[Research advances on the role and mechanism of chitosan-based wound dressing in wound healing].

The skin is the first barrier to maintain the stability of internal environment of the body and resist harmful factors of external environment, and is easily damaged because of various external factors. When full-thickness skin defects reach a certain level, it is difficult for the skin to repair itself, so wound dressings are needed to promote wound healing. Seeking an ideal dressing that can promote wound healing has long been a hot research topic. Chitosan is a unique biopolysaccharide polymer with good biocompatibility, biodegradability, antibacterial activity, and thermal stability, which has great potential in the development and application of wound dressings. Based on the introduction of properties of chitosan, this article reviews the role and mechanism of chitosan-based wound dressings in wound healing, and summarizes the hemostatic effect, antibacterial effect, delivery effect, and tissue regeneration promotion effect of chitosan, aiming to provide a certain reference for the research and development of new chitosan-based wound dressings in the future.

Dioscin ameliorates methotrexate-induced liver and kidney damages via adjusting miRNA-145-5p-mediated oxidative stress.

Dioscin, one natural product, has various pharmacological actions. However, its effects on methotrexate (MTX)-induced hepatorenal damages still remain unknown. In the present study, the data manifested that dioscin restored the viabilities of L-02 and NRK-52E cells, reduced ALT, AST, Cr, BUN levels, and ameliorated histopathological changes of liver and kidney. Besides, dioscin decreased ROS levels in cells, and adjusted SOD, MDA, GSH and GSH-Px levels in rats. Dioscin reduced the expression levels of miR-145-5p which directly targeted Sirt5, and then regulated the expression levels of SOD1, Nrf2, Gst, Keap1, HO-1, GCLC and NQO1. MiR-145-5p mimic in cells deteriorated ROS levels and decreased Sirt5 expression to accentuate oxidative stress by regulating the expression levels of SOD1, Nrf2, Keap1, which were all reversed by dioscin. Moreover, MTX-induced hepatorenal damage were worsened in mice by Sirt5 siRNA or miR-145-5p agomir, which were also alleviated by dioscin. Dioscin relieved MTX-induced hepatorenal damages through regulating miR-145-5p-medicated oxidative stress, which should be considered as one effective drug to treat the disorder in future.

Suppression of microRNA-101 attenuates hypoxia-induced myocardial H9c2 cell injury by targeting DIMT1-Sp1/survivin pathway.

The article "Suppression of microRNA-101 attenuates hypoxia-induced myocardial H9c2 cell injury by targeting DIMT1-Sp1/survivin pathway, by Z.-X. Guo, F.-Z. Zhou, W. Song, L.-L. Yu, W.-J. Yan, L.-H. Yin, H. Sang, H.-Y. Zhang, published in Eur Rev Med Pharmacol Sci 2018; 22 (20): 6965-6976-DOI: 10.26355/eurrev_201810_16167-PMID: 30402863" has been withdrawn from the authors due to some inaccuracies. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16167.

MiR-23a-5p exacerbates intestinal ischemia-reperfusion injury by promoting oxidative stress via targeting PPAR alpha.

MiR-23a-5p is involved in the occurrence and development of some serious diseases, but its effects on intestinal ischemia-reperfusion (II/R) injury is unclear. In this research, the hypoxia/reoxygenation (H/R) model on IEC-6 cells and II/R model in mice were used. The data showed that the ROS level in model group was significantly increased compared with control group. The level of intestinal MPO was increased and serum SOD was decreased in mice compared with sham group. Moreover, the expression levels of miR-23a-5p in model groups were obviously increased in vitro and in vivo, while the expression levels of PPARα, FOXO3α, PGC-1α, Nrf2, CAT, NQO1, HO-1 and SOD2 were significantly decreased. The double luciferase reporter gene assay showed that there was binding site between miR-23a-5p and PPARα. When miR-23a-5p was inhibited or PPARα gene was overexpressed, H/R-caused cell damage was alleviated and ROS level was decreased compared with NC group. PPARα expression level was increased, accompanied by the increased levels of FOXO3α, PGC-1α, Nrf2, CAT, NQO1, HO-1 and SOD2. After enhancing miR-23a-5p expression or silencing PPARα gene, H/R-caused cell damage was further aggravated compared with NC group, and ROS level was increased associated with the decreased levels of FOXO3α, PGC-1α, Nrf2, CAT, NQO1, HO-1 and SOD2. Our study demonstrated that miR-23a-5p exacerbated II/R injury by promoting oxidative stress via targeting PPARα, which should be considered as one new drug target to treat II/R injury.

