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3. Truncated TDP‐43 proteoforms diagnostic of frontotemporal dementia with TDP‐43 pathology.

Author

Forgrave, Lauren M., Moon, Kyung‐Mee, Hamden, Jordan E., Li, Yun, Lu, Phoebe, Foster, Leonard J., Mackenzie, Ian R. A., and DeMarco, Mari L.

Abstract

INTRODUCTION: Biomarkers of TDP‐43 pathology are needed to distinguish frontotemporal lobar degeneration with TDP‐43 pathology (FTLD‐TDP) from phenotypically related disorders. While normal physiological TDP‐43 is not a promising biomarker, low‐resolution techniques have suggested truncated forms of TDP‐43 may be specific to TDP‐43 pathology. To advance biomarker efforts for FTLD‐TDP, we employed a high‐resolution structural technique to characterize TDP‐43 post‐translational modifications in FTLD‐TDP. METHODS: High‐resolution mass spectrometry was used to characterize TDP‐43 proteoforms in brain tissue from FTLD‐TDP, non‐TDP‐43 dementias and neuropathologically unaffected cases. Findings were then verified in a larger cohort of FTLD‐TDP and non‐TDP‐43 dementias via targeted quantitative mass spectrometry. RESULTS: In the discovery phase, truncated TDP‐43 identified FTLD‐TDP with 85% sensitivity and 100% specificity. The verification phase revealed similar findings, with 83% sensitivity and 89% specificity. DISCUSSION: The concentration of truncated TDP‐43 proteoforms—in particular, in vivo generated C‐terminal fragments—have high diagnostic accuracy for FTLD‐TDP. Highlights: Discovery: Truncated TDP‐43 differentiates FTLD‐TDP from related dementias.Verification: Truncated TDP‐43 concentration has high accuracy for FTLD‐TDP.TDP‐43 proteoforms <28 kDa have highest discriminatory power for TDP‐43 pathology. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Consensus-Based Best Practice Guidelines for the Management of Spinal Deformity and Associated Tumors in Pediatric Neurofibromatosis Type 1: Screening and Surveillance, Surgical Intervention, and Medical Therapy

Author

Xu, Amy L., Suresh, Krishna V., Gomez, Jaime A., Emans, John B., Larson, A. Noelle, Cahill, Patrick J., Andras, Lindsay M., White, Klane K., Miller, Daniel J., Murphy, Joshua S., Groves, Mari L., Belzberg, Allan J., Hwang, Steven W., Rosser, Tena L., Staedtke, Verena, Ullrich, Nicole J., Sato, Aimee A., Blakeley, Jaishri O., Schorry, Elizabeth K., Gross, Andrea M., Redding, Gregory J., and Sponseller, Paul D.

Published
2023
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6. Antibody response durability following three-dose coronavirus disease 2019 vaccination in people with HIV receiving suppressive antiretroviral therapy

Author

Lapointe, Hope R., Mwimanzi, Francis, Cheung, Peter K., Sang, Yurou, Yaseen, Fatima, Speckmaier, Sarah, Barad, Evan, Moran-Garcia, Nadia, Datwani, Sneha, Duncan, Maggie C., Kalikawe, Rebecca, Ennis, Siobhan, Young, Landon, Ganase, Bruce, Omondi, F. Harrison, Umviligihozo, Gisele, Dong, Winnie, Toy, Junine, Sereda, Paul, Burns, Laura, Costiniuk, Cecilia T., Cooper, Curtis, Anis, Aslam H., Leung, Victor, Holmes, Daniel, DeMarco, Mari L., Simons, Janet, Hedgcock, Malcolm, Prystajecky, Natalie, Lowe, Christopher F., Romney, Marc G., Barrios, Rolando, Guillemi, Silvia, Brumme, Chanson J., Montaner, Julio S.G., Hull, Mark, Harris, Marianne, Niikura, Masahiro, Brockman, Mark A., and Brumme, Zabrina L.

Published
2023
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7. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview.

Author

Delaby, Constance, Teunissen, Charlotte E., Blennow, Kaj, Alcolea, Daniel, Arisi, Ivan, Amar, Elodie Bouaziz, Beaume, Anne, Bedel, Aurélie, Bellomo, Giovanni, Bigot‐Corbel, Edith, Bjerke, Maria, Blanc‐Quintin, Marie‐Céline, Boada, Mercè, Bousiges, Olivier, Chapman, Miles D, DeMarco, Mari L., D'Onofrio, Mara, Dumurgier, Julien, Dufour‐Rainfray, Diane, and Engelborghs, Sebastiaan

Abstract

Introduction: The current practice of quantifying cerebrospinal fluid (CSF) biomarkers as an aid in the diagnosis of Alzheimer's disease (AD) varies from center to center. For a same biochemical profile, interpretation and reporting of results may differ, which can lead to misunderstandings and raises questions about the commutability of tests. Methods: We obtained a description of (pre‐)analytical protocols and sample reports from 40 centers worldwide. A consensus approach allowed us to propose harmonized comments corresponding to the different CSF biomarker profiles observed in patients. Results: The (pre‐)analytical procedures were similar between centers. There was considerable heterogeneity in cutoff definitions and report comments. We therefore identified and selected by consensus the most accurate and informative comments regarding the interpretation of CSF biomarkers in the context of AD diagnosis. Discussion: This is the first time that harmonized reports are proposed across worldwide specialized laboratories involved in the biochemical diagnosis of AD. [ABSTRACT FROM AUTHOR]

Published
2022
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8. Dectin‐1 signaling in neutrophils up‐regulates PD‐L1 and triggers ROS‐mediated suppression of CD4+T cells

Author

Deerhake, M. Elizabeth, Cardakli, Emre D., and Shinohara, Mari L.

Abstract

Dectin‐1 is known to drive proinflammatory cytokine production by macrophages and dendritic cells which promotes Th17 CD4+T cell responses in the setting of fungal infection. However, the role of Dectin‐1 signaling in neutrophils and its impact on CD4+T cells is not well understood. In this study, we found that neutrophils stimulated with a Dectin‐1 agonist diminish CD4+T cell viability in a rapid and reactive oxygen species (ROS)‐dependent manner. Furthermore, Dectin‐1 promoted neutrophil PD‐L1 expression via Syk and Card9 signaling, along with other immune‐checkpoint factors in a neutrophil‐biased manner. Although neutrophil PD‐L1 did not significantly impact disease severity in experimental autoimmune encephalomyelitis (EAE), we found that CNS‐infiltrated neutrophils potently up‐regulate PD‐L1 expression. Furthermore, a subset of PD‐L1+neutrophils was also found to express MHC‐II during EAE. In summary, we found that Dectin‐1 elicits a biphasic neutrophil response in which (1) T‐cell suppressive ROS is followed by (2) up‐regulation of PD‐L1 expression. This response may serve to limit excess CD4+T cell‐driven inflammation in infection or autoimmunity while preserving host‐defense functions of neutrophils. Summary sentence: Mechanisms by which Dectin‐1 signaling in neutrophils promotes a cellular phenotype with T cell‐suppressive properties. Mechanisms by which Dectin‐1 signaling in neutrophils promotes a cellular phenotype with T cell‐suppressive properties.

Published
2022
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9. Spinal screening, malignancy, medical therapy, and surgical correction of deformity in pediatric patients with neurofibromatosis type 1: a systematic review

Author

Suresh, Krishna V., Xu, Amy L., Groves, Mari L., and Sponseller, Paul D.

Abstract

The objective of this systematic review was to synthesize evidence regarding spinal screening recommendations, types of spinal and thoracic neurofibromatosis type 1 (NF1) tumors, medical therapy for NF1-associated neoplasms, and treatment with magnetically controlled growing rods (MCGRs) or cervical kyphosis correction in pediatric patients with NF1.We queried PubMed, Embase, Cochrane Library, Web of Science, Scopus, Clinicaltrials.gov, and medRxiv for studies reporting spinal screening recommendations, prognosis, and medical therapy for NF1-associated spinal tumors and MCGR use or cervical kyphosis correction in pediatric NF1 patients, yielding 758 publications, 33 of which were included.There is no consensus on spinal screening interval. Computed tomography is recommended for postoperative monitoring. Patients with gangliomas and spinal neurofibromas had nearly complete symptom resolution after resection. Plexiform neurofibromas were most commonly treated with resection and laminectomy; some patients reported tumor enlargement after intervention. Malignant nerve sheath tumors have high rates of metastasis even after chemoradiation and resection. MEK-inhibitors produced limited regression in tumor size. Sirolimus and thalidomide reduced tumor size but caused more severe adverse effects than MEK-inhibitors. Improvements in major curves and T1–T12 height gain were reported after MCGR intervention. Anteroposterior arthrodesis produced the greatest correction of dystrophic cervical kyphosis.There may be value in establishing standardized spinal screening protocols for pediatric NF1 patients. Surgical correction of NF1-associated spinal deformity is effective, though current medical therapies for spinal tumors have limited success. Areas for further investigation include determining appropriate screening intervals, choice of medical therapy for spinal tumors, and long-term outcomes of MCGRs. Level of Evidence: IV.

Published
2022
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10. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview.

