[Adsorption Performance of Walnut Green Husk Biochar for Heavy Metals].

The biochars of WP300, WP500, and WP700 were prepared by pyrolyzing walnut green husk under 300℃, 500℃, and 700℃ with the oxygen-free condition for removing Pb2+, Cu2+, and Cd2+ in an aqueous solution. The results revealed that WP500 prepared under the medium pyrolysis temperature achieved the best adsorption performance for heavy metals, and the highest removal efficiency was reached when the solution pH was 8, in which the removal efficiency of Pb2+, Cu2+, and Cd2+ were 97.87%, 99.78%, and 71.15%, respectively. The required biochar dosage for heavy metal removal varied under different adsorption conditions. In the single-metal system, the optimal dosage for WP500 in the Pb2+, Cu2+, and Cd2+ solutions was 1.3 g·L-1, 2.1 g·L-1, and 1.9 g·L-1, respectively, whereas in the pollution metals system, the optimal biochar dosage was 5.1 g·L-1. In addition, the adsorption capacity of WP500 for the three heavy metals followed the order of Pb2+>Cu2+>Cd2+ under the single and combined-metals system, indicating that there were no synergistic or antagonistic effects among these three adsorbates. The fitting results of the adsorption isotherm model suggested that various immobilization methods existed in adsorption process between WP500 and Pb2+, Cu2+, and Cd2+. The kinetic fitting results suggested that the main reaction between WP500 and Pb2+, Cu2+, and Cd2+ was chemical adsorption. The mechanisms of WP500 for heavy metals involved pore-filling, electrostatic attraction, ion-exchange, mineral precipitation, complexation, and π-π electron donor-accepter interaction. To conclude, this study offered a new insight for the resource utilization of the waste walnut green husk.

The N6-Methyladenosine (m6A) Methylation Gene YTHDF1 Reveals a Potential Diagnostic Role for Gastric Cancer.

PURPOSE: Gastric cancer (GC) is aggressive cancer with a high mortality rate worldwide. N6-methyladenosine (m6A) RNA methylation is related to tumorigenesis, which is dynamically regulated by m6A modulators ("writer," "eraser," and "reader"). We conducted a comprehensive analysis of the m6A genes of GC patients in TCGA datasets to identify the potential diagnostic biomarkers. MATERIALS AND METHODS: We analyzed the expression profile of m6A genes in the TCGA cohort and constructed a diagnostic-m6A-score (DMS) by the LASSO-logistic model. In addition, by consensus cluster analysis, we identified two different subgroups of GC risk individuals by the expression profile of m6A modulators, revealing that YTHDF1's expression variation profile in GC diagnosis. We also performed RT-qPCR and WB verification in 17 pairs of GC specimens and paired adjacent non-tumor tissues and GC cell lines, and verified the expression trend of YTHDF1 in five GEO GC datasets. YTHDF1 expression and clinical features of GC patients were assessed by the UALCAN. RESULTS: The DMS with high specificity and sensitivity (AUC = 0.986) is proven to distinguish cancer from normal controls better. Moreover, we found that the expression profile variation of YTHDF1 was significantly associated with the high-risk subtype of GC patients. RT-qPCR and Western blot results are consistent with silicon analysis, revealing that YTHDF1's potential oncogene role in GC tumor. CONCLUSION: In conclusion, we developed the m6A gene-based diagnostic signature for GC and found that YTHDF1 was significantly correlated with the high-risk subtype of GC patients, suggesting that YTHDF1 might be a potential target in GC early diagnosis.

Dysregulated N6-methyladenosine methylation writer METTL3 contributes to the proliferation and migration of gastric cancer.

