Dual-Site Biomacromolecule Doped Poly(3, 4-Ethylenedioxythiophene) for Bosting Both Anticoagulant and Electrochemical Performances.

Poly(3, 4-ethylenedioxythiophene) (PEDOT) as a new generation of intelligent conductive polymers, is attracting much attention in the field of tissue engineering. However, its water dispersibility, conductivity, and biocompatibility are incompatible, which limit its further development. In this work, biocompatible electrode material of PEDOT doped with sodium sulfonated alginate (SS) which contains two functional groups of sulfonic acid and carboxylic acid per repeat unit of the macromolecule. The as dual-site doping strategy simultaneously boosts anticoagulant and electrochemical performances, for example, good hydrophilicity (water contact angle of 59.40°), well dispersibility (dispersion solution unstratified in 30 days), high conductivity (4.45 S m-1), and enhanced anticoagulant property (extended activated partial thrombin time value of 59.0 s), forming an adjustable PEDOT: biomacromolecule interface; this fills the technical gap of implantable bioelectronics in terms of coagulation and thrombosis risk. At the same time, the assembled all-in-one supercapacitor with anticoagulant properties is prepared by PEDOT: sodium sulfonated alginate as electrode material and sodium alginate hydrogel as electrolyte layer. The dual-site doping strategy provides a new opinion for the design and optimization of functional conductive polymers and its applications in implantable energy storage fields.

Analysis of the incidence and mortality trends of esophageal cancer in cancer registry areas of China and Japan.

This study aims to analyze the prevalence trend of esophageal cancer in Japan and China to provide suggestions for the prevention and treatment of esophageal cancer. The results showed that the incidence rate for the years 2010-2018 significantly decreased with an APC of 5.66%, and the mortality rate from 2010 to 2015 had an APC of -5.87% in China. However, the incidence rate of Japanese women showed an upward trend, with an APC of 4.09% from 2010 to 2019. The mortality rate of esophageal cancer in Japan showed a downward trend, with an APC of -2.96% from 2010 to 2021. From 2010 to 2018, Chinese esophageal squamous cell carcinoma accounted for the highest proportion, accounting for 85.96%, with the largest distribution in the middle, accounting for 47.25%. Patients are mostly diagnosed at stage III, and the relative survival rate from 2012 to 2015 was 30.3%. Japan also has the highest proportion of squamous cell carcinoma, and the lesions are also mostly located in the middle segment. While Japanese esophageal cancer patients are mostly diagnosed at stage I, and the relative survival rate was 41.5% in Japan from 2009 to 2011. The results of this article indicate that the current prevalence of esophageal cancer in China and Japan is generally declining, and the quality of life of patients is gradually improving, but effective screening and prevention strategies are still needed to reduce the burden of this disease.

Anti-PD-1/PD-L1 therapy for colorectal cancer: Clinical implications and future considerations.

Colorectal cancer (CRC) is the third most prevalent cancer in the world. The PD-1/PD-L1 pathway plays a crucial role in modulating immune response to cancer, and PD-L1 expression has been observed in tumor and immune cells within the tumor microenvironment of CRC. Thus, immunotherapy drugs, specifically checkpoint inhibitors, have been developed to target the PD-1/PD-L1 signaling pathway, thereby inhibiting the interaction between PD-1 and PD-L1 and restoring T-cell function in cancer cells. However, the emergence of resistance mechanisms can reduce the efficacy of these treatments. To counter this, monoclonal antibodies (mAbs) have been used to improve the efficacy of CRC treatments. mAbs such as nivolumab and pembrolizumab are currently approved for CRC treatment. These antibodies impede immune checkpoint receptors, including PD-1/PD-L1, and their combination therapy shows promise in the treatment of advanced CRC. This review presents a concise overview of the use of the PD-1/PD-L1 blockade as a therapeutic strategy for CRC using monoclonal antibodies and combination therapies. Additionally, this article outlines the function of PD-1/PD-L1 as an immune response suppressor in the CRC microenvironment as well as the potential advantages of administering inflammatory agents for CRC treatment. Finally, this review analyzes the outcomes of clinical trials to examine the challenges of anti-PD-1/PD-L1 therapeutic resistance.

