Water quality characteristics and ecological risk evaluation of a landscaped river replenished by three reclaimed water sources in Qingdao, China.

The water crisis may be solved by utilizing reclaimed water. Three reclaimed water sources have restored the lower sections of the Licun River, forming a landscaped river. In this paper, the river's water quality was monitored for a year, and the ecological concerns were analyzed using luminescent bacteria, chlorella, and zebrafish. The results indicated that although basic water quality indicators like COD and ammonia fluctuated along the river, the classification of water quality was primarily affected by factors such as flow rate and water depth. Under experimental conditions, the toxic inhibitory effect of river water on luminescent bacteria, chlorella, and zebrafish was related to the treatment process of reclaimed water. It was found that the reclaimed water produced by the MBR, along with the UV disinfection process, showed no detectable toxicity. In contrast, the MBBR process, when combined with coagulation, sedimentation, filtration, ozonation, and chlorination, seemed to be the source of this toxicity. Along the river, the results of water quality assessments and ecological risk assessments were different, indicating that both should be conducted to evaluate rivers replenished with reclaimed water.

Heat Shock Protein Inhibitors Show Synergistic Antibacterial Effects with Photodynamic Therapy on Caries-Related Streptococci In Vitro and In Vivo.

Caries are chronic infections in which the cariogenic biofilm plays a critical role in disease occurrence and progression. Photodynamic therapy (PDT) is a new effective treatment that is receiving wide attention in the antibacterial field, but it can lead to the upregulation of heat shock proteins (HSPs), which enhances bacterial resistance. Herein, we incorporated HSP inhibitors with PDT to evaluate the effect on Streptococcus mutans, Streptococcus sobrinus, and Streptococcus sanguinis under planktonic conditions and on cariogenic biofilms. Additionally, a model of caries was established in 2-week-old rats, and anticaries properties were evaluated by Keyes' scoring. Importantly, the combination of HSP inhibitors and PDT had outstanding efficiency in inhibiting the growth of tested Streptococcus strains and the formation of either monomicrobial or multispecies biofilms in vitro. In addition, the quantity of colonized streptococci and the severity of carious lesions were also distinctly suppressed in vivo. Overall, the synergistic application of HSP inhibitors and PDT has promising potential in the prevention and treatment of dental caries. IMPORTANCE Effective therapies for the prevention and control of caries are urgently needed. Cariogenic streptococci play a key role in the occurrence and progression of caries. Recently, photodynamic therapy has been demonstrated to have good antibacterial efficiency, but it can cause a heat shock response in bacteria, which may weaken its practical effects. We indicate here an effective therapeutic strategy of combining heat shock protein inhibitors and photodynamic therapy, which shows excellent inhibition toward three dominant streptococci related to caries and suppression of carious progression in a rat model. Further development for clinical application is promising.

Profiling the oral microbiomes in patients with Alzheimer's disease.

OBJECTIVES: To analyse the characteristics of the oral microbiomes and expected to find biomarkers about Alzheimer's disease (AD). SUBJECTS AND METHODS: AD patients (n = 26) and cognitive intact people (n = 26) were examined for cognition, depression, oral health and collected saliva and gingival crevicular fluid (GCF) in the morning. Full-length 16S rRNA gene was amplified and sequencing was performed using the PacBio platform. RESULTS: The predominant bacterium of salivary microbiome and periodontal microbiome from AD patients was Streptococcus oralis and Porphyromonas gingivalis, respectively. With respect to ß diversity analysis, there was a significance difference in periodontal microbiome between AD patients and cognitively intact subjects. The relative abundance of Veillonella parvula significantly increased in oral microbiomes from AD patients. Interestingly, the dominant species were different between early-onset AD and late-onset AD patients. Moreover, the predominant species were changed as the clinical severity of AD. Furthermore, the correlation analysis revealed that V. parvula was associated with AD in both saliva and GCF and that P. gingivalis was associated with AD only in GCF. CONCLUSIONS: In this study, the microbiome community of oral microbes was altered in AD patients and periodontal microbiome was sensitive to cognition changes. Moreover, V. parvula and P. gingivalis were associated with AD.

