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1.
Medicine (Baltimore) ; 98(40): e17460, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31577775

RESUMO

BACKGROUND: This study aimed to perform a network meta-analysis to evaluate the therapeutic effect and safety of various modalities in treating advanced hepatocellular carcinoma (HCC). Typically, the modalities of interest were comprised of sorafenib, transarterial chemoembolization (TACE), sorafenib combined with TACE, TACE combined with traditional Chinese medicine (TCM), and sorafenib combined with hepatic arterial infusion chemotherapy (HAIC). METHODS: Potentially eligible studies were systemically retrieved from the electronic databases (including PubMed and Cochrane Library) up to September 2018. The overall survival (OS) associated with the 5 modalities of interest enrolled in this study was compared by means of network meta-analysis. Meanwhile, major adverse events (AEs) were also evaluated. RESULTS: The current network meta-analysis enrolled 7 published randomized controlled trials (RCTs), and the pooled results indicated that the TACE-TCM regimen displayed the highest efficacy in treating advanced HCC, followed by HAIC-sorafenib. By contrast, the TACE alone and sorafenib alone regimens had the least efficacy. Relative to other regimens of interest, the TACE-TCM regimen was associated with less incidence of treatment-associated AEs. CONCLUSION: The TACE-TCM regimen was associated with higher treatment responses in advanced HCC patients than those of the other regimens of interest.

2.
J Environ Manage ; 252: 109642, 2019 Oct 03.
Artigo em Inglês | MEDLINE | ID: mdl-31586745

RESUMO

Hexametaphosphate intercalated green rust (hexa-P GR) was fabricated by a coprecipitation process in an anaerobic environment to improve the adsorption of hexa-P GR for Cr(VI) and the total Cr under various aqueous conditions. Three kinetic models including the pseudo-first-order, intraparticle, and Elovich were appropriate in describing the adsorption of hexa-P GR towards Cr(VI) and the total Cr. The maximum mono-layer adsorption capacities (mg/g) of hexa-P GR for Cr(VI) at pH of 2 and 7 were 87.64 and 92.25, respectively, with the theoretical maximum capacity (mg/g) of 52.73 being obtained at pH of 7. Some competing cations existing in solutions such as Al3+, Ca2+, and Mg2+ would consume more hexa-P GR to remove Cr species. The neutral and weak alkaline environment was conducive to the hexa-P GR reuse, while the strong alkaline environment was beneficial to the removal of the total Cr. The orthogonal variables including the initial pH, the flow rate, and the Cr(VI) concentration all significantly influenced Cr removal. The sequences of reaction pathways referring to the adsorption of hexa-P GR differently occurred in various pH conditions.

3.
J Nephrol ; 2019 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-31595420

RESUMO

BACKGROUND: Cardiac surgery-associated acute kidney injury (CSA-AKI) is associated with high risk for complications and mortality. Whether renin-angiotensin system (RAS) inhibitor should be continued or withdrawn in patients with long-term use before cardiac surgery has been lack of consensus. METHODS: We performed this prospective observational cohort study and recruited cardiac surgery patients in the surgical intensive care units between 2000 and 2011. These patients were divided into users and non-users of RAS inhibitor. Propensity score matching and multivariable models were performed to investigate the association between renal outcome, mortality, and preoperative use of RAS inhibitor. RESULTS: Preoperative use of RAS inhibitor was identified as the independent protective factor for AKI development (OR 0.41, 95% CI 0.23, 0.63), AKI severity (stage 3 vs. stage 1, OR 0.35, 95% CI 0.18, 0.69), and renal recovery (OR 3.41, 95% CI 1.84, 5.36). Nevertheless, there was no significant protective effect of RAS inhibitor on in-hospital dialysis, in-hospital mortality, and ensuing development of chronic kidney disease (CKD) after AKI. We created a prediction model of CSA-AKI and indicated that preoperative use of RAS inhibitor provided more protective effect in low-risk than high-risk population. CONCLUSION: Preoperative use of RAS inhibitor was associated with less AKI development and severity, and higher renal recovery. Although more risk reduction of AKI development was shown in low-risk group by our prediction model, continued use of RAS inhibitor before cardiac surgery could provide protective effect in all patients.

