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591.
Shai I Pischon T Hu FB Ascherio A Rifai N Rimm EB 《Obesity (Silver Spring, Md.)》2006,14(11):2099-2106
Objective: We examined the association of circulating levels of soluble intercellular adhesion molecules (sICAM‐1) and soluble vascular cell adhesion molecules (sVCAM‐1) with coronary heart disease (CHD) risk factors and whether the adhesion molecules alone, and in combination, can serve as predictors of coronary CHD. Research Methods and Procedures: Among 18,225 men from the Health Professional Follow‐up Study who provided blood in 1994, we documented 266 incidents of non‐fatal myocardial infarction or fatal CHD during 6 years of follow‐up. The cases were matched 1:2 with non‐cases on age, smoking, and month of blood draw. We found both adhesion molecules directly associated with BMI, inflammatory biomarkers, and triglycerides and inversely associated with high‐density lipoprotein and alcohol intake (p < 0.05). After adjustment for C‐reactive protein, cholesterol‐to‐high‐density lipoprotein ratio, age, smoking, BMI, physical activity, alcohol intake, history of diabetes, parental history of CHD, aspirin use, antihypertensive drug use, and fasting status, the relative risk of CHD was 1.69 [95% confidence interval (CI), 1.14 to 2.51] for sICAM‐1 and 1.34 (95% CI, 0.91 to 1.96) for sVCAM‐1, when comparing the top quintile with the lower four quintiles. Control for other inflammatory or lipid biomarkers did not appreciably attenuate the associations. When we cross‐classified participants based on their sICAM‐1 and sVCAM‐1 levels, only the men in the top quintile of both biomarkers [relative risk = 2.39 (95% CI, 1.45 to 3.91)] had a significantly elevated risk of CHD (P interaction = 0.01, multivariate model). Discussion: sICAM‐1 and sVCAM‐1 are directly associated with obesity and other CHD risk factors. The combination of high levels of both adhesion molecules might be associated with the development of CHD, independent of other CHD risk factors. 相似文献
592.
Guo-Qiang Bi Vadim Bolshakov Guojun Bu Catherine M Cahill Zhou-Feng Chen Graham L Collingridge Robin L Cooper Jens R Coorssen Alaa El-Husseini Vasco Galhardo Wen-Biao Gan Jianguo Gu Kazuhide Inoue John Isaac Koichi Iwata Zhengping Jia Bong-Kiun Kaang Mikito Kawamata Satoshi Kida Eric Klann Tatsuro Kohno Min Li Xiao-Jiang Li John F MacDonald Karim Nader Peter V Nguyen Uhtaek Oh Ke Ren John C Roder Michael W Salter Weihong Song Shuzo Sugita Shao-Jun Tang Yuanxiang Tao Yu Tian Wang Newton Woo Melanie A Woodin Zhen Yan Megumu Yoshimura Ming Xu Zao C Xu Xia Zhang Mei Zhen Min Zhuo 《Molecular pain》2006,2(1):1-22
Understanding basic neuronal mechanisms hold the hope for future treatment of brain disease. The 1st international conference on synapse, memory, drug addiction and pain was held in beautiful downtown Toronto, Canada on August 21–23, 2006. Unlike other traditional conferences, this new meeting focused on three major aims: (1) to promote new and cutting edge research in neuroscience; (2) to encourage international information exchange and scientific collaborations; and (3) to provide a platform for active scientists to discuss new findings. Up to 64 investigators presented their recent discoveries, from basic synaptic mechanisms to genes related to human brain disease. This meeting was in part sponsored by Molecular Pain, together with University of Toronto (Faculty of Medicine, Department of Physiology as well as Center for the Study of Pain). Our goal for this meeting is to promote future active scientific collaborations and improve human health through fundamental basic neuroscience researches. The second international meeting on Neurons and Brain Disease will be held in Toronto (August 29–31, 2007). 相似文献
593.
Nader Riyahi-Alam Zhaleh Behrouzkia Alexander Seifalian Soheila Haghgoo Jahromi 《Biological trace element research》2010,137(3):324-334
Nanosized materials of gadolinium oxide can provide high-contrast enhancement in magnetic resonance imaging (MRI). The aim
of this research was to characterize a novel emulsion composed of a silicon-based nanocomposite polymer (NCP) and gadolinium
(III) oxide (Gd2O3) nanoparticles. The size and morphological structure of this nanoparticle are determined by particle size analysis device
(zeta sizer) and transmission electronic microscope. We determined composition of Gd2O3 nanoparticles with energy dispersive X-ray analysis (EDXA) and magnetic resonance signal by T
1-weighted MRI. Cytotoxicity of Gd2O3 nanoparticles in SK-MEL-3 cancer cells was evaluated. Zeta sizer showed Gd2O3 nanoparticles to be 75 nm in size. EDXA indicated the two main chemical components of gadolinium-nanocomposite polymer emulsion:
gadolinium and silicon and MRI also showed a significantly higher incremental relaxivity for Gd2O3 nanoparticles compared to Magnevist (conventional contrast agent). In such concentrations, the slope of R1 relaxivity (1/T
1) vs. concentration curve of Magnevist and Gd2O3 were 4.33, 7.98 s−1 mM−1. The slope of R2 relaxivity (1/T
2) vs. concentration curve of Magnevist and Gd2O3 were 5.06, 13.75 s−1 mM−1. No appreciable toxicity was observed with Gd2O3 nanoparticles. Gadolinium-nanocomposite polymer emulsion is well characterized and has potential as a useful contrast agent
for magnetic resonance molecular imaging. 相似文献
594.
