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BACKGROUND AND STUDY AIMS: Currently, an increasing amount of experimental data is available on newly discovered biomarkers in inflammatory bowel diseases (IBD), but the role of these biomarkers is often questionable due to their limited sensitivity. Therefore, this study aimed to build a diagnostic tool incorporating a panel of serum biomarkers into a computational algorithm to identify patients with IBD and differentiate those with Crohn's disease (CD) from those with ulcerative colitis (UC). PATIENTS AND METHODS: We studied sera from 192 CD patients, 118 UC patients, 60 non-IBD controls and 60 healthy controls. Indirect immunofluorescence (IIF) assays were utilized to determine several serum biomarkers previously associated with IBD, and the decision tree algorithm was used to construct the diagnosis model. Performances of models were evaluated by prediction accuracy, precision, AUC and Matthews's correlation coefficient (MCC). The "Inflammatory Bowel Disease Multi-omics Database (IBDMDB)" cohorts were used to validate the model as external validation set. RESULTS: The prediction rates were determined and compared for decision tree models after each data was developed using C5.0, C&RT, QUEST and CHAID. The C5.0 and CHAID algorithms, which ranked top for the prediction rate in the IBD vs. non-IBD model and the CD vs. UC model, respectively, were utilized for final pattern analysis. The final decision tree model achieved higher classification accuracy than the approach based on conservative marker combinations (sensitivity 75.0% vs. 79.5%, specificity 93.8% vs. 78.3% for differentiating IBD from non-IBD; and sensitivity 84.3% vs. 73.4%, specificity 92.5% vs. 54.9% for differentiating CD from UC, respectively). The model prediction consistency was 93% (28/30) in the external validation set. CONCLUSION: The decision-tree-based approach used in this study, based on serum biomarkers, has shown to be a valid and useful approach to identifying IBD and differentiating CD from UC.
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Objectives: Portal hypertension (PH) frequently gives rise to severe and life-threatening complications, including hemorrhage accompanied by the rupture of esophageal and gastric varices. In contrast to the guidelines for the management of PH in adults, the optimal endoscopic management of variceal bleeding for secondary prophylaxis in children remains unclear. The present study evaluated the efficacy and safety of endoscopic variceal ligation (EVL) and endoscopic sclerotherapy (EST) to control gastroesophageal variceal bleeding in children. Methods: This retrospective study included children with gastroesophageal variceal bleeding who underwent EST or EVL at Xinhua Hospital, Shanghai Jiaotong University School of Medicine, between February 2013 and March 2020. Short-term hemostasis rate and long-term rebleeding rate were evaluated. Adverse events related to the procedures, such as esophageal ulcer, esophageal stricture, abnormal embolization, pneumonia and perforation, were also recorded. Results: EVL (n = 8) and EST (n = 13) were performed successfully in all pediatric patients diagnosed with moderate to severe esophageal varices concurrent with gastric varices. Hemostasis was achieved during episodes of upper gastrointestinal bleeding. The mean volume of each single aliquot of cyanoacrylate injected was 0.3 ± 0.1â ml (range: 0.1-0.5â ml). Varices were eradicated in six (75%) of the eight patients who underwent EVL after a median 2 (range: 1-4) procedures and a median time of 3.40 months (range: 1.10-13.33 months). Eleven (52.4%) of the 21 patients developed rebleeding events, with the mean duration of hemostasis being 11.1 ± 11.6 months (range 1.0-39.2 months). No treatment-related complications, for example, distal embolism, occurred except for abdominal pain in one patient (4.8%). Conclusions: EST, alone or in combination with EVL, is an effective and safe method of managing gastroesophageal variceal hemorrhage in children undergoing secondary prophylaxis.