4.
Biosci Rep ; 2019 Sep 03.
Artigo em Inglês | MEDLINE | ID: mdl-31481528

RESUMO

Diabetic nephropathy (DN) is the common complications of diabetes mellitus, but the efficacy of available treatments for the prevention of DN is still unsatisfactory. In this study, we aimed to explore the effect of Danggui buxue tang (DGT) on the proliferation of high glucose (HG)-induced mesangial cells and accumulation of extracellular matrix in mesangial cells. We found DGT upregulated the expression of GAS5 and IKK dose-dependently in mouse mesangial cells (SV40 MES-13). We found DGT participated in the expression IKK and the activity of nuclear transcription factor-κB (NF-κB) via GAS5, and proved that lncRNA GAS5 was positively related with IKK. And we proved GAS5 regulated the expression of IKK and the activity of NF-κB. In addition, DGT inhibited viability of MES-13 cells and extracellular matrix related proteins (laminin, fibronectin and collagen IV) via GAS5. Moreover, we proved GAS5 regulated the viability of SV40 MES-13 cells and extracellular matrix related proteins through NF-κB pathway. DGT inhibited the proliferation of mesangial cells and accumulation of extracellular matrix via GAS5/NF-κB, therefore, DGT could be an effective treatment for the prevention of DN.

5.
Biomolecules ; 9(9)2019 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-31514306

RESUMO

In the last couple of decades, there has been a growing optimism surrounding the potential transformative use of human mesenchymal stem cells (MSCs) and human-induced pluripotent stem cells (iPSCs) for regenerative medicine and disease treatment. In order for this to occur, it is first essential to understand the mechanisms underpinning their cell-fate specification, which includes cell signaling via gap junctional intercellular communication. Here, we investigated the role of the prototypical gap junction protein, connexin43 (Cx43), in governing the differentiation of iPSCs into MSCs and MSC differentiation along the adipogenic lineage. We found that control iPSCs, as well as iPSCs derived from oculodentodigital dysplasia patient fibroblasts harboring a GJA1 (Cx43) gene mutation, successfully and efficiently differentiated into LipidTox and perilipin-positive cells, indicating cell differentiation along the adipogenic lineage. Furthermore, the complete CRISPR-Cas9 ablation of Cx43 from iPSCs did not prevent their differentiation into bona fide MSCs or pre-adipocytes, strongly suggesting that even though Cx43 expression is upregulated during adipogenesis, it is expendable. Interestingly, late passage Cx43-ablated MSCs senesced more quickly than control cells, resulting in failure to properly differentiate in vitro. We conclude that despite being upregulated during adipogenesis, Cx43 plays no detectable role in the early stages of human iPSC-derived MSC adipogenic differentiation. However, Cx43 may play a more impactful role in protecting MSCs from premature senescence.

6.
Semin Nephrol ; 39(5): 421-430, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31514906

RESUMO

Acute kidney injury is a major health care problem. Improving recognition of those at risk and highlighting those who have developed AKI at an earlier stage remains a priority for research and clinical practice. Prediction models to risk-stratify patients and electronic alerts for AKI are two approaches that could address previously highlighted shortcomings in management and facilitate timely intervention. We describe and critique available prediction models and the effects of the use of AKI alerts on patient outcomes are reviewed. Finally, the potential for prediction models to enrich population subsets for other diagnostic approaches and potential research, including biomarkers of AKI, are discussed.

