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N-acetylcysteine (NAC), an anti-oxidant, does not improve bone mechanical properties in a rat model of progressive chronic kidney disease-mineral bone disorder.
Allen MR, Wallace J, McNerney E, Nyman J, Avin K, Chen N, Moe S
(2020) PLoS One 15: e0230379
MeSH Terms: Acetylcysteine, Animals, Antioxidants, Caseins, Chronic Kidney Disease-Mineral and Bone Disorder, Disease Models, Animal, Disease Progression, Glycation End Products, Advanced, Humans, Kidney, Lipid Peroxidation, Male, Mutation, Nuclear Proteins, Oxidative Stress, Parathyroid Hormone, Rats, Tibia, X-Ray Microtomography
Show Abstract · Added March 25, 2020
Individuals with chronic kidney disease have elevated levels of oxidative stress and are at a significantly higher risk of skeletal fracture. Advanced glycation end products (AGEs), which accumulate in bone and compromise mechanical properties, are known to be driven in part by oxidative stress. The goal of this study was to study effects of N-acetylcysteine (NAC) on reducing oxidative stress and improving various bone parameters, most specifically mechanical properties, in an animal model of progressive CKD. Male Cy/+ (CKD) rats and unaffected littermates were untreated (controls) or treated with NAC (80 mg/kg, IP) from 30 to 35 weeks of age. Endpoint measures included serum biochemistries, assessments of systemic oxidative stress, bone morphology, and mechanical properties, and AGE levels in the bone. CKD rats had the expected phenotype that included low kidney function, elevated parathyroid hormone, higher cortical porosity, and compromised mechanical properties. NAC treatment had mixed effects on oxidative stress markers, significantly reducing TBARS (a measure of lipid peroxidation) while not affecting 8-OHdG (a marker of DNA oxidation) levels. AGE levels in the bone were elevated in CKD animals and were reduced with NAC although this did not translate to a benefit in bone mechanical properties. In conclusion, NAC failed to significantly improve bone architecture/geometry/mechanical properties in our rat model of progressive CKD.
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19 MeSH Terms
Modeling human disease: a mouse model of acute kidney injury to chronic kidney disease progression after cardiac arrest.
Terker AS, de Caestecker M
(2020) Kidney Int 97: 22-24
MeSH Terms: Acute Kidney Injury, Animals, Cardio-Renal Syndrome, Disease Progression, Heart Arrest, Humans, Inflammation, Mice, Renal Insufficiency, Chronic
Show Abstract · Added May 10, 2020
Matsushita et al. describe a model of acute kidney injury to chronic kidney disease progression in mice surviving cardiac arrest: mice develop severe acute kidney injury that initially recovers but is followed by the onset of impaired renal function on longer-term follow-up. These findings suggest that distinct cardiorenal toxicities and/or injury dynamics are operative in this cardiac arrest model that do not occur in traditional models of acute kidney injury, providing new opportunities for therapeutic and biomarker discovery for an important clinical problem.
Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.
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9 MeSH Terms
AGA Technical Review on Gastric Intestinal Metaplasia-Natural History and Clinical Outcomes.
Gawron AJ, Shah SC, Altayar O, Davitkov P, Morgan D, Turner K, Mustafa RA
(2020) Gastroenterology 158: 705-731.e5
MeSH Terms: Biopsy, Disease Progression, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
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14 MeSH Terms
Breast Cancer Dormancy in Bone.
Clements ME, Johnson RW
(2019) Curr Osteoporos Rep 17: 353-361
MeSH Terms: Animals, Bone Marrow, Bone Neoplasms, Breast Neoplasms, Disease Models, Animal, Disease Progression, Female, Humans, Mice, Neoplasm Metastasis, Signal Transduction, Tumor Microenvironment
Show Abstract · Added March 3, 2020
PURPOSE OF REVIEW - The goal of this review is to summarize recent experimental and clinical evidence for metastatic latency and the molecular mechanisms that regulate tumor dormancy in the bone.
