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1.
Mol Cancer ; 19(1): 26, 2020 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-32020881

RESUMO

BACKGROUND: Although trastuzumab provides significant clinical benefit for HER2-positive breast cancers, responses are limited by the emergence of resistance. Recent evidence suggests that long noncoding RNAs (lncRNAs) play important roles in tumorigenesis and chemoresistance. However, the regulatory mechanism of lncRNAs in trastuzumab resistance is not well established to date. In this research, we identified the differentially expressed lncRNA and investigated its regulatory role in trastuzumab resistance of breast cancer. METHODS: LncRNA microarray and qRT-PCR were performed to identify the dysregulated lncRNAs. Transmission electron microscopy, differential ultracentrifugation and qRT-PCR were used to verify the existence of exosomal AFAP1-AS1 (actin filament associated protein 1 antisense RNA 1). Bioinformatics prediction, RNA fluorescence in situ hybridization (RNA-FISH) and immunoprecipitation assays were performed to identify the direct interactions between AFAP1-AS1 and other associated targets, such as AU-binding factor 1 (AUF1) and ERBB2. Finally, a series gain- or loss-functional assays were done to prove the precise role of AFAP1-AS1 in trastuzumab resistance. RESULTS: AFAP1-AS1 was screened out due to its higher expression in trastuzumab-resistant cells compared to sensitive cells. Increased expression of AFAP1-AS1was associate with poorer response and shorter survival time of breast cancer patients. AFAP1-AS1 was upregulated by H3K27ac modification at promoter region, and knockdown of AFAP1-AS1 reversed trastuzumab resistance. Moreover, extracellular AFAP1-AS1 secreted from trastuzumab resistant cells was packaged into exosomes and then disseminated trastuzumab resistance of receipt cells. Mechanically, AFAP1-AS1 was associated with AUF1 protein, which further promoted the translation of ERBB2 without influencing the mRNA level. CONCLUSION: Exosomal AFAP1-AS1 could induce trastuzumab resistance through associating with AUF1 and promoting ERBB2 translation. Therefore, AFAP1-AS1 level may be useful for prediction of trastuzumab resistance and breast cancer treatment.

2.
Mol Ther ; 2020 Jan 21.
Artigo em Inglês | MEDLINE | ID: mdl-32027844

RESUMO

The major obstacles for the efficacy of tumor immunotherapies are their immune-related systemic adverse events. Therefore, tumor tropism property and pro-inflammatory ability of mesenchymal stem cells (MSCs) could be utilized in combination to potentiate local immunity for cancer eradication. We previously observed that MSCs with the type III histone deacetylase silent information regulator 2 homologue 1 (Sirt1) overexpression displayed a pro-inflammatory capacity. However, the anti-tumor effect of Sirt1-overexpressing MSCs and the role of Sirt1 in regulating the pro-inflammatory capacity of MSCs still need to be clarified. In this study, utilizing the hepatic metastasis model of colorectal carcinoma, we demonstrated that Sirt1-overexpressing MSCs significantly exerted anti-tumor activity through increasing the number of CD8+ T cells. Furthermore, Sirt1 did not affect chemokine secretion in MSCs induced by inflammatory cytokines, but impaired the immunosuppressive ability of MSCs through suppressing inflammatory cytokine-stimulated inducible nitric oxide synthase (iNOS) production via deacetylating p65. iNOS overexpression negated the anti-tumor effect of Sirt1-overexpressing MSCs. Collectively, our data defined Sirt1 as the critical regulator for modulating the pro-inflammatory ability of MSCs, and they suggested that Sirt1-overexpressing MSCs secreting chemokines but little iNOS under the inflammatory milieu were capable of attracting immune cells to close proximity without suppressing their proliferation, thereby achieving a potent anti-tumor effect.