Fariba Khodagholi Bahareh Eftekharzadeh Nader Maghsoudi Parisa Fathi Rezaei 《Molecular and cellular biochemistry》2010,337(1-2):39-51
Increased oxidative stress is a widely accepted factor in the development and progression of Alzheimer’s disease. Here, we introduce chitosan, an antioxidant oligosaccharide, as a protective agent against H2O2/FeSO4-induced cell death in the NT2 neural cell line. Chitosan not only protects the neurons against cell death, as measured by MTT and caspase-3 activity, but also decreases amyloid β formation. NT2 neurons can be used to elucidate the relationship between oxidative stress and Aβ formation. We induced Aβ formation through oxidative stress in NT2 neurons and studied the effect of chitosan. We demonstrate that chitosan can be neuroprotective by suppressing Aβ formation. We further show that chitosan exerts its protective effect by up-regulation of HO-1, γ-GCS, Hsp-70, and Nrf2, while it inhibits activation of caspase-3 and NF-κB. Chitosan or chitosan derivatives have potential value as neuroprotective agents, particularly with regard to oxidative stress. 相似文献
595.
Stabilization of transcription factor Nrf2 by tBHQ prevents oxidative stress-induced amyloid β formation in NT2N neurons 总被引:1,自引:0,他引:1
Alzheimer's disease (AD) a progressive neurodegenerative disorder of later life, is characterized by brain deposition of amyloid β-protein (Aβ) plaques, accumulation of intracellular neurofibrillatory tangles, synaptic loss and neuronal cell death. There is significant evidence that oxidative stress is a critical event in the pathogenesis of AD. 相似文献
596.
Nader Chaparzadeh Maria Lucia D'Amico Ramazan-Ali Khavari-Nejad Riccardo Izzo Flavia Navari-Izzo 《Plant Physiology and Biochemistry》2004,42(9):695-701
To gain a better insight into long-term salt-induced oxidative stress, some physiological parameters in marigold (Calendula officinalis L.) under 0, 50 and 100 mM NaCl were investigated. Salinity affected most of the considered parameters. High salinity caused reduction in growth parameters, lipid peroxidation and hydrogen peroxide accumulation. Under high salinity stress, a decrease in total glutathione and an increase in total ascorbate (AsA + DHA), accompanied with enhanced glutathione reductase (GR, EC 1.6.4.2) and ascorbate peroxidase (APX, EC 1.11.1.11) activities, were observed in leaves. In addition, salinity induced a decrease in superoxide dismutase (SOD, EC 1.15.1.1) and peroxidase (POX, EC 1.11.1.7) activities. The decrease in dehydroascorbate reductase (DHAR, EC 1.8.5.1) and monodehydroascorbate reductase (MDHAR, EC 1.6.5.4) activities suggests that other mechanisms play a major role in the regeneration of reduced ascorbate. The changes in catalase (CAT, EC 1.11.1.6) activities, both in roots and in leaves, may be important in H2O2 homeostasis. 相似文献
597.
Glycogen phosphorylase from macroplasmodia of Physarum polycephalum was purified 76-fold to homogeneity. The native enzyme migrated as a single protein band on analytical disc gel electrophoresis coinciding with phosphorylase activity. After reduction in the presence of sodium dodecylsulfate one protein band was detectable which corresponded to an Mr of 93 000. The molecular weight of the native enzyme determined by gel sieving or gradient-polyacrylamide gel electrophoresis was 172000 and 186000, respectively. The enzyme contained about 1 mol pyridoxal 5'-phosphate and less than 0.1 mol covalently bound phosphate per mol subunit. The amino acid composition of the enzyme was determined. In the direction of phosphorolysis the kinetic data were determined by initial velocity studies, assuming a rapid equilibrium random mechanism. Glucose 1-phosphate and GDP-glucose were competitive inhibitors toward phosphate and noncompetitive to glycogen. 5'-AMP, a weak activator of the enzyme, counteracted the glucose-1-phosphate inhibition completely. Physarum phosphorylase was compared with phosphorylases from other sources on the basis of chemical and kinetic properties. No evidence for the presence of phosphorylated forms has yet been found. 相似文献
598.