Ginsenoside Rb3 inhibits osteoclastogenesis via ERK/NF-κB signaling pathway in vitro and in vivo.

OBJECTIVE: The objective of the study was to determine the anti-osteoclastogenic potential of ginsenoside Rb3 for the treatment of periodontitis. METHODS: The anti-osteoclastogenic effect was determined using RANKL-induced RAW264.7 cells and murine bone marrow-derived macrophages followed by TRAP and phalloidin staining. Expression of osteoclastogenesis-related genes and proteins were examined by qPCR and WB. Activation of signaling pathways was detected by WB and IHC techniques. Experimental periodontitis rat model was built up by gingival injections of P. gingivalis LPS. After 21 days of Rb3 treatment, rats were sacrificed for micro-CT, IHC, H&E, and TRAP staining analyses. RESULTS: Rb3 dramatically inhibits RANKL-induced osteoclastogenesis. Nfatc1, Mmp9, Ctsk, Acp5 mRNA, and MMP9, CTSK proteins were dose-dependently downregulated by Rb3 pretreatment. WB results revealed that Rb3 suppressed activations of p38 MAPK, ERK, and p65 NF-κB, and the inhibition of ERK was most pronounced. Consistently, IHC analysis revealed that p-ERK was highly expressed in alveolar bone surface, blood vessels, odontoblasts, and gingival epithelia, which were notably suppressed by Rb3 treatment. H&E staining and micro-CT analyses showed that Rb3 significantly attenuated gingivitis and alveolar bone resorption in rats. CONCLUSION: Rb3 inhibits RANKL-induced osteoclastogenesis and attenuates P. gingivalis LPS-induced gingivitis and alveolar bone resorption in rats via ERK/NF-κB signaling pathway.

HIV-1 Tat drives the Fabp4/NF-κB feedback loop in microglia to mediate inflammatory response and neuronal apoptosis.

Fatty acid-binding proteins (FABPs) are relevant to multiple neurodegenerative diseases. However, the roles and mechanisms of FABPs in HIV-associated neurocognitive disorder (HAND) remain yet unclear. In this study, cultured BV-2 microglial cells and HT-22 neuronal cells were used for in vitro experiments and HAND mouse models were constructed through intracerebroventricular injection of lentiviral vectors for in vivo experiments. FABP expression was determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot. The interrelationship between Fabp4 and NF-κB signaling was investigated using chromatin immunoprecipitation, qRT-PCR, and Western blot. The role of Fabp4 in regulating inflammatory response was determined using qRT-PCR, enzyme-linked immunosorbent assay, Western blot, and immunofluorescence staining. Cell viability and apoptosis were analyzed using cell counting kit-8 assay and flow cytometry assay, respectively. Our results suggested an upregulation of Fabp4 expression in the presence of Tat. Tat-induced Fabp4 expression was directly regulated by NF-κB p65, followed by, Fabp4 facilitating Tat-activated NF-κB signaling pathway. We also observed that Fabp4 knockdown in microglial cells significantly suppressed inflammatory response and neuronal apoptosis both in vitro and in vivo. In conclusion, the presence of Tat in microglial cells results in Fabp4 and NF-κB to form a positive feedback loop leading to exacerbate inflammatory response and neuronal apoptosis.

Application of Ginsenoside Rd in Periodontitis With Inhibitory Effects on Pathogenicity, Inflammation, and Bone Resorption.

Periodontitis is a worldwide oral disease induced by the interaction of subgingival bacteria and host response and is characterized by local inflammation, bone resorption, and tooth loss. Ginsenoside Rd (Rd) is a biologically active component derived from Panax ginseng and has been demonstrated to exert antibacterial and anti-inflammatory activities. This study aims to investigate the inhibitory efficiency of Rd towards Porphyromonas gingivalis (P. gingivalis), periodontal inflammatory response, and osteoclastogenesis in vitro and to further validate the results in a mouse periodontitis model, thus, evaluate the potential effects of Rd on the control and prevention of periodontitis. According to the results, Rd exerted excellent antibacterial activities against planktonic P. gingivalis, along with attenuating P. gingivalis virulence and inhibiting its biofilms. Meanwhile, the inflammatory cytokine production and osteoclastogenesis were remarkably inhibited by Rd both in vitro and in vivo. Furthermore, Rd efficiently ameliorated the subgingival P. gingivalis abundance and suppressed the alveolar bone resorption in vivo as well. In conclusion, Rd has the potential to be developed as a promising medication in the control and prevention of periodontitis.

