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Although the anaerobic reduction of azo dyes is ecofriendly, high ammonia consumption remains a significant challenge. This work enriched a mixed nitrogen-fixing bacteria consortium (NFBC) using n-Fe3O4 to promote the anaerobic reduction of methyl orange (MO) without exogenous nitrogen. The enriched NFBC was dominated by Klebsiella (80.77 %) and Clostridium (17.16 %), and achieved a 92.7 % reduction of MO with an initial concentration of 25 mg·L-1. Compared with the control, the consortium increased the reduction efficiency of MO, cytochrome c content, and electron transport system (ETS) activity by 11.86 %, 89.86 %, and 58.49 %, respectively. When using 2.5 g·L-1 n-Fe3O4, the extracellular polymeric substances (EPS) of NFBC were present in a concentration of 85.35 mg·g-1. The specific reduction rates of MO by NFBC were 2.26 and 3.30 times faster than those of Fe(II) and Fe(III), respectively, while the enrichment factor of the ribosome pathway in NFBC exceeded 0.75. Transcriptome, carbon consumption, and EPS analyses suggested that n-Fe3O4 stimulated carbon metabolism and secreted protein synthesized by the mixed culture. The latter occurred due to the increased activity of consortium and the content of redox substances. These findings demonstrate that n-Fe3O4 promoted the efficiency of mixed nitrogen-fixing bacteria for removing azo dyes from wastewater. This innovative approach highlights the potential of integrating nanomaterials with biological systems to effectively address complex pollution challenges.
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Nanodrug delivery systems (NDDS) have been proposed to improve the targeting and bioavailability of chemotherapy drugs. The approach of drug loading via physical adsorption is facile to operate; however, there exists a risk of premature leakage. Coupling the drug molecules with the carrier through chemical reactions can guarantee the stability of the drug delivery process, yet the preparation procedure is relatively intricate. In this research, a kind of Prussian blue nanocage (PB Cage) was fabricated, and the phase change material, 1-pentadecanol, was used as the gating material to solidify 5-fluorouracil (5-FU) inside the nanocage. Upon irradiation with near-infrared (NIR) light, the temperature of the PB Cage can rise rapidly. When the temperature exceeds 43 °C, 1-pentadecanol undergoes a solid-liquid phase transition and subsequently releases 5-FU to inhibit DNA synthesis. Meanwhile, the photothermal therapy (PTT) mediated by the PB Cage is also capable of ablating tumor cells. The NDDS constructed based on PB has achieved the precise release of 5-FU triggered by NIR light, which may avoid side effects on normal tissues. Moreover, the combination of chemotherapy and photothermal therapy can efficaciously suppress the proliferation of tumor cells.
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Pd-based electrodes are recognized to facilitate effective electrochemical hydrodechlorination (EHDC) as a result of their superior capacity for atomic hydrogen (H*) generation. However, challenges such as electrode stability, feasibility of treating complex matrices, and high cost associated with electrode synthesis hinder the application of Pd-based electrodes for EHDC. In this work, we investigated the feasibility of degrading 2,4-dichlorophenol (2,4-DCP) by EHDC employing Pd-loaded activated carbon particles, prepared via a simple wet-impregnation method, as a flow cathode (FC) suspension. Compared to other Pd-based EHDC studies, a much lower Pd loading (0.02-0.08 mg cm-2) was used. Because of the excellent mass transfer in the FC system, almost 100% 2,4-DCP was hydrodechlorinated to phenol within 1 h. The FC system also showed excellent performance in treating complex water matrices (including hardness ion-containing wastewater and various other chlorinated organics such as 2,4-dichlorobenzoic acid and trichloroacetic acid) with a relatively low energy consumption (0.26-1.56 kW h m-3 mg-1 of 2,4-DCP compared to 0.32-7.61 kW h m-3 mg-1 of 2,4-DCP reported by other studies). The FC synthesized here was stable over 36 h of continuous operation, indicating its potential suitability for real-world applications. Employing experimental investigations and mathematical modeling, we further show that hydrodechlorination of 2,4-DCP occurs via interaction with H*, with no role of direct electron transfer and/or HOâ¢-mediated processes in the removal of 2,4-DCP.
