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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]

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]

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]

Cancer stemness represents a major source of development and progression of colorectal cancer (CRC). c-Met critically contributes to CRC stemness, but how c-Met is activated in CRC remains elusive. We previously identified the lipolytic factor ABHD5 as an important tumour suppressor gene in CRC. Here, we show that loss of ABHD5 promotes c-Met activation to sustain CRC stemness in a non-canonical manner. Mechanistically, we demonstrate that ABHD5 interacts in the cytoplasm with the core subunit of the SET1A methyltransferase complex, DPY30, thereby inhibiting the nuclear translocation of DPY30 and activity of SET1A. In the absence of ABHD5, DPY30 translocates to the nucleus and supports SET1A-mediated methylation of YAP and histone H3, which sequesters YAP in the nucleus and increases chromatin accessibility to synergistically promote YAP-induced transcription of c-Met, thus promoting the stemness of CRC cells. This study reveals a novel role of ABHD5 in regulating histone/non-histone methylation and CRC stemness. This study reveals an unrecognized role of ABHD5 in regulating colon cancer stemness via controlling YAP methylation and nuclear localization, further explaining the molecular mechanism through which ABHD5 functions as a tumour suppressor gene in colon cancer. [ABSTRACT FROM AUTHOR]

Cancer stemness represents a major source of development and progression of colorectal cancer (CRC). c-Met critically contributes to CRC stemness, but how c-Met is activated in CRC remains elusive. We previously identified the lipolytic factor ABHD5 as an important tumour suppressor gene in CRC. Here, we show that loss of ABHD5 promotes c-Met activation to sustain CRC stemness in a non-canonical manner. Mechanistically, we demonstrate that ABHD5 interacts in the cytoplasm with the core subunit of the SET1A methyltransferase complex, DPY30, thereby inhibiting the nuclear translocation of DPY30 and activity of SET1A. In the absence of ABHD5, DPY30 translocates to the nucleus and supports SET1A-mediated methylation of YAP and histone H3, which sequesters YAP in the nucleus and increases chromatin accessibility to synergistically promote YAP-induced transcription of c-Met, thus promoting the stemness of CRC cells. This study reveals a novel role of ABHD5 in regulating histone/non-histone methylation and CRC stemness. This study reveals an unrecognized role of ABHD5 in regulating colon cancer stemness via controlling YAP methylation and nuclear localization, further explaining the molecular mechanism through which ABHD5 functions as a tumour suppressor gene in colon cancer. [ABSTRACT FROM AUTHOR]

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]

Purpose: Soil microorganisms play an indispensable role in the material and energy cycle of grassland ecosystems. The abundance of these organisms vary according to environmental factors, such as time of year and soil depth. There have been few studies on the transformation of soil microbial communities in degraded typical steppe according to these temporal and spatial changes. In this study, we analyze the community structure and diversity of soil bacteria and fungi, and the impact of these changing temporal and spatial factors upon the community structure. Methods: From May to September 2018, we collected 90 soil samples from different depths (10, 20, and 30 cm) from the typical degraded steppe area of Xilingol. We carried out studies on soil physical and chemical properties and soil microbial diversity using high-throughput sequencing technology. Results: We found that depth significantly affected abundance and diversity of bacteria and fungi. Bacteria and fungi diversity at 10 cm was higher than that at 20 cm and 30 cm. The abundance of Acidobacteria, Proteobacteria, Actinomycetes, Ascomycetes, and Basidiomycetes varies significantly with depth. In addition, soil pH increased significantly with increasing depth, while soil organic matter (SOM), available nitrogen (AN), volume water content of soil (VWC), and soil temperature (ST) decreased significantly with increasing depth. Finally, the depth, total organic carbon (TOC), and AN had a significant impact on the bacterial and fungal communities’ abundance (p < 0.05). Conclusions: Spatial heterogeneity (in soil depth) is more significant than the time of year (month) in predicting changes in microbial community composition and soil properties. SOM, VWC, and the abundance of Proteobacteria and Actinomycetes positively correlate with soil depth, while pH and the abundance of Acidobacteria, Ascomycetes, and Basidiomycetes negatively correlate with soil depth. We speculate that SOM and VWC account for the variations in the abundance of Acidobacteria and Proteobacteria, while pH causes variations in the abundance of Actinomycetes, Ascomycetes and Basidiomycota. [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]

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]

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]

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]

These authors contributed equally: Yan Gu, Yanrong Chen, Lai Wei, Shuang Wu. Correction to: I Nature Communications i https://doi.org/10.1038/s41467-021-26967-5, published online 18 November 2021 This Article contains an error in Figure 2j. [Extracted from the article]

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]

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]

XPA, a zinc-finger DNA-binding protein, play an important role in both global genome and transcription-coupled repair pathways. XPA −4G>A polymorphism was identified in the 5′ noncoding region, located four nucleotides upstream of the ATG start codon. Previous studies have shown that this polymorphism may affect mRNA tertiary structure and stability and play a role in susceptibility to cancer. However, the results remained controversial. To derive a more precise estimation of association between this polymorphism and risk of different types of cancer, we performed a meta-analysis based on 36 case-control or case-cohort studies, including a total of 11,700 cases and 15,033 controls. We used odds ratios with 95% confidence intervals to assess the strength of the association. Overall, no significantly elevated cancer risk was found in all genetic models when eligible studies were pooled into the meta-analysis. In the stratified analyses, we found that individuals with A-allele had a higher risk of lung cancer (AA versus GG: OR = 1.25, 95% CI = 1.09-1.43; recessive model: OR = 1.31, 95% CI = 1.16-1.48). When stratified by ethnicity, significantly elevated risks were observed among Asian populations (AA versus GG: OR = 1.31, 95% CI = 1.01-1.70; dominant model: OR = 1.14, 95% CI = 1.00-1.30). This meta-analysis suggests that XPA −4G>A polymorphism is associated with increased lung cancer risk and may be a low-penetrant risk factor in Asian ethnicity for cancer development. [ABSTRACT FROM AUTHOR]

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]

Oligo‐microarray can be fabricated on modified surface of glass slides involving immobilization of oligonucleotides. In this study, glass slides were modified with acrylic acid‐co‐acrylamide copolymer and EDC (1‐ethyl‐3(3‐dimethylaminopropyl)‐carbodiimide)/NHS (N‐hydroxysuccinimide) by covalent linkage method, and covalent immobilization of unmodified oligonucleotide on the glass surface was achieved. The platform with binding of stable and sensitive oligonucleotides was prepared for oligo‐microarray fabrication. An optimum concentration of 0.5 g/L was used for spotting. The lengths of 26 to 70 mer oligonucleotides were immobilized on the surface efficiently. The spots were ∼160 nm in diameter and their mean value of fluorescent intensity was measured in the range of 3.2 × 104 to 7.3 × 104 after hybridization. The modified glass surface was scanned by SEM and the dendritic structure was observed. Results showed that the process of preparation of the modified glass surface was simple and cost effective, and the modified surface can be used for the oligo‐microarray fabrication and also attachment of protein, PNA etc. © 2008 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2008 [ABSTRACT FROM AUTHOR]

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]