MicroRNA-142-3p attenuates hepatic ischemia/reperfusion injury via targeting of myristoylated alanine-rich C-kinase substrate.

MiR-142-3p as one key molecule in oncogenesis and inflammation plays crucial roles in hepatic fibrosis, hepatocellular carcinoma and other liver disease. However, there have no literatures to report its effects on hepatic ischemia-reperfusion (HI/R) injury. In the present work, hypoxia reoxygenation (H/R) models on AML12 and HepG2 cells, and ischemia/reperfusion model in mice were established. The methods of real-time PCR, dual luciferase reporter, mimic, inhibitor, agomir, antagomir and siRNA transfection assays were used. The expression levels of miR-142-3p were decreased in model groups in vitro and in vivo compared with control group or Sham group, which directly targeted MARCKS to regulate its expression. Then, MARCKS activated p38/JNK signal, up-regulated NF-κB expression to accelerate inflammation, and inhibited PI3K/AKT signal to promote apoptosis. Moreover, miR-142-3p mimic in vitro and agomir in vivo lowered the expression levels of MARCKS, thereby alleviating apoptosis and inflammation to relieve HI/R injury. Furthermore, miR-142- 3p inhibitor in vitro and antagomir in vivo up-regulated the expression levels of MARCKS to aggravate HI/R damage via promoting inflammation and apoptosis. Consistently, MARCKS siRNA markedly inhibited HI/R injury by restraining apoptosis and inflamm- ation in mice. MiR-142-3p played a considerable part in adjusting HI/R injury by targeting MARCKS, and miR-142-3p/MARCKS should be a new therapeutic target for HI/R injury.

[Comparison of two epidemic patterns of COVID-19 and evaluation of prevention and control effectiveness: an analysis based on Guangzhou and Wenzhou].

Objective: To compare the epidemiological characteristics of COVID-19 in Guangzhou and Wenzhou, and evaluate the effectiveness of their prevention and control measures. Methods: Data of COVID-19 cases reported in Guangzhou and Wenzhou as of February 29, 2020 were collected. The incidence curves of COVID-19 in two cities were constructed. The real time reproduction number (R(t)) of COVID-19 in two cities was calculated respectively. Results: A total of 346 and 465 confirmed COVID-19 cases were analysed in Guangzhou and Wenzhou, respectively. In two cities, most cases were aged 30-59 years (Guangzhou: 54.9%; Wenzhou: 70.3%). The incidence curve peaked on 27 January, 2020 in Guangzhou and on 26 January, 2020 in Wenzhou, then began to decline in both cities. The peaks of imported COVID-19 cases from Hubei occurred earlier than the peak of COVID-19 incidences in two cities, and the peak of imported cases from Hubei occurred earlier in Wenzhou than in Guangzhou. In early epidemic phase, imported cases were predominant in both cities, then the number of local cases increased and gradually took the dominance in Wenzhou. In Guangzhou, the imported cases was still predominant. Despite the different epidemic pattern, the R(t) and the number of COVID-19 cases declined after strict prevention and control measures were taken in Guangzhou and in Wenzhou. Conclusion: The time and scale specific differences of imported COVID-19 resulted in different epidemic patterns in two cities, but the spread of the disease were effectively controlled after taking strict prevention and control measures.

[Risk assessment and early warning of imported COVID-19 in Guangdong province].

