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Anionic redox activity can trigger structural instability in Li‐rich Mn‐based cathodes. Lattice oxygen activity can be tuned through liquid acid‐induced spinel phases and oxygen vacancies. However, the liquid‐acid‐modified surface is still attacked by the electrolyte. Besides, the underlying mechanism of spinel phase suppression of lattice oxygen activity is controversial. Here, a solid acid strategy for modification is proposed and the underlying mechanism is investigated in detail. Unique solid acid can in situ generate an interface protection layer and remarkably stabilize the structure. Theoretical calculations and experimental characterizations reveal that the spinel phase suppresses the irreversible loss of lattice oxygen by decreasing the O 2p non‐bonding energy level and enriching electrons at the layered/spinel phase interface. The inert layer on the surface prevents highly active On− from being attacked by electrolytes. The obtained material exhibits significantly reduced irreversible lattice oxygen release and improved electrochemical performance. After 300 cycles, a slow capacity fading of 0.177 mAh g−1 per cycle and suppressed voltage fading are achieved. This study reveals the regulation method and mechanism for the anion activity of oxide cathodes in next‐generation Li‐ion batteries. [ABSTRACT FROM AUTHOR]

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Objective To systematically review the overall status of postoperative recurrence in patients with atypical meningiomas. Methods China National Knowledge Infrastructure,Wanfang Database,Chinese Biomedical Literature Database,VIP Database,PubMed,Embase,Web of Science,and Cochrane Library were searched for collection of the relevant literature on the recurrence of atypical meningioma from database establishment to July 2021.Two investigators independently screened the literature,extracted data,and assessed the risk of bias of the included studies,and then performed a meta-analysis by using R 5.0. Results A total of 29 studies involving 3122 patients were included in this study.The meta-analysis showed that the overall postoperative recurrence rate of atypical meningioma was 38%.The subgroup analysis showed that the tumor recurrence rate of patients ≥60 years old and<60 years old was 51% and 40%,respectively,with no significant difference.The tumor recurrence rates in male and female patients were 42% and 44%,respectively,which showed no significant difference.The recurrence rates of the patients with parasagittal meningiomas,brain tissue infiltration,Ki-67>8%,mitotic count ≥6/10 high-power fields,and tissue necrosis were 52%,47%,63%,53%,and 69%,respectively.The recurrence rate after subtotal tumor resection was as high as 58%,and the patients who received radiotherapy had higher tumor recurrence rate than that those who did not receive radiotherapy (38% vs. 29%, P =0.007). Conclusions The current evidence demonstrates that atypical meningioma has a high recurrence rate after surgery.It is essential to pay more attention and take corresponding measures to improve the tumor-free survival rate of the patients.

Prostate cancer (PCa), as a malignant tumor originating in the prostate glandular epithelium, has become a global "killer" that threatens the health of elderly men. PCa-related studies have been focusing on the progression mechanisms and treatment strategies of the malignancy, particularly on the role of long non-coding RNA (lncRNA) in recent years. The lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a key role in the progression and treatment of PCa, as well as in its metastasis and invasion and cell proliferation. lncRNA MALAT1 not only influences the biological characteristics of PCa, but also has a regulatory effect on the medicinal treatment of the disease, its action mechanisms involving ceRNA and AR signaling pathways. This review focuses on the relationship between lncRNA MALAT1 and PCa, aiming to provide a new research direction for the diagnosis and treatment of the malignancy.

The distribution and vertical variation of phosphorus forms in sediments along Xiangxi River were analyzed with Hedley classification method, meanwhile the influences of physical and chemical properties of overlying and interstitial water on the release of phosphorus in sediment were discussed. The major findings showed that the pH values in the overlying and interstitial water increased from 4.72 to 8.55, and were slightly acidic in summer, while weak alkaline in other seasons. The redox potential of sediment was in the reduction state overall. The annual variation range of total phosphorus (TP) content in the overlying and interstitial water, and that in the sediment was 0.02-0.48 mg·L -1 and 0.48-1.45 g·kg -1 , respectively. The distribution features of TP content in the sediment were the same with those in the interstitial water along the Xiangxi River. It was interesting that the content of TP in the interstitial water in spring and summer was higher than that in autumn and winter, but that in the sediment of Xiangxi River was opposite. The content of different phosphorus (P) forms decreased successively:HCl-P (HCl extracted phosphorus)> Res-P (residual phosphorus)> NaOH-P (NaOH extracted phosphorus)> NaHCO 3 -P (NaHCO 3 extracted phosphorus)> H 2 O-P (water-soluable phosphorus). The reductive environment of the interface between sediment and overlying water, and pH of water in spring (weak alkaline) and summer (slightly acidic), were conducive to phosphorus release from sediment into overlying water, increasing the eutrophication risk. TP content in the interstitial water was closely related to that in sediment. The PO 4 3- -P in 4 sampling areas diffused from the interstitial water into the overlying water with diffusive fluxes in the range of 0.01-0.04 mg·(m 2 ·d) -1 . All of these findings indicated that sediments is an important source of nutrient for the overlying water.

