[Research Progress in Electrochemical Detection and Removal of Micro/Nano Plastics in Water].

Micro/nano plastics （M/NPs） are widely dispersed in the soil， atmosphere， and water environment due to their small particle size， easy adsorption， and strong migration， and have been detected in all major water bodies in recent years. As a type of emerging pollutant， the physiological toxicity of M/NPs has a great impact on human health. The current bottleneck in this research field lies in the precise detection and efficient removal of M/NPs. Electrochemical technology， owing to its advantages of simple portability， sensitivity， and low cost in the detection of M/NPs， has the advantages of environmental friendliness， controllable reaction， and high efficiency in the removal of M/NPs， demonstrating enormous application potential. Based on the pollution status of M/NPs， the application of electrochemical technology to the detection and removal of M/NPs in the water environment was elaborated and summarized. The electrochemical sensing methods of M/NPs and the principles and characteristics of sensor recognition of M/NPs were analyzed. The removal efficiency and influencing factors of M/NPs in water by electro-flocculation， electro-adsorption， electro-oxidation， and electro-reduction technologies were also discussed. The results indicated that the detection of M/NPs particles using electrochemical sensing methods exhibited good characterization performance， and M/NPs could be efficiently removed through electrochemical techniques such as electrocoagulation， electro-adsorption， electro-oxidation， and electro-reduction. The influencing factors of electrochemical technology on the detection and removal of M/NPs were mainly related to sensor devices， electrode materials， material interface regulation， parameter conditions， and reactor systems. In the future， researchers should focus on the design of sensors， the development of electrode materials， and the optimization of reaction processes， which are expected to realize the application of M/NPs from laboratory detection and removal to actual water bodies.

Inhibitory effects of phthalate esters (PAEs) and phthalate monoesters towards human carboxylesterases (CESs).

Phthalate esters (PAEs), accompanied by phthalate monoesters as hydrolysis metabolites in humans, have been widely used as plasticizers and exhibited disruptive effects on the endocrine and metabolic systems. The present study aims to investigate the inhibition behavior of PAEs and phthalate monoesters on the activity of the important hydrolytic enzymes, carboxylesterases (CESs), to elucidate the toxicity mechanism from a new perspective. The results showed significant inhibition on CES1 and CES2 by most PAEs, but not by phthalate monoesters, above which the activity of CES1 was strongly inhibited by DCHP, DEHP, DiOP, DiPP, DNP, DPP and BBZP, with inhibition ratios exceeding 80%. Kinetic analyses and in vitro-in vivo extrapolation were conducted, revealing that PAEs have the potential to disrupt the metabolism of endogenous substances catalyzed by CES1 in vivo. Molecular docking results revealed that hydrogen bonds and hydrophobic contacts formed by ester bonds contributed to the interaction of PAEs towards CES1. These findings will be beneficial for understanding the adverse effect of PAEs and phthalate monoesters.

Inhibition of aflatoxins on UDP-glucuronosyltransferases (UGTs).

Aflatoxins have been recognized as the most harmful mycotoxins leading to various toxic effects. The present study aims to determine the inhibition behavior of aflatoxins on the activity of the important phase II metabolizing enzymes, UDP-glucuronosyltransferases (UGTs), based on in vitro incubation system of recombinant human UGTs-catalyzed glucuronidation of 4-methylumbelliferone (4-MU). 100 µM AFB1 and AFG1 exhibited extensive inhibition towards UGT isoforms especially UGT1A7 and UGT1A8, with the inhibition ratios to be 71.38%, 72.95% and 72.79% for AFB1 to UGT1A7, AFB1 to UGT1A8 and AFG1 to UGT1A8, respectively. Molecular docking results showed that hydrogen bonds and hydrophobic contacts of the particular structure consisting of double furan ring with double bond contributed to the interaction of aflatoxins and UGTs. Kinetics analysis, including inhibition types and kinetics parameters (Ki), and in vitro-in vivo extrapolation (IVIVE) indicated that there might be a medium possibility of inhibition on UGTs by aflatoxins in vivo. In conclusion, the present study indicated that aflatoxins could possibly disturb endogenous metabolism by inhibiting the activity of UGTs so as to exhibit toxic effects.

