Search

The identification of drug-target interactions (DTI) is a valuable step in the drug discovery and repositioning process. However, traditional laboratory experiments are time-consuming and expensive. Computational methods have streamlined research to determine DTIs. The application of deep learning methods has significantly improved the prediction performance for DTIs. Modern deep learning methods can leverage multiple sources of information, including sequence data that contains biological structural information, and interaction data. While useful, these methods cannot be effectively applied to each type of information individually (e.g., chemical structure and interaction network) and do not take into account the specificity of DTI data such as low- or zero-interaction biological entities. To overcome these limitations, we propose a method called MFA-DTI (Multi-feature Fusion Adopted framework for DTI). MFA-DTI consists of three modules: an interaction graph learning module that processes the interaction network to generate interaction vectors, a chemical structure learning module that extracts features from the chemical structure, and a fusion module that combines these features for the final prediction. To validate the performance of MFA-DTI, we conducted experiments on six public datasets under different settings. The results indicate that the proposed method is highly effective in various settings and outperforms state-of-the-art methods. • A novel DTI prediction model that explores both the graph and structural features of drugs and proteins is proposed. • A graph processing algorithm for biological networks is designed. • A module for generating sequence structure vectors is developed. • The results on 6 public datasets show it outperforms existing methods in all observed metrics. [ABSTRACT FROM AUTHOR]

• Establishment of gene editing technologies in tilapia enhances our knowledges on fish reproductive endocrinoogy. • Transcription factors Dmrt1 and Foxl3 are key factors involved in germ cell fate decision and sexual plasticity. • Blockage of estrogen synthesis rescues the male to female sex reversal of amhy and gsdf but not dmrt1 mutants. • The deficiency of steroid hormones, such as androgen, DHP and cortisol, impairs reproduction as revealed by gene editing. The Nile tilapia (Oreochromis niloticus), with a system of XX/XY sex determination, is a worldwide farmed fish with a shorter sexual maturation time than that of most cultured fish. Tilapia show a spawning cycle of approximately 14 days and can be artificially propagated in the laboratory all year round to obtain genetically all female (XX) and all male (XY) fry. Its genome sequence has been opened, and a perfect gene editing platform has been established. With a moderate body size, it is convenient for taking enough blood to measure hormone level. In recent years, using tilapia as animal model, we have confirmed that estrogen is crucial for female development because 1) mutation of star2 , cyp17a1 or cyp19a1a (encoding aromatase, the key enzyme for estrogen synthesis) results in sex reversal (SR) due to estrogen deficiency in XX tilapia, while mutation of star1 , cyp11a1 , cyp17a2 , cyp19a1b or cyp11c1 affects fertility due to abnormal androgen, cortisol and DHP levels in XY tilapia; 2) when the estrogen receptors (esr2a / esr2b) are mutated, the sex is reversed from female to male, while when the androgen receptors are mutated, the sex cannot be reversed; 3) the differentiated ovary can be transdifferentiated into functional testis by inhibition of estrogen synthesis, and the differentiated testis can be transdifferentiated into ovary by simultaneous addition of exogenous estrogen and androgen synthase inhibitor; 4) loss of male pathway genes amhy , dmrt1 , gsdf causes SR with upregulation of cyp19a1a in XY tilapia. Disruption of estrogen synthesis rescues the male to female SR of amhy and gsdf but not dmrt1 mutants; 5) mutation of female pathway genes foxl2 and sf-1 causes SR with downregulation of cyp19a1a in XX tilapia; 6) the germ cell SR of foxl3 mutants fails to be rescued by estrogen treatment, indicating that estrogen determines female germ cell fate through foxl3. This review also summarized the effects of deficiency of other steroid hormones, such as androgen, DHP and cortisol, on fish reproduction. Overall, these studies demonstrate that tilapia is an excellent animal model for studying reproductive endocrinology of fish. [ABSTRACT FROM AUTHOR]