Accumulating evidence implies that N6-methyladenosine (m6A) methylation participated in the tumorigenesis of gastric cancer (GC). Here we synthetically analyzing the prognostic value and expression profile of seven m6A methylation-relevant genes through silico analysis of sequencing data downloaded from The Cancer Genome Atlas, Kaplan-Meier plotter, and Gene Expression Omnibus database. We explored the methyltransferase-like 3 (METTL3) expression in GC cell line and tumor tissues by reverse transcription quantitative polymerase chain reaction and western blot analysis. The m6A methylation status of total RNA was measured by m6A RNA methylation quantification kit. Small interfering RNA was used to establish METTL3 knockdown cell lines. We also measure the proliferation and migration capability GC cell. Furthermore, we detect the epithelial cell mesenchymal transition marker and m6A methylation level after METTL3 knock down. Our result revealed that METTL3 was significantly increased in GC tissues compared with control in big crowd data sets. Survival analysis showed that METTL3 serve as a poor prognostic factor for GC patients. The expression level of METTL3 gradually increased with the progress of tumor stage and grade. GFI1 is an important transcription factor associated with METTL3. We verified the up-trend of METTL3 in messenger RNA and protein expression and observed a significant increase in the m6A methylation status of total RNA in the GC cells and tissues. METTL3 knockdown inhibited total RNA m6A methylation level, as well as cell proliferation and migration capacity. Moreover, METTL3 knockdown decreased α-smooth muscle actin. Taken together, our finding revealed that m6A methylation writer METTL3 serve as an oncogene in tumorigenesis of GC.

[Effect of Electroacupuncture on Expression of Ghrelin and mRNA Expression of Its Receptor in Functional Dyspesia Rats].

OBJECTIVE: To explore the effect of electroacupuncture (EA) on the expression of Ghrelin and mRNA expression of its receptor in functional dyspepsia (FD) rats. METHODS: Totally 80 rats were divided into the normal group, the model group, the drug therapy group, and the EA group according to random digit table, 20 in each group. FD model was duplicated by clipping tail modeling. Drug containing cisapride [2 mL/100 g, 0.09 g/(kg x d)] was administered to rats in the drug therapy group from the 3rd day after successful modeling, once per day. EA at Zusanli (ST36) (0.3-0.5 cun) and Taichong (LR3) (0.1-0.2 cun) was performed in the EA group. The twirling of needle was performed to the subsidence of needle, and then the needle was connected to HANS-200A Acupoint Nerve Stimulating Device using disperse-dense wave at 2 Hz, 2 mA, 30 min each time, once per day. Six days consisted of one therapeutic course, two courses in total with an interval of one day. The intestinal propulsive rate of ink was observed. Ghrelin protein expression in gastric tissue was detected by Western blot. mRNA expression of growth hormone secretagogue receptor (GHS-R) in stomach, hypothalamus, and hippocampus was detected using Real-time PCR respectively. RESULTS: Compared with the normal group, the intestinal propulsive rate of ink, Ghrelin protein expression in gastric tissue, mRNA expression of GHS-R in stomach, hypothalamus, and hippocampus decreased in the model group (P < 0.05, P < 0.01). Compared with the model group, the intestinal propulsive rate of ink, Ghrelin protein expression in gastric tissue, mRNA expression of GHS-R in stomach, hypothalamus, and hippocampus increased in the EA group (P < 0.01); mRNA expression of GHS-R in stomach, hypothalamus, and hippocampus increased in the drug therapy group (P < 0.01). Compared with the drug therapy group, Ghrelin protein expression in gastric tissue, mRNA expression of GHS-R in hypothalamus increased in the EA group (P < 0.05, P < 0.01). CONCLUSION: EA could regulate Ghrelin content and GHS-R mRNA expression of FD rat hypothalamus, hippocampus, and gastric tissue, and promote the intestinal propulsive rate of ink.

Correlation of AIM2 expression in peripheral blood mononuclear cells from humans with acute and chronic hepatitis B.

The AIM2 (absent in melanoma 2) protein promotes host defenses against invading viruses and pathogenic bacteria through corresponding adapter molecules leading to the initiation of innate immune responses. We investigated the expression of AIM2 in peripheral blood mononuclear cells (PBMCs) from patients with acute hepatitis B (AHB) and chronic hepatitis B (CHB) during different clinical phases, and analyzed the correlation between AIM2 and clinical profiles in these groups. This study indicated that there is higher expression of AIM2, IL-1ß, and IL-18 in AHB compared with expression in CHB. The expression of AIM2 mRNA was significantly negatively correlated with serum hepatitis B virus (HBV) load, HBeAg, and significantly positively correlated with IL-1ß and IL-18 in AHB patients and CHB patients with immune clearance, which suggests that AIM2 expression is correlated with the immune clearance of HBV in the host. We summarized that there is a higher immune status in AHB, and a lower immune response in CHB. This suggests that the down-regulation of AIM2 may be associated with the chronic development of HB.