Simulation of the mechanical behavior of osteons using artificial gravity devices in microgravity.

Aviation medical research shows that disuse osteoporosis will occur after long-term space flight. Even with countermeasures such as exercise and drug treatments, this outcome cannot be avoided in flight. In recent years, the application of artificial gravity devices that change the mechanical microenvironment of bone in microgravity have shown promise in mitigating the risk of disuse osteoporosis. Considering the existence of osteocytes, a fluid-solid coupling finite element model for osteons with two-stage pore structure (Haversian canal, lacunar-canalicular system) was established. In order to study the changes in the mechanical behavior of osteocytes under the action of various artificial gravity (AG) devices, including long-arm centrifuge (LAC), short-arm centrifuge (SAC), and a lower body negative pressure (LBNP) chamber. In addition, the difference in pulsating pressure and static pressure stress caused by the gravity gradient under the AG devices was examined. The simulation results showed that the AG devices could effectively improve the stress level of osteocytes in microgravity. The mechanical microenvironment of osteocytes that was provided by the LAC was closest to that of the Earth's gravitational field. The mechanical stimulation on osteocytes was not significantly improved by the SAC, but from a practical viewpoint, it occupied less space than the LAC. The LBNP chamber created a higher level of stress for osteocytes. Therefore, the LAC was an ideal device for replacing Earth's gravitational field, except for the practical limitations of its physical size. In contrast, the LBNP device had the greatest application potential in training for its expansibility and convenience.

[Therapeutic effects and mechanisms of Opuntia dillenii Haw on atherosclerosis of rats].

The research aimed to investigate the therapeutic effects and mechanisms of Opuntia dillenii Haw polysaccharide (OPS) on atherosclerosis of rats. First atherosclerotic rat models were established by high-fat and high-calcium diet. Thirty days later, the rats were treated with low dosage of OPS (0.2 g x kg(-1) x d(-1)) or high dosage of OPS (0.4 g x kg(-1) x d(-1)) by intraperitoneal injection for 60 days continuously. At the end of treatment, thoracic aorta rings were prepared and vasorelaxation of rat thoracic aorta in different experiment groups were determined by using 620M multi wire myograph system in vitro. Blood and livers of rats were collected. Then plasma levels of total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL) of rats were separately determined using whole automatic biochemical analyzer; protein level of hepatic apolipoprotein B (ApoB) and that of hepatic diglyceride acyltransferase (Dgat1) were measured by Western Blot technique. Results showed that the ability of rat thoracic aorta to relax decreased markedly in the model group compared with that in the normal group, and significant differences existed in vasorelaxation ratios induced by different concentrations of carbamylcholine chloride (Carb) between these two groups (P < 0.01). After OPS treatment, the ability of rat thoracic aorta to relax improved markedly, the vasorelaxation ratios induced by Carb at 5 and 10 µmol x L(-1) were respectively 0.34 ± 0.08 and 0.62 ± 0.15 in the group treated with low dosage of OPS, while the ratios induced by Carb at 1 and 5 µmol x L(-1) were respectively 0.54 ± 0.08 and 0.98 ± 0.02 in the group treated with high dosage of OPS, which were all significantly different with those in the model group (P < 0.01). Plasma contents of TC, TG and LDL reduced significantly by the treatments both with low and high dosages of OPS compared with those in the model group (P < 0.01). Protein level of hepatic ApoB and that of hepatic Dgat1 decreased significantly after the treatment with high dosage of OPS compared with those in the model group (P < 0.01). These results indicate that OPS can markedly improve the vasorelaxation of thoracic aorta of atherosclerotic rats and has significant anti-atherosclerotic effect; inhibiting the expression of ApoB and Dgat1 and thus decreasing the amounts of TC, LDL and TG serving as one of the molecular mechanisms of its antiatherosclerosis effect.

Increased CD4+CD25+ regulatory T cells correlate with poor short-term outcomes in hepatitis B virus-related acute-on-chronic liver failure patients.