3.
Sci Total Environ ; 711: 135087, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32000338

RESUMO

Oxygen has not been purposely introduced to the autotrophic denitrification systems and simultaneous nitrification/autotrophic denitrification (SNAD) has not been proposed. In this study, oxygen was introduced into a micro-electrolysis-enhanced Fe0-supported autotrophic denitrification (mFe0AD) system. The nitrogen removal performance was investigated and the application potential of iron-scraps-supported simultaneous nitrification/mFe0AD was evaluated. The results showed that Fe0AD was surprisingly enhanced by oxygen together with nitrification at average dissolved oxygen (DO) of 0.08-1.56 mg/L. The ammonia oxidizing bacterial, nitrite oxidizing bacteria, facultative autotrophic denitrificans, and iron compounds transformation bacteria were markedly enriched. Average denitrification rate shifted from 0.116 to 0.340 kg N/(m3·d) with increase of average total nitrogen removal efficiency from 31.4% to 90.5%. Oxygen could enhance the biological conversion and storage of iron compounds, which was capable of reducing the coating of Fe0 surface.The accelerating of oxygen on  Fe0 passivation appeared when increasing the average DO from 1.56 to 2.17 mg/L. Therefore, the SNAD was recommended to be operated at the DO range of 0.08-1.56 mg/L. ME significantly enhanced Fe0AD, and the utilization of iron-scraps reduced its cost. The denitrification rate is comparable with methanol supported heterotrophic denitrification with 58.9% reduction on the cost. The iron-scraps supported SNAD is competitive in both denitrification rate and costs in the ammonia contaminated low-carbon water treatment.

4.
Artigo em Inglês | MEDLINE | ID: mdl-32048119

RESUMO

PURPOSE: To identify the disease gene in 40 patients with female infertility due to oocyte maturation arrest. METHODS: Genomic DNA was extracted from peripheral blood of 40 patients and their family members. Whole-exome sequencing was performed on the patients, and the PATL2 mutations were identified and confirmed by Sanger sequencing. Harmfulness of the mutations was analyzed by SIFT, Polyphen-2, Mutation Taster, and M-CAP software, and we used western immunoblotting analysis to check the effect of mutations on PATL2 protein expression in vitro. RESULTS: Two novel missense mutations c.1528C>A (p.Pro510Thr) and c.1376C>A (p.Ser459Tyr) in PATL2 were identified in three patients (7.5%) from two consanguineous families in our cohort. We found that mutations in PATL2 resulted in variable oocyte phenotypes, including GV arrest, MI arrest, and morphologic abnormalities. Western immunoblotting analysis showed that the expression levels of the two novel mutant PATL2 proteins decreased significantly. CONCLUSIONS: We identified two novel PATL2 mutations that caused oocyte maturation arrest and abnormal morphology, and variable phenotypes in patients.

5.
ACS Chem Neurosci ; 2020 Feb 12.
Artigo em Inglês | MEDLINE | ID: mdl-32049477

RESUMO

Mitophagy is an important process for removing damaged mitochondria in cells, the dysfunction of which has been directly linked to an increasing number of neurodegenerative disorders. However, the details of mitophagy in prion diseases still need to be deeply explored. In this study, we identified more autophagosomes and large swelling mitochondria structures in the prion infected cultured cell line SMB-S15 by transmission electron microscopy, accompanying with the molecular evidences of activated autophagic flux. Western blots illustrated that the levels of Pink1 and Parkin, particularly in the mitochondrial fraction, were increased in SMB-S15 cells, whereas the levels of mitochondrial membrane proteins TIMM44, TOMM20 and TIMM23 were decreased. The amount of the whole polyubiquitinated proteins decreased but that of phosphor-polyubiquitinated proteins increased in SMB-S15 cells. The level of MFN2 in SMB-S15 cells were downregulated but its polyubiquitinated form upregulated. Knock-down of the expressions of Pink1 and Parkin by the individual SiRNAs in SMB-S15 cells reduced autophagic activity but seemed not to influence the expressions of TOMM20 and TIMM23. Moreover, we also demonstrated that the brain levels of Pink1 and Parkin in the mice infected with scrapie strains 139A and ME7 were remarkably increased at the terminal stage of the disease by Western blot and immunohistochemical (IHC) assays. Immunofluorescent assays (IFA) revealed that Pink1 signals widely colocalized with GAFP- Iba1- and NeuN positive cells in the brains of scrapie infected mice. IHC assays with serial sections of the brain tissues infected with agents 139A and ME7 mice showed more Pink1 and Parkin positive cells located at the areas with more PrPSc deposit. These results suggest that an activated mitophagy in prion infected cells and prion infected experimental mice, probably via enhanced Pink-Parkin pathway.

