A hidden demethylation pathway removes mercury from rice plants and mitigates mercury flux to food chains.

Dietary exposure to methylmercury (MeHg) causes irreversible damage to human cognition and is mitigated by photolysis and microbial demethylation of MeHg. Rice (Oryza sativa L.) has been identified as a major dietary source of MeHg. However, it remains unknown what drives the process within plants for MeHg to make its way from soils to rice and the subsequent human dietary exposure to Hg. Here we report a hidden pathway of MeHg demethylation independent of light and microorganisms in rice plants. This natural pathway is driven by reactive oxygen species generated in vivo, rapidly transforming MeHg to inorganic Hg and then eliminating Hg from plants as gaseous Hg°. MeHg concentrations in rice grains would increase by 2.4- to 4.7-fold without this pathway, which equates to intelligence quotient losses of 0.01-0.51 points per newborn in major rice-consuming countries, corresponding to annual economic losses of US$30.7-84.2 billion globally. This discovered pathway effectively removes Hg from human food webs, playing an important role in exposure mitigation and global Hg cycling.

New insights into HgSe antagonism: Minor impact on inorganic Hg mobility while potential impacts on microorganisms.

Selenium (Se) is a crucial antagonistic factor of mercury (Hg) methylation in soil, with the transformation of inorganic Hg (IHg) to inert mercury selenide (HgSe) being the key mechanism. However, little evidence has been provided of the reduced Hg mobility at environmentally relevant doses of Hg and Se, and the potential impacts of Se on the activities of microbial methylators have been largely ignored. This knowledge gap hinders effective mitigation for methylmercury (MeHg) risks, considering that Hg supply and microbial methylators serve as materials and workers for MeHg production in soils. By monitoring the mobility of IHg and microbial activities after Se spike, we reported that 1) active methylation might be the premise of HgSe antagonism, as higher decreases in MeHg net production were found in soils with higher constants of Hg methylation rate; 2) IHg mobility did not significantly change upon Se addition in soils with high DOC concentrations, challenging the long-held view of Hg immobilization by Se; and 3) the activities of iron-reducing bacteria (FeRB), an important group of microbial methylators, might be potentially regulated by Se addition at a dose of 4 mg/kg. These findings provide empirical evidence that IHg mobility may not be the limiting factor under Se amendment and suggest the potential impacts of Se on microbial activities.

Demystify esophageal submucosal tumor: angiomas.

A 51-year-old man presented to the gastroenterology department with a history of abdominal discomfort. Computed tomography was unremarkable. Upper gastrointestinal endoscopy showed a submucosal mass lesion at the esophagus, with a 36cm distance from the incisors. The esophageal submucosal mass lesion with mixed echo was confirmed by endoscopic ultrasound (EUS). Endoscopic submucosal dissection (ESD) was performed, and the mass lesion was resected in a whole piece. Histopathological examination showed lymphatic and blood vessels, which demonstrated an esophageal vascular tumor. Further immunohistochemistry revealed tumor cells that stained positive for CD34 and D2-40.

Identification of Key Genes and FUNCTIONAL Pathway in Radioresistance of Non-Small Cell Lung Cancer.

Purpose: For better understanding of radiotherapy resistance and its potential mechanism. Methods: We established radioresistance cell lines of non-small cell lung cancer (NSCLC) followed by microarray analysis. 529 differentially expressed genes (DEGs) were then screened between radiation resistant cell lines compared with the sensitive cell lines. The biological functions and enrichment pathways of the above DEGs were identified using Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) enrichment analyses. Gene Set Enrichment Analysis (GSEA) revealed that the radiation resistance group had the most gene sets enriched in altered immune response, such as TNF signaling pathway, when compared to the radiation sensitive group. Protein-protein interaction (PPI) network was carried out through the STRING database, and then five hub genes (CXCL10, IFIH1, DDX58, CXCL11, RSAD2) were screened by Cytoscape software. RT-PCR confirmed the expression of the above hub genes. ChIP-X Enrichment Analysis showed that STAT1 might be the transcription factor of the above hub genes. Considering that PD-L1 could be activated by STAT1 in a variety of tumors and ultimately lead to immune exhaustion, RT-PCR and Western blot verified the expression level of PD-L1. Results: Five hub genes (CXCL10, IFIH1, DDX58, CXCL11, RSAD2) were screened and verified to be highly expressed in radioresistance group, STAT1 might be the transcription factor of the above hub genes. Our study found that the expression level of PD-L1 was increased after radiotherapy resistance. Conclusion: Although immune system activation occurs followed by radiation resistance, we hypothesized that the upregulation of PD-L1 expression caused by STAT1 activation might be one of the mechanisms of radiotherapy resistance.