BACKGROUND: The roles of CD4(+)CD25(+) regulatory T cells (Treg) in chronicity of hepatitis B virus (HBV) infection have been confirmed. We aimed to explore alteration of Treg in patients with HBV-related acute-on-chronic liver failure (ACLF). METHODS: Thirty-two HBV-related ACLF patients, 44 chronic hepatitis B patients, and 41 healthy controls were recruited. We detected frequencies of peripheral Treg and intrahepatic forkhead winged helix transcription factor (Foxp3)(+) cells. Inhibitory activity of Treg was assessed by functional suppression assays. Serum interferon-γ and interleukin-10 were also determined. RESULTS: Peripheral Treg and intrahepatic Foxp3(+) cells were more markedly increased in ACLF than chronic hepatitis B and controls (all p < 0.001), and the Foxp3(+) cells located predominantly in the portal areas. The Treg frequency was positively correlated with HBV DNA load, international normalized ratio, model of end stage liver disease score, and serum interleukin-10 level in ACLF patients. Functional assays in vitro demonstrated that ACLF patients exhibited higher suppressive effects of Treg on proliferations of autologous CD4(+)CD25(-) T cells than controls. On logistic regression, prolonged international normalized ratio and higher peripheral Treg frequency predicted 30-day survival of ACLF. CONCLUSION: The patients with HBV-related ACLF exhibit increased amounts of Treg, of which redistribution from periphery to liver seems to modulate liver inflammation. Higher Treg amounts are associated with more severe liver disease in ACLF, and its level in combination with international normalized ratio may assist prediction of short-term outcomes of HBV-related ACLF.

[The clinical classification method research of keloid].

OBJECTIVE: To explore the clinical classification method of keloids and providing a thread for the treatment of keloids. METHODS: To summarize the 600 cases of keloid patients we accepted and diagnosed from November 2004 to October 2012, and filling in keloid patients information sheet, recording the keloids form by photographs, analyzing the treatment, putting forward the classification method of keloids in clinic. RESULTS: According to the position and quantity that keloids grow, the keloid patients are divided into four major categories:one in single site, one in each site, more than one in single site and more than one in each site; According to the area and thickness of keloids, the keloid single lesion is divided into four subclasses: type of small area and thin, type of small area and thick, type of large areas and thin,type of large areas and thick; According to the number of lesions, keloid multiple lesions is divided into two subgenera: isolated multiple and dispersion multiple, different kinds of keloids suit different methods of treatment. CONCLUSION: The clinical classification method of keloids can be used to provide thought for the treatment of keloids, and have a good application value.

[Reconstruction of traumatic ear defect by retro-auricular expanded flap and cartilage graft].

OBJECTIVE: To investigate the therapeutic effect of retro-auricular expanded flap and cartilage graft for reconstruction of traumatic ear defect. METHODS: From Aug. 2008 to Aug. 2010, 10 cases of traumatic ear defects were treated with retro-auricular expanded flap and cartilage graft. The expanders (volume, 50 ml) were implanted subcutaneously at retro-auricular area on the first stage. Then the expansion began at 1 week after operation until the volume reached 60 ml. On the second stage, the ear defects were reconstructed with the expanded flaps, rib cartilage framework, as well as skin graft. RESULTS: All the wounds healed primarily without any complication. The patients were followed up for 6 months to 2 years with satisfactory cosmetic results. Good symmetry was achieved. CONCLUSIONS: It is an effective and reliable method to reconstruct traumatic ear defect by retro-auricular expanded flap and cartilage graft.

Transforming growth factor-ß1 phage model peptides isolated from a phage display 7-mer peptide library can inhibit.