Poloxamer 407 Combined with Polyvinylpyrrolidone To Prepare a High-Performance Poly(ether sulfone) Ultrafiltration Membrane.

At present, the design and fabrication of polymer membranes with high permeability and good retention ability are still huge challenges. In this study, the commercial Poloxamer 407 (Pluronic F127) is selected as a multifunctional additive, and polyvinylpyrrolidone is used as a pore-forming agent to modify the poly(ether sulfone) membrane by liquid-liquid phase conversion technology to prepare an ultrafiltration membrane with excellent performance. The hydrophobic poly(propylene oxide) segment in Poloxamer 407 guarantees that this copolymer can be firmly anchored to the poly(ether sulfone) matrix, and the hydrophilic poly(ethylene oxide) segments in Poloxamer 407 impart a stronger hydrophilic nature to the modified membrane surface. Therefore, the permeability and hydrophilicity of the modified membrane are significantly improved and the modified membrane also has good stability. When the amount of Poloxamer 407 added to the casting solution reached 0.6 g, the water flux of the modified membrane was as high as 368 L m-2 h-1, and the rejection rate of bovine serum albumin was close to 98%. In the test to isolate organic small molecule dyes, the retention rate of the modified membrane to Congo red is 94.27%. In addition, the modified membrane shows an excellent water flux recovery rate and antifouling ability. It performs well in subsequent cycle tests and long-term membrane life tests and can be used repeatedly. Our work has resulted in poly(ether sulfone) membranes with good performance, which show great potential in the treatment of biomedical wastewater and the removal of industrial organic dye wastewater, it provides ideas for the development and application of amphiphilic polymer materials.

Network Pharmacological Study of Compound Kushen Injection in Esophageal Cancer.

AIM: To provide new methods and ideas for the clinical application of integrated traditional Chinese and Western medicine in the treatment of esophageal cancer. BACKGROUND: Traditional Chinese medicine compound Kushen injection (CKI) has been widely used in the clinic with adjuvant radiotherapy and chemotherapy. However, the mechanism of action of CKI as adjuvant therapy for esophageal cancer has not yet been described. METHODS: This study is based on network pharmacology, data mining, and molecular docking technology to explore the mechanism of action of CKI in the treatment of esophageal cancer. We obtained the effective ingredients and targets of CKI from the traditional Chinese medicine system pharmacology database and analysis platform (TCMSP) and esophageal cancer-related genes from the Online Mendelian Inheritance in Man (OMIM) and GeneCards databases. RESULTS: CKI mainly contains 58 active components. Among them, the top 5 active ingredients are quercetin, luteolin, naringenin, formononetin, and beta-sitostero. The target protein of the active ingredient was matched with the genes associated with esophageal cancer. The active ingredients targeted 187 esophageal cancer target proteins, including AKT1, MAPK1, MAPK3, TP53, HSP90AA1, and other proteins. Then, we enriched and analyzed the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) and used AutoDockVina to dock the core targets and compounds. Finally, PyMOL and Ligplot were used for data visualization. CONCLUSION: This study provides a new method and ideas for the clinical application of integrated traditional Chinese and Western medicine in the treatment of esophageal cancer.

Baicalein Inhibits the Progression and Promotes Radiosensitivity of Esophageal Squamous Cell Carcinoma by Targeting HIF-1A.

