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4,621 result(s) for "Ding, Ping"
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Heterojunction photocatalysts for degradation of the tetracycline antibiotic: a review
Antibiotic pollution is a major health issue inducing antibiotic resistance and the inefficiency of actual drugs, thus calling for improved methods to clean water and wastewater. Here we review the recent development of heterojunction photocatalysis and application in degrading tetracycline. We discuss mechanisms for separating photogenerated electron–hole pairs in different heterojunction systems such as traditional, p–n, direct Z-scheme, step-scheme, Schottky, and surface heterojunction. Degradation pathways of tetracycline during photocatalysis are presented. We compare the efficiency of tetracycline removal by various heterojunctions using quantum efficiency, space time yield, and figures of merit. Implications for the treatment of antibiotic-contaminated wastewater are discussed.
Nearly ferromagnetic spin-triplet superconductivity
Spin-triplet superconductors potentially host topological excitations that are of interest for quantum information processing. We report the discovery of spin-triplet superconductivity in UTe₂, featuring a transition temperature of 1.6 kelvin and a very large and anisotropic upper critical field exceeding 40 teslas. This superconducting phase stability suggests that UTe₂ is related to ferromagnetic superconductors such as UGe₂, URhGe, and UCoGe. However, the lack of magnetic order and the observation of quantum critical scaling place UTe₂ at the paramagnetic end of this ferromagnetic superconductor series. A large intrinsic zero-temperature reservoir of ungapped fermions indicates a highly unconventional type of superconducting pairing.
Examining the factors influencing academic performance of medical technology students in e-learning: A questionnaire survey
In an era of rapid digital development, e-learning has become a significant trend in the educational field. Medical technology students need to acquire extensive theoretical knowledge and practical skills. E-learning can enhance learning experiences, improving students’ understanding and application abilities. This study examined the impact of learning motivation, learning approaches, and learning burnout on the academic performance of medical technology students in an e-learning environment. This study conducted a quantitative survey on 37 medical technology students. The questionnaires included learning motivations, learning methods, and burnout, and responses provided on a 5-point Likert scale. First, the 37 students were categorized into three groups based on their academic performance. Then, differences between these groups were analyzed using the Kruskal-Wallis test, and correlations between academic performance and questionnaire variables were calculated using Spearman correlation analysis. It revealed that motivation varies among different academic performance levels. Furthermore, in the high-grade group, self-efficacy (r = -0.502, p = 0.047), monitoring studying (r = 0.494, p = 0.032), and emotional exhaustion (r = 0.514, p = 0.024) were correlated to academic performance. In the middle-grade group, self-efficacy for learning and performance was correlated to academic performance (r = 0.858, p = 0.001). In the low-grade group, academic performance was correlated to depth approach (r = 0.826, p = 0.022) and organized studying (r = 0.833, p = 0.020). This study, through a quantitative survey, found significant differences in learning motivation, learning methods, and learning burnout among medical technology students with different academic performance levels. High-grade students demonstrated higher levels of emotional exhaustion, which may reflect feelings of overextension and academic burnout in e-learning environments; the academic performance of the middle-grade group was related to intrinsic motivation; and low-grade students showed a stronger correlation between their learning methods in e-learning and their academic performance. These insights underscore the necessity for personalized learning strategies to enhance educational outcomes effectively.