BACKGROUND: Transforming growth factor-ß1 (TGF-ß1) is known to have a role in keloid formation through the activation of fibroblasts and the acceleration of collagen deposition. The objective of this current study was to isolate TGF-ß1 phage model peptides from a phage display 7-mer peptide library to evaluate their therapeutic effect on inhibiting the activity of keloid fibroblasts. METHODS: A phage display 7-mer peptide library was screened using monoclonal anti-human TGF-ß1 as the target to obtain specific phages containing ectogenous model peptides similar to TGF-ß1. Enzyme-linked immunosorbent assay (ELISA) was performed to select monoclonal phages with good binding activity, which underwent DNA sequencing. MTT assay and apoptosis assessment were used to evaluate the biological effects of the phage model peptides on keloid fibroblasts. Immunofluorescence assay was employed to show the binding affinity of the model peptides on phages causing keloid fibroblasts. Quantitative real-time PCR analysis was carried out to detect the expressions of nuclear factor κB (NF-κB) mRNA, connective tissue growth factor (CTGF) mRNA and TGF-ß receptor II (TßRII) mRNA in keloid fibroblasts. RESULTS: Specific phages with good results of ELISA were beneficiated. Four phage model peptides were obtained. The data of MTT showed that TGF-ß1 and one phage model peptide (No. 4) could promote keloid fibroblasts proliferation, however, three phage model peptides (No. 1 - 3) could inhibit keloid fibroblasts proliferation. The results of apoptosis assessment showed that the three phage model peptides could slightly induce the apoptosis in keloid fibroblasts. The data of immunofluorescence assay revealed that the model peptides on phages rather than phages could bind to keloid fibroblasts. The findings of quantitative real-time PCR analysis suggested that the expressions of NF-κB mRNA and CTGF mRNA in the three phage model peptide groups decreased, while the expression of TßRII mRNA slightly increased. CONCLUSIONS: Three phage model peptides isolated from a phage display 7-mer peptide library can inhibit keloid fibroblasts proliferation and induce the apoptosis in keloid fibroblasts. They can inhibit the activity of keloid fibroblasts by blocking TGF-ß1 binding to its receptor and then regulating the expressions of NF-κB, CTGF and TßRII.

[Study of TGF-ß1 phage model peptides on inhibiting keloid fibroblasts proliferation].

OBJECTIVE: To isolate the transforming growth factor-beta 1 (TGF-ß1) phage model peptides from phage 12-mer display peptide library to inhibit the proliferation of keloid fibroblasts. METHODS: The phage display 12-mer peptide library was screened for 4 rounds with monoclonal anti-human TGF-ß1 as the target to yield the specific phage model peptides. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used for the quantitative determination of cellular proliferation. Apoptosis was detected by the Annexin V-FITC/PI apoptosis detection kit and the cells were analyzed with flow cytometry. Immunofluorescent assay was employed to show the binding affinity of model peptides for keloid fibroblasts. Quantitative real-time polymerase chain reaction (PCR) was performed to detect the expressions of nuclear factor kappa B (NF-κB) and connective tissue growth factor (CTGF). RESULTS: Ten phage model peptides were obtained and they were similar to TGF-ß1, TGF-ß2, TGF-ß receptor II (TßRII), TGF-ß-induced factor, NF-κB or mitogen-activated protein kinase (MAPK). The results of MTT showed that four phage model peptides (No. 7 - 10) could inhibit the proliferation of keloid fibroblasts (P < 0.05). The results of apoptotic assessment showed that phage model peptides (No. 7 - 10) could slightly trigger the late apoptotic stage of keloid fibroblasts. The data of immunofluorescence assay revealed that the model peptides on phages rather than phages could bind to keloid fibroblasts. The findings of quantitative real-time PCR analysis suggested that the relative expression of NF-κB decreased in phage model peptides groups (No. 7 - 10). The quantitative expression was 0.28, 0.26, 0.46 and 0.30 respectively versus the negative control group. The relative expression of CTGF decreased in phage model peptides groups (No. 7 - 10). The quantitative expression was 0.26, 0.60, 0.34 and 0.17 respectively versus the negative control group. CONCLUSION: Four phage model peptides (No. 7 - 10) isolated from phage display 12-mer peptide library can inhibit the proliferation of keloid fibroblasts via regulating the expressions of NF-κB and CTGF.

Keratinocyte growth factor phage model peptides can promote epidermal cell proliferation without tumorigenic effect.

