LINC00942 Alleviates NaAsO2-induced Apoptosis by Promoting GSH Synthesis Through Targeting miR-214-5p.

The mechanism of arsenic-induced liver toxicity is not fully understood. This study aimed to investigate the role of LINC00942 in arsenic-induced hepatotoxicity by regulating miR-214-5p. As the exposure dose of NaAsO2 gradually increases, cell viability, intracellular GSH content, ΔΨm, and the protein levels of GCLC and GCLM were reduced significantly. Apoptosis rate, ROS, and expression of apoptosis-related and NF-κB pathway proteins increased. The expression of LINC00942 was increased, while the expression of miR-214-5p was decreased. After suppressing LINC00942 levels, NaAsO2 exposure further decreased cell viability, intracellular GSH content, ΔΨm, GCLC protein, and miR-214-5p expression. The apoptosis rate, ROS, and apoptosis-related and NF-κB pathway proteins further increased. miR-214-5p is targeted and negatively regulated by LINC00942. After miR-214-5p was overexpressed, NaAsO2 further decreased cell viability, intracellular GSH content, ΔΨm, and GCLC protein expression compared to NaAsO2 exposure. The apoptosis rate, ROS, apoptosis-related and NF-κB pathway proteins p65, and IKKß were higher than those exposed to NaAsO2. LINC00942 inhibitor along with miR-214-5p inhibitor combined with NaAsO2 treatment resulted in increased cell viability, GSH, Bcl-2, and GCLC protein expression and decreased apoptosis rate, apoptosis related, p65, IKKß protein, and ΔΨm, as compared to the combined NaAsO2 and si LINC00942 group. NaAsO2 exposure induces oxidative damage and apoptosis in LX-2 cells by activating NF-κB and inhibiting GSH synthesis. During this process, the expression level of LINC00942 increases, targeting to reduce the level of miR-214-5p, then weakening the effect of NaAsO2 on NF-κB, thereby alleviating cellular oxidative damage and playing a protective role.

Correlation between the development of phage resistance and the original antibiotic resistance of host bacteria under the co-exposure of antibiotic and bacteriophage.

Bacteriophages (phages) are viruses capable of regulating the proliferation of antibiotic resistant bacteria (ARB). However, phages that directly cause host lethality may quickly select for phage resistant bacteria, and the co-evolutionary trade-offs under varying environmental conditions, including the presence of antibiotics, remains unclear as to their impact on phage and antibiotic resistance. Here, we report the emergence of phage resistance in three distinct E. coli strains with varying resistance to ß-lactam antibiotics, treated with different ampicillin (AMP) concentrations. Hosts exhibiting stronger antibiotic resistance demonstrated a higher propensity to develop and maintain stable phage resistance. When exposed to polyvalent phage KNT-1, the growth of AMP-sensitive E. coli K12 was nearly suppressed within 18 h, while the exponential growth of AMP-resistant E. coli TEM and super-resistant E. coli NDM-1 was delayed by 12 h and 8 h, respectively. The mutation frequency and mutated colony count of E. coli NDM-1 were almost unaffected by co-existing AMP, whereas for E. coli TEM and K12, these metrics significantly decreased with increasing AMP concentration from 8 to 50 µg/mL, becoming unquantifiable at 100 µg/mL. Furthermore, the fitness costs of phage resistance mutation and its impact on initial antibiotic resistance in bacteria were further examined, through analyzing AMP susceptibility, biofilm formation and EPS secretion of the isolated phage resistant mutants. The results indicated that acquiring phage resistance could decrease antibiotic resistance, particularly for hosts lacking strong antibiotic resistance. The ability of mutants to form biofilm contributes to antibiotic resistance, but the correlation is not entirely positive, while the secretion of extracellular polymeric substance (EPS), especially the protein content, plays a crucial role in protecting the bacteria from both antibiotic and phage exposure. This study explores phage resistance development in hosts with different antibiotic resistance and helps to understand the limitations and possible solutions of phage-based technologies.

The Role of miR-150-5p/SOCS1 Pathway in Arsenic-Induced Pyroptosis of LX-2 Cells.

