Melanoserispenghuana (Lactucinae, Cichorieae, Asteraceae), a new species from North-central Yunnan, China.

In this paper, we describe a new species, Melanoserispenghuana, from Mt. Jiaozi Xueshan located in North-central Yunnan, China. Despite its morphological similarities to M.likiangensis, M.penghuana exhibits distinct differences in leaf texture, shape of terminal lobes, indumentum of leaves, peduncles, and involucres, as well as the length of the achenes. Additionally, the conservation status of this species is classified as Vulnerable through data analysis from two field surveys.

circRARS synergises with IGF2BP3 to regulate RNA methylation recognition to promote tumour progression in renal cell carcinoma.

As the most prominent RNA modification, N6-methyladenosine (m6 A) participates in the regulation of tumour initiation and progression. Circular RNAs (circRNAs) also play crucial roles in ubiquitous life processes. Whether circRNAs are required for m6 A regulation in renal cell carcinoma (RCC) remains unclear. Meta-analysis and bioinformatics identified that IGF2BP3 was upregulated in RCC and indicated a worse prognosis. IGF2BP3 significantly promoted RCC progression in vitro and in vivo. Mechanistically, circRARS bound to KH1-KH2 domains of IGF2BP3 to enhance m6 A modification recognition. A 12-nt sequence (GUCUUCCAGCAA) was proven to be the IGF2BP3-binding site of circRARS. Additionally, CAPN15, CD44, HMGA2, TNRC6A and ZMIZ2 were screened to be the target genes regulated by the IGF2BP3/circRARS complex in an m6 A-dependent manner. Stabiliser proteins, including HuR, Matrin3 and pAbPC1, were recruited by circRARS, thereby increasing the mRNA stability of the forementioned five target genes. Consequently, the IGF2BP3/circRARS complex facilitated the lipid accumulation of RCC cells and promoted sunitinib resistance via target genes. circRARS synergised with IGF2BP3 to facilitate m6 A recognition, thereby promoting RCC progression. Thus, IGF2BP3 could be a potential biomarker for RCC diagnosis and prognosis and a therapeutic target.

Melanoseriskangdingensis (Lactucinae, Cichorieae, Asteraceae), a new species reported from western Sichuan, China.

Melanoseriskangdingensis, a new species native to western Sichuan, China, is firstly described and illustrated, and its conservation status is also assessed. It bears resemblance to M.macrantha and M.bracteata in terms of morphology; however, there are distinguishing characteristics in terms of their leaf structure, presence of bracts, hairiness of involucre, number of florets, and length of both stamen tube and achene's beak.

circPTPN12 promotes the progression and sunitinib resistance of renal cancer via hnRNPM/IL-6/STAT3 pathway.

Renal cell carcinoma (RCC) is characterized by the difficulties in early diagnosis and the propensity to metastases. For advanced RCC, sunitinib targeted therapy is the clinically recommended first-line drug and the major challenge of sunitinib treatment is adaptive resistance. Therefore, it is imperative to research the mechanisms underlying sunitinib resistance. In this study, we discovered that circPTPN12 was highly expressed in RCC tissues and was associated with poorer clinical outcomes. circPTPN12 could promote the proliferation, migration, invasion, and sunitinib resistance of RCC cells. Mechanistically, circPTPN12 was found to form a complex with hnRNPM, which was involved in the regulation of mRNA processing. The combination with circPTPN12 enhanced the ability of hnRNPM to maintain the stability of IL-6 mRNA and further activated the STAT3 signaling pathway. The study revealed that circPTPN12/hnRNPM/IL-6/STAT3 axis promoted RCC progression and sunitinib resistance, which might be a promising therapeutic target for relieving sunitinib resistance in RCC.

Association between pulmonary hemorrhage and CPAP failure in very preterm infants.