BACKGROUND: Keratinocyte growth factor (KGF) significantly influences epithelial wound healing. The aim of this study was to isolate KGF phage model peptides from a phage display 7-mer peptide library to evaluate their effect on promoting epidermal cell proliferation. METHODS: A phage display 7-mer peptide library was screened using monoclonal anti-human KGF antibody as the target. Enzyme linked immunosorbent assay (ELISA) was performed to select monoclonal phages with good binding activity. DNA sequencing was done to find the similarities of model peptides. Three-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, immunofluorescence assay and quantitative real-time PCR analysis were employed to evaluate the effect of the phage model peptides on epidermal cells. RESULTS: Thirty-three out of fifty-eight (56.9%) of the isolated monoclonal phages exhibited high binding activity by ELISA. Ten of fifteen obtained phage model peptides were similar to KGF or epidermal growth factor (EGF). MTT assay data showed that four (No. 1 - 4) of the ten phage model peptides could promote epidermal cell proliferation. The expression of keratinocyte growth factor receptor (KGFR) mRNA in the KGF control group and the two phage model peptide groups (No. 1 and No. 2) increased. Expression of c-Fos mRNA and c-Jun mRNA in the KGF control group increased, but did not increase in the four phage model peptide groups (No.1 - 4). CONCLUSION: Four phage model peptides isolated from the phage display 7-mer peptide library can safely promote epidermal cell proliferation without tumorigenic effect.

[Expression and function of sphingosine kinases 1 and 2 in human keloid fibroblasts].

OBJECTIVE: To study the expression and function of sphingosine kinase (SphK) 1 and SphK2 in human keloid fibroblasts. METHODS: Specimens of keloid and surrounding normal skin were collected from 12 patients with keloid during operation. Primary fibroblasts were isolated, cultured, and randomly divided into 3 groups: normal skin group, keloid group, and keloid with transforming growth factor (TGF)-beta1 group cultured with TGF-beta1 for 48 h. Immunofluorescence technique was used to detect the location of SphK1 and SphK2 protein. Real-time PCR and Western blotting were used to measure the mRNA and protein expression levels of SphK1 and SphK2. RESULTS: Sphk1 protein was localized primarily in the nuclei of the fibroblasts, and Sphk2 protein was detected both in the cytoplasm and nuclei in the 3 groups. The mRNA and protein levels of Sphk1 in the keloid group were (0.0608 +/- 0.0190) and (0.8308 +/- 0.1093) respectively, both significantly higher than those of the normal skin group [(0.0383 +/- 0.0147) and (0.6800 +/- 0.1126) respectively, both P < 0.05], but significantly lower than those of the keloid fibroblasts with TGF-beta1 group [(0.0790 +/- 0.0280), P < 0.05, and (1.4267 +/- 0.1938), P < 0.01]. There was no significant differences in the Sphk2 mRNA and protein levels among these 3 groups (all P > 0.05). CONCLUSIONS: Sphk1 plays a leading role in keloid pathogenesis. The SphK1 mRNA and protein levels are increased by TGF-beta1 stimulation in keloid fibroblasts, perhaps indicating that Sphk1 is involved in TGF-beta signal transduction pathway.

[Arsenite removal performance by modified GAC].

Two kinds of Fe-Mn oxide impregnated GAC (FM-GAC-1, FM-GAC-2) were prepared and their arsenite removal performance were studied. The adsorption isotherm and reaction kinetic models of arsenite on the two kinds of modified GAC and influence of solution pH, temperature and co-exist anions were investigated in the study. The results showed FM-GAC-1 and FM-GAC-2 can adsorb arsenite effectively, the adsorption capacities were 32.37 mg x g(-1) and 26.67 mg x g(-1) respectively. The adsorb velocity could be predicted well by applying pseudosecond order rate equation and the chemistry reaction process was the limitation of the reaction for both modified GAC. The lower solution pH was benefit to the removal of arsenite. The adsorption capacity of FM-GAC-1 and FM-GAC-2 decreased with temperature increasing. The adsorption processes were spontaneous heat-discharge processes. Some co-exist anions can influence arsenite adsorption on modified GAC when their concentration were 200 times of arsenite. It was found that SiO3(2-), PO3(2-), NO3(-) had a significant negative influence on arsenite removal by FM-GAC-1 and SiO3(2-), CO3(2-) can markedly decrease arsenite adsorption on FM-GAC-2. As a whole, FM-GAC-1 had better arsenite removal performance than FM-GAC-2.