Zinc oxide nanoparticles induce apoptosis and autophagy in human ovarian cancer cells
Zinc oxide nanoparticles (ZnO NPs) are frequently used in industrial products such as paint, surface coating, and cosmetics, and recently, they have been explored in biologic and biomedical applications. Therefore, this study was undertaken to investigate the effect of ZnO NPs on cytotoxicity, apoptosis, and autophagy in human ovarian cancer cells (SKOV3). ZnO NPs with a crystalline size of 20 nm were characterized with various analytical techniques, including ultraviolet-visible spectroscopy, X-ray diffraction, transmission electron microscopy, Fourier transform infrared spectroscopy, and atomic force microscopy. The cytotoxicity, apoptosis, and autophagy were examined using a series of cellular assays. Exposure of cells to ZnO NPs resulted in a dose-dependent loss of cell viability, and the characteristic apoptotic features such as rounding and loss of adherence, enhanced reactive oxygen species generation, and loss of mitochondrial membrane potential were observed in the ZnO NP-treated cells. Furthermore, the cells treated with ZnO NPs showed significant double-strand DNA breaks, which are gained evidences from significant number of γ-H AX and Rad51 expressed cells. ZnO NP-treated cells showed upregulation of p53 and LC3, indicating that ZnO NPs are able to upregulate apoptosis and autophagy. Finally, the Western blot analysis revealed upregulation of Bax, caspase-9, Rad51, γ-H AX, p53, and LC3 and downregulation of Bcl-2. The study findings demonstrated that the ZnO NPs are able to induce significant cytotoxicity, apoptosis, and autophagy in human ovarian cells through reactive oxygen species generation and oxidative stress. Therefore, this study suggests that ZnO NPs are suitable and inherent anticancer agents due to their several favorable characteristic features including favorable band gap, electrostatic charge, surface chemistry, and potentiation of redox cycling cascades.
Effect of Gold Nanoparticles on Luminescence Enhancement in Antibodies for TORCH Detection
Purposes: To explore the optimization method and application of Au-NP-enhanced luminol––H2O2 luminescence system in TORCH (TOX, RV, CMV, HSVI, and HSVII) detection. Method: 4.5 × 10−5 mmol/L gold nano solution was prepared with chloroauric acid as the reducing agent and trisodium citrate as the stabilizer. After curing for 3 days, Au NPs participate in the luminal–H2O2 luminescence system to detect TORCH antibodies and establish the cut off value. SPSS 18.0 software was used to analyze the TORCH antibodies detected by the nano-gold-enhanced luminol luminescence method and TORCH kit. Additionally, its detection performance is studied. Results: The results of a paired t-test for the absorbance values of samples with and without gold nanoparticles showed that there were statistically significant differences (p < 0.001) between the two methods in the detection of TOX, RV, CMV, HSVI, and HSVII. The luminescence values with the addition of gold nanoparticles were significantly higher than those without gold nanoparticles. Using the Au NP–luminol–H2O2 chemiluminescence method, 127 serum samples were tested for TORCH antibodies. The sensitivities were 84.6%, 83.3%, 90.9%, 85.7%, and 84.6%, while the specificities were 94.7%, 96.5%, 96.6%, 97.3%, and 95.6%, respectively. The sensitivity and specificity of the chemiluminescence method enhanced by gold nanoparticles are significantly improved compared to the chemiluminescence method without enhancers. Conclusions: Au NPs participate in the luminal–H2O2 luminescent system. The absorbance, sensitivity, and specificity of TORCH antibodies show that Au NPs can enhance the luminol–H2O2 luminescent system. Au NP–luminol–H2O2 luminescence system has broad application prospects in the detection of eugenics.
Revealing Beta-Diversity Patterns of Breeding Bird and Lizard Communities on Inundated Land-Bridge Islands by Separating the Turnover and Nestedness Components
Beta diversity describes changes in species composition among sites in a region and has particular relevance for explaining ecological patterns in fragmented habitats. However, it is difficult to reveal the mechanisms if broad sense beta-diversity indices (i.e. yielding identical values under nestedness and species replacement) are used. Partitioning beta diversity into turnover (caused by species replacement from site to site) and nestedness-resultant components (caused by nested species losses) could provide a unique way to understand the variation of species composition in fragmented habitats. Here, we collected occupancy data of breeding birds and lizards on land-bridge islands in an inundated lake in eastern China. We decomposed beta diversity of breeding bird and lizard communities into spatial turnover and nestedness-resultant components to assess their relative contributions and respective relationships to differences in island area, isolation, and habitat richness. Our results showed that spatial turnover contributed more to beta diversity than the nestedness-resultant component. The degree of isolation had no significant effect on overall beta diversity or its components, neither for breeding birds nor for lizards. In turn, in both groups the nestedness-resultant component increased with larger differences in island area and habitat richness, respectively, while turnover component decreased with them. The major difference among birds and lizards was a higher relevance of nestedness-resultant dissimilarity in lizards, suggesting that they are more prone to local extinctions derived from habitat fragmentation. The dominance of the spatial turnover component of beta diversity suggests that all islands have potential conservation value for breeding bird and lizard communities.