Mercury transformation processes in nature: Critical knowledge gaps and perspectives for moving forward.

The transformation of mercury (Hg) in the environment plays a vital role in the cycling of Hg and its risk to the ecosystem and human health. Of particular importance are Hg oxidation/reduction and methylation/demethylation processes driven or mediated by the dynamics of light, microorganisms, and organic carbon, among others. Advances in understanding those Hg transformation processes determine our capacity of projecting and mitigating Hg risk. Here, we provide a critical analysis of major knowledge gaps in our understanding of Hg transformation in nature, with perspectives on approaches moving forward. Our analysis focuses on Hg transformation processes in the environment, as well as emerging methodology in exploring these processes. Future avenues for improving the understanding of Hg transformation processes to protect ecosystem and human health are also explored.

Cisplatin Promotes the Efficacy of Immune Checkpoint Inhibitor Therapy by Inducing Ferroptosis and Activating Neutrophils.

The combination of immunotherapy with platinum-based chemotherapy has become the first-line treatment for patients with advanced non-small cell lung cancer (NSCLC) with negative driver gene mutations. However, finding an ideal chemotherapeutic regimen for immunotherapy and exploring the underlying mechanism have noticeably attracted clinicians' attention. In this study, we found that cisplatin induced ferroptosis of tumor cells, followed by N1 neutrophil polarization in the tumor microenvironment, which in turn remodeled the "cold" tumor to a "hot" one through enhancing T-cell infiltration and Th1 differentiation. Based on the important role of tumor ferroptosis in the immune-promoting effect of cisplatin, we noticed that the combination of a ferroptosis activator showed a synergistic effect with chemoimmunotherapy of epidermal growth factor receptor (EGFR)-mutant NSCLC, which would be an effective strategy to overcome immunotherapy resistance in NSCLC patients harboring driver mutations.

Solute Carrier Family 35 Member F2 Regulates Cisplatin Resistance and Promotes Malignant Progression of Pancreatic Cancer by Regulating RNA Binding Motif Protein 14.

We aimed to explore the role of Solute Carrier Family 35 Member F2 (SLC35F2) in pancreatic cancer (PCa) and to further study whether SLC35F2 regulates cisplatin resistance of PCa cells through the modulation of RNA binding motif protein 14 (RBM14) expression. SLC35F2 expression in 60 pairs of PCa tissues and adjacent ones was studied by RT-PCR analysis. Meanwhile, SLC35F2 expression levels in PCa cell lines were also evaluated by qPCR assay. In addition, SLC35F2 knockdown models were constructed in PCa cisplatin-resistant cells. Furthermore, we determined the interaction between SLC35F2 and RBM14 via luciferase assay. The findings of the present study demonstrated that SLC35F2 was significantly upregulated in PCa tissues. High level of SLC35F2 indicated higher incidence of metastasis and shorter survival rates. In vitro cell experiments revealed that knockdown of SLC35F2 suppressed cell invasion and metastasis capacity of cisplatin-resistant PCa cell lines PANC-1/DDP and CFPAC-1/DDP. It was also suggested that the key protein RBM14 in the SLC35F2 knockdown group was remarkably reduced. SLC35F2 can bind to RBM14 specifically. Overexpression of RBM14 partially reversed the effects of knockdown of SLC35F2 on the development of PCa. SLC35F2 expression in PCa tissues and cell lines is remarkably increased. In addition, it was also suggested that SLC35F2 may regulate cisplatin resistance of PCa cells through modulating RBM14 expression. In conclusion, it is conceivable from the study that SLC35F2 was remarkably upregulated in PCa and promoted the malignancy of PCa via regulating RBM14.