This study aims to explore the mechanism of pyroptosis of human hepatocyte LX-2 cells induced by NaAsO2 through the miR-150-5p/SOCS1 pathway. LX-2 cells were transfected with different concentrations of NaAsO2, miR-150-5p inhibitor, and SOCS1 agonist. Cell activity, cell pyroptosis, and the expression of related genes and proteins were detected by scanning electron microscopy, CCK-8, qRT-PCR, western blot, and immunofluorescence. Compared with the control group, 10 µmol/L and 20 µmol/L NaAsO2 significantly elevated the protein expression levels of the pyroptosis-related proteins NLRP3, GSDMD, GSDMD-N, caspase1, and cleaved caspase1 as well as the mRNA levels of NLRP3, GSDMD, caspase1, IL-18, and IL-1ß. The typical pyroptosis with swelling and rupture of the plasma membrane was observed through scanning electron microscopy. The expression of miR-150-5p of the NaAsO2 intervention group increased, while the expression of SOCS1 decreased; then the level of NF-κB p65 elevated. With co-treatment of miR-150-5p inhibitor, SOCS1 agonist, and NaAsO2, the cell pyroptosis was attenuated, and the expressions of NLRP3, caspase1, GSDMD, GSDMD-N, IL-18, IL-1ß, p65 of the group of miR-150-5p inhibitor and NaAsO2 group, and of the group of SOCS1 agonist and NaAsO2 reduced compared with the NaAsO2 group. Arsenic exposure promotes miR-150-5p, inhibits the expression of SOCS1, and activates the NF-κB/NLRP3 pathway in LX-2 cell pyroptosis.

AURKB promotes bladder cancer progression by deregulating the p53 DNA damage response pathway via MAD2L2.

BACKGROUND: Bladder cancer (BC) is the most common urinary tract malignancy. Aurora kinase B (AURKB), a component of the chromosomal passenger protein complex, affects chromosomal segregation during cell division. Mitotic arrest-deficient 2-like protein 2 (MAD2L2) interacts with various proteins and contributes to genomic integrity. Both AURKB and MAD2L2 are overexpressed in various human cancers and have synergistic oncogenic effects; therefore, they are regarded as emerging therapeutic targets for cancer. However, the relationship between these factors and the mechanisms underlying their oncogenic activity in BC remains largely unknown. The present study aimed to explore the interactions between AURKB and MAD2L2 and how they affect BC progression via the DNA damage response (DDR) pathway. METHODS: Bioinformatics was used to analyze the expression, prognostic value, and pro-tumoral function of AURKB in patients with BC. CCK-8 assay, colony-forming assay, flow cytometry, SA-ß-gal staining, wound healing assay, and transwell chamber experiments were performed to test the viability, cell cycle progression, senescence, and migration and invasion abilities of BC cells in vitro. A nude mouse xenograft assay was performed to test the tumorigenesis ability of BC cells in vivo. The expression and interaction of proteins and the occurrence of the senescence-associated secretory phenotype were detected using western blot analysis, co-immunoprecipitation assay, and RT-qPCR. RESULTS: AURKB was highly expressed and associated with prognosis in patients with BC. AURKB expression was positively correlated with MAD2L2 expression. We confirmed that AURKB interacts with, and modulates the expression of, MAD2L2 in BC cells. AURKB knockdown suppressed the proliferation, migration, and invasion abilities of, and cell cycle progression in, BC cells, inducing senescence in these cells. The effects of AURKB knockdown were rescued by MAD2L2 overexpression in vitro and in vivo. The effects of MAD2L2 knockdown were similar to those of AURKB knockdown. Furthermore, p53 ablation rescued the MAD2L2 knockdown-induced suppression of BC cell proliferation and cell cycle arrest and senescence in BC cells. CONCLUSIONS: AURKB activates MAD2L2 expression to downregulate the p53 DDR pathway, thereby promoting BC progression. Thus, AURKB may serve as a potential molecular marker and a novel anticancer therapeutic target for BC.

USP11 promotes glycolysis by regulating HIF-1α stability in hepatocellular carcinoma.

