Effect of Boron Content in LiOH Solutions on the Corrosion Behavior of Zr-Sn-Nb Alloy.

In pressurized water reactors, LiOH may be concentrated in some areas, leading to the accelerated corrosion of fuel claddings. Injecting boric acid into primary coolants can mitigate the accelerated corrosion effect of LiOH on Zircaloys, but the effects of boron content on the corrosion behavior of the Zr-Sn-Nb alloy are still unknown. This work focused on the corrosion and hydrogen absorption behavior at 360 °C/18.6 MPa in 100 mg/kg LiOH solutions with 0 mg/kg, 50 mg/kg, and 200 mg/kg boron contents for up to 510 days, aiming to study the effect of boron content on corrosion resistance in LiOH solutions. Corrosion kinetics, microstructures of oxide films, hydrogen absorption concentrations and hydride morphology were obtained after the test. The results show that injecting boron in LiOH solutions can significantly reduce the corrosion weight gain, hydrogen concentration, and hydrogen length of Zr-Sn-Nb alloys, that is, improving corrosion resistance effectively. During the oxidation of the Zr-Sn-Nb alloy, B3+ and Li+ incorporate in oxide films. The incorporation of Li+ may lead to the generation of oxygen vacancies, which can carry oxygen from the solutions to O/M interface, accelerating corrosion. The incorporation of B3+ in oxide films will slow down the oxidation of Zr-Sn-Nb alloys by reducing the oxygen vacancies caused by Li+ aggregation.

Hydrogen Flux Inhibition of Pd-Ru Membranes under Exposure to NH3.

The hydrogen flux inhibition of Pd-Ru membranes under exposure to 1-10% NH3 at 673-773 K was investigated. The Pd-Ru membranes were characterized by XRD, SEM, XPS, and hydrogen permeation tests. The results show that when exposed to 1-10% NH3 at 723 K for 6 h, the hydrogen flux of Pd-Ru membranes sharply decreases by 15-33%, and the decline in hydrogen flux becomes more significant with increasing temperatures. After the removal of 1-10% NH3, 100% recovery of hydrogen flux is observed. XPS results show that nitrogenous species appear on the membrane surface after NH3 exposure, and the hydrogen flux inhibition may be related to the competitive adsorption of nitrogenous species. By comparing the hydrogen flux of Pd-Ru membranes exposed to 10% NH3 with 10% N2, it is indicated that the rapid decrease in hydrogen flux is due to the concentration polarization and competitive adsorption of nitrogenous species. The competitive adsorption effect is attenuated, while the concentration polarization effect becomes more pronounced with increasing temperature.

Hungatella hathewayi impairs the sensitivity of colorectal cancer cells to 5-FU through decreasing CDX2 expression.

Hungatella hathewayi (H. hathewayi), also known as Clostridium hathewayi, has been reported to be accumulated in the colorectal cancer (CRC) samples. In addition, evidence has demonstrated that inoculation with H. hathewayi promotes the proliferation of colonic epithelial cells in mice. Herein, we explored H. hathewayi role in regulating the 5-fluorouracil (5-FU) resistance in CRC cells, and investigated the underlying mechanisms. H. hathewayi abundance in CRC tissues and the corresponding adjacent normal tissues was tested using qRT-PCR. Both parental and 5-FU resistance CRC cell lines were used to assess H. hathewayi role in regulating the 5-FU resistance of CRC cells using CCK-8, flow cytometry and animal experiments. H. hathewayi abundance was significantly increased in CRC tissues, and the high level of H. hathewayi was linked to lower overall survival rate. H. hathewayi treatment significantly weakened 5-FU effects on inhibiting cell growth and inducing cell apoptosis in CRC HCT116 and HT29 cells. In addition, H. hathewayi enhanced the 5-FU resistance of HCT116/5-FU and HT29/5-FU cells (the 5-FU resistance cell lines). In mechanism, H. hathewayi decreased the expression of CDX2, and increased the expression of nuclear accumulation of ß-catenin. Overexpression of CDX2 abolished H. hathewayi-mediated enhancement in cell growth and inhibition in cell apoptosis in HCT116/5-FU and HT29/5-FU cells, as well as inhibited the expression and nuclear accumulation of ß-catenin. In conclusion, H. hathewayi abundance was increased in CRC tissues, and the high level of H. hathewayi was linked to lower overall survival rate. In mechanisam, H. hathewayi treatment enhanced the 5-FU resistance of CRC cells through modulating CDX2/ß-catenin signaling.