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BACKGROUND: Lactate, previously considered a metabolic byproduct, is pivotal in cancer progression and maintaining the immunosuppressive tumor microenvironment. Further investigations confirmed that lactate is a primary regulator, introducing recently described post-translational modifications of histone and non-histone proteins, termed lysine lactylation. Pancreatic adenocarcinomas are characterized by increased glycolysis and lactate accumulation. However, our understanding of lactylation-related genes in pancreatic adenocarcinomas remains limited. AIM: To construct a novel lactylation-related gene signature to predict the survival of patients with pancreatic cancer. METHODS: RNA-seq and clinical data of pancreatic adenocarcinoma (PDAC) were obtained from the GTEx (Genotype-Tissue Expression) and TCGA (The Cancer Genome Atlas) databases via Xena Explorer, and GSE62452 datasets from GEO. Data on lactylation-related genes were obtained from publicly available sources. Differential expressed genes (DEGs) were acquired by using R package "DESeq2" in R. Univariate COX regression analysis, LASSO Cox and multivariate Cox regressions were produced to construct the lactylation-related prognostic model. Further analyses, including functional enrichment, ESTIMATE, and CIBERSORT, were performed to analyze immune status and treatment responses in patients with pancreatic cancer. PDAC and normal human cell lines were subjected to western blot analysis under lactic acid intervention; two PDAC cell lines with the most pronounced lactylation were selected. Subsequently, RT-PCR was employed to assess the expression of LRGs genes; SLC16A1, which showed the highest expression, was selected for further investigation. SLC16A1-mediated lactylation was analyzed by immunofluorescence, lactate production analysis, colony formation, transwell, and wound healing assays to investigate its role in promoting the proliferation and migration of PDAC cells. In vivo validation was performed using an established tumor model. RESULTS: In this study, we successfully identified 10 differentially expressed lactylation-related genes (LRGs) with prognostic value. Subsequently, a lactylation-related signature was developed based on five OS-related lactylation-related genes (SLC16A1, HLA-DRB1, KCNN4, KIF23, and HPDL) using Lasso Cox hazard regression analysis. Subsequently, we evaluated the clinical significance of the lactylation-related genes in pancreatic adenocarcinoma. A comprehensive examination of infiltrating immune cells and tumor mutation burden was conducted across different subgroups. Furthermore, we demonstrated that SLC16A1 modulates lactylation in pancreatic cancer cells through lactate transport. Both in vivo and in vitro experiments showed that decreasing SLC16A1 Level and its lactylation significantly inhibited tumor progression, indicating the potential of targeting the SLC16A1/Lactylation-associated signaling pathway as a therapeutic strategy against pancreatic adenocarcinoma. CONCLUSION: We constructed a novel lactylation-related prognostic signature to predict OS, immune status, and treatment response of patients with pancreatic adenocarcinoma, providing new strategic directions and antitumor immunotherapies.
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Regulación Neoplásica de la Expresión Génica , Neoplasias Pancreáticas , Microambiente Tumoral , Humanos , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/patología , Neoplasias Pancreáticas/mortalidad , Neoplasias Pancreáticas/inmunología , Neoplasias Pancreáticas/metabolismo , Pronóstico , Línea Celular Tumoral , Microambiente Tumoral/inmunología , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Transportadores de Ácidos Monocarboxílicos/genética , Transportadores de Ácidos Monocarboxílicos/metabolismo , Procesamiento Proteico-Postraduccional , Adenocarcinoma/genética , Adenocarcinoma/patología , Adenocarcinoma/mortalidad , Adenocarcinoma/inmunología , Adenocarcinoma/metabolismo , Ácido Láctico/metabolismo , Simportadores/genética , Simportadores/metabolismo , Proliferación Celular/genética , Perfilación de la Expresión Génica , Masculino , Carcinoma Ductal Pancreático/genética , Carcinoma Ductal Pancreático/mortalidad , Carcinoma Ductal Pancreático/patología , Carcinoma Ductal Pancreático/inmunología , Carcinoma Ductal Pancreático/terapia , Femenino , Animales , TranscriptomaRESUMEN
