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Mailiupian (MLP) is a new patent functional food that consists of Crataegi Fructus, Notoginseng Radix, and Ginkgo Folium, which was reported to be active in improving the microcirculation based on formulation screening. However, whether it is effective in inhibiting thrombus and its mechanism has not been evaluated. Therefore, in the present study, the models of arterial thrombosis induced by FeCl3 and the models of APE by ADP were established to evaluate the antithrombosis effect of MLP. Results showed that MLP markedly reduced the weight and size of wet thrombosis in FeCl3‐induced rats and decreased the recovery time from symptoms of APE mice. MLP was proved to prolong APTT, PT, TT and improve the levels of t‐PA and 6‐keto‐PGF1α significantly, meanwhile, PAI‐1 and TXB2 were reduced apparently. By comparing tail bleeding time, MLP showed antithrombotic effects, but without the risk of bleeding, taking aspirin as a control. Practical applications: Our experiments proved that MLP, a new patent health food, acted on both coagulation and fibrinolytic systems and the platelet aggregation to play antithrombosis roles, providing a theoretical basis for applications of MLP in preventing or curing thrombosis diseases. [ABSTRACT FROM AUTHOR]

Hepatitis C virus (HCV)-induced human hepatocellular carcinoma (HCC) progression may be due to a complex multi-step processes. The developmental mechanism of these processes is worth investigating for the prevention, diagnosis and therapy of HCC. The aim of the present study was to investigate the molecular mechanism underlying the progression of HCV-induced hepatocarcinogenesis. First, the dynamic gene module, consisting of key genes associated with progression between the normal stage and HCC, was identified using the Weighted Gene Co-expression Network Analysis tool from R language. By defining those genes in the module as seeds, the change of co-expression in differentially expressed gene sets in two consecutive stages of pathological progression was examined. Finally, interaction pairs of HCV viral proteins and their directly targeted proteins in the identified module were extracted from the literature and a comprehensive interaction dataset from yeast two-hybrid experiments. By combining the interactions between HCV and their targets, and protein-protein interactions in the Search Tool for the Retrieval of Interacting Genes database (STRING), the HCV-key genes interaction network was constructed and visualized using Cytoscape software 3.2. As a result, a module containing 44 key genes was identified to be associated with HCC progression, due to the dynamic features and functions of those genes in the module. Several important differentially co-expressed gene pairs were identified between non-HCC and HCC stages. In the key genes, cyclin dependent kinase 1 (CDK1), NDC80, cyclin A2 (CCNA2) and rac GTPase activating protein 1 (RACGAP1) were shown to be targeted by the HCV nonstructural proteins NS5A, NS3 and NS5B, respectively. The four genes perform an intermediary role between the HCV viral proteins and the dysfunctional module in the HCV key genes interaction network. These findings provided valuable information for understanding the mechanism of HCV-induced HCC progression and for seeking drug targets for the therapy and prevention of HCC. [ABSTRACT FROM AUTHOR]

• E2F2 and MCM4 were downregulated in the uterus tissues. • Over expression of E2F2 inhibits decidualization via promoting the cell cycle. • E2F2 inhibits E2P4-induced decidualization via regulation of MCM4. Cell cycle modulation is an important event during decidualization. E2F2 is a transcription regulator that plays a vital role in cell cycle regulation. However, the biological role of E2F2 in decidualization has not yet been identified. In this study, estrogen (E2) and progestin (P4)-induced in vitro and in vivo decidualization models were applied. Our data showed that the expression levels of E2F2 and its downstream target MCM4 were downregulated in the uterus tissues of E2P4-treated mice compared with control mice. In hESCs, exposure to E2P4 resulted in a significant decrease in E2F2 and MCM4 expression. E2P4 treatment reduced hESC proliferation and ectopic expression of E2F2 or MCM4 elevated the viability of E2P4-treated hESCs. In addition, ectopic expression of E2F2 or MCM4 restored the expression of G1 phase-associated proteins. The ERK pathway was inactivated in E2P4-treated hESCs. Treatment with ERK agonist Ro 67-7476 restored the expression of E2F2, MCM4, and G1 phase-associated proteins that were inhibited by E2P4. Moreover, Ro 67-7476 retracted the levels of IGFBP1 and PRL that were induced by E2P4. Collectively, our results indicate that E2F2 is regulated by ERK signaling and contributes to decidualization via regulation of MCM4. Therefore, E2F2/MCM4 cascade may serve as promising targets for alleviating decidualization dysfunction. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) can function as tumor suppressors or oncogene promoters during tumor development. In this study, low levels of expression of miR-196b were detected in patients with chronic myeloid leukemia. Bisulfite genomic sequencing PCR and methylation-specific PCR were used to examine the methylation status of the CpG islands in the miR-196b promoter in K562 cells, patients with leukemia and healthy individuals. The CpG islands showed more methylation in patients with chronic myeloid leukemia compared with healthy individuals (P<0.05), which indicated that low expression of miR-196b may be associated with an increase in the methylation of CpG islands. The dual-luciferase reporter assay system demonstrated that BCR-ABL1 and HOXA9 are the target genes of miR-196b, which was consistent with predictions from bioinformatics software analyses. Further examination of cell function indicated that miR-196b acts to reduce BCR-ABL1 and HOXA9 protein levels, decrease cell proliferation rate and retard the cell cycle. A low level of expression of miR-196b can cause up-regulation of BCR-ABL1 and HOXA9 expression, which leads to the development of chronic myeloid leukemia. MiR-196b may represent an effective target for chronic myeloid leukemia therapy. [ABSTRACT FROM AUTHOR]