Author

Delaby, Constance, Teunissen, Charlotte E., Blennow, Kaj, Alcolea, Daniel, Arisi, Ivan, Amar, Elodie Bouaziz, Beaume, Anne, Bedel, Aurélie, Bellomo, Giovanni, Bigot‐Corbel, Edith, Bjerke, Maria, Blanc, Marie‐Céline, Boada, Mercè, Bousiges, Olivier, Chapman, Miles D, DeMarco, Mari L., D'Onofrio, Mara, Dumurgier, Julien, Dufour‐Rainfray, Diane, and Engelborgs, Sebastiaan

Abstract

Background: The quantification of cerebrospinal fluid (CSF) biomarkers (Amyloid beta peptides [Aß1‐40 and Aß1‐42], t‐tau and p‐tau(181)) is progressively implemented in specialized laboratories as an aid for the multidisciplinary diagnosis of Alzheimer's disease (AD). There is however a diversity of practices between centers related to pre‐analytical and analytical conditions, the calculation of ratios between analytes, the applied cut‐off, or the use of interpretation scales. Finally, for the same biochemical profile, the interpretation and reporting of results may differ from one center to another, which may raise questions about the commutability of the tests. So far, no consensus has been reached between the different laboratories involved to define the most appropriate conclusions/comments based on the profile of the quantified biomarkers. This work is an essential step towards a consensual harmonization of clinical reporting after CSF analysis in the context of AD diagnosis, as advocated by the "Biofluid Based Biomarkers PIA" working group of the Alzheimer's Association. Method: We obtained, by means of a questionnaire, a description of the pre‐analytical and analytical protocols and examples of reporting from 40 centers located in 15 countries, i.e. in the majority of countries that have implemented clinical CSF tests for the diagnosis of AD. We then adopted a consensus approach to propose harmonized comments corresponding to different AD CSF biomarker profiles observed in patients. Result: Pre‐analytical procedures were very similar, among the centers. Regarding the analytical part, more than 88% of the laboratories use automatized immunoassays and more than 83% measure Aß1‐40 and compute the Aß1‐42/Aß1‐40 ratio, in addition to the three core biomarkers (Aß1‐42, t‐tau and p‐tau(181)). The cut‐off values of biomarkers used by the different laboratories are widely dispersed. Delay before sending back the results is lower than 1 week in more than 34% of the laboratories. Conclusion: Our results highlight the state of the art in terms of clinical CSF analysis in the context of AD. Harmonization of clinical reporting between different centers could benefit AD care, prevention and treatment strategies, as a common terminology will allow a better assessment of the prevalence of AD and the contribution of biochemical biomarkers to its diagnosis. [ABSTRACT FROM AUTHOR]

Published
2021
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11. International Consensus Statement on the diagnosis, multidisciplinary management and lifelong care of individuals with achondroplasia

Author

Savarirayan, Ravi, Ireland, Penny, Irving, Melita, Thompson, Dominic, Alves, Inês, Baratela, Wagner A. R., Betts, James, Bober, Michael B., Boero, Silvio, Briddell, Jenna, Campbell, Jeffrey, Campeau, Philippe M., Carl-Innig, Patricia, Cheung, Moira S., Cobourne, Martyn, Cormier-Daire, Valérie, Deladure-Molla, Muriel, del Pino, Mariana, Elphick, Heather, Fano, Virginia, Fauroux, Brigitte, Gibbins, Jonathan, Groves, Mari L., Hagenäs, Lars, Hannon, Therese, Hoover-Fong, Julie, Kaisermann, Morrys, Leiva-Gea, Antonio, Llerena, Juan, Mackenzie, William, Martin, Kenneth, Mazzoleni, Fabio, McDonnell, Sharon, Meazzini, Maria Costanza, Milerad, Josef, Mohnike, Klaus, Mortier, Geert R., Offiah, Amaka, Ozono, Keiichi, Phillips, John A., Powell, Steven, Prasad, Yosha, Raggio, Cathleen, Rosselli, Pablo, Rossiter, Judith, Selicorni, Angelo, Sessa, Marco, Theroux, Mary, Thomas, Matthew, Trespedi, Laura, Tunkel, David, Wallis, Colin, Wright, Michael, Yasui, Natsuo, and Fredwall, Svein Otto

Abstract

Achondroplasia, the most common skeletal dysplasia, is characterized by a variety of medical, functional and psychosocial challenges across the lifespan. The condition is caused by a common, recurring, gain-of-function mutation in FGFR3, the gene that encodes fibroblast growth factor receptor 3. This mutation leads to impaired endochondral ossification of the human skeleton. The clinical and radiographic hallmarks of achondroplasia make accurate diagnosis possible in most patients. However, marked variability exists in the clinical care pathways and protocols practised by clinicians who manage children and adults with this condition. A group of 55 international experts from 16 countries and 5 continents have developed consensus statements and recommendations that aim to capture the key challenges and optimal management of achondroplasia across each major life stage and sub-specialty area, using a modified Delphi process. The primary purpose of this first International Consensus Statement is to facilitate the improvement and standardization of care for children and adults with achondroplasia worldwide in order to optimize their clinical outcomes and quality of life.

Published
2022
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13. Neurosurgical Evaluation and Management of Adults with Achondroplasia

Author

Groves, Mari L., Kashanian, Alon, Danielpour, Moise, and Stadler, James A.

Abstract

Much of the current medical discussion for within centers for skeletal dysplasia and specifically patients with achondroplasia focuses on infancy and early childhood. Most neurosurgical concerns arise due to a defect in the endochondral ossification, resulting on early fusion of the synchondrosis. As patients age, the neurosurgical focus shifts from primarily cranial to spinal concerns. Often pediatric neurosurgeons may continue to follow their patients with skeletal dysplasia. However, general adult neurosurgeons and orthopedic surgeons may see these graduated adults in their practice. This article provides a review of the common neurosurgical concerns for patients with achondroplasia.

Published
2022
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14. Neurosurgical Considerations of Neurocutaneous Syndromes

Author

Iyer, Rajiv R., Strahle, Jennifer M., and Groves, Mari L.

Abstract

The phakomatoses are a group of genetic and acquired disorders characterized by neurologic, cutaneous, and often ocular manifestations, thus commonly referred to as neurocutaneous syndromes. In several of these conditions the underlying genetic pathophysiology has been elucidated, which will continue to play an important role in advancing therapeutic techniques. This article focuses on several examples of such neurocutaneous syndromes, with special attention to the relevant neurosurgical considerations of these patients.

Published
2022
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15. Quantitative Profiling of Synuclein Species: Application to Transgenic Mouse Models of Parkinson’s Disease

Author

Singh, Serena, Khayachi, Anouar, Milnerwood, Austen J., and DeMarco, Mari L.

Abstract

Introduction: Improved analytical tools for detailed characterization of synucleins in pre-clinical models of Parkinson’s disease (PD) and related synucleinopathies are needed.Objective: Develop a multiple reaction monitoring (MRM) liquid chromatography tandem mass spectrometry (LC-MS/MS) assay to quantify species-specific sequences and structural heterogeneity in soluble a- and ß-synucleins in brain tissue.Methods: Using a proteolytic digestion workflow, the MRM LC-MS/MS method assayed six proteotypic peptides from the a-synuclein sequence; three unique to mouse or human a-synuclein and three conserved in a- and ß-synuclein. For quantification, we used labeled a-synuclein as the internal standard and an external calibration curve. As proof of concept, the synuclein LC-MS/MS method was applied to brain tissue specimens from M83 transgenic PD mice, which overexpresses human a-synuclein, relative to wild-type littermate controls.Results: The synuclein MRM assay was linear over a wide concentration range (at least one order of magnitude). The assay had several advantages over ligand binding analytical methods, such as western blotting and enzyme-linked immunosorbent assays. These advantages included the ability to: quantify 1) total a-synuclein, 2) combined a- and ß-synucleins, 3) species-specific contributions to total a-synuclein (e.g., in mice expressing both mouse and human a-synuclein), and 4) identify peptide-specific profile differences that may reflect post-translational modifications, all within a single analysis.Conclusion: With improved and expanded analytical characteristics coupled with a streamlined sample preparation workflow, the quantitative synuclein profiling LC-MS/MS assay provides a versatile and efficient platform to characterize synuclein biology in pre-clinical models and the potential for application to human tissues and fluids.

Published
2020
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16. Quantitative Profiling of Synuclein Species: Application to Transgenic Mouse Models of Parkinson’s Disease

Author

Singh, Serena, Khayachi, Anouar, Milnerwood, Austen J., and DeMarco, Mari L.

Abstract

Improved analytical tools for detailed characterization of synucleins in pre-clinical models of Parkinson’s disease (PD) and related synucleinopathies are needed. Develop a multiple reaction monitoring (MRM) liquid chromatography tandem mass spectrometry (LC-MS/MS) assay to quantify species-specific sequences and structural heterogeneity in soluble α- and β-synucleins in brain tissue. Using a proteolytic digestion workflow, the MRM LC-MS/MS method assayed six proteotypic peptides from the α-synuclein sequence; three unique to mouse or human α-synuclein and three conserved in α- and β-synuclein. For quantification, we used labeled α-synuclein as the internal standard and an external calibration curve. As proof of concept, the synuclein LC-MS/MS method was applied to brain tissue specimens from M83 transgenic PD mice, which overexpresses human α-synuclein, relative to wild-type littermate controls. The synuclein MRM assay was linear over a wide concentration range (at least one order of magnitude). The assay had several advantages over ligand binding analytical methods, such as western blotting and enzyme-linked immunosorbent assays. These advantages included the ability to: quantify 1) total α-synuclein, 2) combined α- and β-synucleins, 3) species-specific contributions to total α-synuclein (e.g., in mice expressing both mouse and human α-synuclein), and 4) identify peptide-specific profile differences that may reflect post-translational modifications, all within a single analysis. With improved and expanded analytical characteristics coupled with a streamlined sample preparation workflow, the quantitative synuclein profiling LC-MS/MS assay provides a versatile and efficient platform to characterize synuclein biology in pre-clinical models and the potential for application to human tissues and fluids.