Objective: To assess the imported risk of COVID-19 in Guangdong province and its cities, and conduct early warning. Methods: Data of reported COVID-19 cases and Baidu Migration Index of 21 cities in Guangdong province and other provinces of China as of February 25, 2020 were collected. The imported risk index of each city in Guangdong province were calculated, and then correlation analysis was performed between reported cases and the imported risk index to identify lag time. Finally, we classified the early warming levels of epidemic by imported risk index. Results: A total of 1 347 confirmed cases were reported in Guangdong province, and 90.0% of the cases were clustered in the Pearl River Delta region. The average daily imported risk index of Guangdong was 44.03. Among the imported risk sources of each city, the highest risk of almost all cities came from Hubei province, except for Zhanjiang from Hainan province. In addition, the neighboring provinces of Guangdong province also had a greater impact. The correlation between the imported risk index with a lag of 4 days and the daily reported cases was the strongest (correlation coefficient: 0.73). The early warning base on cumulative 4-day risk of each city showed that Dongguan, Shenzhen, Zhongshan, Guangzhou, Foshan and Huizhou have high imported risks in the next 4 days, with imported risk indexes of 38.85, 21.59, 11.67, 11.25, 6.19 and 5.92, and the highest risk still comes from Hubei province. Conclusions: Cities with a large number of migrants in Guangdong province have a higher risk of import. Hubei province and neighboring provinces in Guangdong province are the main source of the imported risk. Each city must strengthen the health management of migrants in high-risk provinces and reduce the imported risk of Guangdong province.

[Risk assessment of exported risk of COVID-19 from Hubei Province].

Objective: To evaluate the exported risk of COVID-19 from Hubei Province and the imported risk in various provinces across China. Methods: Data of reported COVID-19 cases and Baidu Migration Indexin all provinces of the country as of February 14, 2020 were collected. The correlation analysis between cumulative number of reported cases and the migration index from Hubei was performed, and the imported risks from Hubei to different provinces across China were further evaluated. Results: A total of 49 970 confirmed cases were reported nationwide, of which 37 884 were in Hubei Province. The average daily migration index from Hubei to other provinces was 312.09, Wuhan and other cities in Hubei were 117.95 and 194.16, respectively. The cumulative COVID-19 cases of provinces was positively correlated with the migration index derived from Hubei Province, also in Wuhan and other cities in Hubei, with correlation coefficients of 0.84, 0.84, and 0.81. In linear model, population migration from Hubei Province, Wuhan and other cities in Hubei account for 71.2%, 70.1%, and 66.3% of the variation, respectively. The period of high exported risk from Hubei occurred before January 27, of which the risks before January 23 mainly came from Wuhan, and then mainly from other cities in Hubei. Hunan Province, Henan Province and Guangdong Province ranked the top three in terms of cumulative imported risk (the cumulative risk indices were 58.61, 54.75 and 49.62 respectively). Conclusion: The epidemic in each province was mainly caused by the importation of Hubei Province. Taking measures such as restricting the migration of population in Hubei Province and strengthening quarantine measures for immigrants from Hubei Province may greatly reduce the risk of continued spread of the epidemic.

MicroRNA-27a-3p aggravates renal ischemia/reperfusion injury by promoting oxidative stress via targeting growth factor receptor-bound protein 2.

Renal ischemia-reperfusion (RI/R) injury with high morbidity and mortality is one common clinical disease. Development of drug targets to treat the disorder is critical important. MiR-27a-3p plays important roles in regulating oxidative stress. However, its effects on RI/R injury have not been reported. In this paper, hypoxia/reoxygenation (H/R) models on NRK-52E and HK-2 cells, and RI/R model in C57BL/6 mice were established. The results showed that H/R in vitro decreased cell viability and increased ROS levels in cells, and RI/R caused renal injury and oxidative damage in mice. The expression levels of miR-27a-3p were up-regulated based on real-time PCR and FISH assays in model groups compared with control groups, which directly targeted Grb2 based on dual luciferase reporter assay and co-transfaction test. In addition, miR-27a- 3p markedly reduced Grb2 expression to down-regulate the expression levels of p-PI3K, p-AKT, Nrf2, HO-1, and up-regulate Keap1 expression in model groups. MiR-27a-3p mimics in vitro enhanced H/R-caused oxidative stress via increasing ROS levels and decreasing Grb2 expression to down-regulate PI3K-AKT signal. In contrary, miR-27a-3p inhibitor in vitro significantly reduced H/R-caused oxidative damage via decreasing ROS levels and increasing Grb2 expression to up-regulate PI3K-AKT signal. In vivo, miR-27a- 3p agomir exacerbated RI/R-caused renal damage by decreasing SOD level and increasing Cr, BUN, MDA levels via suppressing Grb2 expression to down-regulate PI3K- AKT signal. However, miR-27a -3p antagomir alleviated RI/R-caused oxidative damage via increasing Grb2 expression to up-regulate PI3k-AKT signal. Grb2siRNA in mice further enhanced RI/R-caused renal injury by increasing Cr, BUN, MDA levels and decreasing SOD level via inhibiting the expression levels of Grb2, Nrf2, HO-1, and increasing Keap1 expression. Our data showed that miR-27a-3p aggravated RI/R injury by promoting oxidative stress via targeting Grb2, which should be considered as one new drug target to treat RI/R injury.