• Fish sex exhibits striking plasticity. • Endogenous estrogen is critical for the ovarian differentiation and maintenance. • Cyp19a1a is a reliable early marker for ovarian differentiation in fishes. Fish sex could be reversed at the undifferentiated stage of gonad by administration of exogenous estrogen (E2) or blockade of endogenous estrogen synthesis with aromatase inhibitors, which is designated as primary sex reversal (PSR). Recent studies have well demonstrated that gonochoristic fish maintain their sexual plasticity after sex determination/differentiation. The differentiated ovary could be transdifferentiated into functional testis, and vice versa, the differentiated testis could be transdifferentiated into ovary. By analyzing these two secondary sex reversal (SSR) models, it was found that induction of male-to-female sex reversal initiates from dorsal (near the blood vessel) to the ventral, while induction of female-to-male sex reversal initiates from the ventral to dorsal. Down regulation of endogenous estrogen is the prerequisite for the ovarian transdifferentiation. However, exogenous estrogen alone is not sufficient for inducing differentiated testis to ovary. Administration of E2 and simultaneous blockage of androgen synthesis could induce testicular transdifferentiation. Therefore, endogenous estrogen is critical for the ovarian differentiation/maintenance and androgen is critical for testicular maintenance. Recently, genetic studies with genome editing technologies also showed that disruption of Cyp19a1a induced testicular development, indicating that cyp19a1a is the key gene essential for estrogen synthesis and ovary differentiation/maintenance. Knockout of male pathway genes or overexpression of female pathway genes could up-regulate cyp19a1a expression and increase estrogen level so as to promote ovary. Conversely, knockout of female pathway genes or overexpression of male pathway genes could down-regulate cyp19a1a expression and decrease estrogen level so as to promote testis (transgenic or knockout sex reversal, TSR). Epigenetic regulation of cyp19a1a play a critical role in natural sex reversal (NSR), but its relation with PSR, SSR and TSR needs further detailed investigations. In all, these studies further highlighted the important roles of endogenous estrogens in fish sex differentiation/maintenance. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction of macrophage-mediated inflammatory response plays a key pathophysiological process in myocardial infarction (MI). Calpains are a well-known family of calcium-dependent cysteine proteases that regulate a variety of processes, including cell adhesion, proliferation, and migration, as well as mitochondrial function and inflammation. CAPNS1, the common regulatory subunit of calpain-1 and 2, is essential for the stabilization and activity of the catalytic subunit. Emerging studies suggest that calpains may serve as key mediators in mitochondria and NLRP3 inflammasome. This study investigated the role of myeloid cell calpains in MI. MI models were constructed using myeloid-specific Capns1 knockout mice. Cardiac function, cardiac fibrosis, and inflammatory infiltration were investigated. In vitro, bone marrow-derived macrophages (BMDMs) were isolated from mice. Mitochondrial function and NLRP3 activation were assessed in BMDMs under LPS stimulation. ATP5A1 knockdown and Capns1 knock-out mice were subjected to MI to investigate their roles in MI injury. Ablation of calpain activities by Capns1 deletion improved the cardiac function, reduced infarct size, and alleviated cardiac fibrosis in mice subjected to MI. Mechanistically, Capns1 knockout reduced the cleavage of ATP5A1 and restored the mitochondria function thus inhibiting the inflammasome activation. ATP5A1 knockdown antagonized the protective effect of Capns1 mKO and aggravated MI injury. This study demonstrated that Capns1 depletion in macrophages mitigates MI injury via maintaining mitochondrial homeostasis and inactivating the NLRP3 inflammasome signaling pathway. This study may offer novel insights into MI injury treatment. [Display omitted] • Calpain activities were significantly upregulated in cardiac macrophages after MI. • Myeloid-specific Capns1 KO alleviated cardiac injury after MI. • Capns1 KO reduced the cleavage of ATP5A1 and restored the Mitochondrial dysfunction in macrophages. [ABSTRACT FROM AUTHOR]