6.
Database (Oxford) ; 20202020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-32047888

RESUMO

RNA-binding proteins (RBPs) play important roles in regulating the expression of genes involved in human physiological and pathological processes, especially in cancers. Many RBPs have been found to be dysregulated in cancers; however, there was no tool to incorporate high-throughput data from different dimensions to systematically identify cancer-related RBPs and to explore their causes of abnormality and their potential functions. Therefore, we developed a database named RBPTD to identify cancer-related RBPs in humans and systematically explore their functions and abnormalities by integrating different types of data, including gene expression profiles, prognosis data and DNA copy number variation (CNV), among 28 cancers. We found a total of 454 significantly differentially expressed RBPs, 1970 RBPs with significant prognostic value, and 53 dysregulated RBPs correlated with CNV abnormality. Functions of 26 cancer-related RBPs were explored by analysing high-throughput RNA sequencing data obtained by crosslinking immunoprecipitation, and the remaining RBP functions were predicted by calculating their correlation coefficient with other genes. Finally, we developed the RBPTD for users to explore functions and abnormalities of cancer-related RBPs to improve our understanding of their roles in tumorigenesis. Database URL: http: //www.rbptd.com.

7.
Chem Commun (Camb) ; 2020 Jan 23.
Artigo em Inglês | MEDLINE | ID: mdl-31970341

RESUMO

Based on the structural programmability and spatial addressability of DNA nanodevices, a target-triggered, enzyme-free 3D DNA walker, comprising of hairpin DNA assembled gold nanoparticles with a local catalytic hairpin assembly reaction, was developed for the highly sensitive detection of intracellular tumor-associated microRNAs.

9.
J Clin Nurs ; 2020 Jan 23.
Artigo em Inglês | MEDLINE | ID: mdl-31972867

RESUMO

AIMS AND OBJECTIVES: To explore the consistency of pain intensity and pain location assessed by nurses and patients in gynaecology undergoing enhanced recovery after surgery pathway. BACKGROUND: Several studies have shown that clinical nurses' assessment of patients' pain is not always accurate. Little is known about the accuracy of nurses' pain assessments for gynaecological patients. Postoperative pain assessment and management is an essential part of enhanced recovery after surgery. DESIGN: Comparative cross-sectional study. METHODS: A total of 160 patients were recruited and only 85 patients and 17 nurses participated. Patients and nurses recorded pain scores (using an 11-point Numeric Rating Scale) and pain location (incision pain, surgical area pain in the abdominal cavity, other pain or no pain) on Pain Assessment Forms at 4 hr after surgery and on the first and second postoperative days. We used the STROBE guidelines to report our study. RESULTS: The patients' pain score was higher than that of nurses from 4 hr to second day after laparoscopic surgery at rest. The pain scores of both nurses and patients decreased over this period of time. All the intraclass correlation coefficients were between 0.214-0.296. At the three time points, surgical area pain in the abdominal cavity and abdominal incision pain were the main pain areas. All the kappa coefficients were between 0.164-0.255. CONCLUSIONS: The consistency of postoperative pain assessment about pain score and pain location between nurses and patients was not high. We should attach importance to systematic pain assessment, and more detailed enhanced recovery after surgery pathways should be developed about pain assessment. RELEVANCE TO CLINICAL PRACTICE: Continuing education for nurses regarding pain assessment is necessary. Nurses should accept the patient's self-reported pain. There should be a step that gives more time for pain assessment in enhanced recovery after surgery pathways.

