Engineering of Cerium Modified TiNb2O7 Nanoparticles For Low-Temperature Lithium-Ion Battery.

Although TiNb2O7 (TNO) with comparable operating potential and ideal theoretical capacity is considered to be the most ideal replacement for negative Li4Ti5O12 (LTO), the low ionic and electronic conductivity still limit its practical application as satisfactory anode for lithium-ion batteries (LIBs) with high-power density. Herein, TNO nanoparticles modified by Cerium (Ce) with outstanding electrochemical performance are synthesized. The successful introduction of Ce3+ in the lattice leads to increased interplanar spacing, refined grain size, more oxygen vacancy, and a smaller lithium diffusion barrier, which are conducive to improve conductivity of both Li+ and electrons. As a result, the modified TNO reaches high reversible capacity of 256.0 mA h g-1 at 100 mA g-1 after 100 cycles, and 183.0 mA h g-1 even under 3200 mA g-1. In particular, when the temperature drops to -20 °C, the cell undergoing 1500 cycles at a high current density of 500 mA g-1 can still reach 89.7 mA h g-1, corresponding to a capacity decay rate per cycle of only 0.033%. This work provides a new way to improve the electrochemical properties of alternative anodes for LIBs at extreme temperature.

The Utilization of Metal-Organic Frameworks and Their Derivatives Composite in Supercapacitor Electrodes.

Up to now, the mainstream adoption of renewable energy has brought about substantial transformations in the electricity and energy sector. This shift has garnered considerable attention within the scientific community. Supercapacitors, known for their exceptional performance metrics like good charge/discharge capability, strong power density, as well as extended cycle longevity, have gained widespread traction across various sectors, including transportation and aviation. Metal-organic frameworks (MOFs) with unique traits including adaptable structure, highly customizable synthetic methods, and high specific surface area, have emerged as strong candidates for electrode materials. For enhancing the performance, MOFs are commonly compounded with other conducting materials to increase capacitance. This paper provides a detailed analysis of various common preparation strategies and characteristics of MOFs. It summarizes the recent application of MOFs and their derivatives as supercapacitor electrodes alongside other carbon materials, metal compounds, and conductive polymers. Additionally, the challenges encountered by MOFs in the realm of supercapacitor applications are thoroughly discussed. Compared to previous reviews, the content of this paper is more comprehensive, offering readers a deeper understanding of the diverse applications of MOFs. Furthermore, it provides valuable suggestions and guidance for future progress and development in the field of MOFs.

Cell cycle deregulation in neurodegenerative diseases.

Background: Cell cycle is critical for a wide range of cellular processes such as proliferation, differentiation and apoptosis in dividing cells. Neurons are postmitotic cells which have withdrawn from the cell division cycle. Recent data show us that inappropriate activation of cell cycle regulators including cyclins, cyclin dependent kinases (CDKs) and endogenous cyclin dependent kinase inhibitors (CDKIs) may take part in the aetiology of neurodegenerative diseases. However, the mechanisms for cell cycle reentry in neurodegenerative disease remain unclear.Methods: Electronic databases such as Pubmed, Science Direct, Directory of Open Access Journals, PLOS were searched for relevant articles.Conclusion: The present work reviews basic aspects of cell cycle mechanism, as well as the evidence showing the expression of cell cycle proteins in neurodegenerative disease. We provide a brief summary of these findings and hope to highlight the interaction between the cell cycle reentry and neurodegenerative diseases. Moreover, we outline the possible signaling pathways. However more understanding of the mechanism of cell cycle is of great importance. Because these represents an alternative target for therapeutic interventions, leading to novel treatments of neurodegenerative diseases.

The protective mechanism of protein kinase R to inhibit neuronal ferroptosis in cerebral injury from subarachnoid hemorrhage.