Bisphenols, including Bisphenol A (BPA), Tetrabromobisphenol A (TBBPA), and Tetrabromobisphenol S (TBBPS), have been widely applied in the production of polycarbonate plastics and epoxy resins and have been detected in the environment worldwide. The frequent detection of bisphenols in maternal and fetal samples has raised concerns about their toxic effects on human embryonic development, especially on the development of the central nervous system. However, the effect of bisphenols on human retinal development is still unknown. In this study, to evaluate the toxicity of bisphenols on early retinal development, human embryonic stem cells were induced to differentiate into retinal organoids that responded to BPA, TBBPA, and TBBPS, at human exposure relevant concentrations. The global gene expression of retinal organoids was analyzed by RNA sequencing (RNA-seq). A set of retinal development-related biological processes, including neuron differentiation, phototransduction, axon guidance, and retina layer formation, were identified in retinal organoids corresponding to different developmental stages. The RNA-seq data also showed that BPA, TBBPA, and TBBPS influenced retinal development by interfering with the Cytokine-cytokine receptor interaction pathway. HSPA6 , HIF1A-AS3 , CDC20B , IL19 , OAS1 , HSPA7 , and RN7SK were dysregulated by these chemicals. Additionally, BPA, TBBPA, and TBBPS exhibited different toxic effects on neural retina development, with TBBPA appearing to exert more toxicity than BPA and TBBPS. Furthermore, three bisphenols exhibited different effects at different stages of neural retina development. The sensitivity of retinal development to bisphenols depends on their developmental stage. This study provides new insights into the deep dissection of retinotoxicity after prenatal bisphenol exposure. [Display omitted] • Bisphenols exerted adverse effects on the early development of the neural system. • Retinal organoids mimic human embryonic retinal development. • Bisphenol exposure disrupted human early embryonic retinal development. • BPA, TBBPA, and TBBPS exhibited similar toxic effects on neural retina development but not always the same. [ABSTRACT FROM AUTHOR]

Existing studies demonstrated that retinoic acid (RA) regulates meiotic initiation via stra8 -independent pathway in teleosts which lack stra8 in their genomes. However, stra8 was recently identified from several fish species including Southern catfish ( Silurus meridionalis ). To explore the existence of stra8 -dependent pathway in RA mediated meiotic initiation in fishes, in the present study, the genes encoding RA synthase aldh1a2 and catabolic enzyme cyp26a1 and cyp26b1 were cloned from the Southern catfish. By immunohistochemistry, Aldh1a2 signal was observed in gonads of both sexes during the meiotic initiation period. By real-time PCR, differentially expressed gene was observed for cyp26a1 , but not for cyp26b1 , in gonads during the meiotic initiation. Administration of exogenous RA or inhibition of endogenous RA degradation by either KET (RA catabolic enzyme inhibitor) or cyp26a1 knockdown using CRISPR/Cas9 induced advanced meiotic initiation in the ovaries as demonstrated by increased Stra8/ stra8 expression and appearance of oocytes. In contrast, treatment with RA synthase inhibitor DEAB resulted in delayed meiotic initiation and Stra8/ stra8 expression in the ovaries, which was rescued by exogenous RA administration. These results indicated that (1) RA triggers the onset of meiosis via stra8 -dependent pathway in stra8 existing teleosts, as it does in tetrapods; (2) exogenous RA can rescue the endogenous RA deficiency; (3) Cyp26a1, instead of Cyp26b1, is the key catabolic enzyme involved in meiosis initiation in teleosts. Taken together, RA might trigger meiotic initiation via stra8 -dependent and -independent pathway in different teleosts. [ABSTRACT FROM AUTHOR]