Understanding the mechanisms underlying metastasis in hepatocellular carcinoma (HCC) is crucial for developing new therapies against this fatal disease. Deubiquitinase ubiquitin-specific protease 11 (USP11) belongs to the deubiquitinating family and has previously been reported to play a critical role in cancer pathogenesis. Although it has been established that USP11 can facilitate the metastasis and proliferation ability of HCC, the underlying regulatory mechanisms are poorly understood. The primary objective of this research was to reveal hitherto undocumented functions of USP11 during HCC progression, especially those related to metabolism. Under hypoxic conditions, USP11 was found to significantly impact the glycolysis of HCC cells, as demonstrated through various techniques, including RNA-Seq, migration and colony formation assays, EdU and co-immunoprecipitation. Interestingly, we found that USP11 interacted with the HIF-1α complex and maintained HIF-1α protein stability by removing ubiquitin. Moreover, USP11/HIF-1α could promote glycolysis through the PDK1 and LDHA pathways. In general, our results demonstrate that USP11 promotes HCC proliferation and metastasis through HIF-1α/LDHA-induced glycolysis, providing new insights and the experimental basis for developing new treatments for this patient population.

NaAsO2 regulates TLR4/MyD88/NF-κB signaling pathway through DNMT1/SOCS1 to cause apoptosis and inflammation in hepatic BRL-3A cells.

The exact molecular mechanism of arsenic-induced liver injury has not been fully elucidated. The aim of the study was to investigate the potential mechanism of NaAsO2-induced cytotoxicity in BRL-3A cells and to provide a basis for the mechanism of arsenic poisoning. BRL-3A cells were treated with different doses of NaAsO2, DNMT1 inhibitor (DC_517), TLR4 inhibitor (TAK-242), and transfection of SOCS1 plasmid. Cell activity, apoptosis, inflammation and protein expression of DNMT1, SOCS1, TLR4, MyD88, and NF-κB were detected by CCK8 assay, Annexin V-FITC and Western blot, respectively. With increasing NaAsO2 doses, BAX and caspase-3 expression increased, Bcl-2 expression decreased, pro-inflammatory factors TNF-α, IL-1ß, and IL-6 increased, and cell activity decreased causing increased apoptosis. When BRL-3A was intervened with 10, and 20 µmol/L NaAsO2, DNMT1 expression was elevated, SOCS1 expression was decreased, and TLR4, MyD88, p-IκBα/IκBα, and p-p65/p65 expression were elevated. After the combination of NaAsO2 and DC_517, compared to the NaAsO2 group, apoptosis and inflammation were attenuated, SOCS1 expression was elevated and TLR4, MyD88, p-IκBα/IκBα and p-p65/p65 expression was decreased. Apoptosis and inflammation were attenuated after co-treatment of SOCS1 high expression with NaAsO2 compared to the NaAsO2 group. In addition, TLR4, MyD88, p-IκBα/IκBα and p-p65/p65 expression was reduced. When NaAsO2 and TAK-242 were combined, apoptosis and inflammation were attenuated. Besides MyD88, p-IκBα/IκBα and p-p65/p65 expression was reduced compared to the NaAsO2 group. We found that NaAsO2 induce apoptosis and inflammation in BLR-3A cells, which may be related to inhibit SOCS1 through regulation of DNMT1 and thus activating the TLR4/MyD88/NF-κB signaling pathway.

Integrated nucleic acid purification technology based on amino-modified centrifugal microfluidic chip.

Nucleic acid detection is an important tool for clinical diagnosis. The purification of the sample is the most time-consuming step in the nucleic acid testing process and will affect the results of the assay. Here, we developed a surface modification-based nucleic acid purification method and designed an accompanying set of centrifugation equipment and chips to integrate the steps of nucleic acid purification on a single platform. The results of experiments with HeLa cells and HPV type 16 as samples showed that the mentioned method had good nucleic acid purification capability and the accompanying equipment greatly simplified the operation of the experimenters in the whole process. Overall, our equipment can improve the efficiency of nucleic acid purification and is suitable for application in larger-scale clinical assays.

FAM171B stabilizes vimentin and enhances CCL2-mediated TAM infiltration to promote bladder cancer progression.