Published
2020
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17. Rfx6 promotes the differentiation of peptide-secreting enteroendocrine cells while repressing genetic programs controlling serotonin production.

Author

Piccand, Julie, Vagne, Constance, Blot, Florence, Meunier, Aline, Beucher, Anthony, Strasser, Perrine, Lund, Mari L., Ghimire, Sabitri, Nivlet, Laure, Lapp, Céline, Petersen, Natalia, Engelstoft, Maja S., Thibault-Carpentier, Christelle, Keime, Céline, Correa, Sara Jimenez, Schreiber, Valérie, Molina, Nacho, Schwartz, Thue W., De Arcangelis, Adèle, and Gradwohl, Gérard

Abstract

Enteroendocrine cells (EECs) of the gastro-intestinal tract sense gut luminal factors and release peptide hormones or serotonin (5-HT) to coordinate energy uptake and storage. Our goal is to decipher the gene regulatory networks controlling EECs specification from enteroendocrine progenitors. In this context, we studied the role of the transcription factor Rfx6 which had been identified as the cause of Mitchell–Riley syndrome, characterized by neonatal diabetes and congenital malabsorptive diarrhea. We previously reported that Rfx6 was essential for pancreatic beta cell development and function; however, the role of Rfx6 in EECs differentiation remained to be elucidated. We examined the molecular, cellular, and metabolic consequences of constitutive and conditional deletion of Rfx6 in the embryonic and adult mouse intestine. We performed single cell and bulk RNA-Seq to characterize EECs diversity and identify Rfx6-regulated genes. Rfx6 is expressed in the gut endoderm; later, it is turned on in, and restricted to, enteroendocrine progenitors and persists in hormone-positive EECs. In the embryonic intestine, the constitutive lack of Rfx6 leads to gastric heterotopia, suggesting a role in the maintenance of intestinal identity. In the absence of intestinal Rfx6, EECs differentiation is severely impaired both in the embryo and adult. However, the number of serotonin-producing enterochromaffin cells and mucosal 5-HT content are increased. Concomitantly, Neurog3-positive enteroendocrine progenitors accumulate. Combined analysis of single-cell and bulk RNA-Seq data revealed that enteroendocrine progenitors differentiate in two main cell trajectories, the enterochromaffin (EC) cells and the Peptidergic Enteroendocrine (PE) cells, the differentiation programs of which are differentially regulated by Rfx6. Rfx6 operates upstream of Arx , Pax6 and Isl1 to trigger the differentiation of peptidergic EECs such as GIP-, GLP-1-, or CCK-secreting cells. On the contrary, Rfx6 represses Lmx1a and Tph1 , two genes essential for serotonin biosynthesis. Finally, we identified transcriptional changes uncovering adaptive responses to the prolonged lack of enteroendocrine hormones and leading to malabsorption and lower food efficiency ratio in Rfx6-deficient mouse intestine. These studies identify Rfx6 as an essential transcriptional regulator of EECs specification and shed light on the molecular mechanisms of intestinal failures in human RFX6-deficiencies such as Mitchell–Riley syndrome. • The lack of Rfx6 impairs the differentiation of peptide-producing enteroendocrine cells. • The number of 5-HT-expressing-cells is increased in Rfx6-deficient intestine. • Intestinal inactivation of Rfx6 leads to lipid malabsorption and decreased food efficiency. [ABSTRACT FROM AUTHOR]

Published
2019
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19. Subventricular zone stem cell niche injury is associated with intestinal perforation in preterm infants and predicts future motor impairment

Author

Epstein, Adrian A., Janos, Sara N., Menozzi, Luca, Pegram, Kelly, Jain, Vaibhav, Bisset, Logan C., Davis, Joseph T., Morrison, Samantha, Shailaja, Aswathy, Guo, Yingqiu, Chao, Agnes S., Abdi, Khadar, Rikard, Blaire, Yao, Junjie, Gregory, Simon G., Fisher, Kimberley, Pittman, Rick, Erkanli, Al, Gustafson, Kathryn E., Carrico, Caroline W.T., Malcolm, William F., Inder, Terrie E., Cotten, C. Michael, Burt, Trevor D., Shinohara, Mari L., Maxfield, Charles M., and Benner, Eric J.

Abstract

Brain injury is highly associated with preterm birth. Complications of prematurity, including spontaneous or necrotizing enterocolitis (NEC)-associated intestinal perforations, are linked to lifelong neurologic impairment, yet the mechanisms are poorly understood. Early diagnosis of preterm brain injuries remains a significant challenge. Here, we identified subventricular zone echogenicity (SVE) on cranial ultrasound in preterm infants following intestinal perforations. The development of SVE was significantly associated with motor impairment at 2 years. SVE was replicated in a neonatal mouse model of intestinal perforation. Examination of the murine echogenic subventricular zone (SVZ) revealed NLRP3-inflammasome assembly in multiciliated FoxJ1+ependymal cells and a loss of the ependymal border in this postnatal stem cell niche. These data suggest a mechanism of preterm brain injury localized to the SVZ that has not been adequately considered. Ultrasound detection of SVE may serve as an early biomarker for neurodevelopmental impairment after inflammatory disease in preterm infants.

Published
2024
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21. International initiative for harmonization of cerebrospinal fluid diagnostic comments in Alzheimer's disease: Developing topics.

Author

Delaby, Constance, Teunissen, Charlotte E, Alcolea, Daniel, Amar, Elodie Bouaziz, Beaume, Anne, Bedel, Aurélie, Bigot‐Corbel, Edith, Bjerke, Maria, Blanc, Marie‐Céline, Bousiges, Olivier, Chapman, Miles D, DeMarco, Mari L, D'Onofrio, Mara, Dufour‐Rainfray, Diane, Engelborghs, Sebastiaan, Esselmann, Hermann, Fogli, Anne, Galloni, Elisabetta, Gondolf, Clémentine, and Grandhomme, Frédérique

Abstract

Background: The quantification of cerebrospinal fluid (CSF) biomarkers (Abeta peptides [Ab1‐40 and Ab1‐42], tau protein and its phosphorylated form phospho‐tau) is progressively implemented in laboratories as an aid for the multidisciplinary diagnosis of Alzheimer disease (AD), DeKosky ST, Alz dementia, 2011, PMID: 21322828. However, no consensus has been defined among the different laboratories involved to adapt the conclusions/comments to the level of quantified CSF biomarkers. As a result, although the analytical methods for such quantification may be similar across the laboratories involved in this clinical task, the conclusions transmitted to the physician in charge (neurologist or psychiatrist) may be quite different. Harmonization of this report is thus necessary so patients' care and research stratification can be similar wherever the analysis is performed. Method: A total of 34 laboratories (involved in CSF biomarkers measurement) across the world accepted to be part of our project of diagnostic's comments harmonization (represented countries: Austria, Belgium, Canada, France, Germany, Italy, Netherland, Poland, Spain, Sweden, United Kingdom, USA). As a first step, we defined the 9 most typical biochemical profiles, according to the level of CSF biomarkers and their combination. For each profile, each laboratory was asked to provide us with the comments/conclusions given in routine clinical practice. We then collected and pooled all the comments in a common file, so that the laboratories could, as a second step, choose and order three of these comments (for each biochemical profile defined), according to their reliability in clinical practice. Result: We are currently analysing the second step‐answers of the laboratories, in order to define a consensual pattern of comments and conclusions that could be implemented in all the laboratories involved in the biochemical diagnosis of AD. Obtained data will be presented. Conclusion: The discrepancies of the comments for AD biochemical diagnosis across laboratories worldwide can be confusing and it is of strong importance to harmonize them (according to the level of quantified biomarkers and other information likely available such as the age, APOE genotype...). Our initiative will likely provide such harmonized pattern of comments/conclusions, thus ensuring equal care of patients across the different diagnostic centres. [ABSTRACT FROM AUTHOR]

Published
2020
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22. Applying the Alzheimer Disease ATN Diagnostic Framework in Atypical Dementia.

Author

Funnell, Clark, Feldman, Howard H., Mackenzie, Ian R.A., and DeMarco, Mari L.

Abstract

Cerebrospinal fluid (CSF) biomarkers amyloid-β and tau have been validated for the antemortem diagnosis of Alzheimer disease (AD) and are included in the AT(N) research framework for AD. Recently, an AT(N) CSF profile has been described for dementia with Lewy bodies (DLB), a disorder which is difficult to distinguish clinically from AD, particularly early in the disease course. Herein we describe a 71-year old male who presented with an atypical dementia syndrome including years of stability after an initial abrupt decline, marked visuospatial dysfunction, and relative sparing of memory. CSF biomarkers combined with the pattern of cognitive symptoms made AD unlikely and were consistent with DLB. This classification was confirmed clinically, with the emergence of classic DLB symptoms, and at postmortem pathologic examination. This case highlights the role for AD CSF biomarkers in facilitating earlier diagnosis of non-Alzheimer neurodegenerative dementias. [ABSTRACT FROM AUTHOR]

Published
2020
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23. The effect of mark enhancement techniques on the presumptive and confirmatory tests for blood.

