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https://www.readbyqxmd.com/read/28918995/cutaneous-adverse-events-of-targeted-therapies-for-hematolymphoid-malignancies
#1
REVIEW
Julia D Ransohoff, Bernice Y Kwong
The identification of oncogenic drivers of liquid tumors has led to the rapid development of targeted agents with distinct cutaneous adverse event (AE) profiles. The diagnosis and management of these skin toxicities has motivated a novel partnership between dermatologists and oncologists in developing supportive oncodermatology clinics. In this article we review the current state of knowledge of clinical presentation, mechanisms, and management of the most common and significant cutaneous AEs observed during treatment with targeted therapies for hematologic and lymphoid malignancies...
July 14, 2017: Clinical Lymphoma, Myeloma & Leukemia
https://www.readbyqxmd.com/read/28859549/traumatic-brain-injury-in-htau-model-mice-enhanced-acute-macrophage-response-and-altered-long-term-recovery
#2
Olga N Kokiko-Cochran, Maha Saber, Shweta Puntambekar, Shane Michael Bemiller, Atsuko Katsumoto, Yu-Shang Lee, Kiran Bhaskar, Richard M Ransohoff, Bruce T Lamb
TBI induces widespread neuroinflammation and accumulation of microtubule associated protein tau (MAPT) - two key pathological features of tauopathies. This study sought to characterize the microglial/macrophage response to TBI in genomic-based MAPT transgenic mice in a Mapt knockout background (called hTau). Two-month-old hTau and age-matched control male and female mice received a single lateral fluid percussion TBI or sham injury. Separate groups of mice were aged to an acute (3 days post-injury [DPI]) or chronic (135 DPI) post-injury time point...
August 31, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28694451/polymorphic-regulation-of-mitochondrial-fission-and-fusion-modifies-phenotypes-of-microglia-in-neuroinflammation
#3
Mitsuhiko Katoh, Bao Wu, Huy Bang Nguyen, Truc Quynh Thai, Ryo Yamasaki, Haiyan Lu, Anna M Rietsch, Musab M Zorlu, Youichi Shinozaki, Yurika Saitoh, Sei Saitoh, Takashi Sakoh, Kazuhiro Ikenaka, Schuichi Koizumi, Richard M Ransohoff, Nobuhiko Ohno
Microglia are the resident macrophages of the central nervous system and play complex roles in the milieu of diseases including the primary diseases of myelin. Although mitochondria are critical for cellular functions and survival in the nervous system, alterations in and the roles of mitochondrial dynamics and associated signaling in microglia are still poorly understood. In the present study, by combining immunohistochemistry and 3D ultrastructural analyses, we show that mitochondrial fission/fusion in reactive microglia is differentially regulated from that in monocyte-derived macrophages and the ramified microglia of normal white matter in myelin disease models...
July 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28679661/glucose-regulated-protein-78-autoantibody-associates-with-blood-brain-barrier-disruption-in-neuromyelitis-optica
#4
Fumitaka Shimizu, Kristin L Schaller, Gregory P Owens, Anne C Cotleur, Debra Kellner, Yukio Takeshita, Birgit Obermeier, Thomas J Kryzer, Yasuteru Sano, Takashi Kanda, Vanda A Lennon, Richard M Ransohoff, Jeffrey L Bennett
Neuromyelitis optica (NMO) is an inflammatory disorder mediated by antibodies to aquaporin-4 (AQP4) with prominent blood-brain barrier (BBB) breakdown in the acute phase of the disease. Anti-AQP4 antibodies are produced mainly in the periphery, yet they target the astrocyte perivascular end feet behind the BBB. We reasoned that an endothelial cell-targeted autoantibody might promote BBB transit of AQP4 antibodies and facilitate NMO attacks. Using monoclonal recombinant antibodies (rAbs) from patients with NMO, we identified two that strongly bound to the brain microvascular endothelial cells (BMECs)...
July 5, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28649618/synergistic-effects-of-influenza-and-1-methyl-4-phenyl-1-2-3-6-tetrahydropyridine-mptp-can-be-eliminated-by-the-use-of-influenza-therapeutics-experimental-evidence-for-the-multi-hit-hypothesis
#5
Shankar Sadasivan, Bridgett Sharp, Stacey Schultz-Cherry, Richard Jay Smeyne
Central Nervous System inflammation has been implicated in neurodegenerative disorders including Parkinson's disease (Ransohoff, Science 353: 777-783, 2016; Kannarkat et al. J. Parkinsons Dis. 3: 493-514, 2013). Here, we examined if the H1N1 influenza virus (Studahl et al. Drugs 73: 131-158, 2013) could synergize with the parkinsonian toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (Jackson-Lewis et al. in Mark LeDoux (ed) Movement Disorders: Genetics and Models: 287-306, Elsevier, 2015) to induce a greater microglial activation and loss of substantia nigra pars compacta dopaminergic neurons than either insult alone...