PURPOSE: To investigate the role and mechanism of protein kinase R (PKR) in subarachnoid hemorrhage (SAH)-mediated ferroptosis. METHODS: A rat SAH model was constructed and treated with PKR inhibitor C16 to observe SAH and neurological impairment in rats and to detect malonaldehyde (MDA), iron ions content, ferritin heavy polypeptide 1 (FTH1) and glutathione peroxidase 4 (GPX4), and other related ferroptosis indicators in brain tissue. RNA sequencing analysis was used to investigate the mechanism of PKR, affecting the ferroptosis network of SAH. RESULTS: SAH caused severe fundic hemorrhage, neurological impairment, MDA and iron ion accumulation, and significant decrease in GPX4 and FTH1 levels in rats. C16 treatment significantly improved the above signs caused by SAH. By RNA-seq analysis, brain tissue of SAH-treated rats with SAH and C16 differentially expressed mRNA target genes enriched in stress response and organic developmental signaling pathways. CONCLUSION: Inhibition of PKR may improve cerebral injury after SAH by inhibiting ferroptosis, and RNA sequencing staged its mechanism of action may be related to the stress response.

Overexpression of miR-99a in hippocampus leads to impairment of reversal learning in mice.

As one of the most common human genetic disorders, Down syndrome (DS) is characterized by a mild-to-moderate cognitive disability, which mainly results from genes overexpression on chromosome 21. The expression of miR-99a, a gene harboring on chromosome 21, is increased by 50 folds in DS brain samples. This study aims to investigate the effect of miR-99a overexpression in the hippocampus on mouse behaviors and explore the underlying mechanisms. Lentivirus vectors were delivered into the hippocampus for focal miR-99a overexpression in mice. Then behaviors were observed by an open field, elevated plus maze, rotarod motor test, and Morris water maze. The genes affected by miR-99a were identified by RNA sequencing (RNA-seq) and confirmed by quantitative RT-PCR (qRT-PCR) in samples isolated from the hippocampus injected with lentivirus-GFP-miR-99a or lentivirus-GFP vectors. It was found that the expression of miR-99a with intrahippocampal delivery of lentivirus-GFP-miR-99a resulted in reversal learning impairment in mice although it had no influence on motor function and anxiety. Meanwhile, RNA-seq results showed that 92 genes including mRNAs and microRNAs were significantly regulated by miR-99a, consistent with qRT-PCR consequence. Moreover, dual-luciferase reporter assay showed that miR-99a could directly bind to the 3'-untranslated regions (3'UTR) of target genes (Clic6 and Kcnj13) with an inhibitory effect on their activity. Furthermore, we also found that miR-99a overexpression affected different biological processes by bioinformatic analyses. Our study showed that miR-99a overexpression in the hippocampus leads to cognitive impairment through regulating the expressions of various genes, which reveals a novel function of miR-99a and provides new insights into understanding the pathophysiologic process of DS.

Development and Multi-Data Set Verification of an RNA Binding Protein Signature for Prognosis Prediction in Glioma.

Objective: Increasing evidence emphasizes the clinical implications of RNA binding proteins (RBPs) in cancers. This study aimed to develop a RBP signature for predicting prognosis in glioma. Methods: Two glioma datasets as training (n = 693) and validation (n = 325) sets were retrieved from the CGGA database. In the training set, univariate Cox regression analysis was conducted to screen prognosis-related RBPs based on differentially expressed RBPs between WHO grade II and IV. A ten-RBP signature was then established. The predictive efficacy was evaluated by ROCs. The applicability was verified in the validation set. The pathways involving the risk scores were analyzed by ssGSEA. scRNA-seq was utilized for evaluating their expression in different glioma cell types. Moreover, their expression was externally validated between glioma and control samples. Results: Based on 39 prognosis-related RBPs, a ten RBP signature was constructed. High risk score distinctly indicated a poorer prognosis than low risk score. AUCs were separately 0.838 and 0.822 in the training and validation sets, suggesting its well performance for prognosis prediction. Following adjustment of other clinicopathological characteristics, the signature was an independent risk factor. Various cancer-related pathways were significantly activated in samples with high risk score. The scRNA-seq identified that risk RBPs were mainly expressed in glioma malignant cells. Their high expression was also found in glioma than control samples. Conclusion: This study developed a novel RBP signature for robustly predicting prognosis of glioma following multi-data set verification. These RBPs may affect the progression of glioma.