RECENT FINDINGS - Tumor dormancy contributes to the progression of metastasis and thus has significant clinical implications for prognosis and treatment. Tumor-intrinsic signaling and specialized bone marrow niches play a pivotal role in determining the dormancy status of bone disseminated tumor cells. Experimental models have provided significant insight into the effects of the bone microenvironment on tumor cells; however, these models remain limited in their ability to study dormancy. Despite recent advances in the mechanistic understanding of how tumor cells remain dormant in the bone for prolonged periods of time, the signals that trigger spontaneous dormancy escape remain unclear. This review highlights the need for further investigation of mechanisms underlying tumor dormancy using clinically relevant models.
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12 MeSH Terms
Non-canonical roles for metabolic enzymes and intermediates in malignant progression and metastasis.
Williams D, Fingleton B
(2019) Clin Exp Metastasis 36: 211-224
MeSH Terms: ATP Citrate (pro-S)-Lyase, Disease Progression, Energy Metabolism, Fatty Acids, Glucose, Glucose-6-Phosphate Isomerase, Glutaminase, Glutamine, Humans, Isocitrate Dehydrogenase, Neoplasm Metastasis, Neoplasms
Show Abstract · Added March 24, 2020
Metabolic alterations are established as a hallmark of cancer. Such hallmark changes in cancer metabolism are characterized by reprogramming of energy-producing pathways and increases in the generation of biosynthetic intermediates to meet the needs of rapidly proliferating tumor cells. Various metabolic phenotypes such as aerobic glycolysis, increased glutamine consumption, and lipolysis have also been associated with the process of metastasis. However, in addition to the energy and biosynthetic alterations, a number of secondary functions of enzymes and metabolites are emerging that specifically contribute to metastasis. Here, we describe atypical intracellular roles of metabolic enzymes, extracellular functions of metabolic enzymes, roles of metabolites as signaling molecules, and epigenetic regulation mediated by altered metabolism, all of which can affect metastatic progression. We highlight how some of these mechanisms are already being exploited for therapeutic purposes, and discuss how others show similar potential.
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Transforming Growth Factor-β in the Acute Kidney Injury to Chronic Kidney Disease Transition.
Gewin LS
(2019) Nephron 143: 154-157
MeSH Terms: Acute Kidney Injury, Animals, Disease Progression, Humans, Renal Insufficiency, Chronic, Signal Transduction, Transforming Growth Factor beta
Show Abstract · Added March 18, 2020
Transforming growth factor-β (TGF-β) is a key profibrotic growth factor that is activated in acute kidney injury (AKI) and associated with cellular responses that lead to the development of chronic kidney disease (CKD). The persistently injured, de-differentiated tubular epithelial cell is an important mediator of the transition from AKI to CKD. TGF-β signaling may perpetuate proximal tubule injury through de-differentiation, cell cycle arrest, and increased susceptibility to apoptosis. In addition, TGF-β signaling promotes macrophage chemotaxis, endothelial injury, and myofibroblast differentiation after AKI. Future studies that block TGF-β signaling after cessation of AKI are needed to better define its role in the progression of acute to chronic renal injury.
© 2019 S. Karger AG, Basel.
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7 MeSH Terms
Chemokines Modulate Immune Surveillance in Tumorigenesis, Metastasis, and Response to Immunotherapy.