Purpose: To explore the mechanism of the effect of baicalein on radioresistance of esophageal cancer, and to provide ideas for the treatment of patients with poor radiotherapy effect of esophageal cancer. Methods: The glycolytic rate assay kit was used to detect the changes in glycolytic metabolism in esophageal cancer cells after treatment with baicalein, and mass spectrometry was used to detect whether baicalein could affect the level of glycolysis-related metabolites in esophageal cancer cells. The binding of baicalein to the target protein was simulated by molecular docking technique, the protein expression level was detected by Western Blot, and the changes in the cell cycle were detected by flow cytometry. Results: Radiation combined with baicalein could significantly inhibit the proliferation and migration of esophageal cancer cells compared with that of 6 Gy rays alone. The results of the glycolytic rate assay showed that baicalein could inhibit the glycolysis of esophageal cancer cells. Metabonomic studies showed that baicalein could affect the expression levels of glycolysis-related metabolites. The results of network pharmacology showed that baicalein could target several key glycolysis enzymes and glycolysis-related proteins, such as HIF-1A. The results of the WB experiment showed that glycolysis-related proteins and cycle-related proteins were down-regulated after baicalein treatment. Conclusion: The main mechanism of baicalein inhibiting radiation resistance of esophageal cancer cells is that targeting HIF-1A protein regulates glucose metabolism and then regulates Cyclin D1/CDK4 axis to change the cell cycle.

The neuroprotective effect of YaoYi-moxibustion on ischemic stroke by attenuating NK-κB expression in rats.

Background: Traditional Chinese medicine (TCM) has become a crucial direction for ischemic stroke treatment. This study sought to explore the underlying roles of YaoYi-moxibustion (YY-moxi) in ischemic stroke. Methods: A total of 75 Sprague-Dawley rats were randomly divided into the following 5 groups: (I) the sham-operated group; (II) the middle cerebral artery occlusion model (MCAO) group; (III) the YY-moxi group; (IV) the antioxidant (N-acetylcysteine, NAC) group; and (V) the NAC + YY-moxi group. After the model had been established, the NAC group received intracerebroventricular injections of NAC, the YY-moxi group received YY-moxi, and the NAC + YY-moxi group received a combination of these 2 interventions. The neurological deficit score was confirmed, and the cerebral infarction was examined by triphenyl tetrazolium chloride (TTC) staining. In the ischemia site of stroke, terminal deoxynucleotidyl transferase-mediated Dutp nick end labeling staining was applied to examine the apoptotic cells. Additionally, the apoptosis-associated genes and protein expressions in the ischemic brains were investigated by the reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR), immunohistochemistry, and western blot analysis. Results: YY-moxi alone and YY-moxi combined with NAC significantly reduced the neurological scores and cerebral infarction area of the MCAO rats. Additionally, YY-moxi alone and the combined application of YY-moxi and NAC improved the pathological status of ischemic brain tissues. Further, we found that YY-moxi alone and YY-moxi in combination with NAC could enhanced the antioxidation ability and reduced the inflammatory response of the MCAO model rats. We also proved that YY-moxi alone and YY-moxi combined with NAC significantly suppressed apoptosis-related proteins in the MCAO model rats. Conclusions: These findings indicate that YY-moxi exerts a protective effect on cerebral ischemic injury by reducing apoptosis. The study suggests that the mechanism may be related to its downregulating the expression of nuclear factor kappa B (NK-κB).

Artesunate Inhibits the Development of Esophageal Cancer by Targeting HK1 to Reduce Glycolysis Levels in Areas With Zinc Deficiency.

Esophageal cancer (EC) threatens many lives in China, especially in areas with high incidences of EC. Our previous studies proved that zinc deficiency (ZD) promotes the cell cycle, thus promoting the progression of EC in areas with a high incidence of EC. Artesunate could inhibit the cell cycle, thereby inhibiting the progression of EC. In this study, we first demonstrated the mechanism by which artesunate inhibits EC in vitro and then demonstrated that artesunate could reverse the ZD-promoted progression of EC before EC occurred in vivo. The results showed that artesunate could inhibit the cell cycle, metastasis, and glycolysis of EC cells. Artesunate could target HK1, promote HK1 degradation, and reduce the levels of HIF-1α and PKM2 expression, which are key glycolysis enzymes. The in vivo results showed that ZD could increase the expression of HK1 and increase the incidence of EC. Artesunate reduced the incidence of EC and decreased the level of HK1 expression before EC occurred. Artesunate has an anti-EC effect by inhibiting aerobic glycolysis and has the potential to be a drug that prevents EC in areas with a high risk of EC.