M6A demethylase fat mass and obesity‐associated protein regulates cisplatin resistance of gastric cancer by modulating autophagy activation through ULK1
Drug resistance is an important factor for treatment failure of gastric cancer. N6‐methyladenosine (m6A) is the predominant mRNA internal modification in eukaryotes. The roles of m6A modification in drug resistance of gastric cancer remains unclear. In the present study, the m6A methylated RNA level was significantly decreased while the expression of m6A demethylase fat mass and obesity‐associated protein (FTO) was obviously elevated in cisplatin‐resistant (SGC‐7901/DDP) gastric cancer cells. Knockdown of FTO reversed cisplatin resistance of SGC‐7901/DDP cells both in vitro and in vivo, which was attributed to the inhibition of Unc‐51‐like kinase 1 (ULK1)‐mediated autophagy. Mechanistically, ULK1 expression was regulated in an FTO‐m6A‐dependent and YTHDF2‐mediated manner. Collectively, our findings indicate that the FTO/ULK1 axis exerts crucial roles in cisplatin resistance of gastric cancer. Knockdown of FTO reversed cisplatin resistance of SGC‐7901/DDP cells both in vitro and in vivo, which were attributed to the inhibition of ULK1 mediated‐autophagy. ULK1 expression was regulated in the FTO‐m6A dependent and YTHDF2‐mediated manner.
Single nucleotide polymorphisms within HLA region are associated with the outcomes of unrelated cord blood transplantation
Cord blood transplantation (CBT) provides a treatment scheme for hematologic diseases and leukemia in both children and adults. However, adverse reactions and transplantation-related death may still occur in patients receiving CBT even when donor and recipient have fully matched HLA in high-resolution HLA typing analysis. Single nucleotide polymorphisms (SNPs) of HLA-related and unrelated genes are known to associate with disease status of patients with unrelated stem cell transplantation. In this study, the genomic regions ranging from 500 base pairs upstream to 500 base pairs downstream of the eight SNPs that were reported as transplantation determinants by Petersdorf et al. were analyzed to evaluate whether genetic variants were associated with the survival status of patients, and the risk for severe (grades 3–4) graft-versus-host disease (GVHD) or cytomegalovirus (CMV) infection/reactivation. The analyses were performed in the mode of recipient genotype, donor genotype, and recipient-donor mismatching, respectively. By analysis of sixty-five patients and their HLA-matched unrelated donors, we found that five SNPs were associated with patient survival which included the recipient genotype with SNPs of rs107822 in the RING1 gene, and rs2070120, rs17220087 and rs17213693 in the HLA-DOB gene; and the recipient-donor mismatching with SNPs of rs9282369 in HLA-DOA gene, and rs2070120, rs17220087 and rs17213693 in the HLA-DOB gene. Five SNPs were associated with the risk for severe GVHD which included the donor genotype with SNPs of rs213210 and rs2523675; the recipient genotype with SNPs of rs9281491 in the HCP5 gene; and the recipient-donor mismatching with SNPs of rs209130 in the TRIM27 gene, and rs986522 in the COL11A2 gene. Six SNPs were related to the risk for CMV infection/reactivation which included the donor genotype with SNPs of rs435766, rs380924, and rs2523957; and the recipient-donor mismatching with SNPs of rs2070120, rs17220087, and rs17213693 in the HLA-DOB gene; and rs435766 and rs380924 in the MICD gene. This study provides the basis for larger analyses and if the results are confirmed, a way of selecting better unrelated CBT candidate donors.