Effect and possible mechanisms of dioscin on ameliorating metabolic glycolipid metabolic disorder in type-2-diabetes.

BACKGROUND: Our previous study revealed that microRNA-125a-5p plays a crucial role in regulating hepatic glycolipid metabolism by targeting STAT3 in type 2 diabetes mellitus (T2DM). Dioscin, a major active ingredient in Dioscoreae nipponicae rhizomes, displays various pharmacological activities, but its role in T2DM has not been reported. PURPOSE: The aim of this study was to investigate the effect of dioscin on T2DM and elucidate its potential mechanism. METHODS: The effect of dioscin on glycolipid metabolic disorder in insulin-induced HepG2 cells, palmitic acid-induced AML12 cells, high-fat diet- and streptozotocin- induced T2DM rats, and spontaneous T2DM KK-Ay mice were evaluated. Then, the possible mechanisms of dioscin were comprehensively evaluated. RESULTS: Dioscin markedly alleviated the dysregulation of glycolipid metabolism in T2DM by reducing hyperglycemia and hyperlipidemia, improving insulin resistance, increasing hepatic glycogen content, and attenuating lipid accumulation. When the mechanism was investigated, dioscin was found to markedly elevate miR-125a-5p level and decrease STAT3 expression. Consequently, dioscin increased phosphorylation levels of STAT3, PI3K, AKT, GSK-3ß, and FoxO1 and decreased gene levels of PEPCK, G6Pase, SREBP-1c, FAS, ACC, and SCD1, leading to an increase in glycogen synthesis and a decrease in gluconeogenesis and lipogenesis. The effects of dioscin on regulating miR-125a-5p/STAT3 pathway were verified by miR-125a-5p overexpression and STAT3 overexpression. CONCLUSIONS: Dioscin showed potent anti-T2DM activity by improving the inhibitory effect of miR-125a-5p on STAT3 signaling to alleviate glycolipid metabolic disorder of T2DM.

[Surface morphology and surface properties of Ti and TiZr implant materials].

Objective: To investigate the effects of hydrophilic treatment on the surface morphology and surface properties of pure titanium and titanium-zirconium alloy implants, and to provide reference for the studies of implant surface modification. Methods: The pure titanium group, the hydrophilic pure titanium group, the titanium zirconium alloy group and the hydrophilic titanium-zirconium alloy group were prepared by sandblasting and acid-etching or hydrophilic sandblasting and acid-etching, (11 specimens in each group). The surface morphology and surface properties of four types of titanium specimens were analyzed by surface contact angle meter, scanning electron microscope (SEM), optical profilometer, atomic force microscope (AFM) and Raman spectrometer. Results: The surface contact angles of hydrophilic pure titanium and hydrophilic titanium-zirconium alloy were 1.6°±0.3° and 1.5°±0.2°, and the surface contact angles of pure titanium and titanium-zirconium alloy were 101.4°±4.6° and 96.2°±3.0°, respectively. SEM showed that the nano-protrusions on the surface of pure titanium and titanium-zirconium alloys were less or even absent, while the nano-protrusions on the surface of hydrophilic pure titanium and hydrophilic titanium-zirconium alloys were relatively more; the nano-protrusions on the surface of hydrophilic pure titanium surface were small and dense relatively, but the nano-protrusions of the hydrophilic titanium-zirconium alloy had large diameters and were dispersed relatively. The optical profiler and AFM showed that the surface roughness of hydrophilic pure titanium and hydrophilic titanium-zirconium alloy was significantly higher than that of pure titanium and titanium-zirconium alloy (P<0.05). Raman spectroscopy showed that only the amorphous TiO(2) was present on the surface of the pure titanium group, while the rutile TiO(2) characteristic peak was observed in the other three groups, but the lateral inhomogeneity was observed. After Raman shift 610 cm(-1), the Raman spectra of four groups were similar. Conclusions: Hydrophilic sandblasting and acid-etching treatment can improve the surface hydrophilicity and surface roughness of pure titanium and titanium zirconium alloy, and improve the surface properties of pure titanium and titanium zirconium alloy implants.