Bioresponsive nanotherapy for preventing dental caries by inhibiting multispecies cariogenic biofilms.

Early childhood caries (ECC) is a public healthcare concern that greatly reduces the quality of life of young children. As a leading factor of ECC, cariogenic biofilms are composed of acidogenic/aciduric pathogens and extracellular polysaccharides (EPSs), creating an acidic and protected microenvironment. Antimicrobial photodynamic therapy (aPDT) is a noninvasive, painless, and efficient therapeutic approach that is suitable for treating ECC. However, due to the hyperfine structure of cariogenic biofilms, most photosensitizers (PSs) could not access and penetrate deeply in biofilms, which dramatically hamper their efficiency in the clinic. Herein, bioresponsive nanoparticle loaded with chlorin e6 (MPP-Ce6) is developed, which largely increases the penetration depth (by over 75%) and retention (by over 100%) of PS in the biofilm compared with free Ce6. Furthermore, MPP-Ce6-mediated aPDT not only kills the bacteria in preformed biofilms but also inhibits multispecies biofilm formation. A rampant caries model is established to mimic ECC in vivo, where the population of cariogenic bacteria is decreased to 10% after MPP-Ce6-mediated aPDT. Importantly, the number and severity of carious lesions are efficiently reduced via Keyes' scoring and micro-CT analysis. This simple but effective strategy can serve as a promising approach for daily oral hygiene in preventing ECC.

Sulfuretted hydrogen ameliorates high dose glucose-induced podocyte apoptosis via orchestrating AMPK/mTOR cascade-mediated anti-apoptotic effects.

BACKGROUND: Podocytes play a pivotal role in the glomerular filtration barrier and contribute to proteinuria and glomerulosclerosis through abnormal apoptosis. Longitudinal studies have indicated the protective properties of hydrogen sulfide (H2S) against neuronal cell apoptosis, whereas the biological function and the underlying molecular mechanism on glucose-induced podocyte apoptosis are largely unknown. METHODS: Herein, we conducted multifaceted biological analyses to verify the potential function of H2S in glucose-induced podocyte apoptosis by examining apoptotic proteins and markers (e.g., caspase 3, Hoechst) and antioxidative effects [e.g., reactive oxygen species (ROS), lipid peroxidation, superoxide dismutase (SOD), catalase (CAT)]. Then, we took advantage of transcriptome sequencing and biological analyses to further determine the potential influence of H2S as well as the accompanying molecular mechanism. RESULTS: In this study, we found that glucose-induced podocyte apoptosis could be largely rescued by H2S via antioxidative responses, which was further confirmed by transcriptome sequencing and bioinformatics analyses. According to apoptotic signaling analysis, the over-activated AMPK/mTOR signaling cascade in glucose-treated podocytes was effectively restrained. CONCLUSIONS: For the first time, we indicated the protective effect and mechanism of H2S in podocytes by restricting glucose-induced apoptosis and suppressing the abnormally activated AMPK/mTOR signaling cascade. Our findings provide new references for podocyte apoptosis-associated diseases and also indicate the potential of H2S administration in clinical trials.

Sub-Thick Electrodes with Enhanced Transport Kinetics via In Situ Epitaxial Heterogeneous Interfaces for High Areal-Capacity Lithium Ion Batteries.