Therapeutic and adverse effects of adrenaline on patients who suffer out-of-hospital cardiac arrest: a systematic review and meta-analysis.

OBJECTIVE: The efficacy and safety of epinephrine in patients with out-of-hospital cardiac arrest (OHCA) remains controversial. The meta-analysis was used to comprehensively appraise the influence of epinephrine in OHCA patients. METHODS: We searched all randomized controlled and cohort studies published by PubMed, EMBASE, and Cochrane Library from the inception to August 2022 on the prognostic impact of epinephrine on patients with OHCA. Survival to discharge was the primary outcome, while the return of spontaneous circulation (ROSC) and favorable neurological outcome were secondary outcomes. RESULTS: The meta-analysis included 18 studies involving 863,952 patients. OHCA patients with adrenaline had an observably improved chance of ROSC (RR 2.81; 95% CI 2.21-3.57; P = 0.001) in randomized controlled studies, but the difference in survival to discharge (RR 1.27; 95% CI 0.58-2.78; P = 0.55) and favorable neurological outcomes (RR 1.21; 95% CI 0.90-1.62; P = 0.21) between the two groups was not statistically significant. In cohort studies, the rate of ROSC (RR 1.62; 95% CI 1.14-2.30; P = 0.007) increased significantly with the adrenaline group, while survival to discharge (RR 0.73; 95% CI 0.55-0.98; P = 0.03) and favorable cerebral function (RR 0.42; 95% CI 0.30-0.58; P = 0.001) were lower than the non-adrenaline group. CONCLUSION: We found that both the randomized controlled trials (RCTs) and cohort studies showed that adrenaline increased ROSC in OHCA patients. However, they were unable to agree on a long-term prognosis. The cohort studies showed that adrenaline had an adverse effect on the long-term prognosis of OHCA patients (discharge survival rate and good neurological prognosis), but adrenaline had no adverse effect in the RCTs. In addition to the differences in research methods, there are also some potential confounding factors in the included studies. Therefore, more high-quality studies are needed to fully confirm the effect of adrenaline on the long-term results of OHCA.

Circular RNA PLCE1 promotes epithelial mesenchymal transformation, glycolysis in colorectal cancer and M2 polarization of tumor-associated macrophages.

Plentiful studies have clarified that circular RNAs (circRNAs) are crucial in colorectal cancer (CRC)'s occurrence and development, but its function has not been fully elucidated. The purpose of this study was to investigate the biological functions of circPLCE1 on epithelial mesenchymal transformation (EMT) and glycolysis in CRC, and tumor-associated macrophage (TAM) polarization. The results affirmed augment of circPLCE1 and γ-Actin Gene (ACTG1) but decline of miR-485-5p in CRC. Knockdown circPCLE1 refrained CRC proliferation, glucose consumption, lactic acid and pyruvate production, M2 macrophage markers (IL-10, MRC1), N-cadherin, Snail, reduced the proportion of CD206+ and CD168+ macrophages, but expedited M1 macrophage markers (TNF-α, IL-6) and E-cadherin, while descending miR-485-5p expedited EMT, glycolysis in CRC and TAM M2 polarization . Additionally, it was affirmed that the repression or motivation of depressive or elevated circPCLE1 on EMT, glycolysis in CRC and TAM M2 polarization were reversed via facilitated ACTG1 and miR-485-5p, separately. Mechanism studies have clarified that circPCLE1 as a competitive endogenous RNA adsorbed miR-485-5p to mediate ACTG1. It was assured that refrained circPCLE1 constrained CRC tumor growth, EMT and TAM M2 polarization. In brief, circPCLE1 expedites EMT, glycolysis in CRC and TAM M2 polarization via modulating the miR-485-5p/ACTG1 axis, and is supposed to be a latent molecular target for CRC therapy later.

The impact of online education on carbon emissions in the context of the COVID-19 pandemic - Taking Chinese universities as examples.