Vilgelm AE, Richmond A
(2019) Front Immunol 10: 333
MeSH Terms: Animals, Antineoplastic Agents, Immunological, Biomarkers, Carcinogenesis, Chemokines, Disease Progression, Humans, Immunologic Surveillance, Immunomodulation, Immunotherapy, Molecular Targeted Therapy, Neoplasm Metastasis, Neoplasm Staging, Neoplasms, Prognosis, Receptors, Chemokine, Treatment Outcome
Show Abstract · Added March 26, 2019
Chemokines are small secreted proteins that orchestrate migration and positioning of immune cells within the tissues. Chemokines are essential for the function of the immune system. Accumulating evidence suggest that chemokines play important roles in tumor microenvironment. In this review we discuss an association of chemokine expression and activity within the tumor microenvironment with cancer outcome. We summarize regulation of immune cell recruitment into the tumor by chemokine-chemokine receptor interactions and describe evidence implicating chemokines in promotion of the "inflamed" immune-cell enriched tumor microenvironment. We review both tumor-promoting function of chemokines, such as regulation of tumor metastasis, and beneficial chemokine roles, including stimulation of anti-tumor immunity and response to immunotherapy. Finally, we discuss the therapeutic strategies target tumor-promoting chemokines or induce/deliver beneficial chemokines within the tumor focusing on pre-clinical studies and clinical trials going forward. The goal of this review is to provide insight into comprehensive role of chemokines and their receptors in tumor pathobiology and treatment.
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17 MeSH Terms
Associations of Unhealthy Food Environment With the Development of Coronary Artery Calcification: The CARDIA Study.
Kelman J, Pool LR, Gordon-Larsen P, Carr JJ, Terry JG, Rana JS, Kershaw KN
(2019) J Am Heart Assoc 8: e010586
MeSH Terms: Adolescent, Adult, Coronary Angiography, Coronary Artery Disease, Coronary Vessels, Disease Progression, Female, Follow-Up Studies, Food Supply, Forecasting, Humans, Incidence, Male, Prospective Studies, Restaurants, Risk Assessment, Risk Factors, United States, Vascular Calcification, Young Adult
Show Abstract · Added April 3, 2019
Background While prior studies have linked the neighborhood environment and development of subclinical atherosclerosis, it is unknown whether living in neighborhoods with greater availability of "unhealthy" food outlets (fast-food chain restaurants and convenience stores) is associated with risk of developing coronary artery calcification ( CAC ). Methods and Results We included 2706 CARDIA study (Coronary Artery Risk Development in Young Adults) participants who underwent CAC measurement during follow-up years 15 (2000-2001), 20 (2005-2006), and 25 (2010-2011). Neighborhood features examined included percentage of all food outlets that were convenience stores and fast-food chain restaurants within a 3-km Euclidean buffer distance from each participant's residence. Econometric fixed effects models, which by design control for all time-invariant covariates, were used to model the longitudinal association between simultaneous within-person change in percentage food outlet and change in CAC . At baseline (year 15), 9.7% of participants had prevalent CAC . During 10 years of follow-up, 21.1% of participants developed CAC . Each 1-SD increase in percentage of convenience stores was associated with a 1.34 higher odds of developing CAC (95% CI : 1.04, 1.72) after adjusting for individual- and neighborhood-level covariates; however, there was no significant association between increased percentage of fast-food chain restaurants and developing CAC (odds ratio=1.15; 95% CI : 0.96, 1.38). There were no significant associations between increases in either food outlet percentage and progression of CAC . Conclusions Our findings suggest that increases in the relative availability of convenience stores in participants' neighborhoods is related to the development of CAC over time.
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20 MeSH Terms
iNKT Cell Activation Exacerbates the Development of Huntington's Disease in R6/2 Transgenic Mice.
Park HJ, Lee SW, Im W, Kim M, Van Kaer L, Hong S
(2019) Mediators Inflamm 2019: 3540974
MeSH Terms: Animals, Brain, Cytokines, Disease Models, Animal, Disease Progression, Galactosylceramides, Genotype, Huntington Disease, Leukocytes, Lymphocyte Activation, Mice, Mice, Knockout, Natural Killer T-Cells
Show Abstract · Added March 26, 2019
Huntington's disease (HD) is an inherited neurodegenerative disorder which is caused by a mutation of the huntingtin (HTT) gene. Although the pathogenesis of HD has been associated with inflammatory responses, if and how the immune system contributes to the onset of HD is largely unknown. Invariant natural killer T (iNKT) cells are a group of innate-like regulatory T lymphocytes that can rapidly produce various cytokines such as IFN and IL4 upon stimulation with the glycolipid -galactosylceramide (-GalCer). By employing both R6/2 Tg mice (murine HD model) and J18 KO mice (deficient in iNKT cells), we investigated whether alterations of iNKT cells affect the development of HD in R6/2 Tg mice. We found that J18 KO R6/2 Tg mice showed disease progression comparable to R6/2 Tg mice, indicating that the absence of iNKT cells did not have any significant effects on HD development. However, repeated activation of iNKT cells with -GalCer facilitated HD progression in R6/2 Tg mice, and this was associated with increased infiltration of iNKT cells in the brain. Taken together, our results demonstrate that repeated -GalCer treatment of R6/2 Tg mice accelerates HD progression, suggesting that immune activation can affect the severity of HD pathogenesis.