The ever-growing portable electronics and electric vehicle draws the attention of scaling up of energy storage systems with high areal-capacity. The concept of thick electrode designs has been used to improve the active mass loading toward achieving high overall energy density. However, the poor rate capabilities of electrode material owing to increasing electrode thickness significantly affect the rapid transportation of ionic and electron diffusion kinetics. Herein, a new concept named "sub-thick electrodes" is successfully introduced to mitigate the Li-ion storage performance of electrodes. This is achieved by using commercial nickel foam (NF) to develop a monolithic 3D with rich in situ heterogeneous interfaces anode (Cu3 P-Ni2 P-NiO, denoted NF-CNNOP) to reinforce the adhesive force of the active materials on NF as well as contribute additional capacity to the electrode. The as-prepared NF-CNNOP electrode displays high reversible and rate areal capacities of 6.81 and 1.50 mAh cm-2 at 0.40 and 6.0 mA cm-2 , respectively. The enhanced Li-ion storage capability is attributed to the in situ interfacial engineering within the NiO, Ni2 P, and Cu3 P and the 3D consecutive electron conductive network. In addition, cyclic voltammetry, charge-discharge curves, and symmetric cell electrochemical impedance spectroscopy consistently reveal improved pseudocapacitance with enhanced transports kinetics in this sub-thick electrodes.

Advanced Tri-Layer Carbon Matrices with π-π Stacking Interaction for Binder-Free Lithium-Ion Storage.

Enabling materials with distinct features toward achieving high-performance energy storage devices is of huge importance but highly challenging. Commercial carbon cloth (CC), because of its appealing chemical and mechanical properties, has been proven to be an excellent conductive substrate for active electrode materials. However, its performance is notably poor when directly used as an electrode in energy storage, due to its low theoretical capacity and surface area. Herein, we successfully endow the CC with enhanced storage capacity via formation of a π-π stacking interaction by integrating electrochemically activated CC (denoted CC/ACC) with biomass-derived carbon (BMDC) (denoted π-CC/ECC@BMDC). The π-CC/ECC@BMDC electrode displays excellent storage performance with a high capacity of 2.53 mAh cm-2 under 0.2 mA cm-2 when used as anode material for lithium ion batteries (LIBs). Due to the induction energy, the negatively charged molecules of the CC/ACC functional groups interact with the BMDC during carbonization, creating the π-π stacking interaction. Based on first-principles calculations, the structural design of the tri-layer carbon enables the movement of electrons around the π-π stacking interaction, which significantly facilitates rapid transportation of electrons, creates three-dimensional (3D) ion tunnels for fast transportation of ions, and improves the electrode's mechanical and electronic properties.

Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS.

Conventional treatments for chronic periodontitis are less effective in controlling inflammation and often relapse. Therefore, it is necessary to explore an immunomodulatory medication as an adjuvant. Ginsenoside Rb3 (Rb3), one of the most abundant active components of ginseng, has been found to possess anti-inflammatory and immunomodulatory properties. Here, we detected the anti-inflammatory effect of Rb3 on Porphyromonas gingivalis LPS-stimulated human periodontal ligament cells and experimental periodontitis rats for the first time. We found that the expression of pro-inflammatory mediators, including IL-1ß, IL-6 and IL-8, upregulated by lipopolysaccharide (LPS) stimulation was remarkably downregulated by Rb3 treatment in a dose-dependent manner at both transcriptional and translational levels. Network pharmacological analysis of Rb3 showed that the mitogen-activated protein kinase (MAPK) signaling pathway had the highest richness and that p38, JNK, and ERK molecules were potential targets of Rb3 in humans. Western blot analysis revealed that Rb3 significantly suppressed the phosphorylation of p38 MAPK and p65 NF-κB, as well as decreased the expression of total AKT. In experimental periodontitis rat models, reductions in alveolar bone resorption and osteoclast generation were observed in the Rb3 treatment group. Thus, we can conclude that Rb3 ameliorated Porphyromonas gingivalis LPS-induced inflammation by inhibiting the MAPK/AKT/NF-κB signaling pathways and attenuated alveolar bone resorption in experimental periodontitis rats.

Pirarubicin-based chemotherapy displayed better clinical outcomes and lower toxicity than did doxorubicin-based chemotherapy in the treatment of non-metastatic extremity osteosarcoma.