Background: Pulmonary hemorrhage (PH) in neonates is a life-threatening respiratory complication. We aimed to analyze the perinatal risk factors and morbidity with PH among very preterm infants in a large multicenter study. Methods: This was a multicenter case-control study based on a prospective cohort. Participants included 3,680 in-born infants with a gestational age at 24-32 weeks (birth weight <1,500 g) who were admitted between January 1, 2019, and October 31, 2021. All infants were divided into two groups, namely, the PH and no-PH groups, at a ratio of 1:2 according to the following factors: gestational age (GA), birth weight (BW), and the Score for Neonatal Acute Physiology with Perinatal extension II (SNAPPE II). Perinatal factors and outcomes were compared between the two groups by logistic regression analyses. Results: A total of 3,680 infants were included in the study, and the number of identified cases of PH was 262 (7.1%). The incidence was 16.9% (136/806) for neonates with extremely low BW (BW < 1,000 g) infants. The multivariate analysis showed that CPAP failure (OR 2.83, 95% CI 1.57, 5.08) was significantly associated with PH. PH was associated with a high likelihood of death (OR 3.81, 95% CI 2.67, 5.43) and bronchopulmonary dysplasia (BPD) (≥grade II) (OR 1.58, 95% CI 1.00, 2.48). Conclusions: In this multicenter case-control study based on a prospective cohort, PH to be common among VLBW infants. PH is associated with significant morbidity and mortality, and perinatal management, especially CPAP failure. Respiratory management strategies to decrease the risk of PH should be optimized.

Restoring the epigenetically silenced lncRNA COL18A1-AS1 represses ccRCC progression by lipid browning via miR-1286/KLF12 axis.

Abnormal accumulation of lipids has been highlighted in the progression of clear cell renal cell carcinoma (ccRCC). However, the underlying mechanism remains unclear. Emerging evidence suggests long noncoding RNAs (lncRNAs) participate in the regulation of lipid metabolism. In this study, we found lncRNA COL18A1-AS1 was downregulated in ccRCC and that higher COL18A1-AS1 expression indicated better prognosis. Decreased COL18A1-AS1 expression was caused by DNA methylation at the CpG islands within its promoter. Restoring the epigenetically silenced COL18A1-AS1 repressed tumor progression, promoted lipid browning and consumption in vitro and in vivo. Mechanistically, COL18A1-AS1 could competitively bind miR-1286 to increase the expression of Krüppel-like factor 12 (KLF12). Downregulation of COL18A1-AS1 in ccRCC resulted in the low expression of KLF12. COL18A1-AS1/KLF12 positively regulated uncoupling protein 1 (UCP1)-mediated lipid browning, which promotes tumor cell "slimming" and inhibits tumor progression. When tumor cell "slimming" occurred, lipid droplets turned into tiny pieces, and lipids were consumed without producing ATP energy. Taken together, our findings on COL18A1-AS1-miR-1286/KLF12 axis revealed a potential mechanism of abnormal accumulation of lipids in ccRCC and could be a promising therapeutic target for ccRCC patients.

TIMP1 Indicates Poor Prognosis of Renal Cell Carcinoma and Accelerates Tumorigenesis via EMT Signaling Pathway.

Renal cell carcinoma (RCC) is one of the most common malignancies in the urinary system. The mortality of advanced RCC remains high despite advances in systemic therapy of RCC. Considering the misdiagnosis of early-stage RCC, the identification of effective biomarkers is of great importance. Tissue inhibitor matrix metalloproteinase 1 (TIMP1), which belongs to TIMP gene family, is a natural inhibitor of the matrix metalloproteinases (MMPs). In this study, we found TIMP1 was significantly up-regulated in cell lines and RCC tissues. Kaplan-Meier analysis revealed that high expression of TIMP1 indicated a poor prognosis. Multivariate analysis further indicated that TIMP1 overexpression was an independent prognostic factor of RCC patients. Furthermore, knockdown of TIMP1 in vitro suppressed the proliferation, migration, and invasion of RCC cells, while upregulating TIMP1 accelerated the proliferation, migration, and invasion of RCC cells. In addition, we also found that TIMP1 prompted the progression of RCC via epithelial-to-mesenchymal transition (EMT) signaling pathway. In conclusion, the present results suggested that TIMP1 indicated poor prognosis of renal cell carcinoma and could serve as a potential diagnostic and prognostic biomarker for RCC.

Inhibition of lncRNA NEAT1 sensitizes medulloblastoma cells to cisplatin through modulating the miR-23a-3p-glutaminase (GLS) axis.