ASPM facilitates colorectal cancer cells migration and invasion by enhancing ß-catenin expression and nuclear translocation.

Increased abnormal spindle-like microcephaly (ASPM) expression has been linked to clinical stage and poor prognosis in cancers, but the molecular mechanisms by which ASPM promotes cell metastasis in colorectal cancer (CRC) has not been identified. This study showed that the abilities of cell migration, invasion, and epithelial-mesenchymal transition (EMT) were attenuated in ASPM-deficient CRC cell lines. Furthermore, we reported that attenuation of ASPM expression inhibited CRC cell metastasis in vivo. Additionally, the expression of ASPM was positively correlated with ß-catenin level in CRC tissues. Mechanistically, ASPM can upregulate ß-catenin transcription by stimulating the ß-catenin promoter and enhancing the nuclear translocation of ß-catenin in CRC cells, which leads to the activation of the Wnt/ß-catenin pathway. Finally, we showed that ASPM effectively induced CRC cell migration and invasion in a ß-catenin-dependent manner.

Clinical study of submucosal tunneling endoscopic resection and endoscopic submucosal dissection in the treatment of submucosal tumor originating from the muscularis propria layer of the esophagus.

Herein, we aimed to evaluate the clinical value and safety of transendoscopic submucosal tunnel tumor resection (STER) and endoscopic submucosal dissection (ESD) for the resection of esophageal submucosal intrinsic muscle tumors. We retrospectively analyzed the clinical data of 68 patients with esophageal submucosal intrinsic muscle tumors treated with STER (STER group, n = 38, March 2018 to January 2020) or ESD (ESD group, n = 30, January 2017 to January 2020) at the First People's Hospital of Lianyungang to compare the treatment efficacy, hospitalization time and costs, and postoperative complications between the 2 groups. All 68 cases were of single lesions. The mean operative duration was shorter in the STER group (53.39 ±â€…11.57 min) than in the ESD group (68.33 ±â€…18.52 min, P < .05). The postoperative hospital stay duration was significantly shorter in the STER group (5.86 ±â€…1.01 days; P < .05) than in the ESD group (8.2 ±â€…3.4 days, P < .05). The mean hospitalization cost was significantly lower in the STER group than in the ESD group (12,468.8 + 4966.8 yuan vs 17,033.3 ±â€…4547.2 yuan; P < .05). Only 1 case of intraoperative perforation occurred in ESD group. There were no other complications in both groups. The wound healed in both groups, and no residual or recurrent tumors were detected during the follow-up period. Both STER and ESD can be used for the treatment of esophageal intrinsic muscular layer (MP) tumors, and STER is safer and more efficient for lesions with a diameter <3.5 cm.

Mechanism of methyltransferase like 3 in epithelial-mesenchymal transition process, invasion, and metastasis in esophageal cancer.

Methyltransferase like 3 (METTL3) has been identified to serve as a definitive inducer in cancer progression. This study sought to analyze the regulatory mechanism of METTL3 in epithelial-mesenchymal transition (EMT), invasion, and metastasis in esophageal cancer (ESCA). The METTL3 expressions in cancer tissues and cells were detected with extensive analysis of its correlation with clinical baseline data. The cells were transfected with sh-RNA-METTL3 and microRNA (miR)-20a-5p mimic, followed by evaluation of invasion, migration, and EMT. The N6-methyladenosine (m6A) level and enrichment of DiGeorge Critical Region 8 (DGCR8) and m6A were observed. The binding relationship between miR-20a-5p and Nuclear Factor I-C (NFIC) was verified, followed by Pearson correlation analysis. A subcutaneous tumor formation assay was conducted prior to observation of lung metastases. Our results revealed that METTL3 was highly expressed in ESCA patients and associated with severe lymph node involvement and distant metastasis. METTL3 downregulation radically inhibited the invasiveness, migration, and EMT. METTL3 elevated the miR-20a-5p expression via improving m6A modification. METTL3 inhibition downregulated the miR-20a-5p expression. Moreover, miR-20a-5p upregulation facilitated ESCA cell invasiveness and migration by targeting NFIC transcription. METTL3 inhibition suppressed tumor growth and lung metastasis in vivo. Overall, METTL3 promoted m6A modification and the binding of DGCR8 to miR-20a-5p to further elevate the miR-20a-5p expression and inhibit NFIC transcription, thus promoting EMT, invasion and migration.