BACKGROUND: Invasion and metastasis are the main causes of unfavourable prognosis in patients diagnosed with bladder cancer. The efficacy of immunotherapy in bladder cancer remains suboptimal due to the presence of an immunosuppressive microenvironment. The novel protein family with sequence similarity 171B (FAM171B) has been identified, but its precise role and mechanism in bladder cancer remain unclear. METHODS: In this study, we conducted an analysis to investigate the associations between FAM171B expression and the prognosis and clinicopathological stage of bladder cancer. To this end, we utilized RNA sequencing data from the TCGA and GEO databases, as well as tumor tissue specimens obtained from our clinical centre. RNA sequencing analysis allowed us to examine the biological function of FAM171B at the transcriptional level in bladder cancer cells. Additionally, we used immunoprecipitation and mass spectrometry to identify the protein that interacts with FAM171B in bladder cancer cells. The effects of FAM171B on modulating tumor-associated macrophages (TAMs) and vimentin-mediated tumor progression, as well as the underlying mechanisms, were clarified by phalloidin staining, immunofluorescence staining, ELISA, RNA immunoprecipitation, flow cytometry and a bladder cancer graft model. RESULTS: FAM171B expression exhibits strong positive correlation with poor survival outcomes and advanced clinicopathological stages in patients with bladder cancer. FAM171B significantly promoted bladder cancer growth and metastasis, accompanied by TAM accumulation in the microenvironment, in vivo and in vitro. Through studies of the molecular mechanism, we found that FAM171B contributes to tumor progression by stabilizing vimentin in the cytoplasm. Additionally, our research revealed that FAM171B enhances the splicing of CCL2 mRNA by interacting with heterogeneous nuclear ribonucleoprotein U (HNRNPU), ultimately leading to increased recruitment and M2 polarization of TAMs. CONCLUSIONS: In this study, we identified FAM171B as a potent factor that promotes the progression of bladder cancer. These findings establish a solid theoretical foundation for considering FAM171B as a potential diagnostic and therapeutic biomarker for bladder cancer.

DUSP2 affects bladder cancer prognosis by down-regulating MEK/ERK and P38 MAPK signaling pathways through PTPN7.

BACKGROUND: As one of the leading causes of cancer death worldwide, bladder cancer (BCa) ranks 12th in incidence rate. Dual Specific Phosphatase 2 (DUSP2) is a member of the bispecific protein phosphatase subfamily. DUSP2 is closely related to the prognosis of cancer, but the role of DUSP2 in bladder cancer is still unclear. This study aims to explore how DUSP2 affects the prognosis of bladder cancer and clarify the important mechanism in bladder cancer. METHODS: Bioinformatics and experiments have detected the anti-tumor effect of DUSP2. Construct a DUSP2 overexpression cell model, and then use protein blotting experiments to verify the efficiency of transfection. The effects of DUSP2 on proliferation, metastasis, apoptosis, epithelial mesenchymal transition (EMT) and immune invasion of bladder cancer cells were detected in vitro or in vivo. In addition, the mechanism of DUSP2 regulating MEK/ERK through PTPN7 pathway and P38 MAPK inhibiting the progression of bladder cancer was also discussed. RESULTS: The expression of DUSP2 was down regulated in bladder cancer samples and cell lines. The overexpression of DUSP2 inhibits the proliferation, metastasis and immune microenvironment of bladder cancer cells. In addition, we confirmed that DUSP2 regulates MEK/ERK and P38 MAPK through PTPN7 pathway to inhibit the progression of bladder cancer. CONCLUSION: DUSP2 inhibits the progression of bladder cancer by regulating PTPN7. These results suggest that DUSP2/PTPN7/MEK/ERK pathway may become a new therapeutic target for bladder cancer.

SQLE Knockdown inhibits bladder cancer progression by regulating the PTEN/AKT/GSK3ß signaling pathway through P53.

Bladder cancer (BCa) is one of the most common malignancies worldwide. However, the lack of accurate and effective targeted drugs has become a major problem in current clinical treatment of BCa. Studies have demonstrated that squalene epoxidase (SQLE), as a key rate-limiting enzyme in cholesterol biosynthesis, is involved in cancer development. In this study, our analysis of The Cancer Genome Atlas, The Genotype-Tissue Expression, and Gene Expression Omnibus databases showed that SQLE expression was significantly higher in cancer tissues than it was in adjacent normal tissues, and BCa tissues with a high SQLE expression displayed a poor prognosis. We then confirmed this result in qRT-PCR and immunohistochemical staining experiments, and our vitro studies demonstrated that SQLE knockdown inhibited tumor cell proliferation and metastasis through the PTEN/AKT/GSK3ß signaling pathway. By means of rescue experiments, we proved that that P53 is a key molecule in SQLE-mediated regulation of the PTEN/AKT/GSK3ß signaling pathway. Simultaneously, we verified the above findings through a tumorigenesis experiment in nude mice. In conclusion, our study shows that SQLE promotes BCa growth through the P53/PTEN/AKT/GSK3ß axis, which may serve as a therapeutic biological target for BCa.