Pirarubicin (THP) is a newer generation anthracycline anticancer drug with antineoplastic efficacy against numerous tumors. Few studies have reported its application and efficiency in anti-osteosarcoma chemotherapeutic strategies. Ninety-six non-metastatic extremity osteosarcoma patients treated with THP or doxorubicin (DOX) in combination with high-dose methotrexate (HDMTX), cisplatin (DDP) and ifosfamide (IFO) within the past 9 years at our hospital were evaluated retrospectively to compare efficacy and side effects. Among the patients, 55.2% were male, 36.5% were ≤14 years old and 59.4% presented with a large tumor (≥1/3 of bone) to our department. The 5-year disease-free survival (DFS) rate of the patients treated with the THP-based chemotherapeutic regimen was 70.2%, significantly higher than that of the DOX-based regimen-treated group (53.1%). The THP-based chemotherapeutic regimen decreased the lung metastatic rate significantly compared with the DOX-based regimen (19.1% vs. 36.7%, P=0.045), as well as the relapse rate (31.9% vs. 49.0%, P=0.067). Both regimens were generally well tolerated. However, while the THP-based chemotherapeutic regimen did not alter toxicity in the hematologic system, liver or kidneys compared with the DOX-based regimen, it showed lower rates of alopecia (63.8% vs. 85.7%, P=0.012), nausea and vomiting (51.1% vs. 79.6%, P=0.003), and mucositis (48.9% vs. 75.6%, P=0.003). THP also resulted in lower cardiac toxicity. Our data demonstrate that the THP-based regimen is better than the DOX-based regimen in terms of the 5-year DFS rate, pulmonary metastasis rate, relapse rate and side effects.

Low expression of cyclic AMP response element modulator-1 can increase the migration and invasion of esophageal squamous cell carcinoma.

Cyclic AMP response element-binding protein (CREB) family can regulate biological functions of various types of cells and has relation with esophageal cancer cell migration and invasion. Cyclic AMP response element modulator-1 (CREM-1) is one member of the family with limited acquaintance. This study was conducted to investigate the effect of CREM-1 on migration and invasion in human esophageal squamous cell carcinoma (ESCC). The expression of CREM-1 protein in ESCC tissues with or without lymph nodes metastasis was determined by western blot. Immunohistochemical analysis of CREM-1 expression were carried out in paraffin-embedded sections of ESCC and correlated with clinical features. The roles of CREM-1 in migration and invasion were studied in TE1 cells through knocking CREM-1 down with siRNA or overexpression of CREM-1 in ECA109 cells. The regulations of CREM-1 on invasion and migration were determined by transwell and wounding healing assay. The effect of CREM-1 on chemotherapy drug was analyzed by Cell counting kit-8 assay. We found that the expression of CREM-1 was significantly downregulated in ESCC tissues with lymph nodes metastasis compared with the tissues without lymph nodes metastasis and was correlated with the clinical features of pathological grade, tumor stage and lymph node metastasis. Moreover, knocking CREM-1 down with siRNA increased cell migration and invasion in human ESCC cell lines TE1 while upregulation of CREM-1 inhibited the motility. Our data suggested that CREM-1 might play an important role in the regulation of tumor metastasis and invasion and serve as a tumor suppressor in human ESCC. We proposed that CREM-1 might be used as a potential therapeutic agent for human ESCC.

CpG island methylator phenotype and Helicobacter pylori infection associated with gastric cancer.