Medulloblastoma (MB) is a commonly occurring brain malignancy in adolescence. Currently, the combination of chemotherapy with subsequent irradiation is a regular therapeutic strategy. However, high dosage of chemotherapy is associated with drug resistance and side effects. The long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1), which is frequently overexpressed in diverse human tumors, is correlated with worse survival rate in cancer patients. Currently, the precise roles of NEAT1 in MB and chemoresistance remain unclear. Our study aimed to investigate the biological functions of NEAT1 in cisplatin-resistant medulloblastoma. We report that NEAT1 was significantly upregulated in medulloblastoma patient specimens. Silencing NEAT1 significantly suppressed MB cell proliferation and sensitized MB cells to cisplatin. In cisplatin-resistant MB cell line, DAOY Cis R, NEAT1 expression, and glutamine metabolism were remarkably upregulated in cisplatin-resistant cells. Under low glutamine supply, cisplatin-resistant cells displayed increased cisplatin sensitivity. Bioinformatical analysis and luciferase assay uncovered that NEAT1 functions as a ceRNA of miR-23a-3p to downregulate its expressions in MB cells. Moreover, miR-23a-3p was apparently downregulated in MB patient tissues and cisplatin resistant MB cells. We identified GLS (glutaminase), a glutamine metabolism enzyme, was directly targeted by miR-23a-3p in MB cells. Rescue experiments demonstrated restoration of miR-23a-3p in NEAT1-overexpressing DAOY cisplatin resistant cells successfully overcame the NEAT1-promoted cisplatin resistance by targeting GLS. In general, our results revealed new molecular mechanisms for the lncRNA-NEAT1-mediated cisplatin sensitivity of MB.

Purification, characterization and partial biological activities of exopolysaccharide produced by Saccharomyces cerevisiae Y3.

In this study, the exopolysaccharide (EPS) from Saccharomyces cerevisiae Y3 was extracted and purified, the preliminary structure characteristics and biological activities was investigated. The S. cerevisiae Y3 EPS was obtained by ethanol precipitation and gel filtration chromatography. MW of purified Y3 EPS was 93,477 Da. High-performance liquid chromatography (HPLC), fourier transform infrared spectroscopy (FT-IR), nuclear magnetic resonance spectroscopy (NMR) and methylation analyses showed that the EPS was a heteropolysaccharide, which composed of 1-α-D mannose (39.8%), 1,2-α-D mannose (19.6%), 1,6-α-D linked mannose (10.4%), 1,3,6-ß-D glucose (27.5%), and 1-ß-D linked glucose (1.9%). Scanning electron microscope (SEM) and atomic force microscope (AFM) further revealed smooth and dense sheet-like structure with reticular configuration. The Congo red test and X-ray diffraction (XRD) reflected an irregular coil conformation and non-crystalline amorphous nature. The EPS exhibited good hydrophilicity, thermal stability and antioxidation ability for DPPH radicals, hydroxyl radicals and NO2-, as well as good prebiotic properties. These results indicated that Y3 EPS could be explored as a promising functional adjunct for application in probiotics and antioxidation.

CircSLC7A6 promotes the progression of Wilms' tumor via microRNA-107/ ABL proto-oncogene 2 axis.

The dysregulation of circular RNAs (circRNAs) has been proved to be involved in the carcinogenesis of various cancers. Nevertheless, the biological function of circSLC7A6 remains unclear in Wilms' tumor (WT). In our study, we found that circSLC7A6 was upregulated in cancerous WT tissues and cells. Cell apoptosis was increased while cell viability, migration, and invasion were repressed by circSLC7A6 silencing. Besides, circSLC7A6 knockdown suppressed WT tumor growth in vivo. miR-107 was identified as a direct target of circSLC7A6, and circSLC7A6 could negatively regulate miR-107 expression. In addition, circSLC7A6 knockdown inhibited WT progression, while the effect was partially abolished by the downregulation of miR-107. Additionally, ABL proto-oncogene 2 axis (ABL2) was verified as a downstream gene of miR-107, and circSLC7A6 could upregulate ABL2 expression by serving as a ceRNA of miR-107. Moreover, functional assays revealed that ABL2 overexpression reversed the impact of circSLC7A6 depletion on cell proliferation, migration, invasion, and apoptosis of WT. In conclusion, the present study demonstrated that circSLC7A6 facilitated WT progression by upregulating ABL2 through inhibiting miR-107 expression. These results suggested that circSLC7A6 might serve as a potential therapeutic target for WT.

The response surface optimization of exopolysaccharide produced by Saccharomyces cerevisiae Y3 and its partial characterization.