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Eletrodos , Filtração , Poluentes Químicos da Água/química , Purificação da Água/métodos , Águas Residuárias/química , Clorofenóis/química , Técnicas EletroquímicasRESUMO
Cancer stem cells (CSCs) are responsible for tumor chemoresistance, and the aryl hydrocarbon receptor (AHR) is indispensable for maintaining CSC characteristics. Here, we aimed to investigate how the interaction between progesterone receptor membrane component 1 (PGRMC1) and AHR contributes to the maintenance of CSC phenotypes in non-small cell lung cancer (NSCLC). Clinical data and tissue microarray analyses indicated that patients with elevated PGRMC1 expression had poorer prognoses. Moreover, PGRMC1 overexpression enhanced CSC phenotypes and chemotherapy resistance in vitro and in vivo by modulating AHR ubiquitination. We then determined the specific interaction sites between PGRMC1 and AHR. Mass spectrometry screening identified tripartite motif containing 56 (TRIM56) as the E3 ligase targeting AHR. Notably, PGRMC1 overexpression inhibited the interaction between TRIM56 and AHR. Overall, our study revealed a regulatory mechanism that involves PGRMC1, AHR, and TRIM56, providing insights for developing CSC-targeting strategies in NSCLC treatment.
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BACKGROUNDS: Gastric carcinoma (GC) is one of the most fatal human malignancies globally, with a median survival time less than 1 year. E-cadherin exerts a crucial role in the development and progression of GC as an adhesive, invasive suppressor gene. Whether reduced E-cadherin has an impact on prognosis, clinicopathological features for GC has been well studied, but no conclusive results has been obtained. METHODS: Eligible studies and relevant data were obtained from PubMed, Elsevier, Embase, Cochrane Library and Web of Science databases until June 30, 2023. A fixed- or random-effects model was used to calculate pooled odds ratios (OR) and 95% confidence intervals (CI). Correlation of E-cadherin expression with overall survival (OS), clinicopathological features and risk factors were evaluated. RESULTS: 36 studies fulfilled the selected criteria. 9048 cases were included. This meta-analysis showed that patients with GC with reduced E-cadherin had unfavourable clinicopathological features and poor OS. The pooled ORs of one-, three- and five-year OS were 0.38 (n = 25 studies, 95%CI: 0.25-0.57, Z = 4.61, P < 0.00001), 0.33 (n = 25 studies, 95% CI: 0.23-0.47, Z = 6.22, P < 0.00001), 0.27 (n = 22 studies, 95% CI: 0.18-0.41, Z = 6.23, P < 0.00001), respectively. Moreover, reduced E-cadherin expression significantly correlated with differentiation grade (OR = 0.29, 95% CI: 0.22-0.39, Z = 8.58, P < 0.00001), depth of invasion (OR = 0.49, 95% CI: 0.36-0.66, Z = 4.58, P < 0.00001), lymphatic node metastasis (OR = 0.49, 95% CI: 0.38-0.64, Z = 5.38, P < 0.00001), distant metastasis (OR = 2.24, 95% CI: 1.62-3.09, Z = 4.88, P < 0.00001), peritoneal metastasis (OR = 2.17, 95% CI: 1.39-3.39, Z = 3.40, P = 0.0007), TNM stage (OR = 0.41, 95% CI: 0.28-0.61, Z = 4.44, P < 0.00001), lymphatic vessel invasion (OR = 1.77, 95% CI: 1.11-2.82, Z = 2.39, P = 0.02), vascular invasion (OR = 1.55, 95% CI: 1.22-1.96, Z = 3.58, P = 0.0003), Lauren type (OR = 0.35, 95% CI: 0.21-0.57, Z = 4.14, P < 0.0001), Borrmann classification (OR = 0.50, 95% CI: 0.25-0.99, Z = 1.97, P = 0.048) and tumor size (≥5 cm vs. <5 cm: OR = 1.73, 95% CI: 1.34-2.23, Z = 4.19, P < 0.0001; ≥6 cm vs. <6 cm: OR = 2.29, 95% CI: 1.51-3.49, Z = 3.87, P = 0.0001). No significant association was observed between reduced E-cadherin expression and liver metastasis, perineural invasion, alcohol consumption, smoking status, familial history, Helicobacter pylori (HP) infection. CONCLUSIONS: The reduced expression of E-cadherin is significantly correlated with poor OS and unfavourable clinicopathological features in GC. The expression level of E-cadherin not only serves as a predictor for disease progression and prognosis in GC but also emerges as a novel therapeutic target.