Suppression of microRNA-101 attenuates hypoxia-induced myocardial H9c2 cell injury by targeting DIMT1-Sp1/survivin pathway.

OBJECTIVE: MicroRNAs (miRNAs) are small single-stranded RNAs in eukaryotic cells, which play important regulatory roles in the pathogenesis of various diseases. We aimed to investigate the effects of miRNA-101 (miR-101) on hypoxia-induced myocardial infarction (MI) cell injury model (myocardial H9c2 cell injury model). The possible target gene of miR-101 was also analyzed. MATERIALS AND METHODS: H9c2 cells were exposed to hypoxia treatment. Cell viability, migration, invasion, apoptosis and the expression of miR-101 were detected using CCK-8 assay, transwell assay, flow cytometer analysis, Western blotting and qRT-PCR, respectively. Then, the effects of miR-101 overexpression or suppression on the cell injury induced by hypoxia were assessed. Dual luciferase reporter assay was used to analyze the possible target gene of miR-101. Finally, the effects of dimethyladenosine transferase 1 homolog (DIMT1), the possible target gene of miR-101, on H9c2 cell injury were investigated. RESULTS: Hypoxia significantly induced H9c2 cell injury. miR-101 was up-regulated after hypoxia induction. Hypoxia-induced cell injury was significantly reversed by miR-101 suppression and exacerbated by miR-101 overexpression. DIMT1 was a direct target gene of miR-101. Knockdown of DIMT1 markedly inhibited the protective effects of miR-101 suppression on hypoxia-induced cell injury by suppressing specific protein 1 (Sp1)/Survivin pathway. CONCLUSIONS: We verified the critical roles of miR-101 in regulating myocardial cell injury induced by hypoxia. DIMT1-mediated the Sp1/Survivin pathway was also involved in this process. Our findings replenished the understanding of the regulatory roles of miRNAs in hypoxia-induced MI cell injury and provided new molecular target for therapy and diagnosis of MI.

Effects of remote ischemic preconditioning on myocardial injury and endothelial function and prognosis after percutaneous coronary intervention in patients with acute coronary syndrome.

OBJECTIVE: To explore the effects of remote ischemic preconditioning on myocardial injury and prognosis after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome. PATIENTS AND METHODS: The study was a single center, prospective, randomized, controlled study. A total of 184 patients with unstable angina undergoing elective PCI were randomly assigned to remote ischemic preconditioning group (induced by four times of 5-min inflations of a blood pressure cuff to 200 mmHg around the upper arm, followed by 5-min intervals of reperfusion at 1 h before PCI therapy) or control group (an uninflated cuff around the arm). Successful completion of the PCI eventually included 130 cases of patients, including 72 cases in the remote ischemic preconditioning group and 58 cases in the control group. CK-MB, cTnI, sICAM-1, sVCAM-1 and Hs-CRP levels were measured at 6 am. of the day operating PCI and at 24 h after PCI in the two groups. Major adverse cardiac events were recorded of two groups of patients in the postoperative 6 months. (MACE, including recurrence of angina pectoris, myocardial infarction and death). RESULTS: There were no statistically significant differences in baseline indicators between the 2 groups. CK - MB, cTnI, sICAM-1, sVCAM-1 and Hs-CRP levels in patients with remote ischemic preconditioning group were significantly lower than those form the control group after PCI (p < 0.05), but there were no significant differences between the occurrence of MACE in the postoperative 6 months (p > 0.05). CONCLUSIONS: Remote ischemic preconditioning can reduce PCI related myocardial injury and protect vascular endothelial function.