MTHFD2 promotes PD-L1 expression via activation of the JAK/STAT signalling pathway in bladder cancer.

Although combination chemotherapy is widely used for bladder cancer (BC) treatment, the recurrence and progression rates remain high. Therefore, novel therapeutic targets are required. Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) contributes to tumourigenesis and immune evasion in several cancers; however, its biological function in BC remains unknown. This study aimed to investigate the expression, prognostic value and protumoural function of MTHFD2 in BC and elucidate the mechanism of programmed death-ligand 1 (PD-L1) upregulation by MTHFD2. An analysis using publicly available databases revealed that a high MTHFD2 expression was correlated with clinical features and a poor prognosis in BC. Furthermore, MTHFD2 promoted the growth, migration, invasion and tumourigenicity and decreased the apoptosis of BC cells in vivo and in vitro. The results obtained from databases showed that MTHFD2 expression was correlated with immune infiltration levels, PD-L1 expression, and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. The expression of MTHFD2, PD-L1 and JAK/STAT signalling pathway-related proteins increased after interferon gamma treatment and decreased after MTHFD2 knockdown. Moreover, addition of a JAK/STAT pathway activator partially reduced the effect of MTHFD2 knockdown on BC cells. Collectively, our findings suggest that MTHFD2 promotes the expression of PD-L1 through the JAK/STAT signalling pathway in BC.

Genetic Analysis and Molecular Identification of the Powdery Mildew Resistance in 116 Elite Wheat Cultivars/Lines.

Powdery mildew, caused by Blumeria graminis f. sp. tritici (Bgt), is a destructive disease worldwide. Host resistance is the preferred method for limiting the disease epidemic, protecting the environment, and minimizing economic losses. In the present study, the reactions to powdery mildew for a collection of 600 wheat cultivars and breeding lines from different wheat-growing regions were tested using the Bgt isolate E09. Next, 116 resistant genotypes were identified and then crossed with susceptible wheat cultivars/lines to produce segregating populations for genetic analysis. Among them, 87, 19, and 10 genotypes displayed single, dual, and multiple genic inheritance, respectively. To identify the Pm gene(s) in those resistant genotypes, 16 molecular markers for 13 documented Pm genes were used to test the resistant and susceptible parents and their segregating populations. Of the 87 wheat genotypes that fitted the monogenic inheritance, 75 carried the Pm2a allele. Three, two, one, and two genotypes carried Pm21, Pm6, Pm4, and the recessive genes pm6 and pm42, respectively. Four genotypes did not carry any of the tested genes, suggesting that they might have other uncharacterized or new genes. The other 29 wheat cultivars/lines carried two or more of the tested Pm genes and/or other untested genes, including Pm2, Pm5, Pm6, and/or pm42. It was obvious that Pm2 was widely used in wheat production, whereas Pm1, Pm24, Pm33, Pm34, Pm35, Pm45, and Pm47 were not detected in any of these resistant wheat genotypes. This study clarified the genetic basis of the powdery mildew resistance of these wheat cultivars/lines to provide information for their rational utilization in different wheat-growing regions. Moreover, some wheat genotypes which may have novel Pm gene(s) were mined to enrich the diversity of resistance source.

Corrigendum to "Anti-tumor effect of AZD8055 against bladder cancer and bladder cancer-associated macrophages" [Heliyon 9(3) (March 2023) e14272].

[This corrects the article DOI: 10.1016/j.heliyon.2023.e14272.].

Anti-tumor effect of AZD8055 against bladder cancer and bladder cancer-associated macrophages.

The increased activity of the mTOR pathway in bladder cancer has been extensively studied, but no satisfactory mTOR inhibitor has been found in bladder cancer. The role of AZD8055, a second-generation mTOR inhibitor, has not been reported in bladder cancer. Herein, we investigated the effects of AZD8055 on bladder cells and their interaction with macrophages in vivo and in vitro. In four bladder cancer cell lines, the phosphorylation of mTOR, AKT and S6K1 was suppressed by AZD8055. AZD8055 inhibited proliferation and induced G1 cell-cycle arrest and apoptosis of bladder cancer cells in a concentration-dependent manner. AZD8055 also inhibits the migration and invasion of bladder cancer cells by blocking EMT and MMP9. In addition, AZD8055 inhibited chemotaxis and M2 phenotype of macrophage after co-culture with bladder cancer cells. These anti-tumor effects of AZD8055 were verified in vivo. Our findings collectively demonstrated that low-dose AZD8055 induces cytotoxicity and apoptosis, and inhibits the Akt/mTOR activation, invasion and migration of bladder cancer. These findings also demonstrate that AZD8055 partially blocked the interactions of bladder cancer cells and macrophages. In conclusion, AZD8055 is a promising mTOR inhibitor for bladder cancer.