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Caderinas , Neoplasias Gástricas , Neoplasias Gástricas/patologia , Neoplasias Gástricas/genética , Neoplasias Gástricas/mortalidade , Neoplasias Gástricas/metabolismo , Humanos , Caderinas/metabolismo , Caderinas/genética , Prognóstico , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Antígenos CD/metabolismo , Antígenos CD/genética , Regulação Neoplásica da Expressão GênicaRESUMO
Dielectric nanostructures exhibit low-loss electrical and magnetic resonance, making them ideal for quantum information processing. In this study, the periodic double-groove silicon nanodisk (DGSND) is used to support the anapole state. Based on the distribution properties of the electromagnetic field in anapole states, the anapoles are manipulated by cutting the dielectric metamaterial. Quantum dots (QDs) are used to stimulate the anapole and control the amplification of the photoluminescence signal within the QDs. By opening symmetrical holes in the long axis of the nanodisk in the dielectric metamaterial, the current distribution of Mie resonance can be adjusted. As a result, the toroidal dipole moment is altered, leading to an enhanced electric field (E-field) and Purcell factor. When the dielectric metamaterial is deposited on the Ag substrate separated by the silicon dioxide (SiO2) layer, the structure exhibits ultra-narrow perfect absorption with even higher E-field and Purcell factor enhancement compared to silicon (Si) nanodisks.
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Creep is the macroscopic manifestation of the process of generation, expansion, and penetration of microscopic cracks in a rock body. In this study, the GDEM continuous-discontinuous numerical simulation software was used to model a rock body containing X-fractured for the purposes of exploring creep crack expansion and rupture in the rock body, analyzing the effects of various factors on X-fractured the rock body under the rule of change of the creep curve, and assessing the influences of the intersection angle of the fracture and other factors on the non-parallel fractured rock body on the creep rupture process. The results show that an X-fractured rock body exhibits a mixed tensile-shear damage mode, with tensile damage being the main type of damage. In the isotropic creep stage of a rock body with X-fractured , the steady-state creep rate initially increases and then decreases as the sub- fracture length increases, with the change of the fracture angle of the creep rate of the w-type; the sub-fracture length of h is 14 mm, the rock body is the first to enter into the accelerated creep stage, for the different fracture intersection angle of the rock body For the rock mass with different fracture angles, the time sequence of entering the accelerated creep stage is consistent with the creep rate; when the fracture intersection angle is 45°, and the sub-fracture length is 12 mm, the rock mass has the largest degree of fragmentation, which has a significant impact on the creep damage; after using a single variable processing, it is found that the fracture intersection angle, the sub-fracture length and other factors compared to the fracture intersection angle has a greater impact on the creep damage of the X-fractured rock body. This paper can provide theoretical basis and reference for the study of rock engineering creep damage law and mechanical properties of X-fractured rock body.
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[This corrects the article DOI: 10.3389/fncel.2022.878673.].
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[This retracts the article DOI: 10.1021/acsomega.3c01296.].
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Several deep learning-based methods have been proposed to extract vulnerable plaques of a single class from intravascular optical coherence tomography (OCT) images. However, further research is limited by the lack of publicly available large-scale intravascular OCT datasets with multi-class vulnerable plaque annotations. Additionally, multi-class vulnerable plaque segmentation is extremely challenging due to the irregular distribution of plaques, their unique geometric shapes, and fuzzy boundaries. Existing methods have not adequately addressed the geometric features and spatial prior information of vulnerable plaques. To address these issues, we collected a dataset containing 70 pullback data and developed a multi-class vulnerable plaque segmentation model, called PolarFormer, that incorporates the prior knowledge of vulnerable plaques in spatial distribution. The key module of our proposed model is Polar Attention, which models the spatial relationship of vulnerable plaques in the radial direction. Extensive experiments conducted on the new dataset demonstrate that our proposed method outperforms other baseline methods. Code and data can be accessed via this link: https://github.com/sunjingyi0415/IVOCT-segementaion.
