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Bioinformatics Analysis of Competing Endogenous RNA Network and Immune Infiltration in Atrial Fibrillation
- Xing Liu, Ke Peng, Guoqiang Zhong, Mingxing Wu, Lei Wang, Iyaswamy Ashok
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- Journal:
- Genetics Research / Volume 2022 / 2022
- Published online by Cambridge University Press:
- 01 January 2024, e50
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Background. There is still no clear understanding of the pathogenesis of atrial fibrillation (AF). For this purpose, we used integrated analysis to uncover immune infiltration characteristics and investigated their relationship with competing endogenous RNA (ceRNA) network in AF. Methods. Three AF mRNA data sets (GSE14975, GSE79768, and GSE41177) were integrated using the SVA method from Gene Expression Omnibus (GEO). Together with AF circRNA data set (GSE129409) and miRNA data set (GSE70887) from GEO database, we built a ceRNA network. Then hub genes were screened by the Cytoscape plug-in cytoHubba from a protein-protein interaction (PPI) network. As well, CIBERSORT was employed to investigate immune infiltration, followed by Pearson correlation coefficients to unravel the correlation between AF-related infiltrating immune cells and hub genes. Ulteriorly, circRNA-miRNA-mRNA regulatory axises that could be immunologically related to AF were obtained. Results. Ten hub genes were identified from the constructing PPI network. The immune infiltration analysis revealed that the number of monocytes and neutrophils was higher, as well as the number of dendritic cells activated and T cells regulatory (Tregs) was lower in AF. Seven hub genes (C5AR1, CXCR4, HCK, LAPTM5, MPEG1, TLR8, and TNFSF13B) were associated with those 4 immune cells (P < 0.05). We found that the circ_0005299–miR-1246–C5AR1 and circRNA_0079284-miR-623-HCK/CXCR4 regulatory axises may be associated with the immune mechanism of AF. Conclusion. The findings of our study provide insights into immuno-related ceRNA networks as potential molecular regulators of AF progression.
120 Fragile X Syndrome Sharing Similar Neural Network Abnormalities as ADHD
- Chunhui Yang, Carolyn Beebe Smith, Guoqiang Xing, Sandeep Gaonkar
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- Journal:
- CNS Spectrums / Volume 23 / Issue 1 / February 2018
- Published online by Cambridge University Press:
- 15 June 2018, p. 76
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Title
Fragile X syndrome sharing similar neural network abnormalities as ADHD
Study Objective(s)The Fragile X syndrome (FXS) phenotype typically involves a variety of psychiatric symptoms, including features of autism, attention deficit/hyperactivity disorder (ADHD), anxiety, and aggression. Studies have shown that ADHD is characterized by multiple functional and structural neural network abnormalities including fronto-striatal, fronto-parieto-temporal, fronto-cerebellar and fronto-limbic networks (Rubia, 2014; Norman, 2017). Studies have shown that ADHD is characterized by a delay in structural brain maturation (Rubia, 2007). Absence of the FMR1 gene product Fragile X mental retardation protein (FMRP) results in FXS, an inherited form of mental retardation. FMRP is an RNA binding protein functioning as a nucleocytoplasmic shuttling. In a knockout mouse model of FXS (Fmr1 null), Qin, et al showed regionally selective effects on cerebral metabolic rates for glucose (rCMRglc) (Qin, 2002) and rates of cerebral protein synthesis (Qin, 2005). In the present study, we asked if there is a relationship between brain regions most vulnerable to the effects of the absence of FMRP in the Fmr1 null mouse, and if the distribution consistent with the structural and functional brain abnormalities in ADHD. We also asked if there is a difference between males and females in the regional distributions and the levels of the FXR mRNAs.
MethodWe used 35S-labeled probes specific for the mRNAs to perform in situ hybridization on brains from male (n=4) and female (n=4) mice at 6 months of age. Flowing hybridization, brain sections were exposed to X-ray film and optical density were measured in nine brain regions on autoradiograms of sections hybridized to the probe.