MiR-200b Suppresses Gastric Cancer Cell Migration and Invasion by Inhibiting NRG1 through ERBB2/ERBB3 Signaling.

PURPOSE: Accumulating evidence indicates that miRNAs (miRs) play crucial roles in the modulation of tumors development. However, the accurately mechanisms have not been entirely clarified. In this study, we aimed to explore the role of miR-200b in the development of gastric cancer (GC). METHODS: Western blot and RT-PCR were applied to detect epithelial-mesenchymal transition (EMT) marker expression and mRNA expression. Transwell assay was used for measuring the metastasis and invasiveness of GC cells. TargetScan system, luciferase reporter assay, and rescue experiments were applied for validating the direct target of miR-200b. RESULTS: MiR-200b was prominently decreased in GC tissues and cells, and its downregulation was an indicator of poor prognosis of GC patients. Reexpression of miR-200b suppressed EMT along with GC cell migration and invasion. Neuregulin 1 (NRG1) was validated as the target of miR-200b, and it rescued miR-200b inhibitory effect on GC progression. In GC tissues, the correlation of miR-200b with NRG1 was inverse. CONCLUSION: MiR-200b suppressed EMT-related migration and invasion of GC through the ERBB2/ERBB3 signaling pathway via targeting NRG1.

Total mercury and methylmercury in human hair and food: Implications for the exposure and health risk to residents in the Three Gorges Reservoir Region, China.

Three Gorges Dam (TGD) is the largest hydroelectric construction in the world, and its potential impacts on the ecological environment and human health risks have invoked considerable global concern. However, as a mercury (Hg) sensitive system, limited work was conducted on the Hg exposure level of local residents around the Three Gorges Reservoir (TGR). Thus, 540 human hair samples and 22 species of local food samples were collected to assess the Hg exposure and human health risk to the residents located in the Three Gorges Reservoir Region (TGRR) and to investigate their dietary exposure to Hg. The results showed that the geometric mean concentrations of total mercury (THg) and methylmercury (MeHg) in hair were 0.42 ± 0.43 µg g-1 and 0.23 ± 0.32 µg g-1, respectively, lower than the reference level (1.0 µg g-1) recommended by the United States Environmental Protection Agency (US EPA), indicating a low level Hg exposure for residents around the TGR. No significant difference in the accumulation of Hg in hair between the gender subgroups was observed, whereas age difference, smoking and alcohol drinking behavior, and fish consumption frequency were significant predictors of hair Hg level. Besides, THg and MeHg of all the investigated food samples did not exceed the corresponding Chinese national standard. The average probable daily intakes (PDIs) of THg and MeHg were 0.032 µg kg-1 day-1 and 0.007 µg kg-1 day-1, which were obviously below the recommended values of 0.57 µg kg-1 day-1 and 0.1 µg kg-1 day-1, respectively. The cereal (mainly rice) contribution of THg (76.0%) and MeHg (74.4%) intakes to the local residents around the TGR was much higher than that of fish (10.7% and 22.9%, respectively) due to the considerable rice consumption. Overall, residents around the TGR were at a low Hg exposure and rice consumption was the major pathway for Hg exposure.