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Abrus cantoniensis Hance (ACH) is an ancient Chinese medicine herb known for its therapeutic effects. This study investigated the potential protective effect of ACH against carbon tetrachloride (CCl4)-induced liver damage in mice. Fifty (n= 50) ICR mice were grouped into five groups. CCl4 was intraperitoneally injected into different mice groups: AM (CCl4 induced), AD (ACH-treated with 25â¯mg/kg), AZ (ACH-treated with 50â¯mg/kg), and AG (ACH-treated with100mg/kg) after every three days for a total of 31 days. The control group was denoted as AC. Additionally, groups AD, AZ, and AG received daily doses of ACH via gavage throughout the study period. According to our findings, ACH administration prominently mitigated liver pathological lesions and the increased liver index induced by CCl4 in mice (p < 0.05). Treatment with ACH resulted in a dose-dependent recovery of GSH-px, SOD, and CAT activities (p < 0.001). Moreover, the levels of TNF-α, MDA, and ALT showed significanlty decreasing trends with various doses of ACH (p < 0.001). Furthermore, 16â¯S rRNA gene sequencing demonstrated that ACH increased the abundance of beneficial genera of Comoclathris, Aureobasidium, and Kazachstania while decreased the presence of pathogenic genera such as Sporobolomyces and Filobasidium. Additionally, ACH treatment ameliorated the changes in liver metabolism due to CCl4 and enhanced the beneficial liver metabolites. In conclusion, ACH shows potential in protecting the liver against oxidative stress and inflammation caused by CCl4 exposure, possibly through its effects on gut microbiota and liver metabolism. Therefore, the use of ACH may offer an effective approach for alleviating CCl4-induced liver injury.
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Abrus , Tetracloreto de Carbono , Doença Hepática Induzida por Substâncias e Drogas , Microbioma Gastrointestinal , Fígado , Camundongos Endogâmicos ICR , Animais , Microbioma Gastrointestinal/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/patologia , Fígado/metabolismo , Camundongos , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Doença Hepática Induzida por Substâncias e Drogas/patologia , Masculino , Tetracloreto de Carbono/toxicidade , Abrus/química , Substâncias Protetoras/farmacologia , Medicamentos de Ervas Chinesas/farmacologia , Estresse Oxidativo/efeitos dos fármacosRESUMO
The glutinous rice starch (GRS) regeneration process could lead to decreased product quality and shorter shelf life. The purpose of this study was to analyze the effect of an ethanol extract of tea (EET) on the regeneration properties of GRS. The microstructure of starch was determined via scanning electron microscopy (SEM), Fourier-transform infrared (FT-IR) spectroscopy was used to determine the microstructure of starch-polyphenol molecular groups, an X-ray diffraction (XRD) instrument was used to determine the starch crystal structure, a differential scanning calorimeter (DSC) was used to determine the thermodynamic properties of starch, and the inhibitory effect of EET on GRS regeneration was comprehensively evaluated. The effect of EET on the in vitro digestion properties of GRS was also determined. The results showed that the addition of EET in GRS resulted in an increase in solubility and swelling power and a decrease in crystallinity and ΔHr. Compared to the control group, when retrograded for 10 days, the ΔHr of GRS with 1%, 2.5%, 5%, and 10% addition of EET decreased by 34.61%, 44.53%, 52.93%, and 66.79%, respectively. Furthermore, the addition of EET resulted in a decrease in the content of RDS and an increase in the content of SDS and RS in GRS. It was shown that the addition of EET could significantly inhibit the retrogradation of GRS, improve the processability, and prolong the shelf life of GRS products.