7.
Protein Pept Lett ; 2019 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-31544687

RESUMO

MicroRNAs (miRNAs) are small, endogenous non-coding RNAs that are involved in post-transcriptional gene regulation of several biological processes, including embryo implantation and placental development. We analyzed miRNAs from the serum of Landrace-Yorkshire Hybrid sows taken on day 14 of pregnancy and non-pregnancy using Illumina sequencing. Bioinformatics software was used to identify the target genes Smad3 and Smad4 of miR-146a-5p. A dual-luciferase reporter system showed that the expression of the Smad3-3'-UTR-W recombinant plasmid in the miR-146a-5p mimic co-transformation group was significantly lower than that in the miR-146a-5p- NC group. The expression of the Smad4-3'-UTR-W recombinant plasmid in the miR-146a-5p mimics co-transformation group was significantly lower than that in the miR-146a-5p-NC group, indicating that Smad3 and Smad4 are the direct target genes of miR-146a-5p. When miRNAs and inhibitors were overexpressed, Smad3 and Smad4 were affected by different levels of miRNAs in regard to mRNA and protein expression. After transfection of BeWo cells with miRNA mimics, mimics-nc, inhibitor and inhibitor-nc, the mRNA expression of the apoptotic genes Caspase-3, BAX and Bcl-2 were measured using qRT-PCR. The results suggest that the miRNAs affect cell apoptosis by regulating their target genes. This study analyzed miRNAs from pregnant sows in order to predict the biological effects induced by these miRNAs and to provide a theoretical basis for regulation of sow pregnancy.

8.
Eur J Pharm Sci ; : 105058, 2019 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-31472255

RESUMO

The biofilm formation of Pseudomonas aeruginosa (P. aeruginosa) is regulated by a phenomenon of quorum sensing (QS). With 5-hydroxyl-3,4-halogenated-5H-furan-2-ones as beginning, analogs bearing alkyl chains, vinyl bromide, or aromatic rings were designed and synthesized. The minimum inhibitory concentration (MIC) of the compounds against P. aeruginosa was assayed and the biofilm inhibition ratio was determined at different concentrations lower than the MIC. C-5 aromatic substituted furanones showed remarkable biofilm formation as well as inhibition of virulence factor production in P. aeruginosa. Fluorescence report analysis identified the QS regulatory mechanism of the most active compound 29. This study provides us a novel candidate for combating drug resistant bacteria strains by merely inhibiting biofilm formation. Without suppressing the regular life cycle of the bacteria, bacterial resistance mechanisms may not be activated.

9.
Int J Mol Sci ; 20(17)2019 Aug 31.
Artigo em Inglês | MEDLINE | ID: mdl-31480430

RESUMO

Breast cancer is regarded worldwide as a severe human disease. Various genetic variations, including hereditary and somatic mutations, contribute to the initiation and progression of this disease. The diagnostic parameters of breast cancer are not limited to the conventional protein content and can include newly discovered genetic variants and even genetic modification patterns such as methylation and microRNA. In addition, breast cancer detection extends to detailed breast cancer stratifications to provide subtype-specific indications for further personalized treatment. One genome-wide expression-methylation quantitative trait loci analysis confirmed that different breast cancer subtypes have various methylation patterns. However, recognizing clinically applied (methylation) biomarkers is difficult due to the large number of differentially methylated genes. In this study, we attempted to re-screen a small group of functional biomarkers for the identification and distinction of different breast cancer subtypes with advanced machine learning methods. The findings may contribute to biomarker identification for different breast cancer subtypes and provide a new perspective for differential pathogenesis in breast cancer subtypes.

10.
Food Res Int ; 125: 108509, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31554065

RESUMO

The differences in bacterial communities and physicochemical characteristics between salted and salt-free yancai samples from Nanfeng County were compared in this study. Total acid, salinity and lactic acid content in salted group were significantly higher than those in salt-free group, whereas pH value as well as the contents of acetic acid, sucrose, glucose and fructose showed no significant difference between the two groups. 20 phyla, 339 genera and 203 species were observed in all yancai samples. Firmicutes and Proteobacteria were the major phyla. Lactobacillus was the predominant genus in both the salted and the salt-free samples, whereas Pediococcus, as the second most abundant genus in the salted samples, was in fairly low abundance in the salt-free samples. Culture-dependent and -independent methods showed that the major lactic acid bacteria in the salted samples were Lactobacillus plantarum, L. pentosus, Pediococcus pentosus and L. brevis, while the salt-free samples were predominated by L. fermentum, L. coryniformis and L. sp. The result indicated that salinity had a significant effect on the bacterial communities in Nanfeng yancai, which will improve our understanding of the bacterial ecology of yancai, as well as the relationships between physicochemical characteristics and the microbiota of yancai.