Author

Stewart, Vanessa, Deacon, Paul, Zahra, Nathalie, Uchimoto, Mari L., and Farrugia, Kevin J.

Subjects
BLOOD testing, CYANOACRYLATES, METHANOL, NUCLEIC acid isolation methods, FORENSIC sciences
Abstract

Abstract An investigation into the effects of physical and chemical enhancement on subsequent presumptive and confirmatory tests for human blood is presented. Human blood was deposited onto porous (white 80 gsm paper and brown envelope) and non-porous (tile and linoleum) substrates in a depletion series (30 depletions on non-porous and 20 on porous) and subjected to three ageing periods; 1, 7 and 28 days. A number of enhancement techniques were tested [fluorescence, black magnetic powder (BMP), iron-oxide black powder suspension (PS), cyanoacrylate (CA) fuming, acid violet 17 (AV17), acid yellow 7 (AY7), ninhydrin, DFO and Bluestar Forensic Magnum (BFM) luminol] to evaluate their potential effects on subsequent presumptive and confirmatory tests. AV17 and Bluestar provided the best enhancement and fully enhanced all depletions in the series. The sensitivity of the Kastle-Meyer (KM) (presumptive), Takayama and RSID-Blood tests (confirmatory) was initially investigated to determine the range of detectable depletions. The KM test detected all depletions, whereas the Takayama test detected up to depletion 6 and RSID-Blood detected up to depletion 20 (paper), 10 (envelope), 15 (tile) and 9 (lino). The abilities of these tests to detect blood after enhancement were then observed. A number of techniques resulted in little to no effect on any of the blood tests, whereas adverse effects were observed for others. Ninhydrin and CA fuming caused weak but instantaneous positive KM results whereas methanol-based AV17 and AY7 delayed the reaction by as much as 1 min. The Takayama test was not very sensitive, therefore, its performance was easily affected by enhancement and negative results were often observed. RSID-Blood tests were largely unaffected by chemical enhancement although a drop in positive results was observed for some of the techniques when compared to positive controls. Using a standard procedure for DNA extraction, all the tested blood samples (before and after enhancement) gave a detectable quantity of DNA and were successfully profiled. Out of the 45 samples processed for DNA profiling, 41 gave full profiles, while the remaining showed allele drop out in one or two loci. Highlights • Strategy to maximise evidence recovery (mark enhancement and blood) and efficiency. • KM test considerably more sensitive than the Takayama and RSID tests. • KM test largely unaffected by most enhancement techniques. • Methanol-based protein stains affected the KM and Takayama tests but not the RSID test. • DNA recovery from bloodstains was still possible after enhancement. [ABSTRACT FROM AUTHOR]

Published
2018
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24. Enterochromaffin 5-HT cells – A major target for GLP-1 and gut microbial metabolites.

Author

Lund, Mari L., Egerod, Kristoffer L., Engelstoft, Maja S., Dmytriyeva, Oksana, Theodorsson, Elvar, Patel, Bhavik A., and Schwartz, Thue W.

Abstract

Objectives 5-HT storing enterochromaffin (EC) cells are believed to respond to nutrient and gut microbial components, and 5-HT receptor-expressing afferent vagal neurons have been described to be the major sensors of nutrients in the GI-tract. However, the molecular mechanism through which EC cells sense nutrients and gut microbiota is still unclear. Methods and results TPH1, the 5-HT generating enzyme, and chromogranin A, an acidic protein responsible for secretory granule storage of 5-HT, were highly enriched in FACS-purified EC cells from both small intestine and colon using a 5-HT antibody-based method. Surprisingly, EC cells from the small intestine did not express GPCR sensors for lipid and protein metabolites, such as FFAR1, GPR119, GPBAR1 (TGR5), CaSR, and GPR142, in contrast to the neighboring GLP-1 storing enteroendocrine cell. However, the GLP-1 receptor was particularly highly expressed and enriched in EC cells as judged both by qPCR and by immunohistochemistry using a receptor antibody. GLP-1 receptor agonists robustly stimulated 5-HT secretion from intestinal preparations using both HPLC and a specific amperometric method. Colonic EC cells expressed many different types of known and potential GPCR sensors of microbial metabolites including three receptors for SCFAs, i.e. FFAR2, OLF78, and OLF558 and receptors for aromatic acids, GPR35; secondary bile acids GPBAR1; and acyl-amides and lactate, GPR132. Conclusion Nutrient metabolites apparently do not stimulate EC cells of the small intestine directly but through a paracrine mechanism involving GLP-1 secreted from neighboring enteroendocrine cells. In contrast, colonic EC cells are able to sense a multitude of different metabolites generated by the gut microbiota as well as gut hormones, including GLP-1. [ABSTRACT FROM AUTHOR]

Published
2018
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25. Erythromyeloid progenitors give rise to a population of osteoclasts that contribute to bone homeostasis and repair

Author

Yahara, Yasuhito, Barrientos, Tomasa, Tang, Yuning J., Puviindran, Vijitha, Nadesan, Puviindran, Zhang, Hongyuan, Gibson, Jason R., Gregory, Simon G., Diao, Yarui, Xiang, Yu, Qadri, Yawar J., Souma, Tomokazu, Shinohara, Mari L., and Alman, Benjamin A.

Abstract

Osteoclasts are multinucleated cells of the monocyte/macrophage lineage that degrade bone. Here, we used lineage tracing studies—labelling cells expressing Cx3cr1, Csf1ror Flt3—to identify the precursors of osteoclasts in mice. We identified an erythromyeloid progenitor (EMP)-derived osteoclast precursor population. Yolk-sac macrophages of EMP origin produced neonatal osteoclasts that can create a space for postnatal bone marrow haematopoiesis. Furthermore, EMPs gave rise to long-lasting osteoclast precursors that contributed to postnatal bone remodelling in both physiological and pathological settings. Our single-cell RNA-sequencing data showed that EMP-derived osteoclast precursors arose independently of the haematopoietic stem cell (HSC) lineage and the data from fate tracking of EMP and HSC lineages indicated the possibility of cell–cell fusion between these two lineages. Cx3cr1+yolk-sac macrophage descendants resided in the adult spleen, and parabiosis experiments showed that these cells migrated through the bloodstream to the remodelled bone after injury.

Published
2020
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27. Maternal nutrition during early and late gestation in gilts and sows under commercial conditions: impacts on maternal growth and litter traits1.

Author

Mallmann, André L, Fagundes, Deivison P, Vier, Carlos E, Oliveira, Gabriela S, Mellagi, Ana P G, Ulguim, Rafael R, Bernardi, Mari L, Orlando, Uislei A D, Cogo, Ricardo J, and Bortolozzo, Fernando P

Abstract

The effects of two different feeding levels, offered in two phases during gestation, on body measurements and litter traits were evaluated in 152 gilts and 551 sows. The treatments consisted of the combination of two gestation phases (phase 1-days 22 to 42; phase 2-days 90 to 110) and two feed amounts (1.8 or 3.5 kg/d). Females were weighed on days 22, 42, 90, and 110 of gestation. Born alive and stillborn piglets were weighed within 12 h of birth. Total placental efficiency (ratio between litter weight and total placental weight) was measured in 518 females. Variables concerning body measurements at days 42 and 90 of gestation were analyzed considering the effects of feed amount, parity order (PO) and its interaction as a 2 × 2 factorial arrangement. Body measurements at day 110 of gestation and litter traits were analyzed considering the effects of feed amounts in phase 1, feed amounts in phase 2, PO and their interactions, as a 2 × 2 × 2 factorial arrangement. As expected, BW, backfat, and caliper units were greater at days 42, 90, and 110 (P ≤ 0.006) for females fed 3.5 kg/d during the previous phase than those fed 1.8 kg. No differences were observed among feed levels in total number of piglets born, mummified fetuses, sum of born alive and stillborn piglets, and within-litter birth weight CV (P ≥ 0.118). The percentage of stillborn piglets was affected by a three-way interaction (feed level at phase 1 × feed level at phase 2 × PO). Gilts fed 1.8 kg/d at phase 1 and 3.5 kg/d at phase 2 had fewer stillborn piglets than the other females (P ≤ 0.004). Birth weight was not affected by feed levels (P ≥ 0.153); however, sows had heavier piglets than gilts (P < 0.001). Females fed 3.5 kg/d during phase 2 tended to have heavier litters (P = 0.054) than those fed 1.8 kg/d. Feeding a high level at phase 2 reduced the occurrence of lightweight piglets in gilts, but not in sows (feed level phase 2 × PO; P = 0.031). Total placental weight, average placental weight, and total placental efficiency were not affected by feed level at phase 1, feed level at phase 2 or interactions (P > 0.14). Sows had total placental weight and average placental weight greater (P ≤ 0.003) than gilts. In conclusion, increasing feed intake during phase 1, phase 2, or both phases resulted in increased maternal BW gain, without expressive effects on litter traits. Feeding 3.5 kg/d to gilts during phase 2 reduced the occurrence of lightweight piglets.