[Spatiotemporal variation analysis and identification of water pollution sources in the Zhangweinan River basin].

In this study, several statistical methods including cluster analysis, seasonal Kendall test, factor analysis/principal component analysis and principal component regression were used to evaluate the spatiotemporal variation of water quality and identify the sources of water pollution in the Zhangweinan River basin. Results of spatial cluster analysis and principal component analysis indicated that the Zhangweinan River basin can be classified into two regions. One is the Zhang River upstream located in the northwest of the Zhangweinan River basin where water quality is good. The other one covers the Wei River and eastern plain of the Zhangweinan River basin, where water is seriously polluted. In this region, pollutants from point sources flow into the river and the water quality changes greatly. Results of temporal cluster analysis and seasonal Kendall test indicated that the study periods may be classified into three periods and two different trends were detected during the period of 2002-2009. The first period was the year of 2002-2003, during which water quality had deteriorated and serious pollution was observed in the Wei river basin and eastern plain of the Zhangweinan River basin. The second period was the year of 2004-2006, during which water quality became better. The year of 2007-2009 is the third period, during which water quality had been improved greatly. Despite that water quality in the Zhangweinan River basin had been improved during the period of 2004-2009, the water quality in the Wei River (southwestern part of the basin), the Wei Canal River and the Zhangweixin River (eastern plain of the basin) is still poor. Principal component analysis and multi-linear regression of the absolute principal component scores showed that the main pollutants of the Zhangweinan River basin came from point source discharge such as heavy industrial wastewater, municipal sewage, chemical industries wasterwater and mine drainage in upstream. Non-point source pollution such as agricultural pollution and runoff pollution caused by heavy rainfalls also showed considerable impact on water quality in the Zhangweinan River basin during flood seasons. These results provide useful information for better pollution control strategies in the Zhangweinan River basin.

Strontium fructose 1,6-diphosphate prevents bone loss in a rat model of postmenopausal osteoporosis via the OPG/RANKL/RANK pathway.

AIM: To evaluate the protective effects of strontium fructose 1,6-diphosphate (FDP-Sr), a novel strontium salt that combined fructose 1,6-diphosphate (FDP) with strontium, on bone in an ovariectomy-induced model of bone loss. METHODS: Eighty female Sprague-Dawley rats were ovariectomized (OVX) or sham-operated. Three months later, the rats were assigned to six groups (10 for each): sham-operated, OVX control, OVX+FDP-Sr (110, 220, or 440 mg/kg), or OVX+strontium ranelate (SR, 180 mg/kg). Drugs were administered orally for 3 months. When the treatment was terminated, the following parameters were assessed: bone mineral density (BMD), the biomechanical properties of the femur and lumbar vertebrae, trabecular histomorphology, serum phosphorus, calcium, bone-specific alkaline phosphatase (B-ALP), tartrate-resistant acid phosphatase 5b (TRACP5b), N-telopeptide of type I collagen (NTx) and a series of markers for oxidative stress. Receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) levels in serum were measured using ELISA and their gene expression levels in the bone were measured using R-T PCR. RESULTS: Treatment with FDP-Sr (220 or 440 mg/kg) or SR (180 mg/kg) significantly increased the BMD and improved the bone microarchitecture and bone strength in OVX rats. The treatments also decreased in the levels of H(2)O(2) and MDA, restored the CAT level in serum and bone marrow, increased the serum B-ALP and decreased NTx and TRACP 5b in OVX rats. Treatment with FDP-Sr decreased the RANKL level, and increased the OPG level in serum in a dose-dependent manner. It also significantly down-regulated the RANKL expression and up-regulated OPG expression in bone marrow. CONCLUSION: FDP-Sr may be an effectve treatment for postmenopausal osteoporosis that acts, in part, via a decrease in osteoclastogenesis through the OPG\RANKL\RANK pathway.

Novel poly(amidoamine)s with pendant primary amines as highly efficient gene delivery vectors.