Comparison of surgical clipping and endovascular coiling in the treatment of oculomotor nerve palsy caused by posterior communicating artery aneurysm.

Oculomotor nerve palsy (ONP) caused by posterior communicating aneurysm (PcomAA) is mainly treated by surgical clipping or endovascular coiling. However, there are still some controversies about which treatment method could provide the more beneficial prognosis. This study aimed to compare ONP recovery rate between surgical clipping and endovascular coiling in patients diagnosed as PcomAA combined with ONP, and explore the potential risk factors of ONP recovery.The clinical data of 152 patients with ONP caused by PcomAA were retrospectively analyzed. Diameter of aneurysm, different treatment methods (surgical clipping or endovascular coiling), subarachnoid hemorrhage (SAH), degree of preoperative ONP, time from ONP onset to treatment, as well as degree of ONP symptom recovery were collected from medical records. All patients were followed up for at least 1 year.One hundred twelve patients underwent surgical clipping and 40 patients received endovascular coiling. There were no significant differences in age, gender, aneurysm diameter, hypertension, dyslipidemia, time from ONP symptom onset to treatment, SAH, and preoperative ONP degree between the 2 groups (all P > .05). Time to complete or partial recovery was 86.7 ±â€Š35.7 days for patients receiving surgical clipping and 132.6 ±â€Š37.5 days for patients receiving endovascular coiling, respectively (Log rank test, P < .001). The recovery rate was 94.6% in the surgical clipping group and 65.0% in the endovascular coiling group. The difference between the two groups was statistically significant (P < .001). Postoperative ONP recovery in the surgical clipping group was significantly superior to that of patients in the endovascular coiling group (HR, 2.625; 95% CI: 1.423-4.841; P = .002). Time from ONP symptom onset to treatment exerted the obvious effect on the ONP prognosis (HR, 0.572; 95% CI: 0.384-0.852; P = .006). In addition, the ONP recovery in patients with SAH before surgery was also independently associated with ONP prognosis (HR, 1.276; 95% CI, 1.043-1.562; P = .018). There was no treatment-related death in either group, and postoperative complications were within the manageable range.The recovery rate and recovery degree of ONP after surgical clipping was significantly better than that of endovascular coiling in PcomAA patients combined with ONP. The postoperative ONP recovery was associated with preoperative spontaneous SAH and time from ONP onset to treatment.

Insight Into the Role of Ferroptosis in Non-neoplastic Neurological Diseases.

Ferroptosis is an iron-dependent form of cell death characterized by the accumulation of intracellular lipid reactive oxygen species (ROS). Ferroptosis is significantly different from other types of cell death including apoptosis, autophagy, and necrosis, both in morphology and biochemical characteristics. The mechanisms that are associated with ferroptosis include iron metabolism, lipid oxidation, and other pathophysiological changes. Ferroptosis inducers or inhibitors can influence its occurrence through different pathways. Ferroptosis was initially discovered in tumors, though recent studies have confirmed that it is also closely related to a variety of neurological diseases including neurodegenerative disease [Alzheimer's disease (AD), Parkinson's disease (PD), etc.] and stroke. This article reviews the definition and characteristics of ferroptosis, the potential mechanisms associated with its development, inducers/inhibitors, and its role in non-neoplastic neurological diseases. We hope to provide a theoretical basis and novel treatment strategies for the treatment of central nervous system diseases by targeting ferroptosis.

Regulatory mechanism of MiR-21 in formation and rupture of intracranial aneurysm through JNK signaling pathway-mediated inflammatory response.