Tremendous progress has been made in the field of toxicology leading to the advance of developmental toxicity assessment. Conventional animal models and in vitro two-dimensional models cannot accurately describe toxic effects and predict actual in vivo responses due to obvious inter-species differences between humans and animals, as well as the lack of a physiologically relevant tissue microenvironment. Human embryonic stem cell (hESC)- and induced pluripotent stem cell (iPSC)-derived three-dimensional organoids are ideal complex and multicellular organotypic models, which are indispensable in recapitulating morphogenesis, cellular interactions, and molecular processes of early human organ development. Recently, human organoids have been used for drug discovery, chemical toxicity and safety in vitro assessment. This review discusses the recent advances in the use of human organoid models, (i.e., brain, retinal, cardiac, liver, kidney, lung, and intestinal organoid models) for developmental toxicity and teratogenicity assessment of distinct tissues/organs following exposure to pharmaceutical compounds, heavy metals, persistent organic pollutants, nanomaterials, and ambient air pollutants. Combining next-generation organoid models with innovative engineering technologies generates novel and powerful tools for developmental toxicity and teratogenicity assessment, and the rapid progress in this field is expected to continue. • Advances in stem cell techniques for toxicity assessment. • Human organoids can decipher the embryonic development and morphogenesis. • Organoid technologies for developmental toxicology assessment. • Advanced next-generation human organoids toward next-level toxicity testing. [ABSTRACT FROM AUTHOR]

• Progresses on fish steroidogenic pathway revealed by gene editing were summarized. • Functional studies confirm role of estrogen, Esr2a and 2b in fish sex determination. • Future directions on mechanism of estrogen on fish sex determination were discussed. The involvement of sex steroids in sex determination and differentiation is relatively conserved among non-mammalian vertebrates, especially in fish. Thanks to the advances in genome sequencing and genome editing, significant progresses have been made in the understanding of steroidogenic pathway and hormonal regulation of sex determination and differentiation in fish. It seems that loss of function study of single gene challenges the traditional views that estrogen is required for ovarian differentiation and androgen is needed for testicular development, but it is not so in essence. Steroidogenic enzymes can be classified into two categories based on expression and enzyme activities in fish. One type, encoded by star2 , cyp17a1 and cyp19a1a , is involved in estrogen production and exclusively expressed in the gonads. Mutation of these genes results in the up-regulation of male pathway genes and sex reversal from genetic female to male. The other type, encoded by the duplicated paralogs of the above genes, including star1 , cyp11a1 , cyp17a2 and cyp19a1b , as well as cyp11c1 gene, is dominantly expressed both in gonads and extra-gonadal tissues. Mutation of these genes alters the steroids (androgen, DHP and cortisol) production and spermatogenesis, fertility, secondary sexual characteristics and sexual behavior, but usually does not affect the sex differentiation. For the estrogen receptors (esr1 , esr2a and esr2b), single mutation failed to, but double and triple mutation leads to sex reversal from female to male, indicating that at least Esr2a and Esr2b are required to mediate the role of estrogen in sex determination proved by gene editing experiments. Taken together, results from gene editing enrich our understanding of steroid synthesis pathways and further confirm the critical role of estrogen in female sex determination by antagonizing the male pathway in fish. [ABSTRACT FROM AUTHOR]

Human enterovirus A71 (EV-A71) is the major causative agent of hand, foot, and mouth disease (HFMD), which may lead to neurological sequelae and even death. Although EV-A71 seriously threatens public health, there remains no efficient drug for the treatment of EV-A71 infection. We previously demonstrated that ROCK1 is a novel host dependency factor for EV-A71 replication and can serve as a target for the development of anti-EV-A71 therapeutics. In this study, we identified a subset of inhibitors with potential anti-EV-A71 activity by virtual screening using ROCK1 as a target. Among the hits, Dasabuvir, an HCV polymerase inhibitor, was found to have the best antiviral activity which is consistent with the ranking scores in Autodock Vina and iGEMDOCK. We found that Dasabuvir efficiently suppressed EV-A71 replication in a dose-dependent manner. Moreover, Dasabuvir not only efficiently suppressed the replication of EV-A71 in RD cells, but also in multiple cell lines, including HEK-293T, Caco-2, HT-29, HepG2, and Huh7. Besides, Dasabuvir alleviated the release of proinflammatory cytokines caused by EV-A71 infection. Notably, Dasabuvir also exhibited antiviral activity of CVA10, indicating it may have broad-spectrum antiviral activity against species Enteroviruses A. Hence, our results further confirm that ROCK1 can be a potential drug target and suggest Dasabuvir could be a clinical candidate for the treatment of EV-A71 infection. • A subset of inhibitors was identified against EV-A71 infection by docking ROCK1. • Dasabuvir suppressed EV-A71 replication in RD cells in a dose-dependent manner. • Dasabuvir efficiently suppressed the replication of EV-A71 in multiple cell lines. • Dasabuvir may exhibited broad-spectrum antiviral activity against species Enteroviruses A. [ABSTRACT FROM AUTHOR]