LINC00662 promotes cell viability and metastasis in esophageal squamous cell carcinoma by sponging miR-340-5p and upregulating HOXB2.

BACKGROUND: Previous studies have shown that lncRNA LINC00662 plays an important role in pathogenesis of malignancies. The purpose of this study was to elucidate the regulatory mechanism of LINC00662 in esophageal squamous cell carcinoma (ESCC). METHODS: In this study, the regulatory mechanism of LINC00662 was investigated by RT-qPCR. MTT, transwell and dual luciferase reporter assays. RESULTS: Upregulation of LINC00662 was found in ESCC and associated with worse clinical outcomes in ESCC patients. More importantly, knockdown of LINC00662 restrained cell proliferation, migration and invasion in ESCC. In addition, LINC00662 acts as a molecular sponge for miR-340-5p in ESCC, and miR-340-5p directly targets HOXB2. HOXB2 expression can be positively regulated by LINC00662 in ESCC. Furthermore, HOXB2 downregulation or miR-340-5p overexpression weakened the carcinogenesis of LINC00662 in ESCC. CONCLUSIONS: LncRNA LINC00662 promotes the progression of ESCC by upregulating HOXB2 by sponging miR-340-5p.

Combination of PD-L1 expression and NLR as prognostic marker in patients with surgically resected non-small cell lung cancer.

Background: In recent years, great improvement has been made in immunotherapies for non-small cell lung cancer (NSCLC). Current data have suggested that Programmed cell death ligand 1 (PD-L1) expression might not be an ideal marker for patient selection in isolation. Evidence has been increasing that alternative markers, such as neutrophil-to-lymphocyte ratio (NLR), a biomarker of systemic inflammation response (SIR) previously associated with outcomes in a variety of cancers including NSCLC, might be a predictor for patient selection and the response to therapy. No reports have examined the prognostic value of combination of PD-L1 expression and inflammatory markers such as NLR in NSCLC. This retrospective study explores the relationship between NLR and PD-L1 expression in NSCLC as well as the prognostic value of combination of PD-L1 expression and NLR. Method: We evaluated tumor PD-L1 expression in 235 surgically resected NSCLC cases by immunohistochemical analysis. Carcinoma cells showing membranous staining for PD-L1 were considered PD-L1-positive cells (Figure 1). Cases with ≥1% tumor membrane staining were considered PD-L1-positive. The association of clinicopathological characteristics with PD-L1 expression was assessed by univariate and multivariate analyses. Moreover, univariate and multivariate analyses were performed to evaluate the predictive impact of PD-L1 expression and other factors on disease-free survival (DFS) and overall survival (OS). Result: PD-L1 protein expression was elevated in 34.0% of patients at cut-off value of 1%. Univariate analyses showed that PD-L1 expression was significantly higher in men (χ2 =5.226, P=0.030), heavy smokers (χ2 =18.650, P<0.001), and patients with squamous cell carcinoma (χ2 =4.036, P=0.045). No correlations were noted between PD-L1 expression and age, EGFR mutation status or clinical stage. No significant correlations between PD-L1 protein expression and NLR were found. Multivariate logistic regression revealed that smoking index ≥400 was independent predictor of PD-L1 expression (odds ratio [OR], 3.375; P < 0.001). The results of univariate survival analyses showed that clinical stage (log-rank χ2 =7.876, P=0.019) was associated with DFS. Smoking index (log-rank χ2 =4.832, P=0.028), clinical stage (log-rank χ2 =7.582, P=0.023) and adjuvant treatment (log-rank χ2 =5.440, P=0.020) were significantly associated with OS. Neither PD-L1 expression nor NLR was found to be associated with DFS or OS. Of interest, when patients were divided in two groups according to combined PD-L1/NLR: patients with PD-L1+/ high NLR as Group 1, other patients as Group 2, Group 1 had significantly shorter DFS as well as OS than Group 2 (DFS: log-rank χ2 =5.231, P=0.022, Figure 2A; OS: log-rank χ2 =4.742, P=0.029, Figure 2B). In the multivariate analysis, Cox proportional hazards regression models showed that, PD-L1+/ high NLR was associated with a significantly shorter DFS and OS (hazard ratio [HR], 1.394, P=0.040; HR, 1.442, P=0.042, respectively). Stratified analysis showed that the prognostic value of combined PD-L1/NLR can only be observed in cases without epidermal growth factor receptor (EGFR) mutations (DFS: log-rank χ2 =5.593, P=0.018, Figure 2C, OS: log-rank χ2 =9.323, P=0.002, Figure 2D). In EGFR mutation subgroup, combination of PD-L1 expression and NLR has no relationship with DFS or OS. Conclusion: We found that combination of PD-L1 expression and NLR may be a promising prognostic indicator, and may also be a good marker for tumor recurrence, especially in the patients with wild-type EGFR.