Imperceptible examination and unideal treatment effect are still intractable difficulties for the clinical treatment of pancreatic ductal adenocarcinoma (PDAC). At present, despite 5-fluorouracil (5-FU), as a clinical first-line FOLFIRINOX chemo-drug, has achieved significant therapeutic effects. Nevertheless, these unavoidable factors such as low solubility, lack of biological specificity and easy to induce immunosuppressive surroundings formation, severely limit their treatment in PDAC. As an important source of energy for many tumor cells, tryptophan (Trp), is easily degraded to kynurenine (Kyn) by indolamine 2,3- dioxygenase 1 (IDO1), which activates the axis of Kyn-AHR to form special suppressive immune microenvironment that promotes tumor growth and metastasis. However, our research findings that 5-FU can induce effectively immunogenic cell death (ICD) to further treat tumor by activating immune systems, while the secretion of interferon-γ (IFN-γ) re-induce the Kyn-AHR axis activation, leading to poor treatment efficiency. Therefore, a metal matrix protease-2 (MMP-2) and endogenous GSH dual-responsive liposomal-based nanovesicle, co-loading with 5-FU (anti-cancer drug) and NLG919 (IDO1 inhibitor), was constructed (named as ENP919@5-FU). The multifunctional ENP919@5-FU can effectively reshape the tumor immunosuppression microenvironment to enhance the effect of chemoimmunotherapy, thereby effectively inhibiting cancer growth. Mechanistically, PDAC with high expression of MMP-2 will propel the as-prepared nanovesicle to dwell in tumor region via shedding PEG on the nanovesicle surface, effectively enhancing tumor uptake. Subsequently, the S-S bond containing nanovesicle was cut via high endogenous GSH, leading to the continued release of 5-FU and NLG919, thereby enabling circulating chemoimmunotherapy to effectively cause tumor ablation. Moreover, the combination of ENP919@5-FU and PD-L1 antibody (αPD-L1) showed a synergistic anti-tumor effect on the PDAC model with abdominal cavity metastasis. Collectively, ENP919@5-FU nanovesicle, as a PDAC treatment strategy, showed excellent antitumor efficacy by remodeling tumor microenvironment to circulate tumor chemoimmunotherapy amplification, which has promising potential in a precision medicine approach.
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Carcinoma Ductal Pancreático , Fluorouracilo , Inmunoterapia , Microambiente Tumoral , Microambiente Tumoral/efectos de los fármacos , Animales , Fluorouracilo/farmacología , Fluorouracilo/uso terapéutico , Ratones , Humanos , Inmunoterapia/métodos , Línea Celular Tumoral , Carcinoma Ductal Pancreático/tratamiento farmacológico , Neoplasias Pancreáticas/tratamiento farmacológico , Metaloproteinasa 2 de la Matriz/metabolismo , Liposomas/química , Quinurenina/metabolismo , Interferón gamma/metabolismo , Indolamina-Pirrol 2,3,-Dioxigenasa/metabolismo , Antineoplásicos/farmacología , Antineoplásicos/uso terapéutico , Antineoplásicos/química , Oxaliplatino/farmacología , Oxaliplatino/uso terapéuticoRESUMEN
BACKGROUND AND STUDY AIMS: Monitoring disease activity in ulcerative colitis (UC) is critical in preventing long-term complications. This study aims to develop a scoring system using non-invasive indicators to predict endoscopic activities for ulcerative colitis (UC) patients. PATIENTS AND METHODS: All enrolled patients with UC admitted to Shanghai Xinhua Hospital between June 2017 and January 2021 were enrolled, and their clinical data were retrospectively collected and a number of serological biomarkers concentrations were analyzed. Patients were categorized into mild and moderate-to-severe disease groups. Univariate and multivariate logistic regression was used to predict moderate-to-severe endoscopic activities, which were then incorporated into a nomogram to establish a prediction scoring model. RESULT: Overall, 231 patients were divided into a mild group (n = 111, 48.0%) and a moderate-to-severe group (n = 120, 52.0%). The following variables were independently associated with the disease severity and were subsequently included into the prediction model: Proteinase 3 antineutrophil cytoplasmic antibody (PR3-ANCA), C-reactive protein (CRP), hemoglobin(Hb), IL-10, stool frequency ≥ 5 times/day and hematochezia. Incorporating these 6 factors, the nomogram showed good discrimination with C-index of 0.819 and reliable calibration. A scoring model was established with the area under the curve 0.818. Moreover, PR3-ANCA and CRP correlated with the duration of hospital stay. CONCLUSION: We developed a predictive model for endoscopic disease activities by using noninvasive factors based on PR3-ANCA, CRP, Hb, IL-10, stool frequency and hematochezia. This prediction model might assist clinicians in managing patients with UC.
