cell RNA sequencing analysis has been usually conducted on post‐traumatic epilepsy (PET) and hereditary epilepsy (HE) patients; however, the transcriptome of patients with traumatic temporal lobe epilepsy has rarely been studied. Materials and Methods: Hippocampus tissues isolated from one patient with PTE and one patient with HE were used in the present study. Single cell isolates were prepared and captured using a 10× Genomics Chromium Single‐Cell 3′ kit (V3) according to the manufacturer's instructions. The libraries were sequenced on an Illumina NovaSeq 6000 sequencing system. Raw data were processed, and the cells were filtered and classified using the Seurat R package. Uniform Manifold Approximation and Projection was used for visualization. Differentially expressed genes (DEGs) were identified based on a p‐value ≤0.01 and log fold change (FC) ≥0.25. Gene Ontology (GO, http://geneontology.org/) and KEGG (Kyoto Encyclopedia of Genes and Genomes, www.genome.jp/kegg) analyses were performed on the DEGs for enrichment analysis. Results: The reads obtained from the 10× genomic platform for PTE and HE were 39.56 M and 30.08 M, respectively. The Q30 score of the RNA reads was >91.6%. After filtering, 7479 PTE cells and 9357 HE cells remained for further study. More than 96.4% of the reads were mapped to GRCh38/GRCm38. The cells were differentially distributed in two groups, with higher numbers of oligodendrocytes (6522 vs. 2532) and astrocytes (133 vs. 52), and lower numbers of microglial cells (2242 vs. 3811), and neurons (3 vs. 203) present in the HE group than in the PTE group. The DEGs in four cell clusters were identified, with 25 being in oligodendrocytes (13 upregulated and 12 downregulated), 87 in microglia cells (42 upregulated and 45 downregulated), 222 in astrocytes (115 upregulated and 107 downregulated), and 393 in neurons (305 upregulated and 88 downregulated). The genes MTND1P23 (downregulated), XIST (downregulated), and RPS4Y1 (upregulated) were commonly expressed in all four cell clusters. The DEGs in microglial cells and astrocytes were enriched in the IL‐17 signaling pathway. Conclusion: Our study explored differences in cells found in a patient with PE compared to a patient with HE, and the transcriptome in the different cells was analyzed for the first time. Studying inflammatory and immune functions might be the best approach for investigating traumatic temporal lobe epilepsy in neurons. [ABSTRACT FROM AUTHOR]

Ellagic acid is one of the most representative natural antioxidants, and is rich in pomegranate peel. In this study, a consecutive countercurrent chromatographic (CCC) separation method was established to improve the preparative efficiency of ellagic acid from pomegranate peel. By optimizing the solvent system, sample size and flow rate, 280 mg of ellagic acid was obtained from 5 g of crude sample from pomegranate peel by CCC after six consecutive injections. Moreover, the values of EC50 for ellagic acid in scavenging ABTS·+ and DPPH· were 4.59 ± 0.07 and 10.54 ± 0.07 μg/ml, respectively, indicating a strong antioxidant activity. This study not only established a high‐throughput method for the preparation of ellagic acid, but also provided a successful example for the development of and research on other natural antioxidants. [ABSTRACT FROM AUTHOR]

The Neoproterozoic evolution of the Jiangnan Orogen is important for understanding the tectonic history of South China. As a volcanic‐sedimentary sequence developed in the Nanhua rift, the Banxi Group preserves the records of important magmatic and tectonic events linked to the assembly and breakup of the Rodinia supercontinent. In this study, we report the results from whole‐rock major‐ and trace‐element concentrations, with zircon LA‐(MC)‐ICP‐MS U‐Pb ages, trace elements and Lu‐Hf isotopic compositions of sandstones from the Banxi Group. The rocks are characterized by high SiO2 (65.88%–82.76%, with an average of 75.50%) contents, moderate (Fe2O3T + MgO) (1.81%–7.78%, mean: 3.79%) and TiO2 (0.39%–0.54%, mean: 0.48%), low K2O/Na2O (0.03–0.40, mean: 0.10) ratios and low Al2O3/SiO2 (0.11–0.24, mean: 0.15) ratios. The sandstones have high ΣREE contents (mean: 179.1 ppm), with chondrite‐normalized REE patterns similar to the upper crust and PAAS, showing enriched LREE ((La/Yb)N mean: 14.85), sub‐horizontal HREE curves and mild Eu (Eu/Eu*: 0.75–0.89, mean: 0.81) negative anomalies. Their geochemical characteristics resemble those of passive continental margin sandstones. Most of the zircons are magmatic in origin and yield a U‐Pb age distribution with three peaks: a major age peak at 805 Ma and two subordinate age peaks at 1990 Ma and 2470 Ma, implying three major magmatic sources. The Neoproterozoic zircons have ɛHf(t) values ranging from –47.4 to 12.4 (mostly –20 to 0), suggesting a mixture of some juvenile arc‐derived material and middle Paleoproterozoic heterogeneous crustal sources. The Hf model ages of middle Paleoproterozoic zircons (∼1990 Ma) with negative ɛHf(t) values (–12.65 to –6.21, Ave. = –9.8) concentrated around the Meso‐Paleoarchean (mean TDMC = 3.3–3.1 Ga). For late Neoarchean detrital zircons (∼2470 Ma), ɛHf(t) values are divided into two groups, one with negative values (–9.16 to –0.6) with model ages of 3.5–2.9 Ga, the other featuring positive values (1.0 to 3.9) with model ages of 2.9–2.7 Ga, recording a crustal growth event at ∼2.5 Ga. Neoproterozoic zircons show volcanic arc affinities with partly intraplate magmatic features. We propose that the Banxi Group formed in a rift basin within a passive continental margin setting, which derived detritus from felsic to intermediate rocks from the Yangtze Block and a small amount of arc volcanic rocks. The middle Paleoproterozoic detrital zircon data suggest Columbia‐aged basement lies beneath the western Jiangnan orogen. [ABSTRACT FROM AUTHOR]