OBJECTIVE: To investigate the regulatory mechanism of micro ribonucleic acid (miR)-21 in the formation and rupture of intracranial aneurysm through the c-Jun N-terminal kinase (JNK) signaling pathway-mediated inflammatory response. METHODS: In the present study, the mice with miR-21 expression deficiency and over-expression in our laboratory were enrolled as the experimental group, while wild-type healthy mice were used as the control group. The mouse model of intracranial aneurysm was established by bilateral carotid artery ligation. The differences in the levels of key genes in the JNK signaling pathway (JNK1 and JNK2) were detected by fluorescence quantitative polymerase chain reaction (qPCR) and western blotting. At the same time, the changes in transcription and translation levels of inflammatory factors, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), in both groups were measured. After the mice were executed by an overdose of anesthesia, the morphology of the aneurysm in different objects was observed by Verhoeff-Van Gieson (EVG) staining and the expressions of TNF-α, JNK1, and JNK2 were determined by immunohistochemistry. RESULTS: Compared with healthy mice, levels of JNK1 and JNK2 in mice with miR-21 deficiency were significantly decreased (P < 0.05) with a significant reduction of inflammatory factors IL-6 and TNF-α (P < 0.05). Compared with healthy mice, levels of JNK1 and JNK2 in mice with miR-21 over-expression were significantly increased (P < 0.05) with significant growing levels of inflammatory factors IL-6 and TNF-α (P < 0.05). The results of EVG staining revealed that the intracranial aneurysm was smaller in mice with miR-21 deficiency [(0.3 ± 0.12) cm] and larger in mice with miR-21 over-expression [(0.8 ± 0.25) cm] and there was a significant difference (P < 0.05). Moreover, the results of immunohistochemistry showed that the expression of TNF-α in intracranial aneurysm was obviously lower in mice with miR-21 deficiency than that in mice with miR-21 over-expression. CONCLUSION: MiR-21 can promote the production of inflammation-related factors through the JNK signaling pathway, leading to the formation and rupture of an intracranial aneurysm.

Peptide interdigitation-induced twisted nanoribbons as chiral scaffolds for supramolecular nanozymes.

Establishing reliable strategies for rationally manipulating the organization of peptide building blocks and thereby precisely creating chiral nanostructures is challenging, while meaningful toward development of advanced functional materials. Here we report on a peptide-interdigitating mechanism for the reliable self-assembly of lipid-inspired amphiphiles (LIPIAs) into robust twisted nanoribbons by grafting domains to one alkyl tail of lipids as an extended element. Peptide interdigitation promoted the self-assembly of LIPIAs into twisted or flat nanoribbons driven by antiparallel or parallel ß-sheet hydrogen bonds, respectively, strongly associated with the connecting direction of the incorporated domains. We found that the LIPIAs containing N-terminus-connected domains with either bulky or small side chain groups formed twisted nanoribbons in a broad pH range, thus implying a sequence- and pH-independent strategy for creation of robust chiral nanostructures. Integrating the resulting twisted nanoribbons with gold nanoparticles led to supramolecular nanozymes exhibiting the excellent catalytic activity and enantioselectivity of asymmetric oxidation of 3,4-dihyroxy-phenylalanine molecules. Our finding demonstrates that the peptide-interdigitating mechanism is a reliable strategy for precise creation of chiral nanostructures serving as chiral matrices for supramolecular nanozymes with improved catalytic performance, thus potentially paving the way towards advanced biomimetic systems resembling natural systems.

Directional molecular sliding movement in peptide hydrogels accelerates cell proliferation.

Adjusting the mechanical cues generated in cellular microenvironments is important for manipulating cell behaviour. Here we report on mechanically dynamic hydrogels undergoing directional domain sliding motion and investigate the effect of the well-defined mechanical motion on accelerating cell proliferation. The mechanically dynamic hydrogels were prepared via self-assembly of an amphiphilic peptide consisting of two alternating polar and nonpolar domains cross-linked by disulfide bonds at a nonsymmetrical position. The cross-linked peptide assembled into entangled nanofibers driven by the hydrophobic collapse involving a partial-length sequence due to the covalent constraint. Reduction of the disulfide bonds led to formation of non-equilibrated peptide bilayers, which underwent directional domain sliding motion along each promoted by the thermodynamically favourable transition from the partial to full hydrophobic collapse. The mechanical cues resulting from the directional domain sliding motion within the mechanically dynamic hydrogels accelerated cell proliferation when incubating cells on the hydrogel, compared to the thermodynamically static counterparts, via a mechanotransduction mechanism as supported by the facilitated translocation of yes-associated proteins into the nucleus of the cells. Our finding demonstrates the great potential of mechanically dynamic hydrogels as new-generation biomimetic extracellular matrices in tissue engineering and regeneration.