While the COVID-19 pandemic has had various impacts on economic and social development, it may have partially reduced human energy use, thereby helping achieve the goals of reducing carbon emissions and promoting carbon neutrality. During the pandemic, online education was widely used to replace traditional education all over the world. There is a lack of empirical studies on whether and to what extent the change of education model can reduce carbon emissions. Taking Chinese universities as cases, this study, concentrating on two main elements - transportation and electricity consumption - constructs a model and calculates the impact of online education on carbon emissions. The results show that online education can significantly reduce energy consumption and lower carbon emissions. In the field of higher education alone, the carbon emissions reduction caused by online education in half a year is equivalent to the total carbon emissions reduction of college students caused by online education during the half-year is equivalent to the total carbon emissions in 1.296 h in China, 2.688 h in the United States, 5.544 h in India, 12 h in Japan and 3.864 h in European countries of OECD. Therefore, this study suggests that the impact of online education on carbon emissions should be further studied, online education should be promoted through legislation and other systemic measures, and the goals of carbon emissions and carbon neutrality should be explored further within the field of education.

Platelet-Derived Mitochondria Display Embryonic Stem Cell Markers and Improve Pancreatic Islet ß-cell Function in Humans.

Diabetes is a major global health issue and the number of individuals with type 1 diabetes (T1D) and type 2 diabetes (T2D) increases annually across multiple populations. Research to develop a cure must overcome multiple immune dysfunctions and the shortage of pancreatic islet ß cells, but these challenges have proven intractable despite intensive research effort more than the past decades. Stem Cell Educator (SCE) therapy-which uses only autologous blood immune cells that are externally exposed to cord blood stem cells adhering to the SCE device, has previously been proven safe and effective in Chinese and Spanish subjects for the improvement of T1D, T2D, and other autoimmune diseases. Here, 4-year follow-up studies demonstrated the long-term safety and clinical efficacy of SCE therapy for the treatment of T1D and T2D. Mechanistic studies found that the nature of platelets was modulated in diabetic subjects after receiving SCE therapy. Platelets and their released mitochondria display immune tolerance-associated markers that can modulate the proliferation and function of immune cells. Notably, platelets also expressed embryonic stem cell- and pancreatic islet ß-cell-associated markers that are encoded by mitochondrial DNA. Using freshly-isolated human pancreatic islets, ex vivo studies established that platelet-releasing mitochondria can migrate to pancreatic islets and be taken up by islet ß cells, leading to the proliferation and enhancement of islet ß-cell functions. These findings reveal new mechanisms underlying SCE therapy and open up new avenues to improve the treatment of diabetes in clinics. Stem Cells Translational Medicine 2017;6:1684-1697.

Sulfate ion (SO4(2-)) release from old and new cation exchange resins used in condensate polishing systems for power plants.

In this study, a dynamic cycle test, a static immersion method and a pyrolysis experiment were combined to examine the characteristics of SO4(2-) released from several new and old cation exchange resins used in condensate polishing systems for power plants. The results show that the quantity and velocity of SO4(2-) released from new and old resins tend to balance in a short time during the dynamic cycle experiment. SO4(2-) is released by 1500H (monosphere super gel type cation exchange resins) and 001 × 7 (gel type cation exchange resins) new and old cation exchange resins, the quantity of which increases according to immersion time. In the pyrolysis experiment, the quantity of SO4(2-) released from resins increases and the pH of the pyrolysis solution transforms from alkaline to acidic with an increase in temperature.

Hepatocyte transplantation ameliorates the metabolic abnormality in a mouse model of acute intermittent porphyria.

Acute intermittent porphyria (AIP) is an autosomal dominant disorder characterized by insufficient porphobilinogen deaminase (PBGD) activity. When hepatic heme synthesis is induced, porphobilinogen (PBG) and 5-aminolevulinic acid (ALA) accumulate, which causes clinical symptoms such as abdominal pain, neuropathy, and psychiatric disturbances. Our aim was to investigate if hepatocyte transplantation can prevent or minimize the metabolic alterations in an AIP mouse model. We transplanted wild-type hepatocytes into PBGD-deficient mice and induced heme synthesis with phenobarbital. ALA and PBG concentrations in plasma were monitored, and the gene transcriptions of hepatic enzymes ALAS1, PBGD, and CYP2A5 were analyzed. Results were compared with controls and correlated to the percentage of engrafted hepatocytes. The accumulation of ALA and PBG was reduced by approximately 50% after the second hepatocyte transplantation. We detected no difference in mRNA levels of PBGD, ALAS1, or CYP2A5. Engraftment corresponding to 2.7% of the total hepatocyte mass was achieved following two hepatocyte transplantations. A lack of precursor production in less than 3% of the hepatocytes resulted in a 50% reduction in plasma precursor concentrations. This disproportional finding suggests that ALA and PBG produced in PBGD-deficient hepatocytes crossed cellular membranes and was metabolized by transplanted cells. The lack of effect on enzyme mRNA levels suggests that no significant efflux of heme from normal to PBGD-deficient hepatocytes takes place. Further studies are needed to establish the minimal number of engrafted hepatocytes needed to completely correct the metabolic abnormality in AIP and whether amelioration of the metabolic defect by partial restoration of PBGD enzyme activity translates into a clinical effect in human AIP.