MAP kinase phosphatase 1 (MKP1) has been identified as an antiapoptotic protein via sustaining mitochondrial function. However, the role of MKP1 in neuroinflammation has not been fully understood. The aim of this study is to figure out the influence of MKP1 in lipopolysaccharide (LPS)‐treated microglia BV‐2 cells and investigate whether MKP1 reduces BV‐2 cell death via modulating endoplasmic reticulum (ER) stress and mitochondrial dysfunction. The results of this study demonstrated that MKP1 was rapidly downregulated after exposure to LPS. However, the transfection of MKP1 adenovirus could reverse cell viability and attenuate LPS‐mediated BV‐2 cell apoptosis. Mechanistically, MKP1 overexpression alleviated ER stress and corrected LPS‐induced calcium overloading. Besides, MKP1 adenovirus transfection also reversed mitochondrial bioenergetics, maintained mitochondrial membrane potential, and blocked mitochondria‐initiated apoptosis signals. Furthermore, we found that MKP1 overexpression is associated with inactivation of mitogen‐activated protein kinase–c‐Jun N‐terminal kinase (MAPK–JNK) pathway. Interestingly, the activation of MAPK–JNK pathway could abolish the protective effects of MKP1 on BV‐2 cells survival and mitochondrial function in the presence of LPS. Altogether, our results identified MKP1 as a primary defender of neuroinflammation via modulating ER stress and mitochondrial function in a manner dependent on MAPK–JNK pathway. These findings may open a new window for the treatment of neuroinflammation in the clinical setting. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction has been found to be associated with neuronal inflammation; however, no effective drug is available to attenuate neuroinflammation via sustaining mitochondrial function. In the current study, experiments were performed to understand the beneficial effects of mitochonic acid 5 (MA‐5) on tumor necrosis factor‐α (TNF‐α)‐mediated neuronal injury and mitochondrial damage. Our data illustrated that MA‐5 pretreatment reduced inflammation response induced by TNF‐α in CATH.a cells. Molecular investigations demonstrated that MA‐5 pretreatment repressed oxidative stress, inhibited endoplasmic reticulum stress, sustained cellular energy metabolism, and blocked cell apoptosis induced by TNF‐α stress. Further, we found that MA‐5 treatment elevated the expression of Sirtuin 3 (Sirt3) and this effect was dependent on the activation of AMP‐activated protein kinase (AMPK) pathway. Blockade of AMPK abolished the promotive action of MA‐5 on Sirt3 and thus mediated mitochondrial damage and cell death. Besides, we also found that MA‐5 treatment augmented Parkin‐related mitophagy and increased mitophagy promoted CATH.a cells survival via improving mitochondrial function. Knockdown of Parkin abolished the beneficial action of MA‐5 on mitochondrial homeostasis and CATH.a cell survival. Altogether, our results confirm that MA‐5 is an effective drug to attenuate neuroinflammation via sustaining mitochondrial damage and promoting CATH.a cell survival. The protective action of MA‐5 on neuronal damage is associated with Parkin‐related mitophagy and the activation of AMPK–Sirt3 pathways. [ABSTRACT FROM AUTHOR]

The article discusses geochemical characteristics of adakitic rocks and mineralization of copper (Cu)-gold (Au) in the Tianzishan Region, Gansu Sheng, China, West Qinling orogenic belt. Topics discussed include formation of adakitic rocks in the high temperature, correlation of most gold and adakite in spatial distribution and temporal of gold deposit in West Qinling orogenic belt, and consists of monzogranite in Tianzishan rocks.