This study aimed to develop a noninvasive, economical and effective subclinical renal damage (SRD) risk assessment tool to identify high-risk asymptomatic people from a large-scale population and improve current clinical SRD screening strategies. Based on the Hanzhong Adolescent Hypertension Cohort, SRD-associated variables were identified and the SRD risk assessment score model was established and further validated with machine learning algorithms. Longitudinal follow-up data were used to identify child-to-adult SRD risk score trajectories and to investigate the relationship between different trajectory groups and the incidence of SRD in middle age. Systolic blood pressure, diastolic blood pressure and body mass index were identified as SRD-associated variables. Based on these three variables, an SRD risk assessment score was developed, with excellent classification ability (AUC value of ROC curve: 0.778 for SRD estimation, 0.729 for 4-year SRD risk prediction), calibration (Hosmer—Lemeshow goodness-of-fit test p = 0.62 for SRD estimation, p = 0.34 for 4-year SRD risk prediction) and more potential clinical benefits. In addition, three child-to-adult SRD risk assessment score trajectories were identified: increasing, increasing-stable and stable. Further difference analysis and logistic regression analysis showed that these SRD risk assessment score trajectories were highly associated with the incidence of SRD in middle age. In brief, we constructed a novel and noninvasive SRD risk assessment tool with excellent performance to help identify high-risk asymptomatic people from a large-scale population and assist in SRD screening. [ABSTRACT FROM AUTHOR]

Early vascular aging (EVA) increases cardiovascular mortality, but its long-term determinants are unknown. We included 2098 participants with ≥4 blood pressure (BP) measurements from childhood to adulthood (from the Hanzhong Adolescent Hypertension Cohort study) to investigate the impact of child-to-adult cumulative BP exposure on EVA patterns in midlife. Participants with EVA had significantly higher long-term BP burden than those with normal vascular age in midlife despite being much younger. Child-to-adult cumulative burden and trends of systolic and diastolic BP were associated with vascular age (standardized regression coefficient [β] =.31 to.53; P <.001 for all). Higher cumulative systolic and diastolic BP exposure significantly increased the risk of EVA in midlife (odds ratio, OR=1.67 to 2.75, P <.05 for all). All associations were independent of socio-demographics and cardiovascular risk factors. Excluding participants who were receiving anti-hypertensive, antidiabetic, or lipid-lowering treatments did not substantially change the above associations. This study, for the first time, reported that high cumulative child-to-adult BP exposure accelerated the vascular aging process. Stabilizing BP across life course could be beneficial to vascular health in the long run. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM) is a complex disease that is caused by an impairment in the secretion of β-cell insulin and by a peripheral resistance to insulin. Most patients suffering from T2DM and from obesity exhibit insulin resistance in the muscles, liver, and fat, resulting in a reduced response of these tissues to insulin. In healthy individuals, pancreatic islet β-cells secrete insulin to regulate the increase in blood glucose levels. Once these β-cells fail to function, T2DM develops. Despite the progress achieved in this field in recent years, the genetic causes for insulin resistance and for T2DM have not yet been fully discovered. The present study aims to characterize T2DM by comparing its gene expression with that of normal controls, as well as to identify biomarkers for early T2DM. Gene expression profiles were downloaded from the Gene Expression Omnibus, and differentially expressed genes (DEGs) were identified for type 2 diabetes. Furthermore, functional analyses were conducted for the gene ontology and for the pathway enrichment. In total, 781 DEGs were identified in the T2DM samples relative to healthy controls. These genes were found to be involved in several biological processes, including cell communication, cell proliferation, cell shape, and apoptosis. We constructed a protein-protein interaction (PPI) network, and the clusters in the PPI were analyzed by using ClusterONE. Six functional genes that may play important roles in the initiation of T2DM were identified within the network. [ABSTRACT FROM AUTHOR]

