scholarly journals Induction of Gut Microbial Tryptamine by SARS-CoV-2 in Nonhuman Primate Model Consistent with Tryptamine-Induced Model of Neurodegeneration

2021 ◽  
pp. 1-6
Author(s):  
Elena L. Paley
Keyword(s):  
Molecular Mechanisms ◽  
Selective Pressure ◽  
Recent Experimental Data ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
Disease Symptoms ◽  
Viral Activity ◽  
Neurodegenerative Process ◽  
Gut Microorganisms ◽  
Selection Of

The author discussed recently the possible molecular mechanisms that cause the COVID-19 disease symptoms. Here the analysis of the recent experimental data supports the hypothesis that production of the gut microbial tryptamine can be induced by the SARS-CoV-2 fecal viral activity due to the selective pressure or positive selection of tryptamine-producing microorganisms. In this report, the author suggests that the mechanism of microbial selection bases on the abilities of tryptamine to affect the viral nucleic acid. In other words, the gut microorganisms producing tryptamine are more resistant to SARS-CoV-2 fecal viral activity than microorganisms producing no tryptamine. Earlier we demonstrated the induction of neurodegeneration by tryptamine in human cells and mouse brain. Furthermore, we were able to uncover the human gut bacteria associated with Alzheimer’s disease (AD) using PCR testing of human fecal samples with the new-designed primers targeting the tryptophan-tryptamine pathway. Likely, SARS-CoV-2 is one of the selective pressure factors in the cascade accelerating the neurodegenerative process in AD. This suggestion is consistent with a higher proportion of AD patients among COVID-19 related victims. Gut microbial tryptamine increase due to the viral infection-induced dysbiosis can synergize and potentiate the tryptamine cytotoxicity, necrotizing ability and other properties as a virulence factor.

scholarly journals An evolutionary perspective of DNA methylation patterns in skeletal tissues using a nonhuman primate model of osteoarthritis

2020 ◽  
Author(s):  
Genevieve Housman ◽  
Ellen E. Quillen ◽  
Anne C. Stone
Keyword(s):  
Dna Methylation ◽  
Nonhuman Primate ◽  
Molecular Mechanisms ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Evolutionary Perspective ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
Knee Oa ◽  
Methylation Patterns

AbstractObjectiveEpigenetic factors, such as DNA methylation, play an influential role in the development of the degenerative joint disease osteoarthritis (OA). These molecular mechanisms have been heavily studied in humans, and although OA affects several other animals in addition to humans, few efforts have taken an evolutionary perspective. This study explores the evolution of OA epigenetics by assessing the relationship between DNA methylation variation and knee OA development in baboons (Papio spp.) and by comparing these findings to human OA epigenetic associations.MethodsGenome-wide DNA methylation patterns were identified in bone and cartilage of the right distal femora from 56 pedigreed, adult baboons (28 with and 28 without knee OA) using the Illumina Infinium MethylationEPIC BeadChip.ResultsSeveral significantly differentially methylated positions (DMPs) and regions (DMRs) were found between tissue types. Substantial OA-related differential methylation was also identified in cartilage, but not in bone, suggesting that cartilage epigenetics may be more influential in OA than bone epigenetics. Additionally, some genes containing OA-related DMPs overlap with and display methylation patterns similar to those previously identified in human OA, revealing a mixture of evolutionarily conserved and divergent OA-related methylation patterns in primates.ConclusionsOverall, these findings reinforce current etiological perspectives of OA and enhance our evolutionary understanding of epigenetic mechanisms associated with OA. This work further establishes baboons as a valuable nonhuman primate model of OA, and continued investigations in baboons will help to disentangle the molecular mechanisms contributing to OA and their evolutionary histories.

Maternal High-Fat Diet Persistently Alters Bone Marrow Immune Cell Proportions and Function in a Nonhuman Primate Model

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 222-OR
Author(s):  
MICHAEL J. NASH ◽  
TAYLOR K. SODERBORG ◽  
RACHEL C. JANSSEN ◽  
ERIC M. PIETRAS ◽  
JACOB E. FRIEDMAN
Keyword(s):  
Bone Marrow ◽  
Nonhuman Primate ◽  
High Fat Diet ◽  
Immune Cell ◽  
High Fat ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
And Function

scholarly journals Reperfusion plus Selective Intra-arterial Cooling (SI-AC) Improve Recovery in a Nonhuman Primate Model of Stroke