ResultsThe highest levels of expression we observed were in the cerebellum, granular layers of the hippocampus. Levels of expression were also high in CA1 pyramidal neurons of hippocampus, amygdala and granule layer of olfactory bulb. We found intermediate levels in the anterior hypothalamus and in cingulate and frontal cortex. Low levels of expression were found in thalamus and caudate. The distribution for the probe was similar in male and female mice, but we found a tendency for male mice to have higher levels than females.
Funding AcknowledgementsNo funding.
Contributors
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- By Ghazi Al-Rawas, Vazken Andréassian, Tianqi Ao, Stacey A. Archfield, Berit Arheimer, András Bárdossy, Trent Biggs, Günter Blöschl, Theresa Blume, Marco Borga, Helge Bormann, Gianluca Botter, Tom Brown, Donald H. Burn, Sean K. Carey, Attilio Castellarin, Francis Chiew, François Colin, Paulin Coulibaly, Armand Crabit, Barry Croke, Siegfried Demuth, Qingyun Duan, Giuliano Di Baldassarre, Thomas Dunne, Ying Fan, Xing Fang, Boris Gartsman, Alexander Gelfan, Mikhail Georgievski, Nick van de Giesen, David C. Goodrich, Hoshin V. Gupta, Khaled Haddad, David M. Hannah, H. A. P. Hapuarachchi, Hege Hisdal, Kamila Hlavčová, Markus Hrachowitz, Denis A. Hughes, Günter Humer, Ruud Hurkmans, Vito Iacobellis, Elena Ilyichyova, Hiroshi Ishidaira, Graham Jewitt, Shaofeng Jia, Jeffrey R. Kennedy, Anthony S. Kiem, Robert Kirnbauer, Thomas R. Kjeldsen, Jürgen Komma, Leonid M. Korytny, Charles N. Kroll, George Kuczera, Gregor Laaha, Henny A. J. van Lanen, Hjalmar Laudon, Jens Liebe, Shijun Lin, Göran Lindström, Suxia Liu, Jun Magome, Danny G. Marks, Dominic Mazvimavi, Jeffrey J. McDonnell, Brian L. McGlynn, Kevin J. McGuire, Neil McIntyre, Thomas A. McMahon, Ralf Merz, Robert A. Metcalfe, Alberto Montanari, David Morris, Roger Moussa, Lakshman Nandagiri, Thomas Nester, Taha B. M. J. Ouarda, Ludovic Oudin, Juraj Parajka, Charles S. Pearson, Murray C. Peel, Charles Perrin, John W. Pomeroy, David A. Post, Ataur Rahman, Liliang Ren, Magdalena Rogger, Dan Rosbjerg, José Luis Salinas, Jos Samuel, Eric Sauquet, Hubert H. G. Savenije, Takahiro Sayama, John C. Schaake, Kevin Shook, Murugesu Sivapalan, Jon Olav Skøien, Chris Soulsby, Christopher Spence, R. ‘Sri’ Srikanthan, Tammo S. Steenhuis, Jan Szolgay, Yasuto Tachikawa, Kuniyoshi Takeuchi, Lena M. Tallaksen, Dörthe Tetzlaff, Sally E. Thompson, Elena Toth, Peter A. Troch, Remko Uijlenhoet, Carl L. Unkrich, Alberto Viglione, Neil R. Viney, Richard M. Vogel, Thorsten Wagener, M. Todd Walter, Guoqiang Wang, Markus Weiler, Rolf Weingartner, Erwin Weinmann, Hessel Winsemius, Ross A. Woods, Dawen Yang, Chihiro Yoshimura, Andy Young, Gordon Young, Erwin Zehe, Yongqiang Zhang, Maichun C. Zhou
- Edited by Günter Blöschl, Technische Universität Wien, Austria, Murugesu Sivapalan, University of Illinois, Urbana-Champaign, Thorsten Wagener, University of Bristol, Alberto Viglione, Technische Universität Wien, Austria, Hubert Savenije, Technische Universiteit Delft, The Netherlands
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- Book:
- Runoff Prediction in Ungauged Basins
- Published online:
- 05 April 2013
- Print publication:
- 18 April 2013, pp ix-xiv
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20 - Psychosocial Stressors as Predisposing Factors to Affective Illness and PTSD: Potential Neurobiological Mechanisms and Theoretical Implications
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- By Robert M. Post, Biological Psychiatry Branch, National Institute of Mental Health, Gabriele S. Leverich, Biological Psychiatry Branch, National Institute of Mental Health, Susan R. B. Weiss, Biological Psychiatry Branch, National Institute of Mental Health, Li-Xin Zhang, Biological Psychiatry Branch, National Institute of Mental Health, Guoqiang Xing, Department of Psychiatry Uniformed Services, National Institute of Mental Health, He Li, Biological Psychiatry Branch, National Institute of Mental Health, Mark Smith, Experimental Station, DuPont, Pharmaceutical National Institute of Mental Health