10.
Cell Death Dis ; 11(1): 70, 2020 Jan 27.
Artigo em Inglês | MEDLINE | ID: mdl-31988281

RESUMO

Previous studies have shown that tumor necrosis factor (TNF)-α is a mediator of hepatotoxicity in liver injury. Moreover, TNF-α has also been reported to have a protective effect in liver regeneration, yet the function of TNF-α during liver injury remains controversial. Here, we report that the concentration of TNF-α determines its functions. High concentrations of TNF-α could aggravate LPS-induced liver injury. However, the TNF-α level was unchanged during APAP-induced liver injury, which exerted a protective effect. We expected that the concentration of TNF-α may affect its function. To test this hypothesis, TNF-α-/- rats or hepatocyte cells were treated with different concentrations of TNF-α. We found low TNF-α could reduce the levels of ALT and AST in the plasma of TNF-α-/- rats and promote the proliferation of hepatocyte cells. However, the levels of ALT and AST increased gradually with increasing TNF-α concentration after reaching the lowest value. Moreover, we showed that TNF-α affects the cell proliferation and cell death of hepatocytes by regulating Yap activity. Low TNF-α promoted Yap1 nuclear translocation, triggering the proliferation of hepatocytes. However, high TNF-α triggered the phosphorylation and inactivation of Yap1, preventing its nuclear import and consequently promoting cell death. Collectively, our findings provide novel evidence that the concentration of TNF-α is an important factor affecting its function in liver injury, which may provide a reference for the clinical treatment of liver injury.

11.
Biomed Pharmacother ; 123: 109724, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31918209

RESUMO

Knee osteoarthritis (KOA) is a chronic degenerative joint disorder characterized by loss of articular cartilage and progressive deterioration, leading to pain and functional limitation. Abnormal biomechanics play a core role in the onset and development of KOA. The aim of this study was to explore whether electroacupuncture (EA) may relieve pain and adjust the biomechanical properties of the extensor-flexor muscles to improve abnormal joint loading, thus alleviating the degradation of cartilage in a rabbit model of KOA. Firstly, a KOA model was induced by immobilization for 6 weeks. Then, different interventions (EA and celecoxib) were applied for 4 weeks. The levels of pain and disability were assessed using the Lequesne MG index. Muscle function, including function of the rectus femoris and biceps femoris, was tested through hematoxylin-eosin staining (HE staining) and use of a microforce tension-torsion instrument. The cartilage was tested using nanoindentation, Safranin O-Fast Green staining, confocal laser scanning microscopy (immunofluorescence), immunohistochemistry and the enzyme-linked immunosorbent assay (ELISA). Finally, we found that EA and celecoxib resulted in lower behavioral and pain scores than the model group. In addition, it improved the function of muscles. Furthermore, those treatments alleviated the rate of cartilage degradation, manifested as increased loss factor without statistical difference and a significant reduction in the Mankin score. This promoted the metabolism of type II collagen in the cartilage layer and drastically reduced the expression of CTX-II in the synovial fluid and peripheral serum. Concisely, EA promotes pain limitation and ameliorates muscular atrophy-induced inappropriate biomechanical loading on the articular cartilage through pain relief and potentiation of muscle function, thus improving cartilage viscoelasticity, as demonstrated by the retarded degradation of type II collagen in our KOA model.

12.
Exp Neurol ; 326: 113176, 2020 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-31926167

RESUMO

Epidemiological studies suggest that chronic periodontitis (CP) is closely associated with the incidence and progression of cognitive impairment. The present study investigated the causal relationship between CP and cognitive decline and the underlying mechanism in mice. Long-term ligature around the left second maxillary molar tooth was used to induce CP in mice. Severe alveolar bone loss and inflammatory changes were observed in gingival tissues, accompanied by progressive cognitive deficits during a 12-month period. We also observed cerebral neuronal and synaptic injury and glial activation in this mouse model of CP. Furthermore, CP mice exhibited significant dysbiosis of the oral and gut microbiota, disruption of the intestinal barrier and blood-brain barrier, increases in the serum contents of proinflammatory cytokines and lipopolysaccharide (LPS), and increases in brain LPS levels, Toll-like receptor 4 (TLR4) expression, nuclear factor-κB (NF-κB) nuclear translocation and proinflammatory cytokine mRNA levels. These results indicate that CP may directly induce progressive cognitive decline and its mechanism is probably related to microbiota-gut-brain axis disorders, LPS/TLR4/NF-κB signaling activation and neuroinflammatory responses in mice. Therefore, the microbiota-gut-brain axis may provide the potential strategy for the prevention and treatment of CP-associated cognitive impairment.