MicroRNA-29b regulates the radiosensitivity of esophageal squamous cell carcinoma by regulating the BTG2-mediated cell cycle.

BACKGROUND: Many patients with esophageal squamous cell carcinoma (ESCC) are inoperable due to old age or advanced stage; thus, radio- and chemotherapy are considered the standard treatments for these patients. However, due to the radiation resistance of tumor cells that may arise during radiotherapy, results are still not satisfactory. The authors' previous studies found that microRNA can affect radiosensitivity, and further microRNA research was conducted to improve the radiosensitivity of ESCC. METHODS: Cells were treated with silent miR-29b (si-miR-29b). Thereafter,proliferation, colony formation, cell cycle, and apoptosis were determined. The luciferase reporting assay was used to confirm the direct interaction between miR-29b and BTG2. Serum samples and clinical follow-up data of 75 elderly or advanced ESCC patients who could not tolerate surgery were collected. RESULTS: The expression level of miR-29 in ESCC serum was closely correlated to radiosensitivity (χ2 =8.36, p < 0.05) and correlated with overall survival (OS; hazard ratio [HR] 0.47, 95% confidence interval [CI] 0.24-0.90). Function assays demonstrated that the number of cell clones increased after radiometry radiation, and the cell cycle was blocked in the G0/G1 phase (from 37.2 to 56.9%) in the si-miR-29b transfection group. Expression of BTG2 was upregulated and expression of cyclin D1 was downregulated (p < 0.05). Transfection of si-BTG2 can reverse this result and restore the expression level of cyclin D1 (p < 0.05). The target gene BTG2 of miR-29b was predicted using a bioinformatics tool and confirmed by dual-luciferase reporter assay. CONCLUSION: Silencing of miR-29b in ESCC cells can increase expression of BTG2 and decrease the level of intracellular cyclin D1, resulting in cell cycle arrest and accumulation in the G0/G1 phase. Because G0/G1-phase cells are insensitive to radiotherapy, the sensitivity of radiotherapy is reduced.

Effect of carbon source on nitrous oxide emission characteristics and sludge properties during anoxic/aerobic wastewater treatment process.

Carbon sources are an important parameter in wastewater treatment processes and are closely related to treatment efficiency and nitrous oxide (N2O) emissions. In this study, three parallel sequencing batch reactors (SBRs) were processed with acetic acid, propionic acid, and a 1:1 mixture of both acids (calculated in COD) to study the effect of carbon sources on N2O generation and sludge properties (including intracellular polymer content, extracellular polymeric substance (EPS) composition, particle size distribution, settleability, and microbial community structure). The results showed that the highest COD, NH4+-N, and TP removal efficiencies (92.2%, 100%, and 82.3%, respectively) were achieved by the reactor with mixed acid as the carbon source, whereas the reactor using acetic acid had the highest TN removal rate (82.6%) and the lowest N2O-N conversion rate (1.4%, based on TN removal). The reactor with the carbon source of mixed acid produced the highest polyhydroxyalkanoate (PHA) content, which led to an increase in N2O generation from the aerobic denitrification pathway. The SBR with mixed acid carbon source also had the highest concentration of EPS, which resulted in the largest particle size and the lowest settleability of sludge flocs among the SBRs. Microbial analysis results revealed that the difference in carbon sources resulted in a variation in the microbial community as well as in the relative abundances of functional microbes involved in biological nitrogen removal processes. The mixed acid promoted the development of ammonia-oxidizing bacteria (AOB), which conducted the primary N2O generation pathway of aerobic denitrification bioreactions. The carbon source of acetic acid promoted the growth of denitrifying bacteria (DNB), which led to the highest TN removal rate. This study provides a comprehensive understanding of the effects of carbon sources on N2O generation and sludge properties for WWTPs.