Three poly(amidoamine)s with pendant primary amines were synthesized by Michael polyaddition of a diamine to N,N-methylenebis(acrylamide). The poly(amidoamine)s with primary and tertiary amines possess a high buffer capacity between pH = 5 and 7, which facilitates the escape of polymer/DNA complexes from endosomes according to the 'proton sponge hypothesis'. In vitro cytotoxicity of poly(amidoamine)s depends on the side-chain structure of the polymer. Polymers 1a-1c can condense plasmid DNA by electrostatic interactions to form nanosized polyelectrolyte complexes with a positive surface charge. In vitro transfection results indicate that the transfection efficiency of polymer 1b under optimized conditions is comparable to that of commercial branched PEI 25,000.

[A study on origin of genetic ethics problem and countermeasure].

The genetic ethical problem is one of problems which are the most disputable or difficult to resolve perfectly in the fields of life science. In these years the research for the problems is being concentrated on the types of genetic ethical problem and the ways to resolve them. But the systematic research for origin of genetic ethical problem is rare to be known. Thus it seems to be short of theoretical support to bring forward corresponding countermeasure. In this paper we focus on the evolving germ of genetic ethical problem and its evolving rule from the twofold views of human biological evolution and cultural evolution. A human being is a double offspring with biological evolution and cultural evolution . And he is a species which has both biological and cultural attribute on the earth. Through comparing and studying human biological evolution , cultural evolution, and characteristics of both biological attribute and cultural attribute, we bring forward a viewpoint that all ethical problems originate from a conflict originating from interplay of human biological evolution and cultural evolution. We intend to seek for the gist of theory and practice in order to research for genetic ethical problem and put forward some corresponding countermeasures. At the same time we'll advance a series of corresponding countermeasures of genetic ethical problem. The final aim in the paper is that not only some of our opinions will be admitted, but also through learning and understanding genetic ethical problem and its origin, the decision-makers and investigators in genetics field will be promoted to have more sense of fate and responsibility , so that the average public are able to misunderstand less and understand more for studying and genetics applying. We all work hard for genetics career to make it in healthy and continuing development and give a lot of happiness to human beings.

Cardioprotective effects of Astragali Radix against isoproterenol-induced myocardial injury in rats and its possible mechanism.

The purpose of the present study was to investigate the effects of the Chinese medical herb Astragali Radix on myocardial injury in vivo and its possible mechanisms. Myocardial injury in rats was induced by the subcutaneous injection of a high dose of isoproterenol for 10 days, and the therapeutic effects of Astragali Radix were observed. Cardiac hemodynamics, heart coefficient and marker enzymes in serum showed that Astragali Radix prevented isoproterenol-induced myocardial damage. Astragali Radix also improved the antioxidant status by decreasing the lipid peroxidative product malondialdehyde and increasing the activity of the antioxidant enzyme superoxide dismutase. The observed depressions in sarcoplasmic reticulum Ca2+-ATPase mRNA and protein expression as well as Ser(16)-phosphorylated phospholamban protein expression in isoproterenol-treated rats were attenuated by Astragali Radix treatment. Moreover, treatment with Astragali Radix showed higher myocardial cAMP content compared with the isoproterenol-alone group. These results suggest that the antioxidant property and partial prevention of changes in protein and gene expression of cardiac sarcoplasmic reticulum Ca2+ regulatory proteins which may be mediated through the cAMP pathway could help to explain the beneficial effects of Astragali Radix on myocardial injury in vivo.

Modification of alterations in cardiac function and sarcoplasmic reticulum by astragaloside IV in myocardial injury in vivo.

