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  • Yin, Honglei  (25)
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  • 1
    Language: English
    In: PLoS ONE, 01 January 2014, Vol.9(11), p.e110773
    Description: Brain derived neurotrophic factor (BDNF) has been known to play an important role in various mental disorders or diseases such as Alzheimer's disease (AD). The aim of our study was to assess whether BDNF promoter methylation in peripheral blood was able to predict the risk of AD. A total of...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 2
    Language: English
    In: PLoS ONE, Nov 3, 2014, Vol.9(11)
    Description: Brain derived neurotrophic factor (BDNF) has been known to play an important role in various mental disorders or diseases such as Alzheimer's disease (AD). The aim of our study was to assess whether BDNF promoter methylation in peripheral blood was able to predict the risk of AD. A total of 44 AD patients and 62 age- and gender-matched controls were recruited in the current case-control study. Using the bisulphite pyrosequencing technology, we evaluated four CpG sites in the promoter of the BDNF. Our results showed that BDNF methylation was significantly higher in AD cases than in the controls (CpG1: p = 10.021; CpG2: p = 0.002; CpG3: p = 0.007; CpG4: p = 0.005; average methylation: p = 0.004). In addition, BDNF promoter methylation was shown to be significantly correlated with the levels of alkaline phosphatase (ALP), glucose, Lp(a), ApoE and ApoA in males (ALP: r = -0.308, p = 0.042; glucose: r = -0.383, p = 0.010; Lp(a): r = 0.333, p = 0.027; ApoE: r = -0.345, p = 0.032;), ApoA levels in females (r = 0.362, p = 0.033), and C Reactive Protein (CRP) levels in both genders (males: r = -0.373, p = 0.016; females: r = -0.399, p = 0.021). Our work suggested that peripheral BDNF promoter methylation might be a diagnostic marker of AD risk, although its underlying function remains to be elaborated in the future.
    Keywords: Mental Disorders – Risk Factors ; Mental Disorders – Forecasts and Trends ; Lipoprotein A – Forecasts and Trends ; Methylation – Forecasts and Trends ; Glucose – Forecasts and Trends ; Apolipoproteins – Forecasts and Trends ; Alzheimer'S Disease – Risk Factors ; Alzheimer'S Disease – Forecasts and Trends ; C-Reactive Protein – Forecasts and Trends
    ISSN: 1932-6203
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Molecular Medicine Reports, 12/2015, Vol.12(6), pp.8282-8288
    Description: Cardiomyocyte hypertrophy is a threat to human health due to the probability of sudden heart failure-induced mortality. Previous studies have demonstrated that nuclear factor of activated T cells cytoplasmic 3 (NFATC3) is important in the process of cardiomyocyte hypertrophy. However, the molecular mechanism underlying the alteration in the expression levels of NFATC3 during cardiomyocyte hypertrophy has remained to be fully elucidated. In order to shed light on the molecular mechanism, the present study employed several approaches, including the measurement of the cell surface area, analysis of the protein/DNA ratio, western blot analysis and a Luciferase reporter assay using isolated rat cardiomyocytes as model. The results showed that expression of microRNA-1 ( miR-1 ) was reduced in patients diagnosed with cardiac hypertrophy and rat cardiomyocytes treated with pro-hypertrophic stimuli. The increase in the expression of miR-1 was able to inhibit the hypertrophic remodeling of cardiomyocytes. The suppression of miR-1 was sufficient to induce cardiomyocyte hypertrophy, and further experiments confirmed that NFATC3 was a target of miR-1 in cardiomyocytes. Forced expression of NFATC3 inhibited the protective activity of miR-1 against hypertrophic stimuli in the cardiomyocytes. These findings provided clarification of the regulatory signaling pathway underlying cardiac hypertrophy, and provided evidence that targeting the miR-1 /NFATC3 pathway may be a promising strategy for the prevention and treatment of heart hypertrophy.
    Keywords: Microrna-1 ; Nuclear Factor Of Activated T Cells Cytoplasmic 3 ; Cardiomyocyte ; Hypertrophy
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 4
    Language: English
    In: Behavioural Brain Research, 30 March 2017, Vol.322, pp.362-367
    Description: To investigate the impact of - and gene single nucleotide polymorphisms (SNPs) and gene- gene interactions on late-onset Alzheimer’s disease (LOAD) risk in Chinese Han population. A total of 880 participants (514 males, 366 females), with a mean age of 81.7 ± 15.9 years old are selected, including 430 LOAD patients and 450 normal participants. Generalized multifactor dimensionality reduction (GMDR) is used to examine interaction among six SNPs, odds ratio (OR) and 95% confident interval (95%CI) are calculated by Logistic regression model. Logistic regression analysis showed that increased LOAD risks are associated with T allele of the rs1155002 polymorphism, adjusted OR (95%CI) = 1.46 (1.12–1.90), and T allele of the rs890293 polymorphism, adjusted OR (95%CI) = 1.65 (1.30–2.06), and G allele of the rs1805192 polymorphism, adjusted OR (95%CI) = 1.70 (1.25–2.27). We also found a potential gene–gene interaction between rs890293 and rs1805192. Participants with GT or TT of rs890293 and CG or GG of rs1805192 genotype have the highest LOAD risk, compared to participants with GG of rs890293 and CC of rs1805192 genotype, OR (95%CI) = 2.22 (1.63 –2.85), after covariates adjustment. rs1155002, rs890293 and rs1805192 polymorphism are associated with increased LOAD risk. Participants with GT or TT of rs890293 and CG or GG of rs1805192 genotype have the highest LOAD risk.