AIM: To investigate the association between the CpG island methylator phenotype (CIMP) and serum Helicobacter pylori (H. pylori) levels for clinical prediction of gastric cancer (GC) progression. METHODS: We analyzed the serum CIMP status of 75 patients with GC using a methylation marker panel and a methylation-specific polymerase chain reaction. Serum samples from 40 healthy persons were examined at the same time. The genes examined were APC, WIF-1, RUNX-3, DLC-1, SFRP-1, DKK and E-cad. H. pylori infection in serum was assayed with an anti-H. pylori immunoglobulin G antibody test and a rapid urease test. RESULTS: The frequencies of high-level methylation in GC tissues for the seven genes were: 48% for APC, 57.33% for WIF-1, 56% for RUNX-3, 50.67% for DLC-1, 52% for SFRP-1, 54.67% for DKK, and 48% for E-cad. The frequencies in GC serum were 30.67% for APC, 34.67% for WIF-1, 37.33% for RUNX-3, 29.33% for DLC-1, 33.33% for SFRP-1, 32% for DKK, and 26.67% for E-cad. CIMP+ (defined as ≥ 3 methylated genes) was associated with 47 (62.67%) GC tissue samples and 44 (58.67%) GC serum samples. CIMP+ was not associated with non-neoplastic mucosal tissues or the serum of healthy persons. Of the 75 GC cases, 51 (68%) were H. pylori+, and 24 (32%) were H. pylori-. Of the 51 H. pylori+ cases, 36 were CIMP+ and 15 were CIMP-. In contrast, for the 24 H. pylori- cases, 11 were CIMP+, and 13 were CIMP-. The difference was significant between the H. pylori+ and H. pylori- groups (χ(2) = 4.27, P < 0.05). Of the 51 H. pylori+ GC patients, 34 were CIMP+ and 17 were CIMP-, while among the 24 H. pylori- GC cases, 10 were CIMP+ and 14 were CIMP-. The difference was significant between the H. pylori+ and H. pylori- groups (χ(2) = 4.21, P < 0.05). A 2-year follow-up showed significant difference in the rates of metastasis and recurrence between H. pylori+/CIMP+ cases and the H. pylori+/CIMP- cases or CIMP- cases associated with H. pylori assayed in serum (P < 0.05). However, there were no significant differences in survival rates between the two groups. CONCLUSION: H. pylori+/CIMP+ cases are associated with higher rates of metastasis and recurrence than H. pylori+/CIMP- cases. Serum may be useful for examining CIMP status.

CpG island methylator phenotype in plasma is associated with hepatocellular carcinoma prognosis.

AIM: To evaluate the clinical significance of CpG island methylator phenotype (CIMP) in plasma and its association with hepatocellular carcinoma (HCC) progress. METHODS: CIMP status of 108 HCC patients was analyzed using a methylation marker panel in tumor tissues and plasma with methylation-specific polymerase chain reaction. Fifteen samples of non-neoplastic liver tissues and 60 of plasma from healthy persons were examined simultaneously. Examined genes included APC, WIF-1, RUNX-3, DLC-1, SFRP-1, DKK and E-cad. RESULTS: The frequencies of high-level methylation in HCC tissue and plasma were at least 15% for the seven genes: APC, 48/108, 44.44% in tissue and 26/108, 24.07% in plasma; WIF-1, 53/108, 49.07% in tissue and 35/108, 32.41% in plasma; RUNX-3, 52/108, 48.14% in tissue and 42/108, 38.89% in plasma; DLC-1, 38/108, 35.18% in tissue and 23/108, 21.30% in plasma; SFRP-1, 40/108, 37.04% in tissue and 31/108, 28.7% in plasma; DKK, 39/108, 36.1% in tissue and 25/108, 23.14% in plasma; and E-cad, 37/108, 34.3% in tissue and 18/108, 16.67% in plasma. CIMP+ (≥ 3 methylated genes) was detected in 68 (60.2%) tumor tissue samples and 62 (57.4%) plasma samples. CIMP was not detected in non-neoplastic liver tissues or plasma of healthy persons. CIMP status in tumor tissues differed significantly in gender, hepatitis B surface antigen, alpha-fetoprotein, and tumor-node-metastasis stage (P < 0.05). Similar results were obtained with plasma samples (P < 0.05). There was no difference in CIMP status in age, presence of hepatitis C virus antibody, cirrhosis, number of nodes, number of tumors, tumor size, or Edmondson-Steiner stage. A one-year follow-up found that the metastatic rate and recurrence rate in the CIMP+ group were significantly higher than in the CIMP- group as assessed with plasma samples (P < 0.05). CONCLUSION: Plasma DNA can be a reliable sample source for CIMP analysis. CIMP in plasma may serve as a molecular marker of late-stage and poor-prognosis HCC.