Investigation of the association between the genetic polymorphisms of the co-stimulatory system and systemic lupus erythematosus
Human leukocyte antigen genes have been shown to have the strongest association with autoimmune disease (AD). However, non-HLA genes would be risk factors of AD. Many genes encoding proteins that are related to T- and B-cell function have been identified as susceptibility genes of systemic lupus erythematosus (SLE). In this study, we explored the correlation between SLE and the genetic polymorphisms of co-stimulatory/co-inhibitory molecules, including CTLA4, CD28, ICOS, PDCD1, and TNFSF4. We found that there were nine single-nucleotide polymorphisms (SNPs) associated with SLE, namely, rs11571315 (TT vs. CT vs. CC: p < 0.001; TT vs. CT: p = 0.001; p = 0.005; TT vs. CT +CC: p < 0.001; TT+CT vs. CC: p = 0.032), rs733618 (CC vs. CT vs. TT: p = 0.002; CC vs. CT: p = 0.001; CC vs. TT: p = 0.018; CC vs. CT + TT: p = 0.001), rs4553808 (AA vs. AG: p < 0.001), rs62182595 (GG vs. AG vs. AA: p < 0.001; GG vs. AG: p < 0.001; GG vs. AG+AA: p < 0.001), rs16840252 (CC vs. CT vs. TT: p < 0.001; CC vs. CT: p < 0.001; CC vs. CT + TT: p < 0.001), rs5742909 (CC vs. CT: p = 0.027; CC vs. CT + TT: p = 0.044), rs11571319 (GG vs. AG vs. AA: p < 0.001, GG vs. AG: p < 0.001; GG vs. AG+AA: p < 0.001), rs36084323 (CC vs. CT vs. TT: p = 0.013, CC vs. TT: p = 0.004; CC vs. CT + TT: p = 0.015; CC +CT vs. TT: p = 0.015), and rs1234314 (CC vs. CG vs. GG: p = 0.005; CC vs. GG: p=0.004; CC+ CG vs. GG: p=0.001), but not in CD28 and ICOS by using the chi-square test. Additionally, rs62182595 and rs16840252 of CTLA and rs1234314 and rs45454293 of TNFSF4 were also associated with SLE in haplotypes. These SLE-related SNPs also had an association with several diseases. It was indicated that these SNPs may play an important role in immune regulation and pathogenic mechanisms.
Exploration of the association between the single-nucleotide polymorphism of co-stimulatory system and rheumatoid arthritis
The human leukocyte antigen (HLA) has been linked to the majority of autoimmune diseases (ADs). However, non-HLA genes may be risk factors for ADs. A number of genes encoding proteins involved in regulating T-cell and B-cell function have been identified as rheumatoid arthritis (RA) susceptibility genes. In this study, we investigated the association between RA and single-nucleotide polymorphisms (SNPs) of co-stimulatory or co-inhibitory molecules in 124 RA cases and 100 healthy controls without immune-related diseases [including tumor necrosis factor superfamily member 4 (TNFSF4), CD28, cytotoxic T-lymphocyte-associated protein 4 (CTLA4), and programmed cell death protein 1 (PDCD1)]. The results showed that there were 13 SNPs associated with RA, including rs181758110 of TNFSF4 (CC vs. CT, = 0.038); rs3181096 of CD28 (TT vs. CC + CT, = 0.035; CC vs. TT, = 0.047); rs11571315 (TT vs. CT, = 0.045), rs733618 (CC vs. TT + CT, = 0.043), rs4553808 (AA vs. AG vs. GG, = 0.035), rs11571316 (GG vs. AG vs. AA, = 0.048; GG vs. AG + AA, = 0.026; GG vs. AG, = 0.014), rs16840252 (CC vs. CT vs. TT, = 0.007; CC vs. CT, = 0.011), rs5742909 (CC vs. CT vs. TT, = 0.040), and rs11571319 of CTLA4 (GG vs. AG vs. AA, < 0.001; GG vs. AG + AA, = 0.048; AA vs. GG + AG, = 0.001; GG vs. AA, = 0.008; GG vs. AG, ≤ 0.001); and rs10204525 (TT vs. CT + CC, = 0.024; TT vs. CT, = 0.021), rs2227982 (AA vs. GG, = 0.047), rs36084323 (TT vs. CT vs. CC, = 0.022; TT vs. CT + CC, = 0.013; CC vs. TT + CT, = 0.048; TT vs. CC, = 0.008), and rs5839828 of PDCD1 (DEL vs. DEL/G vs. GG, = 0.014; DEL vs. DEL/G + GG, = 0.014; GG vs. DEL + DEL/G, = 0.025; DEL vs. GG, = 0.007). Consequently, these SNPs may play an important role in immune regulation, and further research into the role of these SNPs of immune regulatory genes in the pathogenesis of RA is required.