Application of three-dimensional printing individualized titanium mesh in alveolar bone defects with different Terheyden classifications: A retrospective case series study.

OBJECTIVE: To present the results of guided bone regeneration (GBR) with three-dimensional printing individualized titanium mesh (3D-PITM) applied to alveolar bone defects with different Terheyden classifications and the factors affecting the osteogenic outcome. MATERIALS AND METHODS: Fifty-nine patients, presenting with 61 defect sites, were enrolled between 2018 and 2021. GBR+3D-PITM was obtained with simultaneous or second stage implant placement. The complication rate, the success rate of the bone grafting procedure and the survival rate of the implant were documented. Bone gain, thickness of pseudo-periosteum and peri-implant marginal bone loss (MBL) were measured through digital methods by imaging data (CBCT and X-ray). RESULTS: Out of 61 sites, 20 were exposed (exposure rate: 32.8%). The width, height, and volume bone gain at P3 (mesh removal) were 5.22 ± 3.19 mm, 5.01 ± 2.83 mm, and 588.91 ± 361.23 mm3 , respectively. From P2 (3D-PITM+GBR) to P3 , changes in bone gain were not statistically different in the different Terheyden classifications, the occurrence of exposure (p < .001 for all dimensions) and the different type of pseudo-periosteum (p = .030 for width and p = .002 for height) were significantly correlated with the reduction of bone gain. Terheyden classification of the defect sites was significantly associated with the occurrence of exposure (p = .014) and types of the pseudo-periosteum (p = .015). CONCLUSION: The 3D-PITM can be used in alveolar bone defects with different Terheyden classification, but cases with severe vertical bone defects have a greater chance of the 3D-PITM exposure and the exposure can affect the outcome of bone augmentation.

A Novel Electrochemiluminescence Immunosensor Based on Resonance Energy Transfer between g-CN and NU-1000(Zr) for Ultrasensitive Detection of Ochratoxin A in Coffee.

In this study, an electrochemiluminescence (ECL) immunosensor based on nanobody heptamer and resonance energy transfer (RET) between g-C3N4 (g-CN) and NU-1000(Zr) was proposed for ultrasensitive ochratoxin A (OTA) detection. First, OTA heptamer fusion protein was prepared by fusing OTA-specific nanometric (Nb28) with a c-terminal fragment of C4 binding protein (C4bpα) (Nb28-C4bpα). Then, Nb28-C4bpα heptamer with the high affinity used as a molecular recognition probe, of which plenty of binding sites were provided for OTA-Apt-NU-1000(Zr) nanocomposites, thereby improving the immunosensors' sensitivity. In addition, the quantitative analysis of OTA can be achieved by using the signal quenching effect of NU-1000(Zr) on g-CN. As the concentration of OTA increases, the amount of OTA-Apt-NU-1000(Zr) fixed on the electrode surface decreases. RET between g-CN and NU-1000(Zr) is weakened leading to the increase of ECL signal. Thus, OTA content is indirectly proportional to ECL intensity. Based on the above principle, an ultra-sensitive and specific ECL immunosensor for OTA detection was constructed by using heptamer technology and RET between two nanomaterials, with a range from 0.1 pg/mL to 500 ng/mL, and the detection limit of only 33 fg/mL. The prepared ECL-RET immunosensor showed good performance and can be successfully used for the determination of OTA content in real coffee samples, suggesting that the nanobody polymerization strategy and the RET effect between NU-1000(Zr) and g-CN can provide an alternative for improving the sensitivity of important mycotoxin detection.

Characterization and identification of the powdery mildew resistance gene in wheat breeding line ShiCG15-009.