Ticagrelor has been reported to decrease cardiovascular mortality compared with clopidogrel. This benefit cannot be fully explained by the more efficient platelet inhibition. Many studies demonstrated that ticagrelor improved endothelial function, leaving the mechanism elusive though. The present study aims to investigate whether ticagrelor protects against endothelial dysfunction induced by angiotensinII (AngII) through alleviating endoplasmic reticulum (ER) stress. Male Sprague Dawley rats were infused with AngII or vehicle and administrated with ticagrelor or vehicle for 14 days. Reactive oxygen species (ROS) was detected. Aortas from normal mice were incubated with endoplasmic reticulum stress inducer tunicamycin with or without ticagrelor. Vasorecactivity was measured on wire myography. Rat aortic endothelial cells (RAECs) were pretreated with ticagrelor followed by AngII or tunicamycin. Endothelial nitric oxide synthase (eNOS) phosphorylation and ER stress markers were determined by western blotting. Impaired endothelial function, induction of ER stress, reduced eNOS phosphorylation and elevated ROS generation was restored by ticagrelor treatment in vivo. In addition, tunicamycin induced endothelial dysfunction was improved by ticagrelor. In vitro, the induction of ER stress and inhibited eNOS phosphorylation in REACs exposed to AngII as well as tunicamycin was reversed by co-culturing with ticagrelor. In conclusion, ticagrelor protects against AngII-induced endothelial dysfunction via alleviating ER stress. [ABSTRACT FROM AUTHOR]

Sphingosine 1-phosphate (S1P), via binding to its specific receptors of S1PR1, participates in the regulation of both innate and adaptive immunity. Recent reports have identified S1P as a messenger mediating inflammation. However, roles of S1P in Coxsackievirus B3 (CVB3)-induced myocarditis were largely unknown. Here, we investigated the effect of S1P treatment on CVB3-induced myocarditis in vivo. We found that CVB3 infection downregulated S1PR1 expression in spleen and decreased the proportion of invariant natural killer T cells (iNKT) in CD3 positive T cells both in spleen and in blood from left ventricle, which accompanied by severe inflammation lesions and more virus capsid protein (VP1) expression in heart tissue. In comparison, S1P supply upregulated iNKT in the spleen and in blood from left ventricle, which represented the strengthening of anti-inflammatory effects. Indeed, inflammation infiltration, VP1 expression and apoptosis in the myocardium was all downregulated. These results demonstrated that S1P supplement could alleviate CVB3-induced myocarditis. [ABSTRACT FROM AUTHOR]

DNA methylation is one of the important epigenetic mechanisms for modulating gene expression. By performing a genome-wide methylation association analysis of whole peripheral blood from 60 Vogt-Koyanagi-Harada disease (VKH) patients and 60 healthy controls, we depicted the global DNA methylation status of VKH disease. Further pyrosequencing validation in 160 patients and 159 controls identified 3 aberrant CpG sites in HLA gene regions including cg04026937 and cg18052547 (located in HLA-DRB1 region), and cg13778567 (HLA-DQA1). We also identified 9 aberrant CpG sites in non-HLA gene regions including cg13979407, cg21075643, cg24290586, cg10135747 and cg22707857 (BTNL2), cg22155039 (NOTCH4), cg02605387 (TNXB), cg06255004 (AGPAT2) and cg18855195 (RIBC2). Increased mRNA levels of BTNL2, NOTCH4 and TNXB were identified in VKH patients when compared with healthy controls, consistent with the hypomethylated CpG status in these gene regions. Moreover, seven aberrantly methylated CpG sites may serve as a diagnostic marker for VKH disease (AUC = 84.95%, 95%CI: 79.49%–90.41%). • By performing an epigenome-wide association study, we depicted the global DNA methylation profile of VKH disease. • A novel set of aberrant methylation loci that are associated with VKH were idetified. • Aberrantly methylated CpG sites might serve as biomarkers for VKH disease. [ABSTRACT FROM AUTHOR]