Background: The triglyceride-glucose index (TyG index) has emerged as a reliable surrogate marker of insulin resistance associated with arterial stiffness. However, most studies were based on a cross-sectional design, and few studies have evaluated the longitudinal impact of the TyG index on arterial stiffness. This study aimed to investigate the associations of single time point measurement and the long-term trajectory of the TyG index with arterial stiffness in a Chinese cohort. Methods: Data are derived from the Hanzhong Adolescent Hypertension Cohort study. A total of 2480 individuals who participated in the 2017 survey was included in the cross-sectional analysis. A sample of 180 individuals from the sub-cohort with follow-up data in 2005, 2013, and 2017 was enrolled in the longitudinal analysis. The TyG index was calculated as ln (fasting triglyceride [mg/dL] × fasting glucose [mg/dL]/2), and arterial stiffness was determined using brachial-ankle pulse wave velocity (baPWV). The latent class growth mixture modeling method was used to identify the TyG index trajectories from 2005 to 2017. Results: In the cross-sectional analysis, the median age of the study population was 42.8 (39.8, 44.9) years, and 1351 (54.5%) were males. Each one-unit increment in TyG index was associated with a 37.1 cm/s increase (95% confidence interval [CI] 23.7–50.6 cm/s; P < 0.001) in baPWV, and similar results were observed when the TyG index was in the form of quartiles. In the longitudinal analysis, we identified three distinct TyG index trajectories and found that the highest TyG index trajectory carried the greatest odds of increased arterial stiffness, with a fully adjusted odds ratio (OR) of 2.76 (95% CI 1.40, 7.54). Conclusions: Elevated levels of baseline TyG index and higher long-term trajectory of TyG index were independently associated with increased arterial stiffness. Monitoring immediate levels and longitudinal trends of the TyG index may help with the prevention of arterial stiffness in the long run. [ABSTRACT FROM AUTHOR]

Looks at developments in DNA chip technology. Various synonyms of DNA chip; Functions of a DNA chip; Principle of the DNA chip technology; Future applications of the DNA chip.

The pulsatile stress in the microcirculation may contribute to development or progression of chronic kidney disease. However, there is no prospective data confirming whether pulsatile stress in early life affect renal function in middle age. The authors performed a longitudinal analysis of 1738 participants aged 6–15 years at baseline, an ongoing Adolescent Prospective Cohort with a follow‐up of 30 years. The authors evaluated the association between pulsatile stress in childhood and adult subclinical renal damage (SRD), adjusting for related covariates. Pulsatile stress was calculated as resting heart rate × pulse pressure. Renal function was assessed with estimated glomerular filtration rate (eGFR) and urine albumin‐to‐creatinine ratio (uACR). The results showed that pulsatile stress in childhood was associated with adult SRD (Relative Risk, 1.43; p =.032), and the predictive value of combined pulse pressure and heart rate for SRD was higher than either of them alone. The high pulsatile stress in childhood increased the risk of adult SRD in males (RR, 1.92; p =.003), but this association was not found in females (RR, 0.91; p =.729). Further, the participants were categorized into four groups on the basis of pulsatile stress status in childhood and adulthood. Male patients with high pulsatile stress during childhood but normal pulsatile stress as adults still had an increased risk of SRD (RR, 2.04; 95% CI, 1.18–3.54), while female patients did not (RR, 0.96; 95% CI, 0.46–1.99). The study demonstrated that high pulsatile stress in childhood significantly increased the risk of adult SRD, especially in males. Adequate control of pulse pressure and heart rate from childhood, in the long‐term, is very important for preventing kidney damage. [ABSTRACT FROM AUTHOR]

Stage 1 hypertension, newly defined by the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) hypertension guideline, has been the subject of significant interest globally. This study aims to assess the impact of the new blood pressure (BP) stratum on subsequent subclinical cardiovascular outcomes in low‐risk young adults. This longitudinal study consisted of 1020 young adults (47.7% female; ages 18–23 years) free of cardiovascular disease from the Hanzhong Adolescent Hypertension Cohort with up to 25‐year follow‐up since 1992–1995. Outcomes were available through June 2017. Young adults with stage 1 hypertension accounted for 23.7% of the cohort. When it comes to middle adulthood, subjects with early life stage 1 hypertension were more likely to experience BP progression, and they had a 1.61‐fold increased risk of high‐risk brachial‐ankle pulse wave velocity (baPWV) and a 2.92‐fold risk of left ventricular hypertrophy (LVH) comparing with their normotensive counterparts. Among participants without any active treatment in midlife, the risk associated with stage 1 hypertension for BP progression was 2.25 (95% confidence interval [CI] = 1.41–3.59), high‐risk baPWV was 1.58 (95% CI = 1.09–2.79), LVH was 2.75 (95% CI = 1.16–6.48), and subclinical renal damage (SRD) was 1.69 (95% CI = 1.02–2.82) compared with the normal BP group. Overall, young adults with stage 1 hypertension had significantly higher risks for midlife subclinical cardiovascular outcomes than normotensive subjects. BP management targeting low‐risk young adults is of importance from both clinical and public health perspectives. [ABSTRACT FROM AUTHOR]