13.
Artigo em Inglês | MEDLINE | ID: mdl-31953331

RESUMO

As an ideal carotenoids producer, Blakeslea trispora has gained lots of attentions due to its large biomass and high production of ß-carotene and lycopene. However, carotenogenesis regulation in B. trispora still needs to be clarified since few investigations have been conducted at molecular level in B. trispora In this study, the homologous gene of carotenogenesis regulatory gene (crgA) was cloned from the mating type (-) of B. trispora and the deduced CrgA protein was analyzed for its primary structure and domains. In order to clarify the crgA-mediated regulation in B. trispora, we used the strategies of gene knockout and complementation to investigate the effect of crgA expression on the phenotype of B. trispora In contrast to the wild-type strain, the crgA null mutant was defective in sporulation, but accumulated much more ß-carotene (31.2% improvement at the end) accompanied by the enhanced transcription levels of three structural genes (hmgR, carB and carRA) for carotenoids over whole culture time. When the wild-type copy of crgA was complemented into the crgA null mutant, sporulation, transcription level of structural gene and carotenoids production were restored as present in wild-type strain. Gas chromatography-mass spectrometry (GC-MS)-based metabolomic approach and multivariate statistical analyses were performed to investigate the intracellular metabolite profiles. The reduced levels of tricarboxylic acid (TCA) cycle components and some amino acids and enhanced levels of glycolysis intermediates and fatty acids indicate that more metabolic flux was driven into the mevalonate (MVA) pathway, thus the increase of precursors and fat content contributes to the accumulation of carotenoids.IMPORTANCE The zygomycete Blakeslea trispora is an important strain for the production of carotenoids in large scale. However, the regulation mechanism of carotenoid biosynthesis is still not well understood in this filamentous fungus. In the current study, we sought to investigate how crgA influences the expression of structural genes for carotenoids, carotenoid biosynthesis and other anabolic phenotypes. This will lead to a better understanding of global regulation mechanism of carotenoid biosynthesis and facilitate engineering this strain in the future for enhanced production of carotenoids.

14.
Ann Thorac Surg ; 2020 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-31926158

RESUMO

BACKGROUND: Patients undergoing thoracic lung wedge resection could benefit from tubeless strategies. However, postoperative pneumothorax is a primary limiting factor for such strategies. Accordingly, we evaluated the safety and efficacy of the prophylactic use of an air-extraction catheter as an improved drainage strategy and compared the findings with those for chest tube drainage in patients undergoing thoracic wedge resection. METHODS: Patients undergoing thoracic wedge resection between August 2017 and October 2018 were enrolled in this single-center, randomized, open-label, non-inferiority trial. Patients who received an improved drainage strategy involving the use of a prophylactic air-extraction catheter were randomized to the intervention group, while those who underwent routine chest tube drainage were assigned to the control group. Analysis was based on the per protocol population. The primary outcome was the incidence of pneumothorax on postoperative day 1. Secondary outcomes included patient recovery and related complications, including pleural effusion, lung infection, numeric rating scale score for pain, postoperative chest tube/catheter removal, postoperative hospitalization, and chest tube reinsertion. RESULTS: Ninety-six patients were randomized. The baseline demographic and clinical characteristics were similar between groups. The incidence of pneumothorax in the intervention and control groups was 10.0% and 9.1%, respectively (non-inferiority, P = 1.000). In addition, there were no significant between-group differences in secondary outcomes. A significantly lower pain score was observed in the intervention group (P = 0.001). CONCLUSIONS: The improved drainage strategy is non-inferior to standard chest tube drainage after thoracic wedge resection and should be popularized.