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Colitis Ulcerosa , Humanos , Colitis Ulcerosa/diagnóstico , Anticuerpos Anticitoplasma de Neutrófilos , Interleucina-10 , Estudios Retrospectivos , China , Biomarcadores , Proteína C-Reactiva , Hemorragia Gastrointestinal , Índice de Severidad de la EnfermedadRESUMEN
Currently, commercialized infliximab (IFX) has rapidly propelled the clinical treatment of IBD, however, its inherent attributes, such as off-target effects and rapid metabolism, severely limit practical applications. Moreover, high doses injection of IFX can result in IBD treatment failure, which may induce other side effects. In this study, an colon microenvironment-responsive hydrogel (AL/HA hydrogel), consisting of acid-resistant sodium alginate and colon-degraded and targeted hyaluronic acid, was constructed by simple Ca2+/Zn2+ cross-linking. The ion-mediated hydrogel exhibited the protective effect of gastrointestinal tract to avoid early drug leakage, while the inflammation environments showed well-controlled drug release and significant biodegradable behaviors. Additionally, oral hydrogel exhibited long-standing enteritis areas compared with normal mice. Therefore, hydrogel-assisted enteritis treatment has great potential in IBD as an oral agent. After that, IFX was packaged in hydrogel to fabricate a facile oral antibody delivery system to treat IBD. IFX-embedded hydrogel showed remarkable therapeutic effect on IBD compared with free IFX. Surprisingly, oral hydrogel below 7 times IFX achieve the same amount of IFX-infused treatment that will further help alleviate the drawbacks of IFX. Our work elaborated on the efficacy of oral AL/HA@IFX in IBD, providing a guarantee for the future of promoted clinical transformation.
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Colitis Ulcerosa , Colitis , Enteritis , Enfermedades Inflamatorias del Intestino , Animales , Ratones , Infliximab/uso terapéutico , Ácido Hialurónico/uso terapéutico , Fármacos Gastrointestinales/farmacología , Hidrogeles/uso terapéutico , Colitis/tratamiento farmacológico , Enfermedades Inflamatorias del Intestino/tratamiento farmacológico , Enteritis/tratamiento farmacológico , Colitis Ulcerosa/tratamiento farmacológicoRESUMEN
BACKGROUND: Large or transmural defects induced by gastrointestinal endoscopic manipulations are difficult to close, although complete closure is recommended for better recovery. Endoscopic purse-string assisted suturing (EPSS) has been used in clinical practice and has proven to be an effective and safe technique for the closure of large mucosal defects. However, details regarding the efficacy of endoscopic pre-purse-string suture (P-EPSS) are unknown, especially that it offers several advantages over conventional EPSS (C-EPSS). AIM: To elucidate the outcomes of EPSS-assisted closure in different clinical situations, and evaluate the efficacy of P-EPSS. METHODS: This retrospective observational study included a total of 180 patients who underwent closure assisted by P-EPSS (n = 63) or C-EPSS (n = 117) between July 2014 and June 2020. The P-EPSS and C-EPSS groups were compared and the intergroup differences in aspects such as the lesion size, location, and mor-phology, incidence of complete closure, intraoperative perforation, and delayed adverse events were evaluated. Data on the features and clinical course of cases with adverse events were collected for further analysis. RESULTS: Patients with lesion size larger than 3 cm, lesions located at the fundus of stomach, or submucosal tumors originating from the deep mucosa were more likely to undergo P-EPSS-assisted closure. The P-EPSS group showed a sign-ificantly higher proportion of intraoperative perforation (56% vs 17%) and a much shorter procedure time (9.06 ± 6.14 min vs 14.84 ± 7.25 min). Among adverse events, the incidence of delayed perforation (5% vs 4%; P = 0.82) and delayed bleeding (3% vs 4%; P = 0.96) did not differ significantly between the groups. Multivariate analysis revealed that lesions with incomplete closure [odds ratio (OR) = 21.33; 95% confidence interval (CI): 5.45-83.45; P < 0.01] or size greater than 3 cm (OR = 3.14; 95%CI: 1.08-9.18; P = 0.039) showed a statistical tendency to result in an increase in delayed adverse events. CONCLUSION: The present study revealed that EPSS could achieve secure complete closure of mucosal defect. P-EPSS could shorten the procedure and yield complete closure of mucosal defects. Rather than closure-type selection, incomplete closure or lesion size larger than 3 cm were associated with worse outcomes.