Targeting insulin resistance in type 2 diabetes via immune modulation of cord blood-derived multipotent stem cells (CB-SCs) in stem cell educator therapy: phase I/II clinical trial.

BACKGROUND: The prevalence of type 2 diabetes (T2D) is increasing worldwide and creating a significant burden on health systems, highlighting the need for the development of innovative therapeutic approaches to overcome immune dysfunction, which is likely a key factor in the development of insulin resistance in T2D. It suggests that immune modulation may be a useful tool in treating the disease. METHODS: In an open-label, phase 1/phase 2 study, patients (N=36) with long-standing T2D were divided into three groups (Group A, oral medications, n=18; Group B, oral medications+insulin injections, n=11; Group C having impaired ß-cell function with oral medications+insulin injections, n=7). All patients received one treatment with the Stem Cell Educator therapy in which a patient's blood is circulated through a closed-loop system that separates mononuclear cells from the whole blood, briefly co-cultures them with adherent cord blood-derived multipotent stem cells (CB-SCs), and returns the educated autologous cells to the patient's circulation. RESULTS: Clinical findings indicate that T2D patients achieve improved metabolic control and reduced inflammation markers after receiving Stem Cell Educator therapy. Median glycated hemoglobin (HbA1C) in Group A and B was significantly reduced from 8.61%±1.12 at baseline to 7.25%±0.58 at 12 weeks (P=2.62E-06), and 7.33%±1.02 at one year post-treatment (P=0.0002). Homeostasis model assessment (HOMA) of insulin resistance (HOMA-IR) demonstrated that insulin sensitivity was improved post-treatment. Notably, the islet beta-cell function in Group C subjects was markedly recovered, as demonstrated by the restoration of C-peptide levels. Mechanistic studies revealed that Stem Cell Educator therapy reverses immune dysfunctions through immune modulation on monocytes and balancing Th1/Th2/Th3 cytokine production. CONCLUSIONS: Clinical data from the current phase 1/phase 2 study demonstrate that Stem Cell Educator therapy is a safe approach that produces lasting improvement in metabolic control for individuals with moderate or severe T2D who receive a single treatment. In addition, this approach does not appear to have the safety and ethical concerns associated with conventional stem cell-based approaches. TRIAL REGISTRATION: ClinicalTrials.gov number, NCT01415726.

Comparison of two kinds of nanomedicine for targeted gene therapy: premodified or postmodified gene delivery systems.

BACKGROUND: The applications of ligand-polyethylene glycol (PEG)-modified nanocarriers have now emerged, as well as recognized strategies to provide the vectors with active targeting properties. In this research, premodification and postmodification were compared using the same ligand, ie, a novel conjugated mannan-containing PEG and L-α-phosphatidylethanolamine (PE). METHODS: Premodified and postmodified solid lipid nanoparticles were prepared and the characteristics of the two kinds of vehicles were evaluated. The modified vectors were then administered intravenously to rats and the in vivo targeting behavior of the complexes was investigated in liver macrophages. RESULTS: By carefully formulating the carriers with an optimal ratio of mannan-containing PEG-PE, postmodified vehicles displayed more efficient gene expression in rat Kupffer cells both in vitro and in vivo. CONCLUSION: Postmodified gene carriers are superior to premodified gene vectors, although the latter is also promising for targeted gene delivery. This discovery could guide our future research.

Reversal of type 1 diabetes via islet ß cell regeneration following immune modulation by cord blood-derived multipotent stem cells.