15.
J Cardiovasc Pharmacol ; 75(1): 45-53, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31895879

RESUMO

Atherosclerosis is a chronic inflammation condition resulting from the interaction between lipoproteins, monocyte-derived macrophages, T lymphocytes, and other cellular elements in the arterial wall. Macrophage-derived foam cells play a key role in both early and advanced stage of atherosclerosis. Previous studies have shown that berberine could inhibit foam cell formation and prevent experimental atherosclerosis. However, its underlying molecular mechanisms have not been fully clarified. In this study, we explored the cholesterol-lowering effects of berberine in macrophage-derived foam cells and investigated its possible mechanisms in prevention and treatment of atherosclerosis. Here, we demonstrated that berberine could inhibit atherosclerosis in apolipoprotein E-deficient mice and induce cholesterol reduction as well as decrease the content of macrophages. Berberine can regulate oxLDL uptake and cholesterol efflux, thus suppresses foam cell formation. Mechanisms study showed that berberine can suppress scavenger receptor expression via inhibiting the activity of AP-1 and upregulate ATP-binding cassette transporter via activating Nrf2/HO-1 signaling in human macrophage. In summary, berberine significantly inhibits atherosclerotic disease development by regulating lipid homeostasis and suppressing macrophage foam cell formation.

16.
Cell Death Dis ; 11(1): 43, 2020 Jan 22.
Artigo em Inglês | MEDLINE | ID: mdl-31969559

RESUMO

Trastuzumab is commonly used in the treatment of human epidermal growth factor receptor-2 positive (HER-2+) breast cancer, but its efficacy is often limited by the emergence of chemoresistance. Recent studies indicate that exosomes act as vehicles for exchange of genetic cargo between heterogeneous populations of tumor cells, engendering a transmitted drug resistance for cancer development and progression. However, the specific contribution of breast cancer-derived exosomes is poorly understood. In this study, publicly available expression profiling data from breast cancer and bioinformatics analyses were used to screen potential miRNAs in trastuzumab resistance. A series of gain- or loss-functional assays were performed to define the function of miR-567 and ATG5 in trastuzumab resistance and autophagy, both in vitro and in vivo. Our results showed that miR-567 was significantly decreased in trastuzumab-resistant patients compared with responding patients. Moreover, miR-567 was also downregulated in trastuzumab-resistant cells compared with parental cells. Overexpression of miR-567 reversed chemoresistance, whereas silence of miR-567 induced trastuzumab resistance, both in vitro and in vivo. In addition, enhanced miR-567 could be packaged into exosomes, incorporated into receipt cells, suppressing autophagy and reversed chemoresistance by targeting ATG5. To conclude, exosomal miR-567 plays a key role in reversing trastuzumab resistance via regulating autophagy, indicating it may be a promising therapeutic target and prognostic indicator for breast cancer patients.

17.
Mol Med Rep ; 21(1): 360-370, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31939622

RESUMO

The gasdermin (GSDM) superfamily has been demonstrated to consist of several important molecules that modulate multifunctional signal processes, such as cell pyroptosis. In this research, the roles of the GSDM superfamily on the occurrence and prognosis of lung adenocarcinoma (LUAD) were evaluated using integrative bioinformatic analyses and in vitro methods. Here, data from several bioinformatic platforms revealed that GSDMC is significantly upregulated in LUAD tissues and cell lines. Real­time fluorescence quantitative PCR (qPCR) demonstrated that GSDMC was obviously upregulated in radio­resistant LUAD cells, compared with their parental cells. Moreover, upregulated GSDMC expression was confirmed to be an independent indicator of poor first progression (FP) and overall survival (OS) in LUAD patients. DNA methylation analysis showed an evidently negative correlation between GSDMC expression and methylation status of one CpG site (cg05316065) in its DNA sequence. Patients with high methylation values had significantly higher Karnofsky performance scores (KPSs) and prolonged OS rates. Together, we confirmed that overexpression of GSDMC acts as a promising predictive factor for the poor prognosis of LUAD patients.