Astragaloside IV, the primary pure saponin isolated from Astragalus membranaceus has been found to have potent cardioprotective effects. In this study, we aim to investigate if the beneficial effects of astragaloside IV on cardiac function are associated with improvement in sarcoplasmic reticulum Ca(2+)-pump function in myocardial injury in vivo. Myocardial injury in rats was induced by subcutaneous injection of a high dose of isoproterenol, and the therapeutic effect of astragaloside IV was observed. Isoproterenol-treated rats showed widespread subendocardial necrosis, a rise in serum lactate dehydrogenase and creatine kinase, formation of lipid oxide product malondialdehyde and inhibition of left ventricular diastolic and systolic function, which suggested severe myocardial injury and acute heart failure. Moreover, sarcoplasmic reticulum Ca(2+)-uptake ability and Ca(2+)-ATPase (SERCA2a) activity were significantly reduced. And the level of SERCA2a mRNA and protein expression was also markedly decreased, associated with a decrease in Ser(16)-phosphorylated phospholamban protein expression, while total phospholamban level was unchanged in the isoproterenol-treated group compared with controls. However, these biochemical and hemodynamic changes in the acute failing hearts were prevented by treatment of isoproterenol-induced rats with astragaloside IV. Likewise, the observed reductions in sarcoplasmic reticulum Ca(2+)-pump function as well as in SERCA2a mRNA and protein levels and the phosphorylation level of phospholamban in the injured hearts were attenuated by astragaloside IV treatment. These results suggest that the beneficial effect of astragaloside IV on isoproterenol-induced myocardial injury may be due to its ability to prevent changes of SERCA2a and Ser(16)-phosphorylated phospholamban protein expression and, thus, may prevent the depression in sarcoplasmic reticulum Ca(2+) transport and improve cardiac function.

Engagement of PSGL-1 enhances beta(2)-integrin-involved adhesion of neutrophils to recombinant ICAM-1.

AIM: The interactions of selectins and their ligands initiate the process of leukocyte migrating into inflamed tissue. P-selectin glycoprotein ligand 1 (PSGL-1) is the best characterized ligand of selectins, and has been demonstrated to mediate the adhesion of leukocytes to all three selectins in vivo. PSGL-1 not only functions as an anchor molecule to capture the leukocytes to the activated endothelial cells by its interaction with selectins, but also transduces the signals to activate leukocytes. Our present work aimed to investigate the mechanism by which PSGL-1-mediated signal activates neutrophils and enhances the adhesion to the endothelial cells. METHODS: We detected the effects of the engagement of PSGL-1 with monoclonal antibodies (mAb) or P-selectin on the adhesion of neutrophils to the recombinant intercellular adhesion molecule-1 (ICAM-1), and on the expression of beta(2)-integrin. Additionally, the role of cytoskeleton in these process was studied by using inhibitor cytochalasin B. RESULTS: The engagement of PSGL-1 increased the expression of beta(2)-integrin on the surface of neutrophils and enhanced the adhesion of neutrophils to the recombinant ICAM-1. mAb against CD18 impaired the adhesion of PSGL-1-engaged neutrophils to ICAM-1. Moreover, the inhibitor cytochalasin B largely blocked the increase of CD18 expression as well as the adhesion of PSGL-1-engaged neutrophils to ICAM-1. CONCLUSION: The PSGL-1-transduced signals can enhance beta(2)-integrin-involved adhesion of neutrophils to the recombinant ICAM-1, and this process depends on the dynamics of cytoskeleton.

Effects of low-dose capsaicin on L-type calcium current in guinea pig ventricular myocytes.

The purpose of this study was to examine the effects of low-dose capsaicin (CAP) on L-type calcium current (I(Ca-L) ) in guinea pig ventricular myocytes and the underlying mechanism. I(Ca-L) was examined in isolated single guinea pig ventricular myocytes by using whole-cell patch clamp technique. CAP (1-25 nmol/L) increased the voltage-dependently activated peak amplitude of I(Ca-L) and downshifted the current-voltage (I-V) curve. CAP (1, 10, 25 nmol/L) increased the peak amplitude of I(Ca-L) from -9.67+/-0.7 pA/pF to -10.21+/-0.8 pA/pF (P>0.05), to -11.37+/-0.8 pA/pF and to -12.84+/-0.9 pA/pF (P<0.05), respectively. CAP 25 nmol/L shifted the steady-state activation curve of I(Ca-L) to the left and changed half activation potential (V(0.5)) from (-20.76+/-2.0) mV to (-26.71+/-3.0) mV (P<0.05), indicating that low-dose CAP may modify the voltage-dependent activation of calcium channel. Low-dose of CAP did not affect the steady-state inactivation curve of I(Ca-L) or half-recovery time of Ca(2+) channel from inactivation. Ruthenium red (RR, 10 micromol/L), a vanilloid receptor (VR1) blocker, antagonized the effects of low-dose CAP. These results suggest that low-dose CAP increases I(Ca-L) mainly by shifting its steady-state activation curve to the left. Such effects may be mediated by VR1.