MicroRNA­216b inhibits cell proliferation and invasion in glioma by directly targeting metadherin.

Glioma is a well­known aggressive and malignant brain tumor, and accounts for ~30% of all brain and central nervous system tumors. A number of studies have indicated that the abnormal expression of specific microRNAs (miR) serves vital roles in the tumorigenesis and tumor development of human cancer, including glioma. miR­216b has been studied in a number of types of cancer. However, the expression pattern, molecular function and underlying mechanisms of miR­216b in glioma remain unclear. In the present study, it was demonstrated that the level of miR­216b was significantly decreased in glioma tissues and cell lines compared with matched normal tissues and primary normal human astrocytes. The reduced miR­216b expression level was correlated with the Karnofsky Performance Score and the World Health Organization grade of gliomas. Upregulation of miR­216b repressed cell proliferation and invasion in glioma. Additionally, metadherin (MTDH) was identified as a direct target gene of miR­216b in glioma. MTDH expression was demonstrated to be significantly upregulated and inversely associated with miR­216b expression in glioma specimens. MTDH knockdowns could simulate the cellular conditions induced by miR­216b overexpression in glioma cells. In addition, miR­216b regulated phosphatidylinositol 3,4,5­trisphosphate 3­phosphatase and dual­specificity protein phosphatase PTEN/protein kinase B signaling pathways in glioma. These results suggested that miR­216b acted as a tumor suppressor in glioma by directly targeting MTDH and that the miR­216b/MTDH axis may be an effective therapeutic target for the treatment of patients with this disease.

Gas Permeability and Permselectivity of Poly(L-Lactic Acid)/SiOx Film and Its Application in Equilibrium-Modified Atmosphere Packaging for Chilled Meat.

A layer of SiOx was deposited on the surface of poly(L-lactic acid) (PLLA) film to fabricate a PLLA/SiOx layered film, by plasma-enhanced chemical vapor deposition (PECVD) process. PLLA/SiOx film showed Young's modulus and tensile strength increased by 119.2% and 91.6%, respectively, over those of neat PLLA film. At 5 °C, the oxygen (O2 ) and carbon dioxide (CO2 ) permeability of PLLA/SiOx film decreased by 78.7% and 71.7%, respectively, and the CO2 /O2 permselectivity increased by 32.5%, compared to that of the neat PLLA film. When the PLLA/SiOx film was applied to the equilibrium-modified atmosphere packaging of chilled meat, the gas composition in packaging reached a dynamic equilibrium with 6% to 11% CO2 and 8% to 13% O2 . Combined with tea polyphenol pads, which effectively inhibited the microbial growth, the desirable color of meat was maintained and an extended shelf life of 52 d was achieved for the chilled meat.

Novel RGD containing, temozolomide-loading nanostructured lipid carriers for glioblastoma multiforme chemotherapy.

CONTEXT: Glioblastoma multiforme (GBM) is the most common malignant brain tumor originating in the central nervous system. Efficient delivery of therapeutic molecules to the cells and tissues is a difficult challenge. OBJECTIVE: Arginine-glycine-aspartic acid peptide (RGD)-modified nanostructured lipid carriers (NLCs) were used for the delivery of temozolomide (TMZ) into the GBM to provide a new paradigm in gliomatosis cerebri treatment. METHODS: RGD-conjugated polyethylene glycol-b-distearoylphosphatidylethanolamine (PEG-DSPE) was synthesized. RGD containing, TMZ-loaded NLCs (RGD-TMZ/NLCs) were prepared. Their particle size, zeta potential, drug encapsulation efficiency (EE) and drug release behavior were evaluated. In vitro cytotoxicity study of TMZ/NLCs was tested in U87 malignant glioma cells (U87MG cells). In vivo antitumor efficacy of the carriers was evaluated on mice bearing GBM model. RESULTS: The U87MG cells were successfully inhibited by RGD-TMZ/NLCs in vitro. RGD-TMZ/NLCs also displayed the highest antitumor efficacy in vivo than all the other formulations used for comparison. CONCLUSION: RGD-TMZ/NLCs were efficient in selective delivery of TMZ into U87MG cells, and inhibition efficacy is high. These RGD-modified vectors could be a superior drug delivery nano-system to achieve therapeutic efficacy, and this research could be a new promising strategy for treatment in malignant gliomatosis cerebri.