Background: Elevated plasma homocysteine (Hcy) and high-sensitivity C-reactive protein (hsCRP) levels are independent risk factors for cardiovascular diseases. However, it is unclear whether the coexistence of these conditions accelerates the risk of arterial stiffness. Our study aimed to evaluate the association of combined Hcy and hsCRP with arterial stiffness in Chinese middle-aged adults. Material/Methods: We conducted a 12-year longitudinal study in 220 individuals in Hanzhong, China, from 2005 to 2017. The average age at follow-up was 41.83 ± 3.10 years. Demographic information, medical history, anthropometric measurements, and blood pressure as well as urine and fasting blood samples, including Hcy, hsCRP, and brachial-ankle pulse wave velocity (baPWV) were measured and analyzed. Results: BaPWV levels showed a linear growth trend with the increasing of hsCRP (p for trend <0.01). The ORs in the highest quartile compared to the lowest quartile were 1.985 (95% CI 0.776–5.077; p = 0.152) and 3.960 (95% CI 1.468–10.684; p= 0.007) for Hcy and hsCRP, respectively. When Hcy and hsCRP were combined, subjects in both the highest quartile of Hcy and hsCRP (Hcy ≥15.50 μmol/L and hsCRP ≥0.82 μmol/L) had a 12.68-fold increased risk of developing arterial stiffness at the 12-year follow-up compared to those in the lowest quartile of Hcy and hsCRP (Hcy ≤9.91 μmol/L and hsCRP ≤0.19 μmol/L) after adjusting for potential confounders. Conclusions: The present study demonstrated that the combination of elevated serum Hcy and hsCRP may contribute to an increased risk of arterial stiffness. [ABSTRACT FROM AUTHOR]

Background: Dietary sodium affects fluctuations in blood pressure (BP) and vascular function. Cardiotrophin-1 (CT-1), a stress-induced cytokine that belongs to the interleukin 6 family, is released by cells in response to potentially harmful stresses and plays a pivotal role in congestive heart failure, hypertension and arterial stiffness. In this study, we performed a randomized trial to confirm the effects of altered salt intake on the serum CT-1 levels in humans. Methods: Forty-four subjects (18–65 years of age) were selected from a rural community in northern China. All subjects initially maintained a baseline period for 3 days, transitioned to a low-salt (LS) diet for 7 days (3.0 g/day of NaCl) and then a high-salt (HS) diet for an additional 7 days (18.0 g/day of NaCl). Results: For the whole group, the serum CT-1 concentrations were significantly increased in the HS period compared to those of the LS period (293.50 ± 137.70 vs. 360.40 ± 162.83 pg/mL, p = 0.040). The serum CT-1 concentrations significantly decreased from the baseline period to the LS diet (419.91 ± 123.50 to 256.49 ± 109.75 pg/mL, p < 0.01) and significantly increased from the LS to HS diet (256.49 ± 109.75 to 414.39 ± 191.21 pg/mL, p < 0.01). These changes were observed in salt-sensitive (SS) individuals but not in salt-resistant (SR) individuals. In addition, a significant positive relationship was observed between the changes in the CT-1 concentrations and systolic BP as well as the changes in the mean arterial pressure from the LS period to the HS period (r = 0.376, p = 0.012; r = 0.311, p = 0.040). The serum CT-1 concentrations were positively correlated with the 24-h urinary sodium-to-potassium (Na/K) excretion ratios during both of the LS and HS diet intervention periods in SS subjects (r = 0.621, p < 0.01), but this correlation was not evident in SR subjects (r = 0.208, p = 0.107). Conclusions: Our study indicates that variations in dietary salt intake affect the serum CT-1 levels in Chinese adults. [ABSTRACT FROM AUTHOR]

Problems such as air pollution caused by engine burning fossil fuels are becoming increasingly severe. Consequently, the pursuit of clean and efficient energy alternatives, as well as enhancements in the combustion of fossil fuels, have emerged as potential avenues for resolving these challenges. Firstly, a 3D simulation model of the engine is made using the CONVERGE program. Then, the biodiesel-hydrogen (0%, 5%, 10%, and 15%) blends are employed to investigate the combustion processes for the diesel-fuel engine at various loading (50%, 75%, and 100%). Finally, the response surface approach is employed to optimize the biodiesel-hydrogen engines' combustion and emission parameters. The findings demonstrate that combustion pressure and temperature in engine cylinders will also rise as the hydrogen level increases. The hydrogen addition to the engine can enhance its combustion and emission properties. The outcomes prove that 0.656 is the ideal value for multi-objective optimization analysis using the response surface method. The engine reaches optimal working conditions when the hydrogen energy percentage is 6.9%, the load is 100%, and EGR is 7.7%. At this moment, the BSFC, BTE, HC, and NO x emissions were 208.31 g/(kW·h), 41.06%, 340 ppm, and 490 ppm, respectively. • Effects of hydrogen addition on combustion and emission characteristics are investigated in a highland. • The optimization method integrated with the RSM has been developed. • The RME is employed to investigate the multi-objective optimization. • The hydrogen addition fuel plays a very important role. [ABSTRACT FROM AUTHOR]

Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low-sodium diet, a 7-day high-sodium diet, and a 7-day high-sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Plasma pentraxin-3 decreased significantly during the low-salt period compared to baseline (0.57 ± 0.19 ng/mL vs 0.72 ± 0.33 ng/mL, P = .012) and increased during the high-salt period (0.68 ± 0.26 ng/mL vs 0.57 ± 0.19 ng/mL, P = .037). Potassium supplementation inhibited salt-induced increase in pentraxin-3 (0.56 ± 0.21 ng/mL vs 0.68 ± 0.26 ng/mL, P = .015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r = -.349, P = .02), DBP (r = -.414, P = .005), MAP (r = -.360, P = .017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na+ periods (r = .269, P = .012) and a negative relationship with 24 hours urinary potassium excretion during high-salt and high-salt plus potassium periods (r = -.246, P = .02). These correlations remained significant after adjusting for confounders. Pentraxin-3 responses were more prominent in salt-sensitive individuals than salt-resistant individuals. Dietary salt and potassium interventions significantly altered circulating pentraxin-3. [ABSTRACT FROM AUTHOR]

Background/Aims: Elevated serum uric acid (UA) was intimately correlated with vascular stiffness and abnormal ankle brachial index (ABI) in various populations. These correlations lost significance after adjustment for estimated glomerular filtration rate (eGFR), indicating that the association of UA and brachial-ankle pulse wave velocity (baPWV) or ABI might be driven by kidney function. UA is predominantly eliminated through the kidneys, and metabolic disorders can influence the clearance of UA. In this study, we aimed to explore the putative correlation between FEUA and baPWV or ABI to determine to what extent the associations with UA were affected by renal function. Methods: This cross-sectional study enrolled 2351 participants, who underwent general health screening in Hanzhong people’s hospital from March to June of 2017. BaPWV and ABI were measured using a volume-plethysmographic apparatus (BP-203RPEII; Nihon Colin, Tokyo, Japan). FEUA was divided into quartiles: Q1:FEUA≤3.07; Q2: 3.07 9.19. Results: Lower FEUA predicted a higher prevalence of high baPWV and low ABI (p for trend <0.001). The respective ORs for high baPWV from the first to the third quartiles of FEUA were 1.777(1.323, 2.387); 1.561(1.158, 2.104); and 1.680 (1.250, 2.259). The prevalence of low ABI was greatly elevated with the decrement of FEUA [ORs for the first to third FEUA quartiles were 6.977(2.062, 23.610); 5.123(1.475, 17.790); and 2.685(0.709, 10.171), respectively]. The association of FEUA and ABI was independent of related confounding factors. However, the association between FEUA and baPWV was greatly influenced by corresponding confounders, especially gender. The efficacy of FEUA in the prediction of low ABI was stronger than that of serum UA. However, serum UA was more powerful in the prediction of high baPWV. Conclusion: Kidney function exerted a profound influence on the relationship between UA and baPWV or ABI, revealing complex interactions among cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

With the rapid development of industry, the diesel engine as a power source has brought many benefits in promoting economic growth and industrial automation. However, the diesel engine cannot underestimate the harm to air pollution and human health. Therefore, the requirements for the improvement of diesel engine emission standards are higher and higher. Since the introduction of emission regulations to limit the emission of harmful emissions from diesel engines to the environment, the diesel oxidation catalyst (DOC) has been an essential part of the diesel exhaust system. The DOC is one of the most significant catalysts for diesel engine aftertreatment catalysts. Its primary function is to oxidize unburned hydrocarbon (HC) and carbon monoxide (CO) produced in the combustion process into harmless water (H 2 O) and carbon dioxide (CO 2). At the same time, it can also convert nitric oxide (NO) in engine exhaust into nitrogen dioxide (NO 2) for passive regeneration of downstream diesel particulate filter (DPF) and improve the nitrogen oxide (NO x) conversion efficiency of selective catalytic reduction (SCR). This review covers the status, preparation methods, the influence and measures of sulfur dioxide (SO 2) on catalysts, and the methods of developing anti-SO 2 catalysts in the future of DOC. Firstly, the working principle and composition of DOC were discussed. Secondly, the preparation method and process of DOC were introduced. Thirdly, the development trend of DOC was analyzed. Then this paper focused on the impact of SO 2 on DOC and the measures to alleviate SO 2 poisoning. Finally, the possible methods of anti-SO 2 DOC design in the future were prospected. The work in this paper can effectively promote the application of DOC. Based on the work done in this paper, the researchers can efficiently select appropriate DOC according to the future research situation. [Display omitted] • Processes of preparation method and develop are listed. • Optimization applications in diesel engine are investigated. • The future trend of anti SO 2 catalysts is discussed. • Improvement suggestions for performance enhancement of diesel oxidation catalysts are proposed. [ABSTRACT FROM AUTHOR]

