H. Douglas Morris

Dr. H. Douglas Morris

Radiology and Bioengineering, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA
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Research Focus & Metrics

Academic Career Length

38Years (1989-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2003 in Neuroscience
Verified
Journal Article
Closed access
RSRodney Swain
Rodney Swain
AHA.B Harris
A.B Harris
EWE.C Wiener
E.C Wiener
MDM.V Dutka
M.V Dutka
H. Douglas MorrisH. Douglas Morris
H. Douglas Morris
WGW.T Greenough
W.T Greenough

20 April 2011 in Lab Animal
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Journal Article
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TYTal Yardeni
Tal Yardeni
MEMichael Eckhaus
Michael Eckhaus
H. Douglas MorrisH. Douglas Morris
H. Douglas Morris
MHMarjan Huizing
Marjan Huizing
SHShelley Hoogstraten-Miller
Shelley Hoogstraten-Miller

30 September 2015 in Science Translational Medicine
Verified
Journal Article
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WLWenxue Li
Wenxue Li
MLMyoung-Hwa Lee
Myoung-Hwa Lee
LHLisa Henderson
Lisa Henderson
RTRicha Tyagi
Richa Tyagi
MBMuzna Bachani
Muzna Bachani
ANAvindra Nath
Avindra Nath
The role of human endogenous retroviruses (HERVs) in disease pathogenesis is unclear. We show that HERV-K is activated in a subpopulation of patients with sporadic amyotrophic lateral sclerosis (ALS) and that its envelope (env) protein may contribute to neurodegeneration. The virus was expressed in cortical and spinal neurons of ALS patients, but not in neurons from control healthy individuals. Expression of HERV-K or its env protein in human neurons caused retraction and beading of neurites. Transgenic animals expressing the env gene developed progressive motor dysfunction accompanied by selective loss of volume of the motor cortex, decreased synaptic activity in pyramidal neurons, dendritic spine abnormalities, nucleolar dysfunction, and DNA damage. Injury to anterior horn cells in the spinal cord was manifested by muscle atrophy and pathological changes consistent with nerve fiber denervation and reinnervation. Expression of HERV-K was regulated by TAR (trans-activation responsive) DNA binding protein 43, which binds to the long terminal repeat region of the virus. Thus, HERV-K expression within neurons of patients with ALS may contribute to neurodegeneration and disease pathogenesis.

15 February 2016 in Journal of Experimental Medicine
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Journal Article
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VPVladislav Pokatayev
Vladislav Pokatayev
NHNaushaba Hasin
Naushaba Hasin
HCHyongi Chon
Hyongi Chon
SCSusana M. Cerritelli
Susana M. Cerritelli
KSKiran Sakhuja
Kiran Sakhuja
RCRobert Crouch
Robert Crouch
The neuroinflammatory autoimmune disease Aicardi-Goutières syndrome (AGS) develops from mutations in genes encoding several nucleotide-processing proteins, including RNase H2. Defective RNase H2 may induce accumulation of self-nucleic acid species that trigger chronic type I interferon and inflammatory responses, leading to AGS pathology. We created a knock-in mouse model with an RNase H2 AGS mutation in a highly conserved residue of the catalytic subunit, Rnaseh2aG37S/G37S (G37S), to understand disease pathology. G37S homozygotes are perinatal lethal, in contrast to the early embryonic lethality previously reported for Rnaseh2b- or Rnaseh2c-null mice. Importantly, we found that the G37S mutation led to increased expression of interferon-stimulated genes dependent on the cGAS–STING signaling pathway. Ablation of STING in the G37S mice results in partial rescue of the perinatal lethality, with viable mice exhibiting white spotting on their ventral surface. We believe that the G37S knock-in mouse provides an excellent animal model for studying RNASEH2-associated autoimmune diseases.

1 December 2017 in Biological Psychiatry
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Journal Article
Closed access
TSTimothy J. Schoenfeld
Timothy J. Schoenfeld
HMHayley C. McCausland
Hayley C. McCausland
H. Douglas MorrisH. Douglas Morris
H. Douglas Morris
VPVarun Padmanaban
Varun Padmanaban
HCHeather A. Cameron
Heather A. Cameron

16 November 2010 in Magnetic Resonance in Medicine
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Journal Article
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SDSam E. Day
Sam E. Day
MKMikko I. Kettunen
Mikko I. Kettunen
MCMurali Krishna Cherukuri
Murali Krishna Cherukuri
JMJames B. Mitchell
James B. Mitchell
MLMartin J. Lizak
Martin J. Lizak
KBKevin Brindle
Kevin Brindle
We show here that hyperpolarized [1‐13C]pyruvate can be used to detect treatment response in a glioma tumor model; a tumor type where detection of response with 18fluoro‐2‐deoxyglucose, using positron emission tomography, is limited by the high background signals from normal brain tissue. 13C chemical shift images acquired following intravenous injection of hyperpolarized [1‐13C]pyruvate into rats with implanted C6 gliomas showed significant labeling of lactate within the tumors but comparatively low levels in surrounding brain.Labeled pyruvate was observed at high levels in blood vessels above the brain and from other major vessels elsewhere but was detected at only low levels in tumor and brain.The ratio of hyperpolarized 13C label in tumor lactate compared to the maximum pyruvate signal in the blood vessels was decreased from 0.38 ± 0.16 to 0.23 ± 0.13, (a reduction of 34%) by 72 h following whole brain irradiation with 15 Gy. Magn Reson Med, 2011.