Published
2019
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28. Drug therapy, imaging, and other aspects of clinical management change after Alzheimer's biomarker testing in routine practice: Findings from the IMPACT‐AD BC study.

Author

Yang, David, Best, John R., Chambers, Colleen, Feldman, Howard H., Pettersen, Jacqueline A, Henri‐Bhargava, Alexander, Lee, Philip E, Nygaard, Haakon B., Funnell, Clark R, Foti, Dean J, Hsiung, Ging‐Yuek Robin, and DeMarco, Mari L.

Abstract

Background: While previous studies have demonstrated the effect of Alzheimer's disease (AD) CSF testing in changing diagnosis, we lack an understanding of how this testing affects clinical management. Therefore, we assessed changes in clinical management associated with AD CSF biomarker testing when ordered as part of routine clinical management. Method: The 'Investigating the Impact of Alzheimer's Disease Diagnostics in British Columbia' (IMPACT‐AD BC) study (NCT05002699) is a longitudinal study examining the impact of AD CSF testing on clinical management, personal utility and health care economics in British Columbia, Canada. After AD CSF testing was ordered as part of routine care (where the clinical scenario met the appropriate use criteria), the patient and their physician were eligible to participate in the study. The primary outcome was the change in management (pre‐ v. post‐biomarker results) in a composite measure including 1) AD drug therapy, 2) other relevant drug therapy, 3) other diagnostic procedures, and 4) referral or counselling. Result: Participants (n = 129) had a median age of 63 (IQR:58‐68); 49% were female. Cognitive impairment at baseline consisted of 7% with subjective cognitive impairment, 53% with mild cognitive impairment, and 40% with dementia. CSF biomarker profiles were consistent with an amyloid‐beta pathology (i.e., A+) in 72% of cases. Changes in clinical management because of testing occurred in 83% of cases including: referrals and counseling (57%), imaging (47%) and other diagnostic procedures (e.g., neuropsychological testing) (42%), and use of AD drug therapies (40%). For those with a non‐AD pre‐biomarkers diagnosis, 42% were changed to AD post‐biomarkers; for those with an AD pre‐biomarkers diagnosis, 18% were changed to non‐AD post‐biomarkers. Conclusion: This study has revealed substantial changes in clinical management as a direct result of AD CSF biomarker testing in routine care. An understanding of the implications of biomarker testing will in turn help us: improve appropriate utilization, understand the broader impacts on persons living with dementia and on the health care system, and prepare for expanded use of this testing with the availability of disease‐modifying therapeutics. [ABSTRACT FROM AUTHOR]

Published
2022
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29. Identification TDP‐43 fragments specific for frontotemporal lobar degeneration with TDP‐43 inclusions.

Author

Forgrave, Lauren M, Li, Yun, Moon, Kyung‐Mee, Mackenzie, Ian R, Foster, Leonard J, and DeMarco, Mari L.

Abstract

Background: Ante‐mortem biomarkers specific for TDP‐43 pathology are highly desired given the challenge in distinguishing frontotemporal lobar degeneration with TDP‐43 pathology (FTLD‐TDP) from phenotypically related disorders. TDP‐43 post‐translational modifications, like C‐terminal fragments, are regarded as disease‐specific TDP‐43 proteoforms; however, the exact structure of these proteoforms remains unclear. This lack of clarity is due in part to the use of instrumentation and techniques with low structural resolution and the study of small sample sizes. With this in mind, we performed high resolution mass spectrometry (HRMS) analysis of brain tissue from cases with and without TDP‐43 proteinopathy to identify TDP‐43 proteoforms unique to FTLD‐TDP. Method: HRMS was used to determine TDP‐43 proteoform composition in insoluble frontal lobe brain tissue from immunohistochemically‐confirmed FTLD‐TDP (n=13), related dementias (i.e., Alzheimer's disease and FTLD‐tau without TDP‐43 deposits; n=10) and neuropathologically‐unaffected controls (n=3). Brain tissue was fractioned by gel electrophoresis, with HRMS analysis performed on molecular weight regions corresponding to <28 kDa (low molecular weight TDP; L‐TDP), 28‐38 kDa (mid molecular weight TDP; M‐TDP), and 38‐55 kDa (intact TDP; I‐TDP). Result: In all samples tested, the greatest TDP‐43 sequence coverage was observed for I‐TDP, followed by L‐TDP and then M‐TDP. TDP‐43 peptides from L‐TDP were more frequently detected in the FTLD‐TDP cases compared to both sets of controls, whereas no frequency differences were observed for I‐TDP and M‐TDP. Quantitative analysis revealed peptide concentrations from M‐ and L‐TDP were significantly increased in FTLD‐TDP cases compared to controls. The L‐TDP peptides concentrations differentiated FTLD‐TDP cases from related dementias and unaffected controls with 78% sensitivity and 100% specificity. Further, three in vivo cleavage sites of TDP‐43 were identified, which were unique to FTLD‐TDP cases. Conclusion: This is the largest reported proteomics study to date of histology‐confirmed FTLD‐TDP. This is also the first study to include a large number and range of control tissues, and to provide supporting evidence for in vivo cleavage sites including corroboration of the proteolytic fragment recently found in TDP‐43 fibrils. Clarity and consensus on the sequence of TDP‐43 disease‐specific proteoforms will be helpful in advancing biomarker and drug discovery efforts for TDP‐43 proteopathies. [ABSTRACT FROM AUTHOR]

Published
2022
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30. What patients and caregivers do with knowledge of Alzheimer's disease CSF test results: Findings from the IMPACT‐AD BC study.

Author

Patel, Khushbu Jayeshkumar, Yang, David, Chambers, Colleen, Feldman, Howard H., Hsiung, Ging‐Yuek Robin, Nygaard, Haakon B., Best, John R., Dwosh, Emily, Robillard, Julie M., and DeMarco, Mari L.

Abstract

Background: The growing clinical use of the analysis of CSF amyloid‐beta peptides and tau proteins to assist in the diagnosis Alzheimer's disease (AD) highlights an urgent need to understand the impact of this testing on patients, as well as their care partners. We aimed to address this knowledge gap by examining the perspectives of patients who underwent CSF AD biomarker testing as part of routine care, and a family member ('care partner'). Method: Within the 'Investigating the Impact of Alzheimer's Disease Diagnostics in British Columbia' (IMPACT‐AD BC) study (NCT05002699), we conducted semi‐structured telephone interviews with patients that meet the appropriate use criteria for AD CSF biomarker testing and separate interviews with their care partner. A subset of patients (n=33) and care partners (n=31) were interviewed post‐CSF biomarker disclosure and again ∼5 months (median: 4.9 [4.2‐5.3]) after the initial interview. Thematic content analysis was performed to understand the impact of AD biomarker testing on health behaviors, financial and care planning decisions, and resources and support needs. Result: Most patients (94%) rated their decision to undergo testing as "easy", with the remainder noting the decision was neither easy nor difficult. After result disclosure, a few patients (8%) reported feelings of concern, but the majority (80%) reported overall positive feelings from having more information about their brain health, certainty around their diagnosis, and the ability to plan ahead. Regarding actions patients planned to take after learning their test result, many expressed an intention to adopt or continue with healthy behaviors, such as exercise (42%). From the care partners' perspective, many expressed relief at having more diagnostic certainty post‐disclosure, and that this information would help them plan for future care needs. Post‐disclosure, care partners also relayed an increased awareness of future caregiving responsibilities and the need or desire to connect with community resources to help navigate this new role. Additional analyses investigated responses based on patients' amyloid status and disease severity. Conclusion: In summary, individuals undergoing AD CSF biomarker testing and their care partners found that CSF testing provided the information needed to help them make wellbeing decisions and plan their future. [ABSTRACT FROM AUTHOR]

Published
2022
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33. A Qualitative Study of Experiences of Participants in Cardiac Rehabilitation

Author

Yates, Bernice C., Vazquez Hernandez, Mari L., Rowland, Sheri A., Bainter, Denise E., Schulz, Paula, and Hanson, Corrine K.

Abstract

This study examined perceptions of patients and partners in a phase 2 cardiac rehabilitation (CR) within 3 mo of completing the program. Participant perceptions of CR were, overall, very positive. Participants reported that they benefitted from the exercise sessions; however, they wanted more personalized information from the educational sessions.

Published
2018
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35. Virulence profiles of enterotoxigenic Escherichia coli isolated from piglets with post-weaning diarrhea and classification according to fecal consistency.

Author

Sato, José Paulo H., Takeuti, Karine L., Andrade, Mariana R., Koerich, Priscilla K. V., Tagliari, Vinícius, Bernardi, Mari L., Cardoso, Marisa R. I., and Barcellos, David E. S. N.

Abstract

Copyright of Pesquisa Veterinaria Brasileira is the property of Colegio Brasileiro de Patologia Animal - CBPA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2016
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36. Skewing of the population balance of lymphoid and myeloid cells by secreted and intracellular osteopontin

Author

Kanayama, Masashi, Xu, Shengjie, Danzaki, Keiko, Gibson, Jason R, Inoue, Makoto, Gregory, Simon G, and Shinohara, Mari L

Abstract

The balance of myeloid populations and lymphoid populations must be well controlled. Here we found that osteopontin (OPN) skewed this balance during pathogenic conditions such as infection and autoimmunity. Notably, two isoforms of OPN exerted distinct effects in shifting this balance through cell-type-specific regulation of apoptosis. Intracellular OPN (iOPN) diminished the population size of myeloid progenitor cells and myeloid cells, and secreted OPN (sOPN) increase the population size of lymphoid cells. The total effect of OPN on skewing the leukocyte population balance was observed as host sensitivity to early systemic infection with Candida albicans and T cell–mediated colitis. Our study suggests previously unknown detrimental roles for two OPN isoforms in causing the imbalance of leukocyte populations.