Response surface methodology (RSM) was used to optimize the conditions of exopolysaccharides (EPSs) by Saccharomyces cerevisiae Y3. The results indicated that the yield of EPS reached 4.52 ± 0.14 g/L with 10.30% (w/v) sucrose, 0.64% (w/v) yeast extract, liquid volume 141.5 mL, which was 2.40 times the original EPS yield. Y3 EPS contained 83.65 ± 0.16% of total sugars, 15.27 ± 0.26% of uronic acid, 0.78 ± 0.02% of protein and 0.30 ± 0.12% of sulfuric acid groups. Y3 EPS maintained a relatively low viscosity, with intrinsic viscosities of 306.58 mL/g (25 °C) and 200.91 mL/g (35 °C), respectively. The EPS had high water solubility index (WSI), high water holding capacity (WHC) and good emulsifying ability (EA). Meanwhile, the EPS could absorb metal ions such as Cu2+, Fe2+ and Zn2+. In addition, Y3 EPS exhibited good antioxidant properties and coagulated skim milk with a concentration-dependent manner. These results indicated that S. cerevisiae Y3 EPS had applicable prospects in medicine, food, especially the dairy industry.

CENPA promotes clear cell renal cell carcinoma progression and metastasis via Wnt/ß-catenin signaling pathway.

Clear cell renal cell carcinoma (ccRCC) is the most common malignant tumor of the kidney. New and reliable biomarkers are in urgent need for ccRCC diagnosis and prognosis. The CENP family is overexpressed in many types of cancers, but its functions in ccRCC have not been fully clarified. In this paper, we found that several CENP family members were highly expressed in ccRCC tissues. Also, CENPA expression level was related to clinicopathological grade and prognosis by weighted gene co-expression network analysis (WGCNA). CENPA served as a representative CENP family member as a ccRCC biomarker. Further in vitro experiments verified that overexpression of CENPA promoted ccRCC proliferation and metastasis by accelerating the cell cycle and activating the Wnt/ß-catenin signaling pathway. The elevated ß-catenin led by CENPA overexpression translocated to nucleus for downstream effect. Functional recovery experiment confirmed that Wnt/ß-catenin pathway was essential for ccRCC progression and metastasis. Developing selective drugs targeting CENPA may be a promising direction for cancer treatment.

Low Expression Levels of SLC22A12 Indicates a Poor Prognosis and Progresses Clear Cell Renal Cell Carcinoma.

Clear cell renal cell carcinoma (ccRCC) accounts for approximately 4/5 of all kidney cancers. Accumulation of minor changes in the cellular homeostasis may be one cause of ccRCC. Therefore, we downloaded the RNA sequencing and survival data of the kidney renal cell carcinoma (KIRC) cohort from the Cancer Genome Atlas (TCGA) database. After the univariate and multivariate Cox regression analyses, 19 kidney-specific differentially expressed genes (DEGs) were found. Solute Carrier Family 22 Member 12 (SLC22A12) resulted in an independent prognostic predictor for both overall survival (OS) and disease-free survival (DFS). SLC22A12 expression was lower in tumoral tissue compared to normal tissue. Moreover, patients in the SLC22A12 low expression group had a higher pathological stage and worse survival than the high expression group. Additionally, qRT-PCR assay, immunoblotting test (IBT), and immunohistochemical (IHC) analyses of cancer tissues/cells and the corresponding normal controls verified that SLC22A12 is downregulated in ccRCC. Receiver operator characteristic (ROC) curves showed that the low expression level of SLC22A12 could be a good diagnostic marker for ccRCC (AUC=0.7258; p <0.0001). Gene set enrichment analysis (GSEA) showed that SLC22A12 expression levels are related to metabolism, cell cycle, and tumor-related signaling pathways. GO and KEGG analyses revealed that SLC22A12 transports multiple organic compounds, ions, and hormones and participates in the extracellular structure organization. Furthermore, SLC22A12 over-expression in vitro inhibited the proliferation, migration, and invasion of renal cancer cells by regulating PI3K/Akt pathways. Such effects were reversed when knocking out SLC22A12. In summary, as a transporter for many vital metabolites, SLC22A12 may affect tumor cell survival through its impacts on the mentioned metabolites. In conclusion, this study uncovered that SLC22A12 is a promising prognostic and diagnostic biomarker for ccRCC.

Development of a four-gene prognostic model for clear cell renal cell carcinoma based on transcriptome analysis.