11.
Sci Rep ; 9(1): 13904, 2019 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-31554859

RESUMO

The upregulation of ELTD1 ([epidermal growth factor (EGF), latrophilin and seven transmembrane domain-containing 1] on chromosome 1) in tumor cells has been reported in several types of cancer and correlates with poor cancer prognosis. However, the role of ELTD1 in glioma progression remains unknown. In this study, we examined ELTD1 expression levels in human glioma cell lines and in sixteen human gliomas of different grades. The molecular effects of ELTD1 in glioma cells were measured using quantitative polymerase chain reaction (qRT-PCR), Western blotting, Cell proliferation assays, Matrigel migration and invasion assays and brain orthotopic xenografts. We found that high expression levels of ELTD1 were positively associated with cancer progression and poor prognosis in human glioma. Mechanistically, ELTD1 activated the JAK/STAT3/HIF-1α signaling axis and p-STAT3 bound with HIF-1α. Taken together, our data provide a plausible mechanism for ELTD1-modulated glioma progression and suggest that ELTD1 may represent a potential therapeutic target in the prevention and therapy of glioma.

12.
Biomed Pharmacother ; 119: 109413, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31518872

RESUMO

MicroRNA-mediated posttranscriptional regulation is an important epigenetic regulatory mechanism of gene expression, and its dysregulation is involved in the development and progression of a variety of malignancies, including chronic myeloid leukemia (CML). The BCR-ABL1 fusion gene is not only the initiating factor of CML, but it is also an important driving factor for blastic transformation. Tyrosine kinase inhibitors (TKIs) targeting BCR-ABL1 tyrosine kinase activity, represented by imatinib, are currently the first-line treatment for CML. However, due to primary resistance or secondary resistance caused by mutations in the BCR-ABL1 kinase domain, TKIs cannot completely prevent the progression of CML; thus, the study of BCR-ABL1 gene expression regulation is of great significance. In this study, bioinformatics analysis and our results showed that miR-96 could directly bind to the 3'UTR region of BCR-ABL1 to regulate fusion protein expression, thereby regulating its downstream signaling pathway activity. We also found that miR-96 was downregulated during the progression from the chronic phase (CML-CP) to the blast crisis (CML-BC). Downregulation of miR-96 could promote the proliferation and participate in the cell differentiation of CML-BC cells. Additionally, we found that the novel histone deacetylase drug chidamide and the DNA methyltransferase inhibitor decitabine could restore the low expression of miR-96 in CML cells, and there were two abnormal hypermethylated sites in the promoter region of miR-96 in CML, suggesting that its low expression might be at least partially regulated by epigenetic mechanisms. In addition, re-expression of miR-96 could increase the sensitivity of CML-BC cells to imatinib. Thus, miR-96 functions as a tumor suppressor, and re-expression of this microRNA might have therapeutic benefits in CML blastic transformation.