18.
Dalton Trans ; 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31989138

RESUMO

With the in situ-generated [Pb(MCP)4]2+ (HMCP+ = 1-methyl-4-(carboxyl)pyridinium) or [M(phen)3]2+ (M = Co, Fe and Ni; phen = 1,10-phenanthroline) complexes as structural directing agents and charge-balancing ions, we solvothermally synthesized and structurally characterized four new organic-inorganic hybrid iodoplumbates. Compound K2[Pb(MCP)4]Pb3I10 (1) represents the first K+ and [Pb(MCP)4]2+ co-templated hybrid haloplumbate, and exhibits a curve-like anionic layer of [Pb3I10]n4n-. Compounds [M(phen)3]Pb2I6·CH3CN (M = Co (2), Fe (3) and Ni (4)) have isostructural phases, and feature a one-dimensional (1D) [Pb2I6]n2n- anionic chain characteristic of pyramid-like [PbI5] units. The optical property studies show that compounds 1-4 exhibit semiconductor behaviors with the band gaps of 1.98-2.68 eV. In addition, the title compounds exhibited interesting photoelectrical responsive properties, with the photocurrent density in the order of 1 > 3 > 2 > 4. The thermal stabilities of the title compounds 1-4, as well as the theoretical band structure and density of states (DOS) of compounds 1 and 2 have also been studied.

19.
Artigo em Inglês | MEDLINE | ID: mdl-31963197

RESUMO

This study investigated the prevalence and interpersonal correlates of Internet gaming disorders (IGD) among Chinese adolescents. A cross-sectional survey was conducted in two cities (Shanghai and Xi'an) in China. A total of 2666 (Meanage = 12.77 ± 0.75) year-one students from eight middle schools completed a self-reported questionnaire. It tested their levels of IGD, parental psychological control, negative interpersonal events (physical/verbal abuse by parents, verbal abuse by teachers, peer/online bullying), social support from parents/peers, and positive relationships with parents/peers. Results showed that 346 participants (13.0%) were classified as having IGD. Gender, city, single-parent family, family socio-economic status, and mother's education level were significantly associated with the risk of IGD. Logistic regression analyses with and without controlling for the significant background variables showed that the studied interpersonal variables were significantly associated with IGD, respectively. Forward stepwise logistic regression showed that the significant correlates of IGD included parental psychological control, physical/verbal abuse by parents, verbal abuse by teachers, and peer/online bullying. Results highlight the importance of addressing interpersonal risk factors to reduce adolescent IGD. Limitations and implications of this study are discussed.

20.
Fish Physiol Biochem ; 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31993854

RESUMO

Type 1 diabetes is characterized by an increase in blood glucose levels resulting from damage to ß cells in pancreatic islets and the consequent absolute insufficiency of insulin. Animal models of type 1 diabetes were usually established using drugs toxic to ß cells, such as streptozotocin (STZ). To assess the application of zebrafish larvae in diabetes research, we explore the effects of STZ on pancreatic islets and glucose metabolism in zebrafish larvae. STZ was microinjected into the pericardial cavity of zebrafish larvae on alternate days for three times. At 2 days after the whole series of STZ injection (12 dpf), free-glucose level in larvae tissue shows a significant increase, and the fluorescence signal in immunohistochemistry, which indicates the insulin expression, was significantly weaker compared with the solution-injected control. Obvious apoptosis signals were also observed in the location of pancreatic islet, and insulin content decreased to be undetectable in STZ-injected larvae. Gene expression level of ins decreased to half of the solution injection control and that of casp3a was upregulated by 2.20-fold. Expression level of glut2 and gck decreased to 0.312-fold and 0.093-fold, respectively. pck1 was upregulated by 2.533-fold in STZ-injected larvae. By tracking detection, we found the free-glucose level in STZ-injected larvae gradually approached the level of the solution injection control and the insulin content recovered at 6 days post-STZ injection (16 dpf). Consistent with the change of the glucose level, the regeneration rate of the caudal fin in the STZ-injected group decreased initially, but recovered and accelerated gradually finally at 8 days post-amputation (20 dpf). These results indicate the generation of a transient hyperglycemia model due to ß-cell apoptosis caused by STZ, which is abated by the vigorous regeneration ability of ß cells in zebrafish larvae.

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