Necroptosis pathway blockage attenuates PFKFB3 inhibitor-induced cell viability loss and genome instability in colorectal cancer cells.

Cancer cells prone to utilize aerobic glycolysis other than oxidative phosphorylation to sustain its continuous cell activity in the stress microenvironment. Meanwhile, cancer cells generally suffer from genome instability, and both radiotherapy and chemotherapy may arouse DNA strand break, a common phenotype of genome instability. Glycolytic enzyme PFKFB3 (6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3), plays essential roles in variety physiology and pathology processes, and generally maintain high level in cancer cells. Although this protein has been reported to involve in genome instability, its role remains unclear and controversial. Here, we showed that PFK-15, a PFKFB3 inhibitor, obviously induced apoptosis, cell viability loss, and inhibited cell proliferation/migration. Besides, PFK-15 was also found to induce necroptosis, as it not only up-regulated the phosphorylated RIP1, RIP3 and MLKL, but also enhanced the interaction between RIP3 and RIP1/MLKL, all of which are characterization of necroptosis induction. Both genetically and pharmacologically deprivation of necroptosis attenuated the cytotoxic effect of PFK-15. Besides, PFK-15 increased the γ-H2AX level and micronuclei formation, markers for genome instability, and inhibition of necroptosis attenuated these phenotypes. Collectively, the presented data demonstrated that PFK-15 induced genome instability and necroptosis, and deprivation of necroptosis attenuated cytotoxicity and genotoxicity of PFK-15 in colorectal cancer cells, thereby revealing a more intimate relationship among PFKFB3, necroptosis and genome instability.

Silicate-Enhanced Heterogeneous Flow-Through Electro-Fenton System Using Iron Oxides under Nanoconfinement.

Herein, a silicate-enhanced flow-through electro-Fenton system with a nanoconfined catalyst was rationally designed and demonstrated for the highly efficient, rapid, and selective degradation of antibiotic tetracycline. The key active component of this system is the Fe2O3 nanoparticle filled carbon nanotube (Fe2O3-in-CNT) filter. Under an electric field, this composite filter enabled in situ H2O2 generation, which was converted to reactive oxygen species accompanied by the redox cycling of Fe3+/Fe2+. The presence of the silicate electrolyte significantly boosted the H2O2 yield by preventing the O-O bond dissociation of the adsorbed OOH*. Compared with the surface coated Fe2O3 on the CNT (Fe2O3-out-CNT) filter, the Fe2O3-in-CNT filter demonstrated 1.65 times higher kL value toward the degradation of the antibiotic tetracycline. Electron paramagnetic resonance and radical quenching tests synergistically verified that the dominant radical species was the 1O2 or HO· in the confined Fe2O3-in-CNT or unconfined Fe2O3-out-CNT system, respectively. The flow-through configuration offered improved tetracycline degradation kinetics, which was 5.1 times higher (at flow rate of 1.5 mL min-1) than that of a conventional batch reactor. Liquid chromatography-mass spectrometry measurements and theoretical calculations suggested reduced toxicity of fragments of tetracycline formed. This study provides a novel strategy by integrating state-of-the-art material science, Fenton chemistry, and microfiltration technology for environmental remediation.

[Research Progress on Lung Cancer Screening].

Lung cancer is the most common malignant tumor in the world. The five-year survival rate is 19.7%, which seriously threatens human health. Lung cancer screening is an effective measure to reduce lung cancer mortality. Existing studies have shown that screening with low-dose computed tomography (LDCT) can reduce lung cancer deaths by 20%. Currently, lung cancer screening is recommended internationally and nationally. Studying the development status of lung cancer screening helps us to identify the high-risk groups of lung cancer, explore reasonable screening programs, improve the cost-effectiveness of screening and reduce the economic burden. Therefore, this article summarizes the current status of lung cancer screening, the cost-effectiveness of lung cancer screening and the existing problems as follows.
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PRSS8 suppresses colorectal carcinogenesis and metastasis.