13.
Int Immunopharmacol ; 76: 105864, 2019 Aug 31.
Artigo em Inglês | MEDLINE | ID: mdl-31480004

RESUMO

Tumor-associated macrophages (TAMs) are closely related to poor prognosis in triple-negative breast cancer (TNBC). Thus, gaining insight into how TAMs support cancer progression could contribute to effective therapies. We utilized the 4 T1 murine TNBC cell line and murine bone marrow-derived macrophages to assess TAM-mediated pro-proliferative effects in vivo and in vitro. Further, Transcriptional analysis was performed to identify pathways activated in TAM-stimulated 4 T1 cells. We also explored the therapeutic efficacy of combining a mitogen-activated protein kinase kinase (MEK) inhibitor with TAM-targeted therapy using a TNBC mouse model. We found that the presence of TAMs was significantly associated with proliferating cancer cells in a TNBC mouse model. Moreover, RNA sequencing analysis showed that TAMs could enhance mitogen-activated protein kinase (MAPK) pathway activation in 4 T1 cells compared to that in control cells. Further, the depletion of TAMs by clodronate liposomes significantly reduced MAPK pathway activation in vivo. In addition, the blockade of MAPK signaling by a MEK inhibitor repressed TAM-mediated cancer cell proliferation. Most importantly, MEK inhibition combined with macrophage depletion significantly suppressed tumor growth and increased T lymphocyte infiltration in a TNBC model. Our study suggests the possibility that TAM-induced MAPK pathway activation promotes cancer cell proliferation. Thus, MEK inhibition combined with macrophage depletion might represent an effective treatment for TNBC.

14.
J Physiol ; 2019 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-31506936

RESUMO

KEY POINTS: There is a close relationship between skeletal muscle physiology and Ca2+ /calmodulin (CaM) signalling. Despite the effects of Ca2+ /CaM signalling on immune and inflammatory responses having been extensively explored, few studies have investigated the role of CaM pathway activation on the post-injury muscle inflammatory response. In this study, we investigated the role of CaM-dependent signalling in muscle inflammation in cardiotoxin induced myoinjuries in mice. The Ca2+ /calmodulin-dependent protein kinase II (CaMII), Ca2+ /calmodulin-dependent protein kinase IV (CaMKIV), and nuclear factor of activated T cells (NFAT) pathways are likely to be simultaneously activated in muscle cells and in infiltrating lymphocytes and to regulate the immune behaviours of myofibres in an inflammatory environment, and these pathways ultimately affect the outcome of muscle inflammation. ABSTRACT: Calcium/calmodulin (Ca2+ /CaM) signalling is essential for immune and inflammatory responses in tissues. However, it is unclear if Ca2+ /CaM signalling interferes with muscle inflammation. Here we investigated the roles of CaM-dependent signalling in muscle inflammation in mice that had acute myoinjuries in the tibialis anterior muscle induced by intramuscular cardiotoxin (CTX) injections and received intraperitoneal injections of either the CaM inhibitor calmidazolium chloride (CCL) or CaM agonist calcium-like peptide 1 (CALP1). Multiple inflammatory parameters, including muscle autoantigens and toll-like receptors, mononuclear cell infiltration, cytokines and chemokines associated with peripheral muscle inflammation, were examined after the injury and treatment. CALP1 treatment enhanced intramuscular infiltration of monocytes/macrophages into the damaged tibialis anterior muscle and up-regulated mRNA and protein levels of muscle autoantigens (Mi-2, HARS and Ku70) and Toll-like receptor 3 (TLR3), and mRNA levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), Monocyte chemoattractant protein-1 (MCP1), Monocyte chemoattractant protein-3 (MCP3) and Macrophage inflammatory protein-1(MIP-1α) in damaged muscle. In contrast, CCL treatment decreased the intramuscular cell infiltration and mRNA levels of the inflammatory mediators. After CALP1 treatment, a substantial up-regulation in Ca2+ /calmodulin-dependent protein kinase II (CaMKII), Ca2+ /calmodulin-dependent protein kinase IV (CaMKIV) and nuclear factor of activated T cells (NFAT) activity was detected in CD45+ cells isolated from the damaged muscle. More pro-inflammatory F4/80+ Ly-6C+ cells were detected in CD45-gated cells after CALP1 treatment than in those after CCL treatment or no treatment. Consistently, in interferon-γ-stimulated cultured myoblasts and myotubes, CALP1 treatment up-regulated the activities of CaMKII, CaMKIV and NFAT, and levels of class I/II major histocompatibility complexes (MHC-I/II) and TLR3. Our findings demonstrated that CaM-dependent signalling pathways mediate the injury-induced acute muscle inflammatory response.