- Edited by Dante Cicchetti, University of Rochester, New York, Elaine F. Walker, Emory University, Atlanta
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- Book:
- Neurodevelopmental Mechanisms in Psychopathology
- Published online:
- 10 August 2009
- Print publication:
- 04 August 2003, pp 491-525
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Summary
SENSITIZATION IN THE AFFECTIVE DISORDERS
Stressor and Episode Sensitization in the Unmedicated State
At the beginning of the twentieth century, Kraepelin (1921) laid out the fundamentals of the sensitization hypothesis of affective disorders:
the attacks begin not infrequently after the illness or death of near relatives … we must regard all alleged injuries as possibly sparks for the discharge of individual attacks, but the real cause of the malady must be sought in permanent internal changes, which at least very often, perhaps always, are innate … in spite of the removal of the discharging cause, the attack follows its independent development. But, finally, the appearance of wholly similar attacks on wholly dissimilar occasions or quite without external occasion shows that even there where there has been external influence, it must not be regarded as a necessary presupposition for the appearance of the attack.
(pp. 180–181)In this terse and insightful paragraph, he outlines four different components of the sensitization hypothesis: (1) initial episodes of affective illness are often precipitated by psychosocial stressors; (2) as recurrences emerge, later episodes do not require the same psychosocial precipitation, but may occur more spontaneously; (3) episodes tend to occur with a characteristic similarity; and (4) innate neurobiological mechanisms mediate these vulnerabilities and recurrences, and presumably these could occur both on an inherited and an experiential basis.
Other aspects of this sensitization hypothesis are outlined in additional passages from his work.
Developmental vulnerabilities to the onset and course of bipolar disorder
- ROBERT M. POST, GABRIELE S. LEVERICH, GUOQIANG XING, SUSAN R. B. WEISS
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- Journal:
- Development and Psychopathology / Volume 13 / Issue 3 / September 2001
- Published online by Cambridge University Press:
- 27 September 2001, pp. 581-598
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Different types of psychosocial stressors have long been recognized as potential precipitants of both unipolar and bipolar affective episodes and the causative agents in posttraumatic stress disorder (PTSD). New preclinical data have revealed some of the neurobiological mechanisms that could convey the long-term behavioral and biochemical consequences of early stressors. Depending on the timing, quality, quantity, and degree of repetition, maternal deprivation stress in the neonatal rodent can be associated with lifelong anxiety-like behaviors, increases in stress hormones and peptides, and proneness to drug and alcohol administration, in association with acute changes in the rate of neurogenesis and apoptosis (preprogrammed cell death) and decrements in neurotrophic factors and signal transduction enzymes necessary for learning and memory. Patients with bipolar illness who have a history of early extreme adversity (physical or sexual abuse in childhood or adolescence), compared with those without, show an earlier onset of illness, faster cycling frequencies, increased suicidality, more Axis I and Axis II comorbidities (including alcohol and substance abuse), and more time ill in more than 2 years of prospective follow-up. These findings are subject to a variety of interpretations, but to the extent that the more severe course of bipolar illness characteristics are directly and causally related to these early stressful experiences, early recognition and treatment of high-risk children could be crucial in helping to prevent or ameliorate the long-term adverse consequences of these stressors.