Plasma DNA methylation of Wnt antagonists predicts recurrence of esophageal squamous cell carcinoma.

AIM: To detect the effects of plasma DNA methylation of Wnt antagonists/inhibitors on recurrence of esophageal squamous cell carcinoma (ESCC). METHODS: We used methylation-specific polymerase chain reaction to detect hypermethylation of the promoter of four Wnt antagonists/inhibitors (SFRP-1, WIF-1, DKK-3 and RUNX3) using DNA from the plasma of ESCC patients (n = 81) and analyzed the association between promoter hypermethylation of Wnt pathway modulator genes and the two-year recurrence of ESCC. RESULTS: Hypermethylation of SFRP-1, DKK-3 and RUNX-3 was significantly associated with an increased risk of ESCC recurrence (P = 0.001, 0.003 and 0.001 for SFRP-1, DKK-3 and RUNX3, respectively). Patients carrying two to three methylated genes had a significantly elevated risk of recurrence compared with those not carrying methylated genes (odds ratio = 15.69, 95% confidential interval: 2.97-83). The area under the receiver operating characteristic curve (AUC) was 77.1 for ESCC recurrence prediction (sensitivity = 66.67 and specificity = 83.3). When combining methylated genes and the clinical stage, the AUC was 83.69, with a sensitivity of 76.19 and a specificity of 83.3. CONCLUSION: The status of promoter hypermethylation of Wnt antagonists/inhibitors in plasma may serve as a non-invasive prognostic biomarker for ESCC.

Fine structure of the sensilla and immunolocalisation of odorant binding proteins in the cerci of the migratory locust, Locusta migratoria.

Using light and electron microscopy (both scanning and transmission), we observed the presence of sensilla chaetica and hairs on the cerci of the migratory locust, Locusta migratoria L. (Orthoptera: Acrididae). Based on their fine structures, three types of sensilla chaetica were identified: long, medium, and short. Males presented significantly more numbers of medium and short sensilla chaetica than females (p<0.05). The other hairs can also be distinguished as long and short. Sensilla chaetica were mainly located on the distal parts of the cerci, while hairs were mostly found on the proximal parts. Several dendritic branches, enveloped by a dendritic sheath, are present in the lymph cavity of the sensilla chaetica. Long, medium, and short sensilla chaetica contain five, four and three dendrites, respectively. In contrast, no dendritic structure was observed in the cavity of the hairs. By immunocytochemistry experiments only odorant-binding protein 2 from L. migratoria (LmigOBP2) and chemosensory protein class I from the desert locust, Schistocerca gregaria Forsskål (SgreCSPI) strongly stained the outer lymph of sensilla chaetica of the cerci. The other two types of hairs were never labeled. The results indicate that the cerci might be involved in contact chemoreception processes.

The chemosensilla on tarsi of Locusta migratoria (Orthoptera: Acrididae): distribution, ultrastructure, expression of chemosensory proteins.

The chemosensilla on the tarsi of Locusta migratoria were mapped using light microscopy, as well as scanning and transmission electron microscopy. Only chemosensilla chaetica were found on the tarsi. On the basis of their ultrastructure, these can be grouped into three main subtypes: short, long, and sunken sensilla chaetica. Short sensilla chaetica can be further divided into two groups containing 6 or 7 neurons. Long sensilla chaetica are mainly located on the lateral surface of the tarsi. Short sensilla chaetica were mainly found on the dorsal surface of the tarsi. Sunken sensilla chaetica were only found on the ventral surface, such as the pulvilli and arolium. Immunocytochemical localization of chemosensory protein (CSP) was performed on ultrathin sections of chemosensilla on tarsi. The antiserum against LmigCSP-II intensively labeled all three types of sensilla chaetica. Gold granules were concentrated in the outer sensillum lymph surrounding the dendrite sheath, while the inner sensillum lymph containing dendrite branches was never labeled. Massive labeling with the anti-LmigCSP-II was also found in cuticle of the pulvilli on the ventral surface of tarsi.