15.
Int J Oncol ; 2019 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-31485672

RESUMO

Previous studies revealed that the long non­coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) exhibits abnormal expression in numerous cancer types, including breast cancer (BC); however, the regulatory mechanism of NEAT1 in BC remains unclear. In the present study, the effect of NEAT1 on the progression of BC and its regulation mechanism was investigated. The expression levels of NEAT1 and microRNA­107 (miR­107) in BC cells were analyzed using the reverse transcription­quantitative polymerase chain reaction (RT­qPCR). NEAT1 was knocked down in BC cells, and mimics­miR­107 or inhibitor­miR­107 were transfected into BC cells. Subsequently, cell proliferation, invasion and migration, apoptosis and cell cycle distribution were determined. The regulatory mechanism of NEAT1, miR­107 and carnitine palmitoyltransferase­1 (CPT1A) was analyzed using a luciferase reporter assay system, western blotting and RT­qPCR. NEAT1 expression was increased in BC cells, whereas miR­107 expression was decreased, compared with normal mammary gland cells. NEAT1 promoted the progression of BC cells through inhibiting apoptosis­associated genes and promoting cell cycle­ and invasion­associated gene expression, whereas miR­107 served the opposite function. Furthermore, NEAT1 promoted the expression of CPT1A, which was mediated by miR­107. The results of the present study indicate that NEAT1 promotes the expression of CPT1A by inhibiting miR­107 to improve the progression of BC cells; therefore, NEAT1 is a potential therapeutic target of BC.

16.
JAMA Netw Open ; 2(9): e1910915, 2019 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-31539074

RESUMO

Importance: Observational studies have shown associations of birth weight with type 2 diabetes (T2D) and glycemic traits, but it remains unclear whether these associations represent causal associations. Objective: To test the association of birth weight with T2D and glycemic traits using a mendelian randomization analysis. Design, Setting, and Participants: This mendelian randomization study used a genetic risk score for birth weight that was constructed with 7 genome-wide significant single-nucleotide polymorphisms. The associations of this score with birth weight and T2D were tested in a mendelian randomization analysis using study-level data. The association of birth weight with T2D was tested using both study-level data (7 single-nucleotide polymorphisms were used as an instrumental variable) and summary-level data from the consortia (43 single-nucleotide polymorphisms were used as an instrumental variable). Data from 180 056 participants from 49 studies were included. Main Outcomes and Measures: Type 2 diabetes and glycemic traits. Results: This mendelian randomization analysis included 49 studies with 41 155 patients with T2D and 80 008 control participants from study-level data and 34 840 patients with T2D and 114 981 control participants from summary-level data. Study-level data showed that a 1-SD decrease in birth weight due to the genetic risk score was associated with higher risk of T2D among all participants (odds ratio [OR], 2.10; 95% CI, 1.69-2.61; P = 4.03 × 10-5), among European participants (OR, 1.96; 95% CI, 1.42-2.71; P = .04), and among East Asian participants (OR, 1.39; 95% CI, 1.18-1.62; P = .04). Similar results were observed from summary-level analyses. In addition, each 1-SD lower birth weight was associated with 0.189 SD higher fasting glucose concentration (ß = 0.189; SE = 0.060; P = .002), but not with fasting insulin, 2-hour glucose, or hemoglobin A1c concentration. Conclusions and Relevance: In this study, a genetic predisposition to lower birth weight was associated with increased risk of T2D and higher fasting glucose concentration, suggesting genetic effects on retarded fetal growth and increased diabetes risk that either are independent of each other or operate through alterations of integrated biological mechanisms.