    Keywords: Ppar -Γ ; Cyp2j2 ; Snp ; Interaction ; Haplotype ; Anatomy & Physiology
    ISSN: 0166-4328
    E-ISSN: 0166-4328
    E-ISSN: 18727549
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  • 5
    Language: English
    In: Neuroscience Letters, Dec 17, 2013, Vol.557, p.112(6)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neulet.2013.10.024 Byline: Yunliang Wang, Honglei Yin, Jinfeng Li, Yuzhen Zhang, Bing Han, Zhilei Zeng, Nana Qiao, Xiaomei Cui, Jiyu Lou, Jing Li Abstract: acents Identify possible therapeutic mechanisms of curcumin. acents Curcumin improved spatial learning in AD model rats. acents Enhancing the CRMP-2/p-CRMP expression ratio, promoting axonal regeneration. Author Affiliation: (a) Second Affiliated Hospital of Zhengzhou University, Zhengzhou 450014, China (b) The No. 148 Hospital of PLA, Shandong 255300, China Article History: Received 15 July 2013; Revised 10 October 2013; Accepted 11 October 2013
    Keywords: Cognitive Disorders -- Physiological Aspects ; Cognitive Disorders -- Analysis
    ISSN: 0304-3940
    Source: Cengage Learning, Inc.
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  • 6
    Language: English
    In: Neuroscience Letters, 17 December 2013, Vol.557, pp.112-117
    Description: The Alzheimer's disease (AD) brain is characterized by β-amyloid deposition, hyperphosphorylation of microtubule-associated proteins, formation of senile plaques and neurofibrillary tangles, and degeneration of specific neuronal populations. Collapsin response mediator protein 2 (CRMP-2) hyperphosphorylation has been implicated in AD-associated neural process regression and neurofibrillary tangle formation. Curcumin is a promising AD drug with incompletely defined therapeutic mechanisms. One possibility is that curcumin prevents β-amyloid-induced CRMP-2 hyperphosphorylation, thereby protecting against axonal regression and (or) promoting axonal regrowth. We examined spatial learning in the Morris water maze, hippocampal expression levels of CRMP-2 and phosphorylated CRMP-2 (p-CRMP-2) by Western blot, and NF-200 (an axon-specific marker) by immunohistochemistry in Sprague-Dawley rats subjected to a single intrahippocampal injection of Aβ alone or Aβ followed by curcumin (i.p. daily for 7 days). Compared to controls, spatial learning was significantly impaired in these Aβ -injected AD model rats ( 〈 0.05). In addition, hippocampal expression levels of CRMP-2 and NF-200 were reduced while p-CRMP-2 expression was significantly enhanced ( 〈 0.05 for all). Overexpression of p-CRMP-2 was correlated with NF-200 underexpression ( = −0.67308, 〈 0.05), suggesting that Aβ damaged hippocampal axons. Spatial learning deficits were reversed, CRMP-2 and NF-200 expression levels increased, and p-CRMP-2 expression reduced in curcumin-treated rats (all 〈 0.05). We propose that curcumin improves spatial learning by inhibiting CRMP-2 hyperphosphorylation, thus protecting against β-amyloid-induced hippocampal damage or promoting regeneration.
    Keywords: Curcumin ; Amyloid Β Protein ; Crmp-2 ; Axon ; Alzheimer'S Disease ; Medicine ; Anatomy & Physiology
    ISSN: 0304-3940
    E-ISSN: 1872-7972
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  • 7
    Language: English
    In: The American Journal of Chinese Medicine, 2013, Vol.41(1), pp.59-70
    Description: Curcumin, an agent traditionally utilized for its preventative action against tumorigenesis, oxidation, inflammation, apoptosis and hyperlipemia, has also been used in the treatment of Alzheimer's disease (AD). Recent advances in the study of AD have revealed astrocytes (AS) as being key factors in the early pathophysiological changes in AD. Glial fibrillary acidic protein (GFAP), a marker specific to AS, is markedly more manifest during morphological modifications and neural degeneration signature during the onset of AD. Several studies investigating the functionality of curcumin have shown that it not only inhibits amyloid sedimentation but also accelerates the disaggregation of amyloid plaque. Thus, we are interested in the relationship between curcumin and spatial memory in AD. In this study, we intend to investigate the effects of curcumin in amyloid-β (Aβ1-40) induced AD rat models on both the behavioral and molecular levels, that is to say, on their spatial memory and on the expression of GFAP in their hippocampi. Our results were statistically significant, showing that the spatial memory of AD rats improved following curcumin treatment (p 〈 0.05), and that the expression of GFAP mRNA and the number of GFAP positive cells in the curcumin treated rats was decreased relative to the AD group rats (p 〈 0.05). Furthermore, the expression level of GFAP mRNA in hippocampal AS in the AD rats significantly increased when compared with that in the sham control (p 〈 0.05). Taken together, these results suggest that curcumin improves the spatial memory disorders (such disorders being symptomatic of AD) in Aβ1-40-induced rats by down regulating GFAP expression and suppressing AS activity.