Graphene (GR) is one of the most promising candidates for utilization in the electroanalytical field because of its superior electrocatalytic activity, excellent electronic conductivity, and high chemical stability. However, the GR sheets usually tend to stack together with π-π interaction. The spontaneous stacking leads to the aggregation of the GR sheets and imposes a negative feedback in the surface area of the GR, which obviously limits its electrochemical application. In this study, nitrogen-doped porous GR (NPGR) with different pore sizes is prepared by using silica (SiO 2 ) as a template. The NPGR exhibits high surface area and porous structure, fulfilling the requirement for supporting materials. Being a support, the structural uniqueness and N dopants of NPGR facilitate the deposition of Pt nanoparticles (Pt NPs). The Pt NPs/NPGR composites integrate the structural properties of NPGR and catalytic properties of Pt NPs. A selective and sensitive electrochemical sensor was successfully developed for sensitive determination of Tadalafil (TAD), showing a concentration range of 1.30–488.9 μM and limit of detection of 0.268 μM. [ABSTRACT FROM AUTHOR]

Wilms tumor 1 (Wt1) is an essential factor for urogenital system development. Teleosts have two wt1s , named as wt1a and wt1b . In this study, the expression pattern of wt1a and wt1b and their functions on the urogenital system were analyzed by in situ hybridization and CRISPR/Cas9. wt1a was found to be expressed in the glomerulus at 3 dah (days after hatching), earlier than wt1b. wt1a and wt1b were simultaneously expressed in the somatic cells of gonads at 3 dah, while their cell locations were similar, but not identical in adult fish gonads. The wt1a -/- fish displayed pericardial edema and yolk sac edema at 3 dah and subsequently expanded as general body edema at 6 dah, failed to develop glomerulus and died during 6–10 dah, whereas the wt1b -/- fish were phenotypically normal. Immunohistochemical analyses revealed that the germ cell marker Vasa was expressed, while somatic cell genes Cyp19a1a, Amh, Gsdf and Dmrt1 were not expressed in the wt1a -/- gonads at 6 dah. The sex phenotypes of XX and XY in the wt1b -/- fish were not affected. Real-time PCR revealed that the ovarian cyp19a1a expression was up-regulated in XX wt1b -/- fish, compared with XX control at 90 dah. Serum estradiol-17β level was also up-regulated in XX wt1b -/- fish at 90 and 180 dah. The XY wt1b -/- fish had normal serum estradiol-17β and 11-ketotestosterone levels and remained fertile. These results suggest that Wt1a and Wt1b have different functions in the kidneys and gonads of tilapia. [ABSTRACT FROM AUTHOR]

Purpose Previous studies have demonstrated that fibronectin (FN) levels are increased in brain tissues from patients and animals with epilepsy. This study aimed to assess FN levels in cerebrospinal fluid (CSF) and serum samples from patients with epilepsy. Methods Fibronectin levels were assessed in CSF and serum samples from 56 patients with epilepsy (27 and 29 individuals with intractable epilepsy and nonintractable epilepsy, respectively) and 25 healthy controls, using sandwich enzyme-linked immunosorbent assays (ELISA). Results CSF-FN levels were higher in patients with epilepsy (8.07 ± 1.51 mg/l versus 6.20 ± 1.18 mg/l, p < 0.05) than in the control group. In addition, serum-FN levels in the group with epilepsy and in the control group were 236.96 ± 65.7 mg/l and 181.43 ± 72.82 mg/l, respectively, indicating a statistically significant difference (p = 0.01). Interestingly, serum- and CSF-FN levels in individuals with epilepsy were not affected by antiepileptic drug and duration of epilepsy. Of note, the increase of CSF- and serum-FN levels was more pronounced in subjects with intractable epilepsy than in patients with nonintractable epilepsy. Conclusion Serum- and CSF-FN levels constitute a potential clinical diagnostic biomarker for epilepsy and could also be used for differential diagnosis. [ABSTRACT FROM AUTHOR]