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13 MeSH Terms
Spatial distribution of multiple sclerosis lesions in the cervical spinal cord.
Eden D, Gros C, Badji A, Dupont SM, De Leener B, Maranzano J, Zhuoquiong R, Liu Y, Granberg T, Ouellette R, Stawiarz L, Hillert J, Talbott J, Bannier E, Kerbrat A, Edan G, Labauge P, Callot V, Pelletier J, Audoin B, Rasoanandrianina H, Brisset JC, Valsasina P, Rocca MA, Filippi M, Bakshi R, Tauhid S, Prados F, Yiannakas M, Kearney H, Ciccarelli O, Smith SA, Andrada Treaba C, Mainero C, Lefeuvre J, Reich DS, Nair G, Shepherd TM, Charlson E, Tachibana Y, Hori M, Kamiya K, Chougar L, Narayanan S, Cohen-Adad J
(2019) Brain 142: 633-646
MeSH Terms: Adult, Brain, Cervical Cord, Disability Evaluation, Disease Progression, Female, Gray Matter, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Multiple Sclerosis, Multiple Sclerosis, Chronic Progressive, Multiple Sclerosis, Relapsing-Remitting, Spatial Analysis, Spinal Cord, Spinal Cord Diseases, White Matter
Show Abstract · Added March 30, 2020
Spinal cord lesions detected on MRI hold important diagnostic and prognostic value for multiple sclerosis. Previous attempts to correlate lesion burden with clinical status have had limited success, however, suggesting that lesion location may be a contributor. Our aim was to explore the spatial distribution of multiple sclerosis lesions in the cervical spinal cord, with respect to clinical status. We included 642 suspected or confirmed multiple sclerosis patients (31 clinically isolated syndrome, and 416 relapsing-remitting, 84 secondary progressive, and 73 primary progressive multiple sclerosis) from 13 clinical sites. Cervical spine lesions were manually delineated on T2- and T2*-weighted axial and sagittal MRI scans acquired at 3 or 7 T. With an automatic publicly-available analysis pipeline we produced voxelwise lesion frequency maps to identify predilection sites in various patient groups characterized by clinical subtype, Expanded Disability Status Scale score and disease duration. We also measured absolute and normalized lesion volumes in several regions of interest using an atlas-based approach, and evaluated differences within and between groups. The lateral funiculi were more frequently affected by lesions in progressive subtypes than in relapsing in voxelwise analysis (P < 0.001), which was further confirmed by absolute and normalized lesion volumes (P < 0.01). The central cord area was more often affected by lesions in primary progressive than relapse-remitting patients (P < 0.001). Between white and grey matter, the absolute lesion volume in the white matter was greater than in the grey matter in all phenotypes (P < 0.001); however when normalizing by each region, normalized lesion volumes were comparable between white and grey matter in primary progressive patients. Lesions appearing in the lateral funiculi and central cord area were significantly correlated with Expanded Disability Status Scale score (P < 0.001). High lesion frequencies were observed in patients with a more aggressive disease course, rather than long disease duration. Lesions located in the lateral funiculi and central cord area of the cervical spine may influence clinical status in multiple sclerosis. This work shows the added value of cervical spine lesions, and provides an avenue for evaluating the distribution of spinal cord lesions in various patient groups.
© The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For permissions, please email: journals.permissions@oup.com.
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