Published
2017
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37. A binary module for microbiota-mediated regulation of γδ17 cells, hallmarked by microbiota-driven expression of programmed cell death protein 1

Author

Huang, Hsin-I, Xue, Yue, Jewell, Mark L., Tan, Chin Yee, Theriot, Barbara, Aggarwal, Nupur, Dockterman, Jacob, Lin, Yang-Ding, Schroeder, Erin A., Wang, Donghai, Xiong, Na, Coers, Jörn, Shinohara, Mari L., Surana, Neeraj K., and Hammer, Gianna Elena

Abstract

Little is known about how microbiota regulate innate-like γδ T cells or how these restrict their effector functions within mucosal barriers, where microbiota provide chronic stimulation. Here, we show that microbiota-mediated regulation of γδ17 cells is binary, where microbiota instruct in situinterleukin-17 (IL-17) production and concomitant expression of the inhibitory receptor programmed cell death protein 1 (PD-1). Microbiota-driven expression of PD-1 and IL-17 and preferential adoption of a PD-1highphenotype are conserved for γδ17 cells across multiple mucosal barriers. Importantly, microbiota-driven PD-1 inhibits in situIL-17 production by mucosa-resident γδ17 effectors, linking microbiota to their simultaneous activation and suppression. We further show the dynamic nature of this microbiota-driven module and define an inflammation-associated activation state for γδ17 cells marked by augmented PD-1, IL-17, and lipid uptake, thus linking the microbiota to dynamic subset-specific activation and metabolic remodeling to support γδ17 effector functions in a microbiota-dense tissue environment.

Published
2023
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38. 20-αHydroxycholesterol, an oxysterol in human breast milk, reverses mouse neonatal white matter injury through Gli-dependent oligodendrogenesis

Author

Chao, Agnes S., Matak, Pavle, Pegram, Kelly, Powers, James, Hutson, Collin, Jo, Rebecca, Dubois, Laura, Thompson, J. Will, Smith, P. Brian, Jain, Vaibhav, Liu, Chunlei, Younge, Noelle E., Rikard, Blaire, Reyes, Estefany Y., Shinohara, Mari L., Gregory, Simon G., Goldberg, Ronald N., and Benner, Eric J.

Abstract

White matter injuries (WMIs) are the leading cause of neurologic impairment in infants born premature. There are no treatment options available. The most common forms of WMIs in infants occur prior to the onset of normal myelination, making its pathophysiology distinctive, thus requiring a tailored approach to treatment. Neonates present a unique opportunity to repair WMIs due to a transient abundance of neural stem/progenitor cells (NSPCs) present in the germinal matrix with oligodendrogenic potential. We identified an endogenous oxysterol, 20-αHydroxycholesterol (20HC), in human maternal breast milk that induces oligodendrogenesis through a sonic hedgehog (shh), Gli-dependent mechanism. Following WMI in neonatal mice, injection of 20HC induced subventricular zone-derived oligodendrogenesis and improved myelination in the periventricular white matter, resulting in improved motor outcomes. Targeting the oligodendrogenic potential of postnatal NSPCs in neonates with WMIs may be further developed into a novel approach to mitigate this devastating complication of preterm birth.

Published
2023
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39. Poor prognosis despite aggressive treatment in adults with intramedullary spinal cord glioblastoma.

Author

Liu, Ann, Sankey, Eric W., Bettegowda, Chetan, Burger, Peter C., Jallo, George I., and Groves, Mari L.

Abstract

We report our institution’s experience with adult patients who underwent surgery for intramedullary spinal cord glioblastoma. Spine involvement of glioblastoma is rare, representing 7.5% of all intramedullary gliomas and 1–3% of all spinal cord tumors. We performed a retrospective review of five male patients with intramedullary spinal cord glioblastoma who underwent surgical resection from 1990 to 2014. Demographic, operative, and postoperative factors were recorded. The median age at treatment was 31 years (range: 18–61) and all men presented with motor or sensory dysfunction. Two had prior surgical resection of an intramedullary World Health Organization Grade III anaplastic astrocytoma lesion with adjuvant chemoradiation. All tumors were present in the cervical (n = 2; 40%) or thoracic (n = 3; 60%) spine, spanning a median of three levels (range: 2–4). Gross total resection was achieved in three men (60%), and there were no intraoperative mortalities or complications. Although one had improvement in his neurological status postoperatively, all five men died with a median time to death of 20 months (range: 2–31). Adult intramedullary spinal cord glioblastoma is rare, and despite aggressive treatment, prognosis is poor, with a median survival in our series of only 20 months. New treatment strategies are necessary to improve survival in this patient population. [ABSTRACT FROM AUTHOR]

Published
2015
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40. Biomarker Development in COPD

Author

Hollander, Zsuzsanna, DeMarco, Mari L., Sadatsafavi, Mohsen, McManus, Bruce M., Ng, Raymond T., and Sin, Don D.

Abstract

There is a great interest in developing biomarkers to enable precision medicine and improve health outcomes of patients with COPD. However, biomarker development is extremely challenging and expensive, and translation of research endeavors to date has been largely unsuccessful. In most cases, biomarkers fail because of poor replication of initial promising results in independent cohorts and/or inability to transfer the biomarker from a discovery platform to a clinical assay. Ultimately, new biomarker assays must address 5 questions for optimal clinical translation. They include the following: is the biomarker likely to be (1) superior (will the test outperform current standards?); (2) actionable (will the test change patient management?); (3) valuable (will the test improve patient outcomes?); (4) economical (will the implementation of the biomarker in the target population be cost-saving or cost-effective?); and (5) clinically deployable (is there a pathway for the biomarker and analytical technology to be implemented in a clinical laboratory?)? In this article we review some of the major barriers to biomarker development in COPD and provide possible solutions to overcome these limitations, enabling translation of promising biomarkers from discovery experiments to clinical implementation.

Published
2017
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41. An interferon-β-resistant and NLRP3 inflammasome–independent subtype of EAE with neuronal damage

Author

Inoue, Makoto, Chen, Po-han, Siecinski, Stephen, Li, Qi-jing, Liu, Chunlei, Steinman, Lawrence, Gregory, Simon G, Benner, Eric, and Shinohara, Mari L

Abstract

Inflammation induced by innate immunity influences the development of T cell–mediated autoimmunity in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). We found that strong activation of innate immunity induced Nod-like receptor protein 3 (NLRP3) inflammasome–independent and interferon-β (IFNβ)-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate immunity requires the NLRP3 inflammasome and is sensitive to IFNβ treatment. Instead, an alternative inflammatory mechanism, including membrane-bound lymphotoxin-β receptor (LTβR) and CXC chemokine receptor 2 (CXCR2), is involved in type B EAE development, and type B EAE is ameliorated by antagonizing these receptors. Relative expression of Ltbr and Cxcr2 genes was indeed enhanced in patients with IFNβ-resistant multiple sclerosis. Remission was minimal in type B EAE due to neuronal damages induced by semaphorin 6B upregulation on CD4+T cells. Our data reveal a new inflammatory mechanism by which an IFNβ-resistant EAE subtype develops.

Published
2016
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43. Infection and inflammation: New perspectives on Alzheimer's disease

Author

Whitson, Heather E., Colton, Carol, El Khoury, Joseph, Gate, David, Goate, Alison, Heneka, Michael T., Kaddurah-Daouk, Rima, Klein, Robyn S., Shinohara, Mari L., Sisodia, Sangram, Spudich, Serena S., Stevens, Beth, Tanzi, Rudolph, Ting, Jenny P., Garden, Gwenn, Aiello, Alison, Chiba-Falek, Ornit, Heitman, Joseph, Johnson, Kim G., Luftig, Micah, Moseman, Ashley, Rawls, Jonathan, Shinohara, Mari L., Swanstrom, Ronald, and Terrando, Niccolo

Abstract

Neuroinflammation has been recognized as a component of Alzheimer's Disease (AD) pathology since the original descriptions by Alois Alzheimer and a role for infections in AD pathogenesis has long been hypothesized. More recently, this hypothesis has gained strength as human genetics and experimental data suggest key roles for inflammatory cells in AD pathogenesis. To review this topic, Duke/University of North Carolina (Duke/UNC) Alzheimer's Disease Research Center hosted a virtual symposium: “Infection and Inflammation: New Perspectives on Alzheimer's Disease (AD).” Participants considered current evidence for and against the hypothesis that AD could be caused or exacerbated by infection or commensal microbes. Discussion focused on connecting microglial transcriptional states to functional states, mouse models that better mimic human immunity, the potential involvement of inflammasome signaling, metabolic alterations, self-reactive T cells, gut microbes and fungal infections, and lessons learned from Covid-19 patients with neurologic symptoms. The content presented in the symposium, and major topics raised in discussions are reviewed in this summary of the proceedings.