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We investigated the inter- and intra-species differences of leaf vein traits of three dominant Quercus species, Q. wutaishanica, Q. aliena var. acutiserrata, and Q. variabilis of Niubeiling (subtropical humid climate) and Taohuagou (warm temperate semi-humid climate), located in the eastern and western Qinling Mountains. The nine examined leaf vein traits included primary leaf vein width, secondary leaf vein width, mean fine vein width, primary vein density, fine vein density, vein areole diameter, areole density, 3D fine vein surface area, and fine vein volume. We further elucidated the influencing mechanisms and regulatory pathways of biotic and abiotic factors on leaf vein traits. The results showed that species identity had significant effects on eight out of nine leaf vein traits except 3D fine vein surface area, while habitat had significant effects on primary leaf vein width, secondary leaf vein width, vein areole diameter, fine vein density, and areole density. Altitude had significant effects on primary vein density, mean fine vein width, vein areole diameter, fine vein density and areole density. Habitat, tree species identity, and altitude had significantly interactive effects on primary leaf vein density, 3D fine vein surface area, and fine vein volume. There were significant differences in primary leaf vein width, mean fine vein width, areole density, 3D fine vein surface area, fine vein volume, primary vein density of Q. wutaishanica between the two studied habitats, but the differences were only found in secondary leaf vein width and areole density of Q. aliena var. acutiserrata and Q. variabilis. The examined leaf vein traits were influenced both by biotic and abiotic factors, with varying effect sizes. Among the biotic factors, petiole length, leaf length and width ratio had strong effect on leaf vein traits. Among the abiotic factors, climatic and soil factors had high effect size on vein traits, with the former being higher than the latter. Leaf vein traits were affected directly by biotic factors, but indirectly by abiotic factors (soil and climatic factors) via regulating biotic factors (leaf stoichiometry and leaf phenotypic traits).
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Ecossistema , Folhas de Planta , Quercus , Quercus/anatomia & histologia , Folhas de Planta/anatomia & histologia , China , Especificidade da Espécie , AltitudeRESUMO
Methylmercury (MeHg) exposure can cause nerve damage and mitochondrial dysfunction. Mitochondrial dysfunction is mainly mediated by mitochondrial biogenesis and mitochondrial dynamics disorders. Quercetin (QE) plays an important role in activating silencing information regulator 2 related enzyme 1 (SIRT1), and SIRT1 activates peroxisome-proliferator-activated receptor-γ co-activator 1α (PGC-1α), which can regulate mitochondrial biogenesis and mitochondrial dynamics. The main purpose of this study was to explore the alleviating effects of QE on MeHg-induced nerve damage and mitochondrial dysfunction. The results showed that QE could reduce the excessive production of reactive oxygen species (ROS) and the loss of membrane potential induced by MeHg. Meanwhile, QE activated SIRT1 activity and SIRT1/PGC-1α signaling pathway, improved mitochondrial biogenesis and fusion and reduced mitochondrial fission. In summary, we hypothesized that QE prevents MeHg-induced mitochondrial dysfunction by activating SIRT1/PGC-1α signaling pathway.
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Green tides, a globally prevalent marine ecological anomaly observed in coastal regions, have received substantial attention. However, there is limited research on the burial of Ulva prolifera in sediments during the late stages of green tide outbreaks. This study investigates the effect of temperature on U. prolifera buried in sediment over 30 days. The measurements included the length, biomass, relative growth rate, chlorophyll composition and maximum quantum yield (Fv/Fm) of PS II at different stages. The results indicate that at -20 °C, numerous seedlings emerged after 14 days of recovery culture, suggesting the release of spores or gametes; survival was possible from -2 °C to 15 °C; but at 20 °C and 30 °C, all U. prolifera died. The U. prolifera buried in sediment during the late stage of green tide outbreaks may serve as one of the sources for the subsequent year's green tide eruption. This research provides insights into the origins of green tide outbreaks in the southern Yellow Sea.
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Algas Comestíveis , Eutrofização , Ulva , Temperatura , Biomassa , ChinaRESUMO
Microplastics (MPs) and perfluorinated compounds (PFAS) are widespread in the global ecosystem. MPs have the ability to adsorb organic contaminants such as perfluorooctane sulfonate (PFOS), leading to combined effects. The current work aims to explore the individual and combined toxicological effects of polystyrene (PS) and PFOS on the growth and nerves of the freshwater planarian (Dugesia japonica). The results showed that PS particles could adsorb PFOS. PS and PFOS impeded the regeneration of decapitated planarians eyespots, whereas the combined treatment increased the locomotor speed of intact planarians. PS and PFOS caused significant DNA damage, while co-treatment with different PS concentrations aggravated and attenuated DNA damage, respectively. Further studies at the molecular level have shown that PS and PFOS affect the proliferation and differentiation of neoblasts in both intact and regenerating planarians, alter the expression levels of neuronal genes, and impede the development of the nervous system. PS and PFOS not only disrupted the homeostasis of intact planarians, but also inhibited the regeneration of decapitated planarians. This study is the first to assess the multiple toxicity of PS and PFOS to planarians after combined exposure. It provides a basis for the environmental and human health risks of MPs and PFAS.