Hepatitis B virus X protein (HBx) is involved in the pathogenesis of hepatocellular carcinoma (HCC). Overexpression of the transcripts from the P3 and P4 promoters of the insulin-like growth factor-II (IGF-II) gene is observed in HCC. The present study investigated the involvement of HBx in IGF-II overexpression and its epigenetic regulation. Firstly, the effects of HBx on P3 and P4 mRNA expression, the methylation status of the P3 and P4 promoters, and MBD2 expression were analyzed in human HCC cells and HCC samples. Next, interaction between HBx and MBD2 or CBP/p300 was assessed by co-immunoprecipitation, and HBx-mediated binding of MBD2 and CBP/p300 to the P3 and P4 promoters and the acetylation of the corresponding histones H3 and H4 were evaluated by quantitative chromatin immunoprecipitation. Finally, using siRNA knockdown, we investigated the roles of MBD2 and CBP/p300 in IGF-II overexpression and its epigenetic regulation. Our results showed that HBx promotes IGF-II expression via inducing the hypomethylation of the P3 and P4 promoters, and that HBx increases MBD2 expression, directly interacts with MBD2 and CBP/p300, and elevates their recruitment to the hypomethylated P3 and P4 promoters with increased acetylation levels of the corresponding histones H3 and H4. Further results showed that endogenous MBD2 and CBP/p300 are necessary for HBx-induced IGF-II overexpression and that CBP/p300 presence and CBP/p300-mediated acetylation of histones H3 and H4 are partially required for MBD2 binding and its demethylase activity. These data suggest that HBx induces MBD2-HBx-CBP/p300 complex formation via interaction with MBD2 and CBP/p300, which contributes to the hypomethylation and transcriptional activation of the IGF-II-P3 and P4 promoters and that CBP/p300-mediated acetylation of histones H3 and H4 may be a rate-limiting step for the hypomethylation and activation of these two promoters. This study provides an alternative mechanism for understanding the pathogenesis of HBx-mediated HCC.

Cardiovascular disease has been a huge threat to human health. Studies of cardiovascular disease is always an important field of basic medicine. Noncoding RNAs, once thought to be useless, are gaining attention from researchers along with the development of genetics and medical informatics. Most of noncoding RNAs are long noncoding RNA. Evidences suggest that long noncoding RNAs are connected to cardiovascular doisease, yet we still dont know much about their functions and how they work. Here we review the functions and characteristics of long noncoding RNAs and the relationship between long noncoding RNAs and cardiovascular disease. These studies may contribute to better comprehension of the etiology and pathophysiology of cardiovascular disease.

Objective: To investigate the expression of survivin in acute pancreatitis in rats., Methods: Acute pancreatitis was induced in rats by retrograde injection of sodium taurocholate into the pancreaticobiliary duct. The expressions of survivin in the pancreatic tissues was detected by immunohistochemisty, Western blotting and RT-PCR, and the apoptotic ratio of the acinar cells was determined by TUNEL assay., Results: Survivin was not detected in the control group, and in rat models of acute pancreatitis, the expressions of survivin protein and mRNA increased but the apoptotic index of the acinar cells decreased gradually with the severity of inflammation., Conclusion: Survivin is involved in the regulation of acinar cell apoptosis and also the necrosis of the apoptotic acinar cells through its anti-apoptosis activity to aggravate acute pancreatitis, suggesting its value as a promising marker in predicting the severity of acute pancreatitis.

Background: During hepatectomy, a period of ischemia and restoration of the blood supply can result in hepatic ischemia-reperfusion injury (IRI). Current research indicates that erythropoietin (EPO) has a protective effect in animal models of cerebral ischemia, myocardial infarction, and renal IRI. However there is lack of research into the role of EPO in hepatic IRI. This study aimed to explore the role of EPO in hepatic IRI and its possible mechanism of action., Methods: Thirty male Sprague-Dawley rats were divided into three groups: (1) ten rats in the experimental group were given 1000 IU/kg EPO one day before the operation; (2) ten rats in a control group were given normal saline preoperatively as a placebo; and (3) ten rats served as a sham-operated group. Hepatic IRI was induced by occluding the hepatic arteries of the three cephalad hepatic segments and the portal vein for about 45 minutes, while in the sham-operated group only laparotomy was performed. The levels of ALT and AST were tested 24 hours pre- and post-operation. All rats were sacrificed 24 hours after the operation to assess the pathologic changes in the liver and measure the expression of heme oxygenase-1 (HO-1) through Western blotting and RT-PCR., Results: Hepatic IRI was markedly mitigated in the experimental group as compared with the control group. Moreover, the expression of HO-1 at the level of both transcription and protein increased prominently (P<0.05) in the experimental group., Conclusion: These results demonstrate that EPO can up-regulate HO-1 in liver tissues and accordingly decrease hepatic injury through its anti-inflammatory property.

Objective: To investigate the effect of resveratrol on the apoptosis of pancreatic acinar cells in rats with severe acute pancreatitis (SAP) and explore the mechanism of such effect., Method: SD rats with 3.5% sodium taurocholate-induced SAP were treated with resveratrol, and the serum amylase was detected with automatic biochemistry analyzer. The apoptosis of the pancreatic acinar cells in the rats was detected by TUNEL assay, and the expression of Fas and FasL genes was determined by RT-PCR and Western blotting. The pathological changes of the pancreas were observed under optical microscope., Results: Compared with SAP group, the resveratrol-treated rats showed obviously decreased serum amylase and scores for pancreatic histopathological lesions. Resveratrol treatment significantly increased the apoptotic indices of pancreatic acinar cells and the levels of FasL mRNA and protein in rats with SAP., Conclusion: Resveratrol produces important therapeutic effect on SAP in rats by inducing pancreatic acinar cell apoptosis possibly as a result of up-regulated FasL gene expression.