Published
2022
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44. Troubles de la déglutition chez le sujet âgé : quel outil pour prévenir l’iatrogénie médicamenteuse en établissement de santé ? Expérience dans un centre de gériatrie

Author

Bouillot, E., Robert, V., Papailhau, C., Briolant, S., Razafiarizon, M., Adjemout, L., Mari, L., Franqui, C., and Vincentelli, M.-B.

Abstract

Les troubles de la déglutition concernent particulièrement le sujet âgé avec une prévalence de 30 à 40 % en France. L’administration des médicaments sous formes orales sèches (FOS) est ainsi souvent inadaptée, conduisant à l’écrasement des comprimés ou à l’ouverture des gélules de façon inappropriée avec un risque de iatrogénie médicamenteuse. En gériatrie, cette question a toute son importance, et pour sécuriser les pratiques une collaboration pluridisciplinaire associant les équipes médico-pharmaceutique et soignante est nécessaire.

Published
2022
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45. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Author

Klionsky, Daniel J, Abdelmohsen, Kotb, Abe, Akihisa, Abedin, Md Joynal, Abeliovich, Hagai, Acevedo Arozena, Abraham, Adachi, Hiroaki, Adams, Christopher M, Adams, Peter D, Adeli, Khosrow, Adhihetty, Peter J, Adler, Sharon G, Agam, Galila, Agarwal, Rajesh, Aghi, Manish K, Agnello, Maria, Agostinis, Patrizia, Aguilar, Patricia V, Aguirre-Ghiso, Julio, Airoldi, Edoardo M, Ait-Si-Ali, Slimane, Akematsu, Takahiko, Akporiaye, Emmanuel T, Al-Rubeai, Mohamed, Albaiceta, Guillermo M, Albanese, Chris, Albani, Diego, Albert, Matthew L, Aldudo, Jesus, Algül, Hana, Alirezaei, Mehrdad, Alloza, Iraide, Almasan, Alexandru, Almonte-Beceril, Maylin, Alnemri, Emad S, Alonso, Covadonga, Altan-Bonnet, Nihal, Altieri, Dario C, Alvarez, Silvia, Alvarez-Erviti, Lydia, Alves, Sandro, Amadoro, Giuseppina, Amano, Atsuo, Amantini, Consuelo, Ambrosio, Santiago, Amelio, Ivano, Amer, Amal O, Amessou, Mohamed, Amon, Angelika, An, Zhenyi, Anania, Frank A, Andersen, Stig U, Andley, Usha P, Andreadi, Catherine K, Andrieu-Abadie, Nathalie, Anel, Alberto, Ann, David K, Anoopkumar-Dukie, Shailendra, Antonioli, Manuela, Aoki, Hiroshi, Apostolova, Nadezda, Aquila, Saveria, Aquilano, Katia, Araki, Koichi, Arama, Eli, Aranda, Agustin, Araya, Jun, Arcaro, Alexandre, Arias, Esperanza, Arimoto, Hirokazu, Ariosa, Aileen R, Armstrong, Jane L, Arnould, Thierry, Arsov, Ivica, Asanuma, Katsuhiko, Askanas, Valerie, Asselin, Eric, Atarashi, Ryuichiro, Atherton, Sally S, Atkin, Julie D, Attardi, Laura D, Auberger, Patrick, Auburger, Georg, Aurelian, Laure, Autelli, Riccardo, Avagliano, Laura, Avantaggiati, Maria Laura, Avrahami, Limor, Awale, Suresh, Azad, Neelam, Bachetti, Tiziana, Backer, Jonathan M, Bae, Dong-Hun, Bae, Jae-sung, Bae, Ok-Nam, Bae, Soo Han, Baehrecke, Eric H, Baek, Seung-Hoon, Baghdiguian, Stephen, Bagniewska-Zadworna, Agnieszka, Bai, Hua, Bai, Jie, Bai, Xue-Yuan, Bailly, Yannick, Balaji, Kithiganahalli Narayanaswamy, Balduini, Walter, Ballabio, Andrea, Balzan, Rena, Banerjee, Rajkumar, Bánhegyi, Gábor, Bao, Haijun, Barbeau, Benoit, Barrachina, Maria D, Barreiro, Esther, Bartel, Bonnie, Bartolomé, Alberto, Bassham, Diane C, Bassi, Maria Teresa, Bast, Robert C, Basu, Alakananda, Batista, Maria Teresa, Batoko, Henri, Battino, Maurizio, Bauckman, Kyle, Baumgarner, Bradley L, Bayer, K Ulrich, Beale, Rupert, Beaulieu, Jean-François, Beck, George R., Becker, Christoph, Beckham, J David, Bédard, Pierre-André, Bednarski, Patrick J, Begley, Thomas J, Behl, Christian, Behrends, Christian, Behrens, Georg MN, Behrns, Kevin E, Bejarano, Eloy, Belaid, Amine, Belleudi, Francesca, Bénard, Giovanni, Berchem, Guy, Bergamaschi, Daniele, Bergami, Matteo, Berkhout, Ben, Berliocchi, Laura, Bernard, Amélie, Bernard, Monique, Bernassola, Francesca, Bertolotti, Anne, Bess, Amanda S, Besteiro, Sébastien, Bettuzzi, Saverio, Bhalla, Savita, Bhattacharyya, Shalmoli, Bhutia, Sujit K, Biagosch, Caroline, Bianchi, Michele Wolfe, Biard-Piechaczyk, Martine, Billes, Viktor, Bincoletto, Claudia, Bingol, Baris, Bird, Sara W, Bitoun, Marc, Bjedov, Ivana, Blackstone, Craig, Blanc, Lionel, Blanco, Guillermo A, Blomhoff, Heidi Kiil, Boada-Romero, Emilio, Böckler, Stefan, Boes, Marianne, Boesze-Battaglia, Kathleen, Boise, Lawrence H, Bolino, Alessandra, Boman, Andrea, Bonaldo, Paolo, Bordi, Matteo, Bosch, Jürgen, Botana, Luis M, Botti, Joelle, Bou, German, Bouché, Marina, Bouchecareilh, Marion, Boucher, Marie-Josée, Boulton, Michael E, Bouret, Sebastien G, Boya, Patricia, Boyer-Guittaut, Michaël, Bozhkov, Peter V, Brady, Nathan, Braga, Vania MM, Brancolini, Claudio, Braus, Gerhard H, Bravo-San Pedro, José M, Brennan, Lisa A, Bresnick, Emery H, Brest, Patrick, Bridges, Dave, Bringer, Marie-Agnès, Brini, Marisa, Brito, Glauber C, Brodin, Bertha, Brookes, Paul S, Brown, Eric J, Brown, Karen, Broxmeyer, Hal E, Bruhat, Alain, Brum, Patricia Chakur, Brumell, John H, Brunetti-Pierri, Nicola, Bryson-Richardson, Robert J, Buch, Shilpa, Buchan, Alastair M, Budak, Hikmet, Bulavin, Dmitry V, Bultman, Scott J, Bultynck, Geert, Bumbasirevic, Vladimir, Burelle, Yan, Burke, Robert E, Burmeister, Margit, Bütikofer, Peter, Caberlotto, Laura, Cadwell, Ken, Cahova, Monika, Cai, Dongsheng, Cai, Jingjing, Cai, Qian, Calatayud, Sara, Camougrand, Nadine, Campanella, Michelangelo, Campbell, Grant R, Campbell, Matthew, Campello, Silvia, Candau, Robin, Caniggia, Isabella, Cantoni, Lavinia, Cao, Lizhi, Caplan, Allan B, Caraglia, Michele, Cardinali, Claudio, Cardoso, Sandra Morais, Carew, Jennifer S, Carleton, Laura A, Carlin, Cathleen R, Carloni, Silvia, Carlsson, Sven R, Carmona-Gutierrez, Didac, Carneiro, Leticia AM, Carnevali, Oliana, Carra, Serena, Carrier, Alice, Carroll, Bernadette, Casas, Caty, Casas, Josefina, Cassinelli, Giuliana, Castets, Perrine, Castro-Obregon, Susana, Cavallini, Gabriella, Ceccherini, Isabella, Cecconi, Francesco, Cederbaum, Arthur I, Ceña, Valentín, Cenci, Simone, Cerella, Claudia, Cervia, Davide, Cetrullo, Silvia, Chaachouay, Hassan, Chae, Han-Jung, Chagin, Andrei 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Jinxian, Xu, Liang, Xu, Xiaolei, Xu, Yangqing, Xu, Ye, Xu, Zhi-Xiang, Xu, Ziheng, Xue, Yu, Yamada, Takahiro, Yamamoto, Ai, Yamanaka, Koji, Yamashina, Shunhei, Yamashiro, Shigeko, Yan, Bing, Yan, Bo, Yan, Xianghua, Yan, Zhen, Yanagi, Yasuo, Yang, Dun-Sheng, Yang, Jin-Ming, Yang, Liu, Yang, Minghua, Yang, Pei-Ming, Yang, Peixin, Yang, Qian, Yang, Wannian, Yang, Wei Yuan, Yang, Xuesong, Yang, Yi, Yang, Ying, Yang, Zhifen, Yang, Zhihong, Yao, Meng-Chao, Yao, Pamela J, Yao, Xiaofeng, Yao, Zhenyu, Yao, Zhiyuan, Yasui, Linda S, Ye, Mingxiang, Yedvobnick, Barry, Yeganeh, Behzad, Yeh, Elizabeth S, Yeyati, Patricia L, Yi, Fan, Yi, Long, Yin, Xiao-Ming, Yip, Calvin K, Yoo, Yeong-Min, Yoo, Young Hyun, Yoon, Seung-Yong, Yoshida, Ken-Ichi, Yoshimori, Tamotsu, Young, Ken H, Yu, Huixin, Yu, Jane J, Yu, Jin-Tai, Yu, Jun, Yu, Li, Yu, W Haung, Yu, Xiao-Fang, Yu, Zhengping, Yuan, Junying, Yuan, Zhi-Min, Yue, Beatrice YJT, Yue, Jianbo, Yue, Zhenyu, Zacks, David N, Zacksenhaus, Eldad, Zaffaroni, Nadia, Zaglia, Tania, Zakeri, Zahra, Zecchini, Vincent, Zeng, Jinsheng, Zeng, Min, Zeng, Qi, Zervos, Antonis S, Zhang, Donna D, Zhang, Fan, Zhang, Guo, Zhang, Guo-Chang, Zhang, Hao, Zhang, Hong, Zhang, Hong, Zhang, Hongbing, Zhang, Jian, Zhang, Jian, Zhang, Jiangwei, Zhang, Jianhua, Zhang, Jing-pu, Zhang, Li, Zhang, Lin, Zhang, Lin, Zhang, Long, Zhang, Ming-Yong, Zhang, Xiangnan, Zhang, Xu Dong, Zhang, Yan, Zhang, Yang, Zhang, Yanjin, Zhang, Yingmei, Zhang, Yunjiao, Zhao, Mei, Zhao, Wei-Li, Zhao, Xiaonan, Zhao, Yan G, Zhao, Ying, Zhao, Yongchao, Zhao, Yu-xia, Zhao, Zhendong, Zhao, Zhizhuang J, Zheng, Dexian, Zheng, Xi-Long, Zheng, Xiaoxiang, Zhivotovsky, Boris, Zhong, Qing, Zhou, Guang-Zhou, Zhou, Guofei, Zhou, Huiping, Zhou, Shu-Feng, Zhou, Xu-jie, Zhu, Hongxin, Zhu, Hua, Zhu, Wei-Guo, Zhu, Wenhua, Zhu, Xiao-Feng, Zhu, Yuhua, Zhuang, Shi-Mei, Zhuang, Xiaohong, Ziparo, Elio, Zois, Christos E, Zoladek, Teresa, Zong, Wei-Xing, Zorzano, Antonio, and Zughaier, Susu M