Although excessive nitric oxide (NO) induced from iNOS is critical for dysfunction of vascular endothelial cells (ECs) in the diabetic retina, its role on ECs injury remains unknown. RPE (retinal pigment epithelium) is the pigmented cell layer just outside the neurosensory retina that constitutes the blood-retinal-barrier (BRB) with ECs, and also serves as the limiting transport factor that maintains the retinal environment. Dysfunction of the RPE is related to oxidative stress that contributes to the progression of diabetic retina. Using a co-cultural biosystem, we demonstrate that NO generation and iNOS expression was increased in both ECs and RPE cells after high glucose treatment. Increased NO in ECs cocultured with RPE activate the endoplasmic reticulum (ER) and protein kinase RNA (PKR)-like ER kinase (PERK) pathway and involved in ECs apoptosis. Blockade of the iNOS pathway, or depletion of PERK effectively, reverses NO-mediated apoptosis. Our study demonstrates that iNOS and subsequently excessive NO generation in RPE cells can have an unanticipated effect by activating PERK pathways in ECs, resulting in a novel mechanism for vascular endothelium to avoid injury from prolonged hyperglycemia. [ABSTRACT FROM AUTHOR]

• PD-MWCNT nanocomposite containing CMC provided a large number of antibody binding sites. • An electrochemical immunosensor for zearalenone was developed by the U-disk portable potentiostat with smartphone. • zearalenone in feed ingredients and agricultural food was detected using a simple rapid portable immunoassay. Zearalenone (ZEN) has emerged as a global public health concern due to its significant pathogenicity and world-wide distribution in animal feed ingredients and agricultural food. In the study, we report on the design and development of a simple portable immunosensor based on polyamindoamine dendrimer (PD)-multi-walled carbon nanotube (MWCNT) nanocomposite containing carboxymethyl cellulose (CMC) for rapid electrochemical immunoassay of ZEN residual in feed ingredients and agricultural food using U-disk potentiostat with smartphone. A large number of ZEN monoclonal antibody was covalently immobilized onto the electrode surface of nanocomposite owing to abundant carboxyl groups of PD, MWCNT and CMC. Nanocomposite modified screen printed electrode was employed to fabricate a simple rapid portable immunosensor using U-disk potentiostat with smartphone. The electrochemical immunosensor presented a desirable linear relationship ranges from 0.001–100 ng mL−1 with a low detection limit of 0.15 pg mL−1 under the optimal conditions, which was consistent with the results of the immunosensor prepared with glassy carbon electrode on the traditional potentiostat with desktop computer. It is proposed as a simple and robust analytical tool for rapid detection of hazardous substances including ZEN in feed ingredients and agricultural food on the basis of the great performance of the proposed immunosensor. [ABSTRACT FROM AUTHOR]

Abstract: Highly ordered arrays of Cu2ZnSnSe4 nanotubes have been successfully synthesized on fluorine-doped tin oxide glass substrate using ZnO nanorod arrays as sacrificial templates. The structure, morphology and optical properties of the Cu2ZnSnSe4 arrays were characterized by X-ray diffraction, Raman spectrometry, field-emission scanning electron microscopy, transmission electron microscopy, energy dispersive X-ray, and UV–Vis absorption spectroscopy. The diameter and length of the Cu2ZnSnSe4 nanotubes can be adjusted by tuning the diameter and length of the ZnO nanorods. In addition, the effect of the length on the performance of the photoelectrochemical cells was also investigated. [Copyright &y& Elsevier]