The serine protease PRSS8 has shown important physiological and pathological functions, but its roles in cancer initiation and progression are unclear. We developed and dynamically characterized a conditional knockout Prss8fl/fl, p-Villin-Cre+ mouse model. We found that genetic deficiency of the Prss8 gene caused spontaneous colitis and an inflamed rectum at an early age and caused intestinal tumors at a late age, which were linked to increased intestinal cell proliferation and migration but decreased cell differentiation. Increased PRSS8 expression inhibited cancer cell growth and metastasis in nude mice and inhibited cancer cell migration, invasion, colony formation and tumor sphere formation in vitro, but decreased PRSS8 expression facilitated malignancies in vivo and in vitro. Gene profiling on manipulated cancer cells and intestinal epithelial cells of Prss8 mouse models, gene set enrichment analysis and mechanistic studies revealed that PRSS8 targeted the Wnt/ß-catenin, epithelial-mesenchymal transition, and stem cell signaling pathways, which were further supported by the results from the TCGA data mining and validated by immunohistochemical staining on colorectal cancer tissue microarrays. In conclusion, PRSS8 is a novel tumor suppressor that plays critical roles in the suppression of colorectal carcinogenesis and metastasis.

CagA increases DNA methylation and decreases PTEN expression in human gastric cancer.

Gastric cancer is one of the leading causes of cancer-associated mortality worldwide. Cytotoxin­associated gene A (CagA) has been reported to be associated with gastric diseases. Phosphatase and tensin homolog (PTEN) and tet methylcytosine dioxygenase 1 (Tet1) are important tumor­suppressor genes. The present study aimed to investigate the underlying functions of CagA in human gastric cancer, and to explore the associations between CagA, PTEN and Tet1 in gastric cancer. For that purpose, CagA overexpression and Tet1 interference recombinant lentiviral plasmids were constructed. Quantitative polymerase chain reaction (qPCR) was utilized to screen gene expression in HGC­27 human gastric cancer cells overexpressing CagA. qPCR and western blotting were used to detect gene and protein expression, respectively. In addition, the methylation status of PTEN was detected by methylation­specific PCR. The expression levels of PTEN, Tet1, apolipoprotein B mRNA editing enzyme catalytic subunit (APOBEC)3A, APOBEC3C and APOBEC3F were significantly decreased in the CagA overexpression group compared with in the negative control group in HGC­27 cells. Compared with in the negative control group, the mRNA and protein expression levels of PTEN were markedly decreased in cells with Tet1 interference. The decreased expression of PTEN was associated with increased methylation levels in the cells. In addition, the protein expression levels of PTEN were significantly decreased in HGC­27 cells when CagA was overexpressed. The expression levels of PTEN and Tet1 were also markedly decreased in CagA+ gastric cancer tissues compared with in non­cancerous tissues. The decreased expression of PTEN in CagA+ gastric cancer tissues was associated with increased methylation levels. In conclusion, overexpression of CagA significantly decreased the expression of PTEN, Tet1, APOBEC3A, APOBEC3C and APOBEC3F in human gastric cancer. In addition, CagA increased DNA methylation and decreased PTEN expression, which was reversed by Tet1 overexpression. The present study may facilitate future therapeutic approaches targeting human gastric cancer.

Xanthohumol induces apoptosis via caspase activation, regulation of Bcl-2, and inhibition of PI3K/Akt/mTOR-kinase in human gastric cancer cells.