Effect of heparin on production of transforming growth factor (TGF)-beta1 and TGF-beta1 mRNA expression by human normal skin and hyperplastic scar fibroblasts.

Heparin affects both dermal fibroblast proliferation and collagen and may mediate these effects by altering the levels of transforming growth factor-beta1 (TGF-beta1) production and TGF-beta1 mRNA expression as a wound healing modulator. The purpose of this study is to probe the effect of heparin on TGF-beta1 and TGF-beta1 mRNA production by human normal skin and hyperplastic scar fibroblasts. This research investigates the effect of heparin on TGF-beta1 and TGF-beta1 mRNA production by human normal skin and hyperplastic scar fibroblasts with exposure to 0 microg/mL, 100 microg/mL, 300 microg/mL, or 600 microg/mL heparin for 24, 48, 72, or 96 hours in a serum-free in vitro model. Levels of TGF-beta1 in the supernatants and TGF-beta1 mRNA expression of fibroblasts were determined by enzyme-linked immunosorbent assay (ELISA) and real time RT-PCR, respectively. Heparin (300 microg/mL and 600 microg/mL) stimulated TGF-beta1 production by normal skin (26% to 83%) and hyperplastic scar fibroblasts (63% to 85%), with statistical significance (P < 0.05) at various time points. Heparin (300 microg/mL and 600 microg/mL) also stimulated TGF-beta1 mRNA expression by normal skin (12% to 53%) and hyperplastic scar fibroblasts (33% to 52%), with statistical significance (P < 0.05) at various time points. These effects of heparin on normal skin and hyperplastic scar fibroblasts may have implications for hyperplastic scar formation and wound healing in vivo.

[Effects of recombinant adenovirus-mediated double suicide genes on implanted human keloid: experiment with athymic mice].

OBJECTIVE: To detect the effects of the recombinant adenovirus-mediated double suicide genes constructed by Escherichia coli cytosine deaminase (CD)/5-fluorocytosine (5-Fc) and herpes simplex virus-thymidine kinase (HSV-TK)/ganciclovir (GCV)-CDglyTK on implanted human keloids and mechanisms thereof. METHODS: Twenty nude mice were implanted with human keloid obtained during operation so as to establish mouse keloid models and then were randomly divided into 4 equal groups: Group A, injected with normal saline (NS) into the keloid once per 3 days for 18 days totally, Group B injected with NS into the keloid and injected intraperitoneally with 5-Fc and GCV; Group C injected with CDglyTK into the keloid, and Group D injected with CDglyTK into the keloid and 5-Fc and GCV injected intraperitoneally. The volume of the implanted keloid tissue was measured 2, 7, 14, 21, 28, 35, and 42 days after operation. On day 42 the keloid tissues were removed to undergo morphological examination, TUNEL method was used to examine the apoptosis of the fibroblasts, and the expression of Bcl-2 and BAX, products of apoptosis-related genes, were detected by immunohistochemistry. RESULTS: Compared to those before treatment the volume of the implanted keloid of Group D began to decrease since 14 days after treatment time-dependently (all P < 0.05), and the volumes of the other 3 groups continued to increase and peaked on days 21, 14, or 7 respectively (all P < 0.05). Microscopy showed infiltration of a larger quantity of histiocyte in the keloid tissue, and more obvious collagen disorganization and apoptosis of fibroblasts in Group D than in the other 3 groups. The protein expression of Bcl-2 was more remarkable and the protein expression of BAX was less remarkable in Group D than in the other 3 groups. CONCLUSIONS: The recombinant adenovirus-mediated double suicide gene therapy is effective on the implanted keloid tissue. The main mechanism may be induction of apoptosis in the keloid fibroblasts.