Electrophysiological effects of capsaicin on guinea pig papillary muscles.

The cardiac electrophysiological effects of capsaicin (CAP) were examined in guinea pig papillary muscles using intracellular microelectrode technique. The results obtained are as follows: (1) the duration of action potential (APD) in normal papillary muscles was decreased by CAP (30, 60, 120 micromol/L) in a concentration-dependent manner; (2) in partially depolarized papillary muscles, 60 micromol/L CAP not only reduced APD, but also decreased the amplitude of action potential, overshoot and maximal velocity of phase 0 depolarization; (3) pretreatment with L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) could completely block the effects of CAP (60 micromol/L); (4) pretreatment with ruthenium red (20 micromol/L), a vanilloid receptor (VR) blocker, did not affect the actions of capsaicin on papillary muscles. All these results suggest that the effects of CAP on papillary muscles are likely due to a decrease in calcium influx which is not mediated by VR.

Electrophysiologic effects of capsaicin on pacemaker cells in sinoatrial nodes of rabbits.

AIM: To study the electrophysiologic effects of capsaicin on isolated pacemaker cells in sinoatrial (SA) nodes of rabbits and its possible action mechanism(s). METHODS: Parameters of action potential (AP) in SA node were recorded using intracellular microelectrode technique. RESULTS: By perfusion with capsaicin (10 micromol/L), the amplitude of action potential (APA) and maximal rate of depolarization (Vmax) were decreased from (55+/-4) mV to (49+/-4) mV (P<0.05) and from (2.4+/-0.5) V/s to (1.7+/-0.2) V/s (P<0.05). The velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF) were decreased from (91+/-34) mV/s to (70+/-30) mV/s (P<0.01) and from (186+/-14) beat/min to (162+/-10) beat/min (P<0.01). The absolute value of maximal diastolic potential (MDP) was decreased from (49+/-3) mV to (44+/-2) mV (P<0.01). However, the duration of 90 % repolarization of action potential (APD90) was prolonged from (149+/-21) ms to (167+/-27) ms (P<0.01). Pretreatment with ruthenium red (RR, 10 micromol/L), a vanilloid receptor (VR1) blocker, did not affect the effects of capsaicin on SA node cells. Both elevation of calcium concentration (5 mmol/L) in superfusate and application of L-type Ca2+ channel agonist Bay-K-8644 (0.5 micromol/L) antagonized the effects of capsaicin on pacemaker cells. Beta-adrenergic agonist isoproterenol (Iso, 20 nmol/L) inhibited the capsaicin-induced prolongation of repolarization and decrease of MDP. CONCLUSION: Capsaicin exerted a negative chronotropic action and induced a delayed repolarization of pacemaker cells in SA nodes of rabbits. These effects were likely due to reduction in calcium influx and/or potassium efflux, but were not mediated by VR1.

Electrophysiological effects of phytoestrogen genistein on spontaneous activity of rabbit atrioventricular node cells.

The purpose of this study was to determine the electrophysiological effects of genistein (GST) on spontaneous activity of atrioventricular (AV) node and the underlying mechanism(s). Action potentials in AV node cells were recorded using intracellular microelectrode technique. GST not only reduced the amplitude of action potential (APA), maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization (VDD), and rate of spontaneous firing (RSF), but also prolonged 90% duration of action potential (APD(90)) in a concentration-dependent manner. The effects of GST (50 micromol/L) could be blocked completely by pretreatment with Bay K8644 (0.25 micromol/L), an agonist of L-type calcium channel. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L), a nitric oxide (NO) synthase inhibitor, did not affect the effects of GST on AV node cells. Elevation of Ca(2+) concentration (5 mmol/L) in superfusate antagonized the effects of GST (50 micromol/L). These results suggest that GST exerted a negative electrophysiological effects of spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but had no association with NO release.