An electrochemical sensor is developed in this work based on the new perovskite-type nanomaterial LaNiTiO-FeO for sensitive determination of o-phenylenediamine (OPD). As-synthesized materials and the surface of as-fabricated electrochemical sensor are characterized by X-ray diffraction, atomic force microscope, and electrochemical impedance spectroscopy, respectively. The results of characterizations depict that the sample is of nanoscaled complex oxides consisting of perovskite structure and spinel structure, and has good conductive properties. The construction and experimental conditions of the electrochemical sensor are also optimized. The electrochemical properties of OPD at glassy carbon electrode modified with LaNiTiO-FeO are investigated in alkaline solution (NaOH). The new electrochemical sensor exhibits high electrocatalytic activity and stability in NaOH, and a promotion of electrochemical oxidation of OPD at low potentials can be obviously observed. A wide linear range is obtained from 1.0 × 10 to 7.0 × 10 M with a relative low detection limit of 0.15 μM (S/N = 3) under optimal conditions. Furthermore, the sensor exhibits reliable results for the determination of OPD in commercial samples. [ABSTRACT FROM AUTHOR]

Ornithine decarboxylase antizyme (OAZ) has recently emerged as a potential therapeutic target in various malignant tumors because it plays vital roles in cellular functions including proliferation, differentiation, apoptosis and genomic stability. Therefore, there is a significant interest in discovering its function in chronic myeloid leukemia (CML). Firstly, OAZ1 mRNA was measured by qRT-PCR in 43 cases with CML and 23 controls, and we demonstrated that it is significantly down-regulated in CML patients. To further understand its functions in CML pathogenesis, OAZ1 was overexpressed, and the human leukemia PCR array analysis was used to monitor the expression of key genes commonly involved in leukemia development, classification and therapeutic response. We found several favorable up-regulation factors including CXCL10, DAPK1 and IKZF3. In conclusion, OAZ1 may be a useful therapeutic target in CML due to its potential ability to induce erythroid differentiation and cell apoptosis. These functions were proven to be associated with several gene changes that were directly or indirectly caused by OAZ1. The mechanism of how OAZ1 affects other genes remains to be elucidated. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Purpose: The association between Toll-like receptor 2 (TLR2) −196 to −174del polymorphism and Toll-like receptor 4 (TLR4) polymorphisms (Asp299Gly, Thr399Ile, and 3725G>C) and gastric cancer risk are still conflicting. For better understanding of the effects of these four polymorphisms on gastric cancer risk, a meta-analysis was performed. Methods: An extensive search was performed to identify all case-control studies investigating such associations. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the relationship. Results: A total of 21 studies (3,436 cases and 4,239 controls) were found to be eligible for meta-analysis. In the overall analysis, a significantly increased risk was observed in TLR4 Asp299Gly polymorphism (G allele vs. A allele: OR=1.84, 95%CI: 1.41, 2.39; GA vs. AA: OR=1.89, 95%CI: 1.43, 2.48; Recessive model: OR=1.90, 95%CI: 1.44, 2.49) and TLR4 Thr399Ile polymorphism (T allele vs. C allele: OR=1.97, 95%CI: 1.22, 3.18; TC vs. CC: OR=1.94, 95%CI: 1.19, 3.15; Recessive model: OR=1.98, 95%CI: 1.21, 3.21), whereas no associations were found in any genetic models of TLR2 −196 to −174del and TLR4 3725G>C polymorphisms. Similar results were found in the subgroup analyses by ethnicity. However, we detected that A allele carriers of the TLR4 Asp299Gly polymorphism might have an increase risk of gastric cancer in the Helicobacter pylori-positive population (G allele vs. A allele: OR=2.01, 95%CI: 1.22, 3.31). Conclusion: The results of this meta-analysis indicate that the TLR4 Asp299Gly and Thr399Ile polymorphisms are risk factors for gastric cancer development. [ABSTRACT FROM AUTHOR]