Relation between blood pressure variability and early renal damage in hypertensive patients.

OBJECTIVE: The objective of the present study was to observe the relation between blood pressure variability (BPV) and early renal damage in hypertensive patients. PATIENTS AND METHODS: A total of 118 hypertensive patients were consecutively selected. General parameters including sex, age, duration, and grade of hypertension, antihypertensive drugs taken, smoking status, blood sugar, blood lipid level, body mass index, indexes of 24-h ambulatory blood pressure monitoring and renal function including cystatin C (CysC), serum creatinine (SCr), angiotensin II (Ang II), microalbuminuria (mALb), and urine creatinine (UCr) were measured. Glomerular filtration rate (eGFR), endogenous creatinine clearance rate (Ccr), and urine albumin/creatinine ratio (UACR) were calculated by CysC level, SCr level, and mALb and UCr level respectively. The 24-h ambulatory blood pressure monitoring indexes included 24-h mean systolic blood pressure variability (24h-SBPV), 24-h mean diastolic blood pressure variability (24h-DBPV), day mean systolic blood pressure variability (d-SBPV), day mean diastolic blood pressure variability (d-DBPV), night mean systolic blood pressure variability (n-SBPV), and night mean diastolic blood pressure variability (n-DBPV). RESULTS: Sixty-four hypertensive patients (54.24%) were non-dipper, and the baseline data of the two groups were comparable. The 24h-SBPV, 24h-DBPV, d-DBPV, n-SBPV and SCr, eGFR, and Ccr of the two groups showed no significant differences. The d-SBPV, n-DBPV, CysC, and Ang II of the non-dipper group were significantly higher than those of the dipper group (p<0.05). The mALb in both groups increased and was more obvious in the non-dipper group. UACR of the non-dipper group was significantly higher than that of dipper group (p<0.05), while UCr showed no difference. By Pearson correlation, d-SBPV and n-DBPV correlated positively (p<0.05) with CysC, Ang II, mALb, and UACR. CONCLUSIONS: BPV of hypersensitive patients, especially the d-SBPV and n-DBPV, was closely related to indexes of early renal damage including CysC, Ang II, mALb, and UACR.

Identification and functional characterization of microRNAs reveal a potential role in gastric cancer progression.

PURPOSE: To investigate the potential candidate microRNA (miRNA) biomarkers for the clinical diagnosis, classification, and prognosis of gastric cancer (GC). METHODS: We use bioinformatics overlapping subclasses analysis to find the tumor grade and lymphatic metastasis-related GC specific miRNAs from the Cancer Genome Atlas (TCGA) database. Then, we further investigated these GC specific miRNAs distributions in different GC clinical features and their correlations overall survival on the basis of GC patients' information and their related RNA sequencing profile from TCGA. Finally, we randomly selected some of key miRNAs use qRT-PCR to confirm the reliability and validity. RESULTS: 22 GC specific key miRNAs were identified (Fold-change >2, P < 0.05), 11 of them were discriminatively expressed with tumor size, grade, TNM stage and lymphatic metastasis (P < 0.05). In addition, nine miRNAs (miR-196b-5p, miR-135b-5p, miR-183-5p, miR-182-5p, miR-133a-3p, miR-486-5p, miR-144-5p, miR-129-5p and miR-145-5p) were found to be significantly associated with overall survival (log-rank P < 0.05). Finally, four key miRNAs (miR-183-5p, miR-486-5p, miR-30c-2-3p and miR-133a-3p) were randomly selected to validation and their expression levels in 53 newly diagnosed GC patients by qRT-PCR. Results showed that the fold-changes between TCGA and qRT-PCR were 100 % in agreement. We also found miR-183-5p and miR-486-5p were significantly correlated with tumor TNM stage (P < 0.05), and miR-30c-2-3p and miR-133a-3p were associated with tumor differentiation degree and lymph-node metastasis (P < 0.05). These verified miRNAs clinically relevant, and the bioinformatics analysis results were almost the same. CONCLUSION: These key miRNAs may functions as potential candidate biomarkers for the clinical diagnosis, classification and prognosis for GC.