Nanostructured lipid carriers based temozolomide and gene co-encapsulated nanomedicine for gliomatosis cerebri combination therapy.

BACKGROUND: Co-delivery of gene and anticancer drug into the same cancer cells or tissues by multifunctional nanocarriers may provide a new paradigm in cancer treatment. In this study, nanostructured lipid carriers (NLCs) were constructed as multifunctional nanomedicine for co-delivery of enhanced green fluorescence protein plasmid (DNA) and temozolomide (TMZ). METHODS: TMZ- and DNA-loaded NLCs (TMZ/DNA-NLCs) were prepared. Their particle size, zeta potential, gene-loading capacity (GL) and drug encapsulation efficiency (EE) were evaluated. In vitro cytotoxicity study TMZ/DNA-NLCs was tested in U87 malignant glioma cells (U87 MG cells). In vivo gene transfection and anti-tumor efficacy of the carriers were evaluated on mice bearing malignant glioma model. RESULTS: The optimum TMZ/DNA-NLCs formulations with the particle size of 179 nm and with a +23 mV surface charge; got 91% of GL and 83% of EE. The growth of U87 MG cells in vitro was obviously inhibited. TMZ/DNA-NLCs also displayed the highest gene transfection efficiency and the best antitumor activity than other formulations in vivo. CONCLUSION: The results demonstrated that TMZ/DNA-NLCs were efficient in selective delivery to malignant glioma cells. Also TMZ/DNA-NLCs transfer both drug and gene to the gliomatosis cerebri, enhance the antitumor capacity and gene transfection efficacy. Thus, TMZ/DNA-NLCs could prove to be a superior co-delivery nanomedicine to achieve therapeutic efficacy and this report could be a new promising strategy for treatment in malignant gliomatosis cerebri.

[Significance of the R.E.N. A.L. nephrometry scoring system in renal tumour of T1 stage].

OBJECTIVE: To evaluate the application value of R.E.N. A.L. nephrometry score for surgery type decisions of T1 stage renal tumor. METHODS: Clinical data including image data, surgery type and prognosis etc were collected retrospectively for 122 cases from January 2010 to December 2012. There were 76 male and 46 female patients and they were 29-82 years (mean 51 years). The body mass index was (22.8 ± 3.9) kg/m(2). The patients were undergoing surgical excision with renal tumor of T1 stage. The R.E.N. A.L. nephrometry score was analyzed to evaluate their relationships to surgery type (RN or NSS) and the approach of NSS (ONSS or LNSS) using chi-square tests, Fisher's exact tests, and logistic regressions analysis. RESULTS: All surgery had been completed. The surgery included RN of 45 patients, LNSS of 45 patients and ONSS of 32 patients. The R.E.N. A.L. nephrometry score was significantly associated with the type of surgery (χ(2) = 27.89, P < 0.05), and the NSS approach (χ(2) = 12.87, P < 0.05). When the scores less than 7 points, it is majorly treated by nephron sparing surgery (92.9%), and when the scores more than 9 points, it is majorly treated by radical nephrectomy (69.4%). Individual component scores were analyzed to evaluate that they were all related to surgery type (χ(2) = 7.00-14.57, P < 0.05), and the individual component N associated the surgery type mostly. Furthermore, individual component R,E,N and L were statistically significant predictors of the NSS approach (χ(2) = 4.92-15.07, P < 0.05). CONCLUSION: The R.E.N. A.L. nephrometry scoring system provides a simple, useful, and stable system to character the salient renal anatomy of T1 stage, and can provide the best surgery approach.