Abstract: Chronic myeloid leukemia (CML) is associated with overexpression of BCR-ABL1, a nonreceptor tyrosine kinase critical for malignant transformation. We investigated whether non-coding microRNAs (miRNAs) targeting BCR-ABL1 mRNA contribute to the pathogenesis of CML. Indeed, miR-30a targeted BCR-ABL1 and was underexpressed in bone marrow from CML patients. In K562 leukemia cells, overexpression of miR-30a reduced ABL1 and BCR-ABL1 protein expression, decreased proliferation, and arrested cell cycle progression between G1 and S. These findings strongly suggest that miR-30a acts as a tumor suppressor by downregulating ABL1 and BCR-ABL1 expression. Upregulation of miR-30a in hematopoietic cells may have therapeutic efficacy against CML. [Copyright &y& Elsevier]

Abstract: Outbreaks of hand, foot, and mouth disease caused by enterovirus 71 (EV71) have become considerable threats to the health of infants and young children. To identify the cellular long noncoding RNAs (lncRNAs) involved in the host response to EV71 infection, we performed comprehensive lncRNA and mRNA profiling in EV71-infected rhabdomyosarcoma cells through microarray. We observed the differential expression of more than 4800 lncRNAs during infection. Further analysis showed 160 regulated enhancer-like lncRNA and nearby mRNA pairs, as well as 313 regulated Rinn’s lncRNA [M. Guttman I. Amit, M. Garber, C. French, M.F. Lin, D. Feldser, M. Huarte, O. Zuk, B.W. Carey, J.P. Cassady, M.N. Cabili, R. Jaenisch, T.S. Mikkelsen, T. Jacks, N. Hacohen, B.E. Bernstein, M. Kellis, A. Regev, J.L. Rinn, E.S. Lander. Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals. Nature 458 (2009) 223–227, A.M. Khalil, M. Guttman, M. Huarte, M. Garber, A. Raj, D. Rivea Morales, K. Thomas, A. Presser, B.E. Bernstein, A. van Oudenaarden, A. Regev, E.S. Lander, J.L. Rinn. Many human large intergenic noncoding RNAs associate with chromatin-modifying complexes and affect gene expression. Proc. Natl. Acad. Sci. USA 106 (2009) 11667–11672] and nearby mRNA pairs. The results provided information for further research on the prevention and treatment of EV71 infection, as well as on distinguishing severe and mild EV71 cases. [Copyright &y& Elsevier]

The oncogene, microRNA-155, is significantly elevated in GBM (glioblastoma multiforme), regulating multiple genes associated with cancer cell proliferation, apoptosis and invasiveness. Thus, miR-155 can theoretically become a target for enhancement of the chemotherapy in cancer. Down-regulating miR-155 to enhance the effect of taxol has not been studied in human GBM. Human GBM U251 cells were treated with taxol and the miR-155 inhibitor alone or in combination. IC50 values were dramatically decreased in cells treated with miR-155 inhibitor combined with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR-155 inhibitor significantly enhanced apoptosis in U251 cells. The data suggest that miR-155 blockage increased the chemosensitivity to taxol in GBM cells, making combined treatment an effective therapeutic strategy for controlling the growth by inhibiting EAG1 expression. [ABSTRACT FROM AUTHOR]

Abstract: Chromodomain helicase DNA binding protein 5 (CHD5) is a potent tumor suppressor that serves as a master regulator of a tumor-suppressive network. Examination of the role played by CHD5 in a wide range of human cancers is warranted. In this study, we focused on the epigenetic modification and tumor-suppressive role of CHD5 in lung cancer. We measured CHD5 mRNA and protein expression in lung cancer cells, lung cancer tissues, and their corresponding noncancerous lung tissues using real-time PCR and Western blot analysis. We then determined the methylation status of the CHD5 promoter in these samples using methylation-specific sequencing and analyzed CHD5 re-expression in lung cancer cells treated with or without 5-aza-2-deoxycytidine, an inhibitor of DNA methylation. Next, the lung cancer cell clones stably expressing EGFP-CHD5 protein or EGFP protein, respectively, were obtained and the effects of restored CHD5 expression on cell proliferation, colony formation, and tumorigenicity were assessed. CHD5 expression ranged from low to absent in the lung cancer cell lines and tissues examined; the CHD5 promoter was hyperethylated in these samples. Treatment with 5-aza-dC resulted in a localized decrease in methylation density and an increase in CHD5 expression. Clonogenicity and tumor growth were abrogated in A549 and H1299 cells upon restoration of CHD5 expression. A significant reduction in clonogenicity was observed; an average of 47.83±4.6% reduction for A549-EGFP-CHD5 was observed compared to A549-EGFP, and an average of 56.39±5.3% reduction for H1299-EGFP-CHD5 was observed compared to H1299-EGFP. A549-EGFP exhibited an average tumor size of 452.3±36.5mm3, whereas A549-EGFP-CHD5 exhibited an average tumor size of only 57.7±18.5mm3. Thus, our findings indicate that CHD5 is a potential tumor suppressor gene that is inactivated via an epigenetic mechanism in lung cancer. [Copyright &y& Elsevier]