Colorimetric detection of DNA damage by using hemin-graphene nanocomposites.

A colorimetric method for detection of DNA damage was developed by using hemin-graphene nanosheets (H-GNs). H-GNs were skillfully synthesized by adsorping of hemin on graphene through π-π interactions. The as-prepared H-GNs possessed both the ability of graphene to differentiate the damage DNA from intact DNA and the catalytic action of hemin. The damaged DNA made H-GNs coagulated to different degrees from the intact DNA because there were different amount of negative charge exposed on their surface, which made a great impact on the solubility of H-GNs. As a result, the corresponding centrifugal supernatant of H-GNs solution showed different color in the presence of 3,3',5,5'-tetramethylbenzidine (TMB) and H2O2, which could be discriminated by naked eyes or by ultraviolet (UV)-visible spectrometer. Based on this, the damaged effects of styrene oxide (SO), NaAsO2 and UV radiation on DNA were studied. Results showed that SO exerted most serious damage effect on DNA although all of them damaged DNA seriously. The new method for detection of DNA damage showed good prospect in the evaluation of genotoxicity of new compounds, the maximum limit of pesticide residue, food additives, and so on, which is important in the fields of food science, pharmaceutical science and pesticide science.

XPS and biocompatibility studies of titania film on anodized NiTi shape memory alloy.

A dense titania film is fabricated in situ on NiTi shape memory alloy (SMA) by anodic oxidation in a Na(2)SO(4) electrolyte. The microstructure of the titania film and its influence on the biocompatibility of NiTi SMA are investigated by scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), inductively coupled plasma mass spectrometry (ICPMS), hemolysis analysis, and platelet adhesion test. The results indicate that the titania film has a Ni-free zone near the surface and can effectively block the release of harmful Ni ions from the NiTi substrate in simulated body fluids. Moreover, the wettability, hemolysis resistance, and thromboresistance of the NiTi sample are improved by this anodic oxidation method.

Microstructural characteristics and biocompatibility of a Type-B carbonated hydroxyapatite coating deposited on NiTi shape memory alloy.

Microstructural characteristics and biocompatibility of a Type-B carbonated hydroxyapatite (HA) coating prepared on NiTi SMA by biomimetic deposition were characterized using XRD, SEM, XPS, FTIR and in vitro studies including hemolysis test, MTT cytotoxicity test and fibroblasts cytocompatibility test. It is found CO(3)(2-) groups were present as substitution of PO(4)(3-) anions in HA crystal lattice due to Type-B carbonate. The growth of Type-B carbonated HA coating in SBF containing HCO(3)(-) ions is stable during all periods of biomimetic deposition. The carbonated HA coating has better blood compatibility than the chemically-polished NiTi SMA. There was a good cell adhesion to this HA coating surface and cell proliferation in the vicinity of the coating was better than that for the chemically-polished NiTi SMA. Thus biomimetic deposition of this carbonated HA coating is a promising way to improve the biocompatibility of NiTi SMA for implant applications.

Enhancement of apoptosis of human hepatocellular carcinoma SMMC-7721 cells through synergy of berberine and evodiamine.

Berberine and evodiamine, two kinds of alkaloids, have been reported to show many activities. In the present paper, inhibitory activities of the two compounds and their mixtures on human hepatocellular carcinoma SMMC-7721 cells were investigated, and the inhibitory rates, apoptosis, cell cycle distribution and tumor necrosis factor-alpha (TNF-alpha) were all tested and described. The results indicate that the mixtures of the two compounds showed the highest inhibition effect (50.00%) as compared with berberine and evodiamine used individually (20.24% and 16.33%, respectively) over 48 h. Through fluorescence microscope and flow cytometry (FCM) analysis, the cell apoptosis and cell cycle distribution of SMMC-7721 induced by the synergy of the two compounds was made evident. Furthermore, the TNF-alpha value in the mixture treated group was much higher (p<0.05) than in the other two groups. Thus, the combined use of berberine and evodiamine could significantly enhance the apoptosis of SMMC-7721 cells, which will be useful to further anti-cancer therapy and research.