Neuron-Specific Enolase Is an Independent Prognostic Factor in Resected Lung Adenocarcinoma Patients with Anaplastic Lymphoma Kinase Gene Rearrangements.

BACKGROUND An extensive body of research reveals the clinical value of serum tumor markers in lung cancer patients, including carcinoembryonic antigen (CEA), squamous cell carcinoma antigen (SCCA), cytokeratin-19 fragments (Cyfra21-1), and neuron-specific enolase (NSE), but little is known about the clinical properties of these serum tumor markers in anaplastic lymphoma kinase (ALK)-positive lung cancer patients. MATERIAL AND METHODS We retrospectively analyzed 54 patients harboring ALK rearrangements and 520 patients without ALK rearrangements, and all these patients were treated exclusively by surgery between 2011 and 2016. RESULTS NSE level (P=0.007 for OS) was identified as an independent prognostic factor among patients with resected ALK-positive adenocarcinoma of the lung. CONCLUSIONS A high level of NSE is associated with worse outcome among resected lung adenocarcinoma patients harboring ALK rearrangements.

PIM1 kinase promotes cell proliferation, metastasis and tumor growth of lung adenocarcinoma by potentiating the c-MET signaling pathway.

The proto-oncogene PIM1 plays essential roles in proliferation, survival, metastasis and drug resistance in hematopoietic and solid tumors. Although PIM1 has been shown to be associated with lymph node metastasis and poor prognosis in non-small cell lung cancer, its underlying molecular mechanisms in this context are still unclear. Here we show that PIM1 is frequently overexpressed in lung adenocarcinomas, and its expression level is associated with c-MET expression and poor clinical outcome. We further demonstrate that PIM1 may regulate c-MET expression via phosphorylation of eukaryotic translation initiation factor 4B (eIF4B) on S406. Depletion of PIM1 decreased cell proliferation, migration, invasion and colony formation in vitro, as well as reduced tumor growth in vivo. And these effects were partially abrogated by restoring of c-MET expression. Our study implicates a promising therapeutic approach in lung adenocarcinoma patients with PIM1 and c-MET overexpression.

PD-L1 is a Prognostic Biomarker in Resected NSCLC Patients with Moderate/high Smoking History and Elevated Serum SCCA Level.

Programmed cell death-1 (PD-1) -targeted immunotherapy has become a promising treatment paradigm for patients with advanced non-small cell lung cancer (NSCLC). Clinical responses to checkpoint inhibition therapy in NSCLC have been associated with programmed death-1 ligand 1 (PD-L1) expression. However, the association between the expression of PD-L1 and PD-L2 and the clinicopathological features and patient outcomes in NSCLC remain unclear. We retrospectively analyzed 364 patients (158 squamous cell carcinoma and 206 adenocarcinoma) who underwent complete resection between 2009 and 2012. Expression of PD-L1 and PD-L2 was determined by immunohistochemistry. Correlations between PD-L1/PD-L2 expression and the clinicopathological features and survival parameters were analyzed and prognostic factors were identified. PD-L1 expression was significantly associated with moderate/heavy smoking history and serum squamous cell carcinoma antigen (SCCA) levels. Multivariate analysis showed patients with high PD-L1 expression had significantly shorter disease free survival (DFS, HR 1.411, P = 0.025) and overall survival (OS, HR 1.659, P = 0.004) than those with low PD-L1 expression at a 50% cutoff value. No significant association was found between PD-L2 expression and patient postoperative survival. Further stratification analysis revealed that in patients with moderate/heavy smoking history, elevated serum SCCA level, and squamous cell carcinoma, PD-L1 expression was associated with significantly shorter DFS and OS. Therefore, PD-L1 expression was correlated with moderate/heavy smoking history and elevated serum SCCA level in NSCLC patients, and was an independently poor predictor of survival.