Abstract: Magnetic targeting, a promising therapeutic strategy for localizing systemically delivered drug to target tissue, is limited by magnetic attenuation. To satisfy the need of deep magnetic targeting, a special apparatus in which the magnetic flux density can be focused at a distance from the pole was designed. To test the aggregation property of this apparatus, we observed the accumulation of 500-nm paramagnetic particles as flowing through a tube served as a model of blood vessels. The relationship of the accumulation of the paramagnetic particles, the magnetic flux density, the magnetic field gradient and the fluid velocity was studied by theoretical considerations. [Copyright &y& Elsevier]

Abstract: The miniaturization of biological and chemical analytical devices by micro-electro-mechanical-systems (MEMS) technology has posed a vital influence on such fields as medical diagnostics, microbial detection and other bio-analysis. Among many miniaturized analytical devices, the polymerase chain reaction (PCR) microchip/microdevices are studied extensively, and thus great progress has been made on aspects of on-chip micromachining (fabrication, bonding and sealing), choice of substrate materials, surface chemistry and architecture of reaction vessel, handling of necessary sample fluid, controlling of three or two-step temperature thermocycling, detection of amplified nucleic acid products, integration with other analytical functional units such as sample preparation, capillary electrophoresis (CE), DNA microarray hybridization, etc. However, little has been done on the review of above-mentioned facets of the PCR microchips/microdevices including the two formats of flow-through and stationary chamber in spite of several earlier reviews [Zorbas, H. Miniature continuous-flow polymerase chain reaction: a breakthrough? Angew Chem Int Ed 1999; 38 (8):1055–1058; Krishnan, M., Namasivayam, V., Lin, R., Pal, R., Burns, M.A. Microfabricated reaction and separation systems. Curr Opin Biotechnol 2001; 12:92–98; Schneegaβ, I., Köhler, J.M. Flow-through polymerase chain reactions in chip themocyclers. Rev Mol Biotechnol 2001; 82:101–121; deMello, A.J. DNA amplification: does ‘small’ really mean ‘efficient’? Lab Chip 2001; 1: 24N–29N; Mariella, Jr. R. MEMS for bio-assays. Biomed Microdevices 2002; 4 (2):77–87; deMello AJ. Microfluidics: DNA amplification moves on. Nature 2003; 422:28–29; Kricka, L.J., Wilding, P. Microchip PCR. Anal BioAnal Chem 2003; 377:820–825]. In this review, we survey the advances of the above aspects among the PCR microfluidic devices in detail. Finally, we also illuminate the potential and practical applications of PCR microfluidics to some fields such as microbial detection and disease diagnosis, based on the DNA/RNA templates used in PCR microfluidics. It is noted, especially, that this review is to help a novice in the field of on-chip PCR amplification to more easily find the original papers, because this review covers almost all of the papers related to on-chip PCR microfluidics. [Copyright &y& Elsevier]

Describes the design and application of 60mer oligonucleotide microarray in SARS coronavirus detection. Diagnostic capability of the microarray; Results indicating that the genome of SARS coronavirus can be detected in parallel by the 60mer oligonucleotide microarray which can improve the positive ratio of the diagnosis.

Study Objectives:Sleep disorders are a common symptom of Parkinson’s disease (PD) and they significantly impair the sleep quality of the PD patients. However, there is no conclusive evidence to support the relation between PD and the prevalence of obstructive sleep apnea (OSA). The purpose of this meta-analysis review is to evaluate the association between PD and the prevalence of OSA. Methods:A comprehensive literature search was conducted on PubMed and Embase through July 2013. Only studies that referred to PD and the prevalence of OSA and that met the selection criteria were included in the analysis. The odds ratios (ORs) were used to evaluate the relationship of PD and the prevalence of OSA by the fixed-effect model. Results:Five eligible studies were analyzed in this study including 322 cases and 6,361 controls. The pooled-analysis showed the OR to be 0.60 (95% confidence interval (CI): 0.44 to 0.81, P = 0.001) and I2 = 0.0% (χ2 = 3.90, P = 0.420) in the fixed-effect model. Conclusions:Although we only included five small sample studies that indicated high homogeneity in the heterogeneity test, the results suggest that there is a significant negative association between PD and the prevalence of OSA; PD patients generally have a reduced prevalence of OSA. According to our analysis, these results are primarily due to the lower BMI of PD patients when compared with the general population controls. [ABSTRACT FROM AUTHOR]