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Resección Endoscópica de la Mucosa , Gastroscopía , Humanos , Estudios de Factibilidad , Gastroscopía/efectos adversos , Técnicas de Sutura/efectos adversos , Resección Endoscópica de la Mucosa/efectos adversos , Resección Endoscópica de la Mucosa/métodos , Mucosa Intestinal/diagnóstico por imagen , Mucosa Intestinal/cirugía , Suturas/efectos adversos , Estudios Retrospectivos , Resultado del TratamientoRESUMEN
The low immunogenicity, insufficient infiltration of T lymphocytes, and dismal response to immune checkpoint blockade therapy pose major difficulties in immunotherapy of pancreatic cancer. Photoimmunotherapy by photodynamic therapy (PDT) can induce an antitumor immune response by triggering immunogenic cell death in the tumor cells. Notwithstanding, PDT-driven oxygen consumption and microvascular damage can further aggravate hypoxia to exaggerates glycolysis, leading to lactate accumulation and immunosuppressive tumor microenvironment. Herein, a supramolecular prodrug nanoplatform codelivering a photosensitizer and a prodrug of bromodomain-containing protein 4 inhibitor (BRD4i) JQ1 for combinatory photoimmunotherapy of pancreatic cancer are demonstrated. The nanoparticles are fabricated by host-guest complexation between cyclodextrin-grafted hyaluronic acid (HA-CD) and adamantine-conjugated heterodimers of pyropheophorbide a (PPa) and JQ1, respectively. HA can achieve active tumor targeting by recognizing highly expressed CD44 on the surface of pancreatic tumors. PPa-mediated PDT can enhance the immunogenicity of the tumor cells and promote intratumoral infiltration of the cytotoxic T lymphocytes. Meanwhile, JQ1 combats PDT-mediated immune evasion through inhibiting expression of c-Myc and PD-L1, which are key regulators of tumor glycolysis and immune evasion. Collectively, this study presents a novel strategy to enhance photoimmunotherapy of the pancreatic cancer by provoking T cells activation and overcoming adaptive immune resistance.
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BACKGROUND: Inflammatory bowel disease (IBD) is a self-destructive intestinal disease whose etiology is unclear but complex and the effective treatment is deficient. Increasing evidences have indicated that immune dysfunction and epithelial-mesenchymal transition (EMT)-related intestinal mucosal barrier impaired hold critical position in the pathogenesis of IBD. Artemisinin (ART) is a sesquiterpenoid compound extracted from Chinese herbal medicine which has good immunomodulatory effects. Studies have shown that artemisinin and its analogues have therapeutic effects on a variety of tumors and immune-related disorders. The purpose of current study was to research the effect and mechanism about artemisinin-induced macrophage polarization to M2 phenotype and inhibiting the process of EMT. METHODS: In vitro, the anti-inflammatory effect of artemisinin is mainly verified by RAW264.7 cells and tissue (colon tissue and PBMC) from CD patients with active intestinal inflammation. RAW264.7 cells stimulated with LPS to induce inflammatory state and ART were used as therapeutic treatment in different concentration. Then the expression levels of pro-inflammatory factors, macrophage polarization and ERK pathway were analyzed. Colon tissue and PBMC from CD patients were treated with ART in different concentrations and macrophage polarization, pro-inflammatory factors expression, EMT-related protein were analyzed. In vivo, DSS-induced colitis mice were treated by ART for seven days. The DAI score was calculated and the colons and spleens were harvested after the animals were sacrificed. The expression of macrophage markers and EMT-related markers in the intestines of mice in each group were monitored by qPCR and western blot. RESULT: ART treatment could decrease the levels of pro-inflammatory coefficient expressed in theRAW264.7 cells and human PBMC. Moreover, ART could ameliorate the intestinal inflammation in vivo through down-regulating the expression of pro-inflammatory factors, promoting macrophage polarization to M2 phenotype and inhibiting the process of EMT. CONCLUSION: Taken together, our findings demonstrated that artemisinin might ameliorate inflammation by inducing macrophage polarization to M2 phenotype and inhibiting the process of EMT, suggesting that ART may be applied to the rehabilitation of IBD in the future.