Mechanism of Biological Compatibility of Water-Soluble Yb3+, Er3+ Codoped NaYF4 Nanoparticles.

Water soluble NaYF4 nanocrystals codoped with 20 mol% Yb3+, 2 mol% Er3+ were prepared by a facile solvothermal approach using polyvinylpyrrolidone (PVP) as a surfactant. As a potential material for luminescent probes, in votroeffects of upconversion nanoparticles (UCNPs) on human aenocarcinoma (SGC-7901) cells with different concentrations were observed. These effects range from cell viability, mitochondrial membrane potential (MMP), reactive oxygen species (ROS) production, AnnexinV-FITC-propidium iodide (PI) apoptosis detection, and cell cycles. Our results demonstrated that the cells treated with UCNPs showed a decrease in cell viability accompanied the decreased MMP and the release of ROS. When treated with 400 µg/mL UCNPs, AnnexinV-FITC-PI apoptosis detection showed the UCNPs induced apoptosis, the cell cycle indicated the UCNPs suppressor cells in the G1 phase obviously, thereby reducing cell activity.

Giant cystic lymphangioma originating from the cardia of the stomach: A case report.

Cystic lymphangiomas are rare benign tumors involving the neck, head, and axilla, and most frequently occur in children before the age of 5 years. In the present study, the case of a giant cystic lymphangioma originating in the cardia of the stomach was reported in an 18-year-old female complaining of abdominal distention. Contrast-enhanced computed tomography and endoscopic ultrasonography revealed a large, multilobulated cystic mass located between the cardia and esophagogastric junction with a diameter of 4.0 cm. The lesion was successfully removed by endoscopic submucosal dissection. Subsequent immunohistochemical analysis of the lymphatic endothelium-specific O-linked sialoglycoprotein D2-40 confirmed the diagnosis of cystic lymphangioma. No complications associated with the tumor dissection occurred, and the patient did not report any further complaints or any signs of recurrence at 6- and 18-month follow-up. The present case demonstrates that a diagnosis of cystic lymphangioma should be considered in non-pediatric patients suffering aspecific abdominal complaints.

Organic two-photon nanoparticles modulate reactive oxygen species, intracellular calcium concentration, and mitochondrial membrane potential during apoptosis of human gastric carcinoma SGC-7901 cells.

OBJECTIVES: To investigate the biocompatibility of human gastric carcinoma cells (SGC-7901) with organic two-photon nanoparticles (NPs). RESULTS: Different concentrations of NPs were incubated with SGC-7901 cells for different times. The levels of cell apoptosis, reactive oxygen species (ROS), intracellular calcium, and mitochondrial membrane potential (MMP) were measured by staining the SGC-7901 cells with Annexin V-FITC/PI, 2',7'-dichlorofluorescin diacetate, Fluo-3 AM, and Rhodamine 123, followed by the flow cytometry assay. NPs at <4 µg/ml, did not have any significant effect on apoptosis, necrosis, generation of ROS, increase of intracellular Ca(2+) concentration or decrease of MMP in SGC-7901 cells, but >4 µg/ml had a major effects on all the above mentioned parameters. CONCLUSION: 2,5,2',5'-Tetra(4-N,N-diphenylamine styryl) biphenyl NPs can be used at an appropriate concentration as a safe drug carrier or imaging marker and may serve as an effective tool for developing a photodynamic cancer therapy.