Published
2016
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46. Transcriptional and Functional Characterization of the G Protein-Coupled Receptor Repertoire of Gastric Somatostatin Cells

Author

Egerod, Kristoffer L., Engelstoft, Maja S., Lund, Mari L., Grunddal, Kaare V., Zhao, Mirabella, Barir-Jensen, Dominique, Nygaard, Eva B., Petersen, Natalia, Holst, Jens J., and Schwartz, Thue W.

Abstract

In the stomach, somatostatin (SST) acts as a general paracrine negative regulator of exocrine secretion of gastric acid and pepsinogen and endocrine secretion of gastrin, ghrelin, and histamine. Using reporter mice expressing red fluorescent protein (RFP) under control of the SST promotor, we have characterized the G protein-coupled receptors expressed in gastric Sst-RFP-positive cells and probed their effects on SST secretion in primary cell cultures. Surprisingly, besides SST, amylin and PYY were also highly enriched in the SST cells. Several receptors found to regulate SST secretion were highly expressed and/or enriched. 1) The metabolite receptors calcium-sensing receptor and free fatty acid receptor 4 (GPR120) functioned as positive and negative regulators, respectively. 2) Among the neurotransmitter receptors, adrenergic receptors α1a, α2a, α2b, and β1were all highly expressed, with norepinephrine and isoproterenol acting as positive regulators. The muscarinic receptor M3 acted as a positive regulator, whereas M4 was conceivably a negative regulator. 3) Of the hormone receptors, the GLP-1 and GIP receptors, CCKb (stimulated by both CCK and gastrin) and surprisingly the melanocortin MC1 receptor were all positive regulators. 4) The neuropeptide receptors for calcitonin gene-related peptide, adrenomedullin, and vasoactive intestinal peptide acted as positive regulators, no effect was observed using galanin and nociceptin although transcripts for the corresponding receptors appeared highly expressed. 5) The SST receptors 1 and 2 functioned in an autocrine negative feedback loop. Thus, the article provides a comprehensive map of receptors through which SST secretion is regulated by hormones, neurotransmitters, neuropeptides and metabolites that act directly on the SST cells in the gastric mucosa.

Published
2015
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47. Research Resource: A Chromogranin A Reporter for Serotonin and Histamine Secreting Enteroendocrine Cells

Author

Engelstoft, Maja S., Lund, Mari L., Grunddal, Kaare V., Egerod, Kristoffer L., Osborne-Lawrence, Sherri, Poulsen, Steen Seier, Zigman, Jeffrey M., and Schwartz, Thue W.

Abstract

Chromogranin A (ChgA) is an acidic protein found in large dense-core secretory vesicles and generally considered to be expressed in all enteroendocrine cells of the gastrointestinal (GI) tract. Here, we characterize a novel reporter mouse for ChgA, ChgA-humanized Renilla reniformis(hr)GFP. The hrGFP reporter was found in the monoamine-storing chromaffin cells of the adrenal medulla, where ChgA was originally discovered. hrGFP also was expressed in enteroendocrine cells throughout the GI tract, faithfully after the expression of ChgA, as characterized by immunohistochemistry and quantitative PCR analysis of fluorescence-activated cell sorting-purified cells, although the expression in the small intestine was weak compared with that of the stomach and colon. In the stomach, hrGFP was highly expressed in almost all histamine-storing enterochromaffin (EC)-like cells, at a lower level in the majority of serotonin-storing EC cells and ghrelin cells, in a small fraction of somatostatin cells, but was absent from gastrin cells. In the small intestine, the hrGFP reporter was selectively, but weakly expressed in EC cells, although not in any peptide-storing enteroendocrine cells. In the colon, hrGFP was exclusively expressed in EC cells but absent from the peptide-storing enteroendocrine cells. In contrast, in the pancreas, hrGFP was expressed in β-cells, α-cells, and a fraction of pancreatic polypeptide cells. It is concluded that ChgA-hrGFP in the GI tract functions as an effective reporter, particularly for the large populations of still poorly characterized monoamine-storing enteroendocrine cells. Furthermore, our findings substantiate the potential function of ChgA as a monoamine-binding protein that facilitates the regulated endocrine secretion of large amounts of monoamines from enteroendocrine cells.

Published
2015
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49. Considering the effect of stem-loop reverse transcription and real-time PCR analysis of blood and saliva specific microRNA markers upon mixed body fluid stains.

Author

Uchimoto, Mari L., Beasley, Emma, Coult, Natalie, Omelia, Emma J., World, Damian, and Williams, Graham

Subjects
GENETIC transcription, REVERSE transcriptase polymerase chain reaction, BLOOD testing, SALIVA analysis, MICRORNA, BIOMARKERS, BODY fluids, FORENSIC sciences
Abstract

Abstract: Forensic RNA analysis is gathering pace with reports of messenger RNA analysis being used in case work, and with microRNA being increasingly researched. Such techniques address a fundamental issue in body fluid identification, namely increased specificity over existing chemical tests, and the incorporation of additional body fluids such as vaginal material. The use of RNA analysis will be of particular value to sex offences, where there can be a mixture of multiple body fluids from different people. The aim of this study was to determine whether microRNA based body fluid identification tests can be applied to mixed body fluid samples. Blood and saliva were acquired from volunteers and underwent total RNA extraction. Mixed samples were prepared using a range of ratios from 1:1 to 10:1. Each mixed sample then underwent a blood–saliva differentiation test developed in-house, which includes stem-loop reverse transcription and real-time PCR analysis. Aliquots following mixture preparation also underwent standard STR analysis, utilising Quantiplex and Next Generation Multiplex kits. Data relating to the development of an in-house blood–saliva differentiation test is presented, in which it has been demonstrated that such a test has a lower limit of detection than the enzymatic equivalent. It has been shown that not only is it possible to determine the presence of more than one body fluid, it is also possible to determine the major body fluid contributor as well as the minor contributor. [Copyright &y& Elsevier]

Published
2013
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50. Influence of tail biting on weight gain, lesions and condemnations at slaughter of finishing pigs.

Author

Marques, Brenda Maria F. P. P., Bernardi, Mari L., Coelho, Carolini F., Almeida, Mirian, Morales, Oscar E., Mores, Tiago J., Borowski, Sandra M., and Barcellos, David E. S. N.

Abstract

The article discusses a study of tail-biting lesions in finishing pigs and its association with weight gain, occurrence of locomotion or respiratory disorders and abscesses during finishing period, and carcass condemnation at slaughter. The evaluation performed within 41-43 days after the commencement of the study showed the healing of tail lesions in 95 percent to 100 percent of the animals. The occurrence of locomotion problems and nodules/abscesses was seen to be associated with the presence of tail-biting lesions, prior to slaughter. The study also found tail-biting lesions to be associated with the presence of abscesses, lung lesions such as pleuritis and embolic pneumonia or arthritis in carcasses, at slaughter.

Published
2012
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