BACKGROUND: Inability to control autoimmunity is the primary barrier to developing a cure for type 1 diabetes (T1D). Evidence that human cord blood-derived multipotent stem cells (CB-SCs) can control autoimmune responses by altering regulatory T cells (Tregs) and human islet ß cell-specific T cell clones offers promise for a new approach to overcome the autoimmunity underlying T1D. METHODS: We developed a procedure for Stem Cell Educator therapy in which a patient's blood is circulated through a closed-loop system that separates lymphocytes from the whole blood and briefly co-cultures them with adherent CB-SCs before returning them to the patient's circulation. In an open-label, phase1/phase 2 study, patients (n=15) with T1D received one treatment with the Stem Cell Educator. Median age was 29 years (range: 15 to 41), and median diabetic history was 8 years (range: 1 to 21). RESULTS: Stem Cell Educator therapy was well tolerated in all participants with minimal pain from two venipunctures and no adverse events. Stem Cell Educator therapy can markedly improve C-peptide levels, reduce the median glycated hemoglobin A1C (HbA1C) values, and decrease the median daily dose of insulin in patients with some residual ß cell function (n=6) and patients with no residual pancreatic islet ß cell function (n=6). Treatment also produced an increase in basal and glucose-stimulated C-peptide levels through 40 weeks. However, participants in the Control Group (n=3) did not exhibit significant change at any follow-up. Individuals who received Stem Cell Educator therapy exhibited increased expression of co-stimulating molecules (specifically, CD28 and ICOS), increases in the number of CD4+CD25+Foxp3+ Tregs, and restoration of Th1/Th2/Th3 cytokine balance. CONCLUSIONS: Stem Cell Educator therapy is safe, and in individuals with moderate or severe T1D, a single treatment produces lasting improvement in metabolic control. Initial results indicate Stem Cell Educator therapy reverses autoimmunity and promotes regeneration of islet ß cells. Successful immune modulation by CB-SCs and the resulting clinical improvement in patient status may have important implications for other autoimmune and inflammation-related diseases without the safety and ethical concerns associated with conventional stem cell-based approaches. TRIAL REGISTRATION: ClinicalTrials.gov number, NCT01350219.

Direct electrochemistry and electrocatalytic activity of hemoglobin at CdTe nanoparticle/nafion film-modified electrode.

Water-soluble CdTe nanoparticles and hemoglobin (Hb) were immobilized on a glassy carbon (GC) electrode with Nafion. The direct electrochemistry of Hb on this surface was studied. The results indicated that CdTe nanoparticles could effectively promote the direct electron transfer of Hb at the interface of a electrode. The average surface coverage of Hb on the surface could be calculated as 2.63 x 10(-9) mol/cm2, the heterogeneous electron transfer rate constant, k, was calculated as 0.068 s(-1) and the transfer coefficient, alpha, was 0.59, further study indicated that immobilized Hb still kept its catalytic activity to H2O2 reduction. The apparent Michaelis-Menten constant was calculated to be 17.7 microM. It was also found that the modified electrode could be used as a sensor for H2O2; the linear range of detection was 5.0 x 10(-6)-4.5 x 10(-5) M, with a detection limit of 8.4 x 10(-7) M. The sensor exhibited high sensitivity, reproducibility and stability.

Electrocatalysis of emodin at multi-wall nanotubes.

In this article, the electrochemical behavior of emodin at multi-wall carbon nanotube modified glassy carbon electrodes (MWNTs/GCE) was studied. The result showed that MWNTs/GCE had high electrocatalytic activity for emodin. And the electrocatalytic redox process was a two-charge-two-proton process. Diffusion coefficient (D(R)) of 8.403 x 10(-5) cm(2) s(-1) of emodin was obtained. Further experiments demonstrated that the oxidative peaks increased linearly with emodin concentrations in the range of 1.0 x 10(-6) to 1.0 x 10(-4) M with a limit of detection of 3.0 x 10(-7) M. This electrochemical method was accurate and reliable, therefore, it might provide a novel way for emodin detection.

Isolation of mouse hepatocytes for transplantation: a comparison between antegrade and retrograde liver perfusion.

We compared antegrade with retrograde liver perfusion when isolating mouse hepatocytes for hepatocyte transplantation. Male mouse hepatocytes were isolated by different perfusion methods and transplanted into the spleen of congeneic female mice. Retrograde perfusion yielded a larger number of cells (4.90 x 10(7)) than antegrade (4.09 x 10(7), p < 0.05), but hepatocytes obtained by antegrade perfusion gave higher engraftment efficiency (p < 0.05). More of the transplanted hepatocytes could be recovered from recipient liver with antegrade perfusion than with retrograde perfusion (p < 0.05). Our results indicate that hepatocytes isolated by antegrade perfusion gave a higher engraftment efficiency.