RNF121 Inhibits Angiogenic Growth Factor Signaling by Restricting Cell Surface Expression of VEGFR‐2
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Armin Maghsoudlou Rosana D. Meyer Kobra Rezazadeh Emad Arafa Jeffrey Pudney Edward Hartsough Nader Rahimi 《Traffic (Copenhagen, Denmark)》2016,17(3):289-300
Ligand stimulation promotes downregulation of RTKs, a mechanism by which RTKs, through the ubiquitination pathway are removed from the cell surface, causing a temporary termination of RTK signaling. The molecular mechanisms governing RTK trafficking and maturation in the endoplasmic reticulum (ER)/Golgi compartments are poorly understood. Vascular endothelial growth factor receptor‐2 (VEGFR‐2) is a prototypic RTK that plays a critical role in physiologic and pathologic angiogenesis. Here we demonstrate that Ring Finger Protein 121 (RNF121), an ER ubiquitin E3 ligase, is expressed in endothelial cells and regulates maturation of VEGFR‐2. RNF121 recognizes newly synthesized VEGFR‐2 in the ER and controls its trafficking and maturation. Over‐expression of RNF121 promoted ubiquitination of VEGFR‐2, inhibited its maturation and resulted a significantly reduced VEGFR‐2 presence at the cell surface. Conversely, the shRNA‐mediated knockdown of RNF121 in primary endothelial cells reduced VEGFR‐2 ubiquitination and increased its cell surface level. The RING Finger domain of RNF121 is required for its activity toward VEGFR‐2, as its deletion significantly reduced the effect of RNF121 on VEGFR‐2. Additionally, RNF121 inhibited VEGF‐induced endothelial cell proliferation and angiogenesis. Taken together, these data identify RNF121 as a key determinant of angiogenic signaling that restricts VEGFR‐2 cell surface presence and its angiogenic signaling. 相似文献
599.
Dina H. Elkobrosy Dalia G. Aseel Elsayed E. Hafez Mohamed A. El-Saedy Asma A. Al-Huqail Hayssam M. Ali Jebril Jebril Saad Shama Nader R. Abdelsalam Ahmed S.M. Elnahal 《Saudi Journal of Biological Sciences》2022,29(5):3617
Potato cyst nematodes caused by Globodera rostochiensis, are quarantine-restricted pests causing significant yield losses to potato growers. The phytohormone ethylene play significant roles in various plant-pathogen interactions, however, the molecular knowledge of how ethylene influences potato–nematode interaction is still lacking. Precise detection of potato-induced genes is essential for recognizing plant-induced systemic resistance (ISR). Candidate genes or PR- proteins with putative functions in modulating the response to potato cyst nematode stress were selected and functionally characterized. Using real-time polymerase chain reaction (RT-PCR), we measured the quantified expression of four pathogenesis-related (PR) genes, PR2, PR3, peroxidase, and polyphenol oxidase. The activation of these genes is intermediate during the ISR signaling in the root tissues. Using different ethylene concentrations could detect and induce defense genes in infected potato roots compared to the control treatment. The observed differences in the gene expression of treated infected plants are because of different concentrations of ethylene treatment and pathogenicity. Besides, the overexpressed or suppressed of defense- related genes during developmental stages and pathogen infection. We concluded that ethylene treatments positively affected potato defensive genes expression levels against cyst nematode infection. The results emphasize the necessity of studying molecular signaling pathways controlling biotic stress responses. Understanding such mechanisms will be critical for the development of broad-spectrum and stress-tolerant crops in the future. 相似文献
600.
Yun Zhao Shoujian Wang Christine M. Sorenson Leandro Teixeira Richard R. Dubielzig Donna M. Peters Simon J. Conway Colin R. Jefcoate Nader Sheibani 《Molecular and cellular biology》2013,33(21):4225-4240
Mutation in CYP1B1 has been reported for patients with congenital glaucoma. However, the underlying mechanisms remain unknown. Here we show increased diurnal intraocular pressure (IOP) in Cyp1b1-deficient (Cyp1b1−/−) mice. Cyp1b1−/− mice presented ultrastructural irregular collagen distribution in their trabecular meshwork (TM) tissue along with increased oxidative stress and decreased levels of periostin (Postn). Increased levels of oxidative stress and decreased levels of Postn were also detected in human glaucomatous TM tissues. Furthermore, Postn-deficient mice exhibited TM tissue ultrastructural abnormalities similar to those of Cyp1b1−/− mice. Administration of the antioxidant N-acetylcysteine (NAC) restored structural abnormality of TM tissue in Cyp1b1−/− mice. In addition, TM cells prepared from Cyp1b1−/− mice exhibited increased oxidative stress, altered adhesion, and decreased levels of Postn. These aberrant cellular responses were reversed in the presence of NAC or by restoration of Cyp1b1 expression. Cyp1b1 knockdown or inhibition of CYP1B1 activity in Cyp1b1+/+ TM cells resulted in a Cyp1b1−/− phenotype. Thus, metabolic activity of CYP1B1 contributes to oxidative homeostasis and ultrastructural organization and function of TM tissue through modulation of Postn expression. 相似文献