This study aimed to develop a prognostic model for clear cell renal cell carcinoma (ccRCC) based on transcriptome analysis. We screened Gene Expression Omnibus (GEO) database and the Cancer Genome Atlas (TCGA) database for gene expression data and clinical characteristics of ccRCC. After differentially expression analysis, we identified 533 key genes of the development of ccRCC. Next, a weighted gene co-expression network analysis (WGCNA) was executed to investigate the association between differentially expressed genes and clinical characteristics. Then, based on protein-protein interaction (PPI) network, least absolute shrinkage and selection operator (LASSO) regression and Cox regression, a four-gene (COL4A5, ABCB1, NR3C2 and PLG) prognostic model has been constructed in TCGA training cohort. Finally, we examined the predictive power of this model with survival analysis and receiver operating characteristic (ROC) curve both in training cohort and in validation cohorts. And we found this model was significantly correlated with infiltrating immune cells. The four-gene prognosis model could be a potential prediction tool with high accuracy and reliability for ccRCC patients.

The Identification of Critical m6A RNA Methylation Regulators as Malignant Prognosis Factors in Prostate Adenocarcinoma.

RNA methylation accounts for over 60% of all RNA modifications, and N6-methyladenosine (m6A) is the most common modification on mRNA and lncRNA of human beings. It has been found that m6A modification occurs in microRNA, circRNA, rRNA, and tRNA, etc. The m6A modification plays an important role in regulating gene expression, and the abnormality of its regulatory mechanism refers to many human diseases, including cancers. Pitifully, as it stands there is a serious lack of knowledge of the extent to which the expression and function of m6A RNA methylation can influence prostate cancer (PC). Herein, we systematically analyzed the expression levels of 35 m6A RNA methylation regulators mentioned in literatures among prostate adenocarcinoma patients in the Cancer Genome Atlas (TCGA), finding that most of them expressed differently between cancer tissues and normal tissues with the significance of p < 0.05. Utilizing consensus clustering, we divided PC patients into two subgroups based on the differentially expressed m6A RNA methylation regulators with significantly different clinical outcomes. To appraise the discrepancy in total transcriptome between subgroups, the functional enrichment analysis was conducted for differential signaling pathways and cellular processes. Next, we selected five critical genes by the criteria that the regulators had a significant impact on prognosis of PC patients from TCGA through the last absolute shrinkage and selection operator (LASSO) Cox regression and obtained a risk score by weighted summation for prognosis prediction. The survival analysis curve and receiver operating characteristic (ROC) curve showed that this signature could excellently predict the prognosis of PC patients. The univariate and multivariate Cox regression analyses proved the independent prognostic value of the signature. In summary, our effort revealed the significance of m6A RNA methylation regulators in prostate cancer and determined a m6A gene expression classifier that well predicted the prognosis of prostate cancer.

Protective effects of catalpol on mitochondria of hepatocytes in cholestatic liver injury.

Cholestasis, which is caused by the obstruction of bile flow, can lead to rapid organ injury, cell apoptosis and necrosis of hepatocytes, and may eventually develop into fibrosis and cirrhosis. Oxidative stress and mitochondrial dysfunction are the key pathogenic signs of hepatic cholestasis. Catalpol has pharmacological activities, including antioxidative and anti­inflammatory effects, and may relieve mitochondrial damage and restore mitochondrial membrane potential. However, the potential roles and mechanisms of catalpol in cholestasis­induced liver injury are not clear. In the present study, liver function­related indexes were measured in the serum of mice by commercial kits. In addition, levels of serum inflammatory factors were detected by ELISA. Hematoxylin and eosin staining was performed to observe histopathological changes, and mitochondrial membrane potential was detected using JC­1 staining. Mitochondrial adenosine triphosphate (ATP), reactive oxygen species (ROS) and malondialdehyde levels were determined using a luciferase reporter kit, flow cytometry and a thiobarbituric acid reactive substance assay kit, respectively. Western blotting was performed to detect the expression levels of apoptosis­related proteins in liver tissues. The findings revealed that catalpol reduced liver damage caused by cholestasis, improved the mitochondrial membrane potential, and increased the ATP content and glutathione content of cholestasis model mice. Moreover, catalpol also reduced the ROS level, inhibited lipid peroxidation, and regulated oxidative stress and apoptotic protein expression. Thus, the present study preliminarily confirmed that catalpol can reduce liver injury in a mouse model of cholestasis through inhibiting oxidative stress and enhancing mitochondrial membrane potential.

Combined microwave ablation and antiangiogenic therapy to increase local efficacy.