17.
ACS Appl Mater Interfaces ; 11(39): 36244-36251, 2019 Oct 02.
Artigo em Inglês | MEDLINE | ID: mdl-31487984

RESUMO

In the work reported in this article, di(methylsulfonyl) ethane (DMSE) was examined as a neoteric S-related electrolyte additive to elevate LiCoO2/electrolyte interfacial stability at 3.0-4.5 V (compared to Li/Li+). DMSE, when added to the electrolyte, can significantly enhance the high-voltage performance of LiCoO2/graphite cells. Meanwhile, capacity retention increased from 20.8 to 66.5% after 100 cycles owing to the adjunction of 0.5 wt % DMSE to the electrolyte (carbonate solvents and lithium salt). The density functional theory calculation results indicate that DMSE has a greater highest occupied molecular orbital energy in contrast to ethylene carbonate, dimethyl carbonate, and ethyl methyl carbonate. Differential capacity versus voltage analysis and linear sweep voltammetry result indicate that DMSE is decomposed in preference to the electrolyte solvents. DMSE's effects are distinguished by electrochemical impedance spectroscopy, Fourier transform infrared spectroscopy, X-ray-diffraction spectroscopy, scanning electron microscopy, transmission electron microscopy, and X-ray photoelectron spectroscopy. The outcomes indicate that the enhanced cycling performance is attributed to the involvement of DMSE in the generation of a thinner film on LiCoO2, which results in lower interfacial impedance and it protects the electrolyte from decomposition at high voltage.

18.
FASEB J ; : fj201900965R, 2019 Sep 16.
Artigo em Inglês | MEDLINE | ID: mdl-31415184

RESUMO

Schwann cells (SCs) play an essential role in nerve injury repair. A striking feature of the cellular response to peripheral nerve injury is the proliferation of SCs. Circular (circ)RNAs are enriched in the nervous system and are involved in physiologic and pathologic processes. However, the potential role of circRNAs in SC proliferation post nerve injury remains largely unknown. Using a sciatic nerve crush model, we obtained an expression profiling of circRNAs in injured sciatic nerves in rats by RNA sequencing and bioinformatics analysis, and we further identified a circRNA [circ-ankyrin repeat and in-between Ring finger (IBR) domain containing 1 (Ankib1)] involved in SC proliferation by the transfection of specific small interfering RNAs. Overexpression of circ-Ankib1, which was specifically and highly enriched in SCs, impaired SC proliferation and axon regeneration following sciatic nerve injury. Mechanistically, increased expression of DEx/H-box helicase 9 (DHX9) postinjury might contribute to the down-regulation of circ-Ankib1, which further suppressed cytochrome P450, family 26, subfamily B, polypeptide 1 expression by sponging miR-423-5p, miR-485-5p, and miR-666-3p, leading to the induction of SC proliferation and nerve regeneration. Taken together, our results reveal a crucial role for circRNAs in regulating proliferation of SCs involved in sciatic nerve regeneration; as such, circRNAs may serve as a potential therapeutic avenue for nerve injury repair.-Mao, S., Zhang, S., Zhou, S., Huang, T., Feng, W., Gu, X., Yu, B. A Schwann cell-enriched circular RNA circ-Ankib1 regulates Schwann cell proliferation following peripheral nerve injury.

19.
Sci Adv ; 5(8): eaax1101, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31453335

RESUMO

Meiosis is a specialized type of cell division that creates haploid germ cells and ensures their genetic diversity through homologous recombination. We show that the H3K4me3 reader ZCWPW1 is specifically required for meiosis prophase I progression in male but not in female germ cells in mice. Loss of Zcwpw1 in male mice caused a complete failure of synapsis, resulting in meiotic arrest at the zygotene to pachytene stage, accompanied by incomplete DNA double-strand break repair and lack of crossover formation, leading to male infertility. In oocytes, deletion of Zcwpw1 only somewhat slowed down meiosis prophase I progression; Zcwpw1-/- oocytes were able to complete meiosis, and Zcwpw1-/- female mice had normal fertility until mid-adulthood. We conclude that the H3K4me3 reader ZCWPW1 is indispensable for meiosis synapsis in males but is dispensable for females. Our results suggest that ZCWPW1 may represent a previously unknown, sex-dependent epigenetic regulator of germ cell meiosis in mammals.

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