    Keywords: Curcumin ; Amyloid-B ; Astrocyte ; Glial Fibrillary Acidic Protein ; Medicine
    ISSN: 0192-415X
    E-ISSN: 1793-6853
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  • 8
    Language: English
    In: Cancer Letters, 28 October 2015, Vol.367(2), pp.122-128
    Description: The transcripts of the gene Colorectal Neoplasia Differentially Expressed (CRNDE) are recognized as long-noncoding RNAs (lncRNAs), which are expressed in specific regions within the human brain, and are the most upregulated lncRNA in gliomas. However, the underlying regulation and function of CRNDE in gliomas are largely unknown. In this study, the upregulation of CRNDE was confirmed in both primary specimens from glioma patients and in vitro with cell lines. Overexpression of specific CRNDE transcript promotes cell growth and migration in vitro while knockdown of CRNDE expression manifests a repressive function during these cellular processes. The growth promoting effect of CRNDE was also demonstrated in a xenograft mouse model. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma. Thus, our results shed a light on utilizing CRNDE as a potential novel therapeutic target for the treatment of glioma.
    Keywords: Lncrna ; Crnde ; Glioma ; Mtor ; Histone Modification ; Medicine
    ISSN: 0304-3835
    E-ISSN: 1872-7980
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  • 9
    Language: English
    In: Molecular Medicine Reports, 2014, Vol.9(5), p.1834(5)
    Description: The inflammatory response has adverse effects on left ventricular (LV) function and remodeling post-myocardial infarction (MI). Interleukin (IL)-33 is considered to have anti-inflammatory properties. The present study examined whether the suppression of inflammation with IL-33 was able to attenuate LV dysfunction and remodeling post-MI. The MI model was induced and the mice were treated with either saline or recombinant IL-33. Inflammatory mediators, LV functional changes and structural remodeling were evaluated. IL-33 significantly suppressed macrophage infiltration and the production of inflammatory cytokines in the myocardium. IL-33 treatment significantly improved LV function, reduced infarct size and infarct wall thinning. MI-induced activation of the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-[kappa]B (NF-[kappa]B) pathways was also suppressed. Our data demonstrated that IL-33 suppresses inflammatory responses and improved LV function and remodeling by inhibiting the p38 MAPK and NF-[kappa]B pathways. IL-33 may be a potential therapeutic target for heart dysfunction post-MI. Key words: IL-33, myocardial infarction, inflammation, cardiac remodeling
    Keywords: Interleukins – Health Aspects ; Heart Attack – Health Aspects ; Anti-Inflammatory Agents – Health Aspects ; Inflammation – Health Aspects
    ISSN: 1791-2997
    E-ISSN: 17913004
    Source: Cengage Learning, Inc.
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  • 10
    Language: English
    In: Molecular Medicine Reports, 11/2015, Vol.12(5), pp.6568-6576
    Description: Schizophrenia (SCZ) is one of the most complex mental illnesses affecting ~1% of the population worldwide. SCZ pathogenesis is considered to be a result of genetic as well as epigenetic alterations. Previous studies have aimed to identify the causative genes of SCZ. However, DNA methylation of long non-coding RNAs (lncRNAs) involved in SCZ has not been fully elucidated. In the present study, a comprehensive genome-wide analysis of DNA methylation was conducted using samples from two male patients with paranoid and undifferentiated SCZ, respectively. Methyl-CpG binding domain protein-enriched genome sequencing was used. In the two patients with paranoid and undifferentiated SCZ, 1,397 and 1,437 peaks were identified, respectively. Bioinformatic analysis demonstrated that peaks were enriched in protein-coding genes, which exhibited nervous system and brain functions. A number of these peaks in gene promoter regions may affect gene expression and, therefore, influence SCZ-associated pathways. Furthermore, 7 and 20 lncRNAs, respectively, in the Refseq database were hypermethylated. According to the lncRNA dataset in the NONCODE database, ~30% of intergenic peaks overlapped with novel lncRNA loci. The results of the present study demonstrated that aberrant hypermethylation of lncRNA genes may be an important epigenetic factor associated with SCZ. However, further studies using larger sample sizes are required.
    Keywords: Schizophrenia ; Dna Methylation ; Protein Coding Gene ; Long Non-Coding Rna
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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