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Ácidos Alcanossulfônicos , Fluorocarbonos , Planárias , Animais , Humanos , Planárias/fisiologia , Microplásticos/toxicidade , Microplásticos/metabolismo , Plásticos/metabolismo , Poliestirenos/toxicidade , Poliestirenos/metabolismo , Ecossistema , Homeostase , Fluorocarbonos/toxicidade , Fluorocarbonos/metabolismoRESUMO
The effectiveness of platelet-rich plasma (PRP) for the treatment of Achilles tendon disorders still needs to be evaluated through a series of prospective studies, but genomic analysis can reveal the existence of complementary PRP treatment options. Based on the 96 platelet activation-related genes in the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, we performed Gene Ontology functional enrichment analysis and KEGG enrichment analysis, pathway correlation analysis, and enrichment mapping to determine the enrichment results of the gene set enrichment analysis and found that the cAMP signalling pathway may be the key to enhancing the effectiveness of PRP treatment. The cAMP signalling pathway interacts with the Rap1 signalling pathway and cGMP-PKG signalling pathway to mediate the entire pathophysiological process of Achilles tendon disease. Moreover, ADCY1-9 may be the key to the activation of the cAMP signalling network. Further based on the data in the Gene Expression Omnibus database, it was found that ADCY4 and ADCY7 may be the players that play a major role, associated with the STAT4-ADCY4-LAMA5 axis and the GRbeta-ADCY7-SEMA3C axis, which is expected to be a complementary target for enhancing the efficacy of PRP in the treatment of Achilles tendon disease.
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BACKGROUND: Neural stem cells (NSCs), especially human NSCs, undergo cellular senescence characterized by an irreversible proliferation arrest and loss of stemness after prolonged culture. While compelling correlative data have been generated to support the oxidative stress theory as one of the primary determinants of cellular senescence of NSCs, a direct cause-and-effect relationship between the accumulation of oxidation-mediated damage and cellular senescence of NSCs has yet to be firmly established. Human SOD1 (hSOD1) is susceptible to oxidation. Once oxidized, it undergoes aberrant misfolding and gains toxic properties associated with age-related neurodegenerative disorders. The present study aims to examine the role of oxidized hSOD1 in the senescence of NSCs. METHODS: NSCs prepared from transgenic mice expressing the wild-type hSOD1 gene were maintained in culture through repeated passages. Extracellular vesicles (EVs) were isolated from culture media at each passage. To selectively knock down oxidized SOD1 in NSCs and EVs, we used a peptide-directed chaperone-mediated protein degradation system named CT4 that we developed recently. RESULTS: In NSCs expressing the hSOD1 from passage 5, we detected a significant increase of oxidized hSOD1 and an increased expression of biomarkers of cellular senescence, including upregulation of P53 and SA-ß-Gal and cytoplasmic translocation of HMGB1. The removal of oxidized SOD1 remarkably increased the proliferation and stemness of the NSCs. Meanwhile, EVs derived from senescent NSCs carrying the wild-type hSOD1 contained high levels of oxidized hSOD1, which could accelerate the senescence of young NSCs and induce the death of cultured neurons. The removal of oxidized hSOD1 from the EVs abolished their senescence-inducing activity. Blocking oxidized SOD1 on EVs with the SOD1 binding domain of the CT4 peptide mitigated its toxicity to neurons. CONCLUSION: Oxidized hSOD1 is a causal factor in the cellular senescence of NSCs. The removal of oxidized hSOD1 is a strategy to rejuvenate NSCs and to improve the quality of EVs derived from senescent cells.