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Antiinflamatorios/farmacología , Artemisininas/farmacología , Colitis/prevención & control , Colon/efectos de los fármacos , Enfermedad de Crohn/tratamiento farmacológico , Citocinas/metabolismo , Transición Epitelial-Mesenquimal/efectos de los fármacos , Mediadores de Inflamación/metabolismo , Macrófagos/efectos de los fármacos , Animales , Colitis/inducido químicamente , Colitis/metabolismo , Colitis/patología , Colon/metabolismo , Colon/patología , Enfermedad de Crohn/metabolismo , Enfermedad de Crohn/patología , Sulfato de Dextran , Modelos Animales de Enfermedad , Femenino , Humanos , Macrófagos/metabolismo , Ratones , Ratones Endogámicos C57BL , Fenotipo , Células RAW 264.7 , Transducción de Señal , Técnicas de Cultivo de TejidosRESUMEN
BACKGROUND: Immunotherapy targeting programmed death-1 (PD-1) or programmed death-ligand-1 (PD-L1) has been shown to be effective in a variety of malignancies but has poor efficacy in pancreatic ductal adenocarcinoma (PDAC). Studies have shown that PD-L1 expression in tumors is an important indicator of the efficacy of immunotherapy. Tumor cells usually evade chemotherapy and host immune surveillance by epigenetic changes. Protein arginine methylation is a common posttranslational modification. Protein arginine methyltransferase (PRMT) 1 is deregulated in a wide variety of cancer types, whose biological role in tumor immunity is undefined. AIM: To investigate the combined effects and underlying mechanisms of anti-PD-L1 and type I PRMT inhibitor in pancreatic cancer in vivo. METHODS: PT1001B is a novel type I PRMT inhibitor with strong activity and good selectivity. A mouse model of subcutaneous Panc02-derived tumors was used to evaluate drug efficacy, toxic and side effects, and tumor growth in vivo. By flow cytometry, we determined the expression of key immune checkpoint proteins, detected the apoptosis in tumor tissues, and analyzed the immune cells. Immunohistochemistry staining for cellular proliferation-associated nuclear protein Ki67, TUNEL assay, and PRMT1/PD-L1 immunofluorescence were used to elucidate the underlying molecular mechanism of the antitumor effect. RESULTS: Cultured Panc02 cells did not express PD-L1 in vitro, but tumor cells derived from Panc02 transplanted tumors expressed PD-L1. The therapeutic efficacy of anti-PD-L1 mAb was significantly enhanced by the addition of PT1001B as measured by tumor volume (1054.00 ± 61.37 mm3 vs 555.80 ± 74.42 mm3, P < 0.01) and tumor weight (0.83 ± 0.06 g vs 0.38 ± 0.02 g, P < 0.05). PT1001B improved antitumor immunity by inhibiting PD-L1 expression on tumor cells (32.74% ± 5.89% vs 17.95% ± 1.92%, P < 0.05). The combination therapy upregulated tumor-infiltrating CD8+ T lymphocytes (23.75% ± 3.20% vs 73.34% ± 4.35%, P < 0.01) and decreased PD-1+ leukocytes (35.77% ± 3.30% vs 6.48% ± 1.08%, P < 0.001) in tumor tissue compared to the control. In addition, PT1001B amplified the inhibitory effect of anti-PD-L1 on tumor cell proliferation and enhanced the induction of tumor cell apoptosis. PRMT1 downregulation was correlated with PD-L1 downregulation. CONCLUSION: PT1001B enhances antitumor immunity and combining it with anti-PD-L1 checkpoint inhibitors provides a potential strategy to overcome anti-PD-L1 resistance in PDAC.
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Antígeno B7-H1 , Neoplasias Pancreáticas , Proteína-Arginina N-Metiltransferasas , Animales , Antígeno B7-H1/antagonistas & inhibidores , Ratones , Ratones Endogámicos C57BL , Neoplasias Pancreáticas/tratamiento farmacológico , Proteína-Arginina N-Metiltransferasas/antagonistas & inhibidoresRESUMEN
On the basis of fluorescent resonance energy transfer, a new fluorophore dyad (L) bearing rhodamine B and naphthalimide was developed as fluorescent ratiometric chemosensor for Hg(2+) in aqueous solution. L exhibited high selectivity and excellent sensitivity towards Hg(2+) with a broad pH span (1.0-8.0) and the detection limit of L was 2.11×10(-8) M. Sensor L for the detection of Hg(2+) was rapid and the recognizing event could complete in 2.5 min. A significant change in the color could be used for naked-eye detection. The selective fluorescence response of L to Hg(2+) is due to the Hg(2+)-promoted ring opening of spirolactam of rhodamine moiety, leading to a cyclization reaction of thiourea moiety. In addition, fluorescence imaging experiments of Hg(2+) in living EC 109 cells demonstrated its value of practical applications in biological systems.