We assessed the effect of xanthohumol (XN) on gastric cancer (GC) in vitro and in vivo. XN reduced the viability of SGC-7901, SNU216, and SNU668 cells, but not GES-1 non-tumorigenic human gastric epithelial cells. XN induced apoptosis in SGC-7901 cells in a concentration-dependent manner by enhancing the numbers of late and early apoptotic cells. XN also downregulated the anti-apoptotic proteins Bcl-XL and Bcl-2 and upregulated the pro-apoptotic proteins Bax, Bid, PARP, and caspase-3. XN induced phosphorylation of PI3K, Akt, and mTOR in SGC7901 cells. Also, XN reduced the tumour volume and weight by inhibiting the phosphorylation of Akt and mTOR. XN-treated tumours had significantly fewer proliferating cells and more apoptotic cells compared with the control. Our data indicate that XN induces apoptosis of human GC cells in vivo. Thus, XN may have potential as an anti-GC agent.

[Emission Inventory of Greenhouse Gas from Urban Wastewater Treatment Plants and Its Temporal and Spatial Distribution in China].

Urban wastewater treatment plants are considered important greenhouse gas resources with massive emissions of carbon dioxide (CO2), methane (CH4), and nitrous oxide (N2O) during operation. Based on the emission factor approach of pollutant reduction, the 2014 emission inventory of greenhouse gases (CO2, CH4, and N2O) from urban wastewater treatment plants in China was established. In addition, the temporal and spatial distribution and influencing factors of greenhouse gas emissions were analyzed in this study. The results showed that total emissions of greenhouse gas from urban wastewater treatment plants in China was 7348.60 Gg (CO2-eq) in 2014, which included CO2, CH4, and N2O emissions of 6054.57 Gg, 27.47 Gg (769.08 Gg, CO2-eq), and 1.98 Gg (524.95 Gg, CO2-eq), respectively. The difference in greenhouse gas emissions among provinces was significant:high emissions appeared in the eastern areas of China, low emissions were observed in the northwest, and hardly any emissions were found in Xizang. From 2005 to 2014, annual greenhouse gas emissions from urban sewage treatment plants in China increased by 229.4%, and the rates of CO2, CH4, and N2O increased by 217.9%, 217.9%, and 520.3%, respectively. The regional economic development level and number of wastewater treatment plants were correlated the most with the emissions of greenhouse gasses, and the per-capita protein supply was closely related with the N2O emission.

Pregnancy-associated plasma protein a in cancer: expression, oncogenic functions and regulation.

Pregnancy-associated plasma protein A (PAPPA) is a protease that plays important roles in pregnancy, but interestingly acts as an oncogene outside of pregnancy. This review summarizes the oncogenic roles of PAPPA, including its expression levels in multiple malignancies, regulatory and signaling interactions, and pro-tumor functions, which include promoting tumor cell proliferation, invasion, migration and metastasis. These PAPPA activities are linked to IGFBP-4 proteolysis, increased IFG bioavailability, and activation of the NF-κB, PI3K/AKT and ERK signaling pathways. Therefore, PAPPA could be used as a biomarker for monitoring cancer development and progression as well as a potential therapeutic target.

[Dynamic expression of antigen MG7 in the gastric cancer and gastric precancerous lesions].

OBJECTIVE: To study the kinetics of MG7 expression in the process of gastric cancer development. METHODS: The expression level of antigen MG7 on gastric mucosa in 406 cases was determined by immunohistochemical techniques. The classification of intestinal metaplasia of gastric mucosa was determined by histochemistry techniques on gastric mucosa in 82 cases. RESULTS: The positive rates of MG7 expression in normal gastric mucosa, intestinal metaplasia and dysplasia of gastric mucosa and gastric cancer all increased gradually (P < 0.01). The positive rates of MG7 expression in superficial gastritis, atrophic gastritis and gastric cancer increased in sequence (P < 0.01). The positive rate of antigen MG7 expression in III intestinal metaplasia of gastric mucosa was significantly different with I and II intestinal metaplasia (P < 0.05). CONCLUSIONS: MG7 was quite specific in gastric cancer thus could be used as a good index in the screening of gastric cancer. Patients with III intestinal metaplasia of gastric mucosa, atrophic gastritis and dysplasia of gastric mucosa should be closely followed in order to improve the early detection on gastric cancer. It seemed that MG7 was clinically valuable in the dynamic follow-up of gastric precursors.