2020 ◽  
Author(s):  
Di Wu ◽  
Yongjuan Fu ◽  
Longfei Wu ◽  
Mitchell Huber ◽  
Jian Chen ◽  
...  
Keyword(s):  
Nonhuman Primate ◽  
Nonhuman Primate Model ◽  
Primate Model

Robotic Assessment of Upper Limb Function in a Nonhuman Primate Model of Chronic Stroke

2021 ◽  
Author(s):  
Yining Chen ◽  
Meredith C. Poole ◽  
Shelby V. Olesovsky ◽  
Allen A. Champagne ◽  
Kathleen A. Harrison ◽  
...  
Keyword(s):  
Upper Limb ◽  
Nonhuman Primate ◽  
Chronic Stroke ◽  
Nonhuman Primate Model ◽  
Limb Function ◽  
Primate Model ◽  
Upper Limb Function

scholarly journals Transcriptomic phases of periodontitis lesions using the nonhuman primate model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jeffrey L. Ebersole ◽  
Radhakrishnan Nagarajan ◽  
Sreenatha Kirakodu ◽  
Octavio A. Gonzalez
Keyword(s):  
Gene Expression ◽  
Nonhuman Primate ◽  
Gingival Crevicular Fluid ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Lesion Detection ◽  
Gingival Tissue ◽  
Specific Gene ◽  
Nonhuman Primate Model ◽  
Primate Model

AbstractWe used a nonhuman primate model of ligature-induced periodontitis to identify patterns of gingival transcriptomic after changes demarcating phases of periodontitis lesions (initiation, progression, resolution). A total of 18 adult Macaca mulatta (12–22 years) had ligatures placed (premolar, 1st molar teeth) in all 4 quadrants. Gingival tissue samples were obtained (baseline, 2 weeks, 1 and 3 months during periodontitis and at 5 months resolution). Gene expression was analyzed by microarray [Rhesus Gene 1.0 ST Array (Affymetrix)]. Compared to baseline, a large array of genes were significantly altered at initiation (n = 6049), early progression (n = 4893), and late progression (n = 5078) of disease, with the preponderance being up-regulated. Additionally, 1918 genes were altered in expression with disease resolution, skewed towards down-regulation. Assessment of the genes demonstrated specific profiles of epithelial, bone/connective tissue, apoptosis/autophagy, metabolism, regulatory, immune, and inflammatory responses that were related to health, stages of disease, and tissues with resolved lesions. Unique transcriptomic profiles occured during the kinetics of the periodontitis lesion exacerbation and remission. We delineated phase specific gene expression profiles of the disease lesion. Detection of these gene products in gingival crevicular fluid samples from human disease may contribute to a better understanding of the biological dynamics of the disease to improve patient management.

scholarly journals Combining QTL Mapping and Gene Expression Analysis to Elucidate the Genetic Control of ‘Crumbly’ Fruit in Red Raspberry (Rubus idaeus L.)

Agronomy ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 794
Author(s):  
Luca M. Scolari ◽  
Robert D. Hancock ◽  
Pete E. Hedley ◽  
Jenny Morris ◽  
Kay Smith ◽  
...  
Keyword(s):  
Genetic Control ◽  
Developmental Disorder ◽  
Molecular Mechanisms ◽  
Developmental Stages ◽  
Microarray Experiment ◽  
Rubus Idaeus ◽  
Red Raspberry ◽  
Genotype By Sequencing ◽  
First Time ◽  
Selection Of

‘Crumbly’ fruit is a developmental disorder in raspberry that results in malformed and unsaleable fruits. For the first time, we define two distinct crumbly phenotypes as part of this work. A consistent crumbly fruit phenotype affecting the majority of fruits every season, which we refer to as crumbly fruit disorder (CFD) and a second phenotype where symptoms vary across seasons as malformed fruit disorder (MFD). Here, segregation of crumbly fruit of the MFD phenotype was examined in a full-sib family and three QTL (Quantitative Trait Loci) were identified on a high density GbS (Genotype by Sequencing) linkage map. This included a new QTL and more accurate location of two previously identified QTLs. A microarray experiment using normal and crumbly fruit at three different developmental stages identified several genes that were differentially expressed between the crumbly and non-crumbly phenotypes within the three QTL. Analysis of gene function highlighted the importance of processes that compromise ovule fertilization as triggers of crumbly fruit. These candidate genes provided insights regarding the molecular mechanisms involved in the genetic control of crumbly fruit in red raspberry. This study will contribute to new breeding strategies and diagnostics through the selection of molecular markers associated with the crumbly trait.

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