Powdery mildew, caused by Blumeria graminis f. sp. tritici (Bgt), is a serious fungal disease that critically threatens the yield and quality of wheat. Utilization of host resistance is the most effective and economical method to control this disease. In our study, a wheat breeding line ShiCG15-009, released from Hebei Province, was highly resistant to powdery mildew at all stages. To dissect its genetic basis, ShiCG15-009 was crossed with the susceptible cultivar Yannong 21 to produce F1, F2 and F2:3 progenies. After genetic analysis, a single dominant gene, tentatively designated PmCG15-009, was proved to confer resistance to Bgt isolate E09. Further molecular markers analysis showed that PmCG15-009 was located on chromosome 2BL and flanked by markers XCINAU130 and XCINAU143 with the genetic distances 0.2 and 0.4 cM, respectively, corresponding to a physic interval of 705.14-723.48 Mb referred to the Chinese Spring reference genome sequence v2.1. PmCG15-009 was most likely a new gene differed from the documented Pm genes on chromosome 2BL since its different origin, genetic diversity, and physical position. To analyze and identify the candidate genes, six genes associated with disease resistance in the candidate interval were confirmed to be associated with PmCG15-009 via qRT-PCR analysis using the parents ShiCG15-009 and Yannong 21 and time-course analysis post-inoculation with Bgt isolate E09. To accelerate the transfer of PmCG15-009 using marker-assisted selection (MAS), 18 closely or co-segregated markers were evaluated and confirmed to be suitable for tracing PmCG15-009, when it was transferred into different wheat cultivars.

Magnetically Driven Modular Mechanical Metamaterials with High Programmability, Reconfigurability, and Multiple Applications.

Shape transformation and motion guidance are emerging research hotspots of mechanical metamaterials. In this case, the key issue is how to improve the programmability and reconfigurability of metamaterials. The magnetically driven method enables materials to accomplish remote, fast, and reversible deformation, so it is desired for improving the programmability and reconfigurability of metamaterials. However, conventional magnetically driven materials are often pure elastomer materials. Their magnetic programming method is single, and their overall shape is unchangeable after fabrication, which limits their programmability and reconfigurability. Herein, this article proposes a kind of magnetically driven, programmable, and reconfigurable modular mechanical metamaterial based on origami and kirigami design mechanisms. The motion and deformation were designed to follow the predefined creases and incisions that could be transformed into each other. This metamaterial enabled more discrete motion and force transmission and integrated the fold of origami, the rotation of kirigami, and the fold guided by cuts. Such designs laid the foundation for complex, three-dimensional structures which could be quickly reassembled and constructed to deal with complex situations. This paper also demonstrated applications of this metamaterial in information storage and manifestation, mechanical logic computing, reconfigurable robotics, deployable mechanisms, and so on. The results indicated that the high programmability and reconfigurability expanded the application potential of the metamaterial for broader needs.

The effect of bone defect size on the 3D accuracy of alveolar bone augmentation performed with additively manufactured patient-specific titanium mesh.

OBJECTIVE: Additively manufactured (3D-printed) titanium meshes have been adopted in the dental field as non-resorbable membranes for guided bone regeneration (GBR) surgery. However, according to previous studies, inaccuracies between planned and created bone volume and contour are common, and many reasons have been speculated to affect its accuracy. The size of the alveolar bone defect can significantly increase patient-specific titanium mesh design and surgical difficulty. Therefore, this study aimed to analyze and investigate the effect of bone defect size on the 3D accuracy of alveolar bone augmentation performed with additively manufactured patient-specific titanium meshes. METHODS: Twenty 3D-printed patient-specific titanium mesh GBR surgery cases were enrolled, in which 10 cases were minor bone defect/augmentation (the planned bone augmentation surface area is less than or equal to 150 mm2 or one tooth missing or two adjacent front-teeth/premolars missing) and another 10 cases were significant bone defect/augmentation (the planned bone augmentation surface area is greater than 150 mm2 or missing adjacent teeth are more than two (i.e. ≥ three teeth) or missing adjacent molars are ≥ two teeth). 3D digital reconstruction/superposition technology was employed to investigate the bone augmentation accuracy of 3D-printed patient-specific titanium meshes. RESULTS: There was no significant difference in the 3D deviation distance of bone augmentation between the minor bone defect/augmentation group and the major one. The contour lines of planned-CAD models in two groups were basically consistent with the contour lines after GBR surgery, and both covered the preoperative contour lines. Moreover, the exposure rate of titanium mesh in the minor bone defect/augmentation group was slightly lower than the major one. CONCLUSION: It can be concluded that the size of the bone defect has no significant effect on the 3D accuracy of alveolar bone augmentation performed with the additively manufactured patient-specific titanium mesh.