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Esclerose Lateral Amiotrófica , Células-Tronco Neurais , Animais , Humanos , Camundongos , Esclerose Lateral Amiotrófica/genética , Senescência Celular , Camundongos Transgênicos , Células-Tronco Neurais/metabolismo , Peptídeos , Superóxido Dismutase/genética , Superóxido Dismutase/metabolismo , Superóxido Dismutase-1/genéticaRESUMO
The expression of microRNA (miRNA) changes in many diseases plays an important role in the diagnosis, treatment, and prognosis of diseases. Spinal cord injury (SCI) is a serious disease of the central nervous system, accompanied by inflammation, cell apoptosis, neuronal necrosis, axonal rupture, demyelination, and other pathological processes, resulting in impaired sensory and motor functions of patients. Studies have shown that miRNA expression has changed after SCI, and miRNAs participate in the pathophysiological process and treatment of SCI. Therefore, quantitative analysis and monitoring of the expression of miRNA were of great significance for the diagnosis and treatment of SCI. Through the SCI-related miRNA chord plot, we screened out miRNA-21-5p and miRNA-let-7a with a higher correlation. However, for traditional detection strategies, it is still a great challenge to achieve a fast, accurate, and sensitive detection of miRNA in complex biological environments. The most frequently used method for detecting miRNAs is polymerase chain reaction (PCR), but it has disadvantages such as being time-consuming and cumbersome. In this paper, a novel SERS sensor for the quantitative detection of miRNA-21-5p and miRNA-let-7a in serum and cerebrospinal fluid (CSF) was developed. The SERS probe eventually formed a sandwich-like structure of Fe3O4@hpDNA@miRNA@hpDNA@GNCs with target miRNAs, which had high specificity and stability. This SERS sensor achieved a wide range of detection from 1 fM to 1 nM and had a good linear relationship. The limits of detection (LOD) for miRNA-21-5p and miRNA-let-7a were 0.015 and 0.011 fM, respectively. This new strategy realized quantitative detection and long-term monitoring of miRNA-21-5p and miRNA-let-7a in vivo. It is expected to become a powerful biomolecule analysis tool and will provide ideas for the diagnosis and treatment of many diseases.
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MicroRNAs , Traumatismos da Medula Espinal , Humanos , Reação em Cadeia da Polimerase , Limite de Detecção , Prognóstico , Traumatismos da Medula Espinal/diagnóstico , Traumatismos da Medula Espinal/genéticaRESUMO
OBJECTIVES: To describe the clinical characteristics of Chinese cystic fibrosis (CF) patients and to investigate the variants of CFTR and their potential pathogenicity. STUDY DESIGN: Chinese patients with potential CF diagnosis were studied. Clinical data were reviewed retrospectively from medical records. Whole exome sequencing and genetic evaluation were conducted to explore potential gene variants. The disruption of the variants to protein structure and function was explored and validated using in vitro experiments and in silico analysis. RESULTS: Four patients were recruited to the study, three of them were diagnosed as CF, and one was diagnosed as CFTR-related disorder. The age at symptom onset for the patients in this study ranged from newborn to 6 years, while the age at diagnosis varied from 3 to 11 years. All four patients exhibited bilateral diffuse bronchiectasis with Pseudomonas aeruginosa infections, and three of them had malnutrition. Finger clubbing was observed in three patients, two of whom displayed mixed ventilatory dysfunction. The CFTR variants spectrum of Chinese children with CF differs from that of Caucasian. A total of six variants were identified, two of which were first reported (c.1219G > T [p.Glu407*] and c.1367delT [p.Ala457Leufs*12]). The nonsense variants c.1219G > T, c.1657C > T and c.2551C > T and the frameshift variant c.1367delT were predicted to introduce premature stop codon and produce shorten CFTR protein, which was also first validated by in vitro truncation assay in this study. The missense variant c.1810A > C was predicted to disrupt the function of the nucleotide-binding domain 1 (NBD1) in the CFTR protein. The splicing variant c.1766 + 5G > T caused skipping of exon 13 and damaged the integrity of CFTR protein. CONCLUSIONS: Our study expands the spectrum of phenotypes and genotypes for CF of Chinese origin, which differs significantly from that of Caucasian. Genetic analysis and counseling are crucial and deserve extensive popularization for the diagnosis ofCF in patients of Chinese origin.