Electrochemical behavior of levodopa at multi-wall carbon nanotubes-quantum dots modified glassy carbon electrodes.

A multi-wall carbon nanotubes (MWNTs)-quantum dots (QDs) composite-modified glassy carbon electrode (GCE) was prepared. The complex was characterized by transmission electron microscopy (TEM). The electrochemical behavior of levodopa at MWNTs and QDs-modified GCEs (MWNTs-QDs/GCE) was studied by cyclic voltammetry (CV) and chronocoulometry (CC). It was found that its electrochemical behavior was a two-charge-two-proton process. The modified electrode had high electrocatalytic activity for levodopa with a standard heterogeneous rate constant of 0.595 cm s(-1), which was greatly increased compared with the values for bare GCE and individual MWNTs modified GCE. The better electrocatalytic activity for levodopa at MWNTs-QDs/GCE may due to a synergistic effect between MWNTs and QDs. This result provides a novel way to promote research on biomicromolecules at nano-dimensions.

Expression of TNF-alpha and VEGF in the esophagus of portal hypertensive rats.

AIM: To investigate the expression of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) in the development of esophageal varices in portal hypertensive rats. METHODS: Thirty male Sprague-Dawley (SD) rats in the model group in which a two-stage ligation of portal vein plus ligation of the left adrenal vein was performed, were divided into three subgroups (M(7), M(14), and M(21)) in which the rats were kiued on the seventh day, the 14(th) d and the 21 d after the complete portal ligation. Thirty male SD rats, which underwent the sham operation in the control group, were also separated into three subgroups (C(7), C(14) and C(21)) corresponding to the models. The expression of TNF-alpha and VEGF in the esophagus of all the six subgroups of rats were measured with immunohistochemical SP technique. RESULTS: The portal pressure in the three model subgroups was significantly higher than that in the corresponding control subgroups (23.82+/-1.83 vs 11.61+/-0.86 cmH(2)O, 20.90+/-3.27 vs 11.43+/-1.55 cmH(2)O and 20.68+/-2.27 vs 11.87+/-0.79 cmH(2)O respectively, P<0.01), as well as the number (9.3+/-1.6 vs 5.1+/-0.8, 11.1+/-0.8 vs 5.4+/-1.3 and 11.7+/-1.5 vs 5.2+/-1.1 respectively, P<0.01) and the total vascular area (78 972.6+/-3 527.8 vs 12 993.5+/-4 994.8 mum(2), 107 207.5+/-4 6461.4 vs 11 862.6+/-5 423.2 mum(2) and 110 241.4+/-49 262.2 vs 11 973.7+/-3 968.5 mum(2) respectively, P<0.01) of submucosal veins in esophagus. Compared to the corresponding controls, the expression of TNF-alpha and VEGF in M(21) was significantly higher (2.23+/-0.30 vs 1.13+/-0.28 and 1.65+/-0.38 vs 0.56+/-0.30 for TNF-alpha and VEGF respectively, P<0.01), whereas there was no difference in M(7) (1.14+/-0.38 vs 1.06+/-0.27 and 0.67+/-0.35 vs 0.50+/-0.24 for TNF-alpha and VEGF respectively, P>0.05) and M(14) (1.20+/-0.25 vs 1.04+/-0.26 and 0.65+/-0.18 vs 0.53+/-0.25 for TNF-alpha and VEGF respectively, P>0.05). And the expression of TNF-alpha and VEGF in M(21) was significantly higher than that in M(7) (2.23+/-0.30 vs 1.14+/-0.38 and 1.65+/-0.38 vs 0.67+/-0.35 for TNF-alpha and VEGF respectively, P<0.01) and M(14) (2.23+/-0.30 vs 1.20+/-0.25 and 1.65+/-0.38 vs 0.65+/-0.18 for TNF-alpha and VEGF respectively, P<0.01), but there was no difference between M(7) and M(14) (1.14+/-0.38 vs 1.20+/-0.25 and 0.67+/-0.35 vs 0.65+/-0.18 for TNF-alpha and VEGF respectively, P>0.05). CONCLUSION: In the development of esophageal varices in portal hypertensive rats, increased TNF-alpha and VEGF may be not an early event, and probably play a role in weakening the esophageal wall and the rupture of esophageal varices.