Purpose: We aim to evaluate the efficacy, safety and survival time of microwave ablation (MWA) with adjuvant antiangiogenic therapy-endostatin in animal models.Material and methods: A total of 40 rabbits successfully implanted with VX2 tumors were randomly assigned to four experimental groups: Group A underwent only microwave ablation of the tumors; Group B received only antiangiogenic drugs endostatin; Group C received endostatin immediately after MWA; Group D followed up without treatment.Results: Two months post-treatment, tumor sizes of Group A and Group C were reduced to 1.936 ± 0.373 cm3 and 1.592 ± 0.382 cm3, respectively. However, tumors grew to 15.091 ± 1.735 cm3 and 47.825 ± 7.664 cm3 in Group B and the control group. Three months post-treatment, tumor sizes in Group A and Group C maintained as 1.395 ± 0.394 cm3 and 1.482 ± 0.305 cm3, significantly smaller than Group B (35.277 ± 6.019 cm3). All animals in the control group died, while four (40%) survived in Group B (Endo Group). The numbers of survivals in Groups A and C were seven (70%) and eight (80%), respectively. The lowest metastasis rate (2/10, 20%) was observed in Group C (combination therapy).Conclusion: The combination of MWA and antiangiogenic therapy triggered a significant reduction in the growth rate and metastases of tumors and may potentially improve survivals.

Thermodynamics and kinetics guided probe design for uniformly sensitive and specific DNA hybridization without optimization.

Sensitive and specific DNA hybridization is essential for nucleic acid chemistry. Competitive composition of probe and blocker has been the most adopted probe design for its relatively high sensitivity and specificity. However, the sensitivity and specificity were inversely correlated over the length and concentration of the blocker strand, making the optimization process cumbersome. Herein, we construct a theoretical model for competitive DNA hybridization, which disclose that both the thermodynamics and kinetics contribute to the inverse correlation. Guided by this, we invent the 4-way Strand Exchange LEd Competitive DNA Testing (SELECT) system, which breaks up the inverse correlation. Using SELECT, we identified 16 hot-pot mutations in human genome under uniform conditions, without optimization at all. The specificities were all above 140. As a demonstration of the clinical practicability, we develop probe systems that detect mutations in human genomic DNA extracted from ovarian cancer patients with a detection limit of 0.1%.

Effects of prophylactic oral ibuprofen on the closure rate of patent ductus arteriosus in premature infants.

The aim of this study was to investigate the effects of prophylactic oral ibuprofen on the closure rate of patent ductus arteriosus (PDA).This was a retrospective study and data on infants born before 36 weeks were collected. The prophylactic group was treated with ibuprofen (10, 5, and 5 mg/kg) from days 1 to 3 after birth, respectively. The conventional group was treated with the same dose of ibuprofen from days 4 to 6 once they were echocardiographically confirmed with PDA on day 3 after birth. The placebo group was treated with 5% glucose.The closure rate of PDA in the prophylactic group significantly increased on day 7 compared with the placebo group (P = .02), but showed no difference compared with the conventional group (P = .12). Serum NT-proBNP in the prophylactic and conventional groups decreased compared with the placebo group (P = .03 vs P = .07).Prophylactic oral ibuprofen can increase the closure rate of PDA in premature infants; however, it showed no significant advantages compared with conventional treatment. Serum NT-proBNP can be used to observe PDA treatment responses in premature infants.

Branch-Migration Based Fluorescent Probe for Highly Sensitive Detection of Mercury.

Detection of heavy metals is of great importance for food safety and environmental analysis. Among various heavy metal ions, mercury ion is one of the most prevalent species. The methods for detection of mercury were numerous, and the T-Hg-T based assay was promising due to its simplicity and compatibility. However, traditional T-Hg-T based methods mainly relied on multiple T-Hg-T to produce enough conformational changes for further detection, which greatly restrained the limit of detection. Hence, we established a branch-migration based fluorescent probe and found that single T-Hg-T could produce strong signals. The sensing mechanism of our method in different reaction modes was explored, and the detection limits were determined to be 18.4 and 14.7 nM in first-order reaction mode and mixed reaction mode, respectively. Moreover, coupled with Endonuclease IV assisted signal amplification, the detection limit could be 1.2 nM, lower than most DNA based fluorometric assays. For practicability, the specificity of our assay toward different interfering ions was investigated and detection of Hg2+ in deionized water and lake water was also achieved with similar recoveries compared to those of atomic fluorescence spectrometry, which demonstrated the practicability of our method in real samples. Definitely, the proposed branch migration probe would be a promising substitution for current DNA probes based on recognition of multiple T-Hg-T and we anticipate it to be widely adopted in food and environmental analysis.