2017: NPJ Parkinson's Disease
https://www.readbyqxmd.com/read/28561022/il-17-induced-notch1-activation-in-oligodendrocyte-progenitor-cells-enhances-proliferation-and-inflammatory-gene-expression
#6
Chenhui Wang, Cun-Jin Zhang, Bradley N Martin, Katarzyna Bulek, Zizhen Kang, Junjie Zhao, Guanglin Bian, Julie A Carman, Ji Gao, Ashok Dongre, Haibo Xue, Stephen D Miller, Youcun Qian, Dolores Hambardzumyan, Tom Hamilton, Richard M Ransohoff, Xiaoxia Li
NOTCH1 signalling contributes to defective remyelination by impairing differentiation of oligodendrocyte progenitor cells (OPCs). Here we report that IL-17 stimulation induces NOTCH1 activation in OPCs, contributing to Th17-mediated demyelinating disease. Mechanistically, IL-17R interacts with NOTCH1 via the extracellular domain, which facilitates the cleavage of NOTHC1 intracellular domain (NICD1). IL-17-induced NOTCH1 activation results in the interaction of IL-17R adaptor Act1 with NICD1, followed by the translocation of the Act1-NICD1 complex into the nucleus...
May 31, 2017: Nature Communications
https://www.readbyqxmd.com/read/28546318/an-environment-dependent-transcriptional-network-specifies-human-microglia-identity
#7
David Gosselin, Dylan Skola, Nicole G Coufal, Inge R Holtman, Johannes C M Schlachetzki, Eniko Sajti, Baptiste N Jaeger, Carolyn O'Connor, Conor Fitzpatrick, Martina P Pasillas, Monique Pena, Amy Adair, David D Gonda, Michael L Levy, Richard M Ransohoff, Fred H Gage, Christopher K Glass
Microglia play essential roles in central nervous system (CNS) homeostasis and influence diverse aspects of neuronal function. However, the transcriptional mechanisms that specify human microglia phenotypes are largely unknown. We examined the transcriptomes and epigenetic landscapes of human microglia isolated from surgically resected brain tissue ex vivo and after transition to an in vitro environment. Transfer to a tissue culture environment resulted in rapid and extensive down-regulation of microglia-specific genes that were induced in primitive mouse macrophages after migration into the fetal brain...
June 23, 2017: Science
https://www.readbyqxmd.com/read/28510302/association-study-of-genetic-variation-in-dna-repair-pathway-genes-and-risk-of-basal-cell-carcinoma
#8
Yuan Lin, Harvind S Chahal, Wenting Wu, Hyunje G Cho, Katherine J Ransohoff, Fengju Song, Jean Y Tang, Kavita Y Sarin, Jiali Han
DNA repair plays a critical role in protecting the genome from ultraviolet radiation and maintaining the genomic integrity of cells. Genetic variants in DNA repair-related genes can influence an individual's DNA repair capacity, which may be related to the risk of developing basal cell carcinoma (BCC). We comprehensively assessed the associations of 2,965 independent single-nucleotide polymorphisms (SNPs) across 165 DNA repair pathway genes with BCC risk in a genome-wide association meta-analysis totaling 17,187 BCC cases and 287,054 controls from two data sets...
September 1, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28499701/should-we-stop-saying-glia-and-neuroinflammation
#9
REVIEW
Roser Masgrau, Carmen Guaza, Richard M Ransohoff, Elena Galea
Central nervous system (CNS) therapeutics based on the theoretical framework of neuroinflammation have only barely succeeded. We argue that a problem may be the wrong use of the term 'neuroinflammation' as a distinct nosological entity when, based on recent evidence, it may not explain CNS disease pathology. Indeed, the terms 'neuroinflammation' and 'glia' could be obsolete. First, unbiased molecular profiling of CNS cell populations and individual cells reveals striking phenotypic heterogeneity in health and disease...
May 9, 2017: Trends in Molecular Medicine
https://www.readbyqxmd.com/read/28448577/correction-selective-chemokine-receptor-usage-by-central-nervous-system-myeloid-cells-in-ccr2-red-fluorescent-protein-knock-in-mice
#10
Noah Saederup, Astrid E Cardona, Kelsey Croft, Makiko Mizutani, Anne C Cotleur, Chia-Lin Tsou, Richard M Ransohoff, Israel F Charo
[This corrects the article DOI: 10.1371/journal.pone.0013693.].
2017: PloS One
https://www.readbyqxmd.com/read/28296380/cd62l-is-not-a-reliable-biomarker-for-predicting-pml-risk-in-natalizumab-treated-r-ms-patients-author-response
#11
COMMENT
Ellen Cahir-McFarland, Richard M Ransohoff, Linda Lieberman, Tatiana Plavina
No abstract text is available yet for this article.
August 30, 2016: Neurology
https://www.readbyqxmd.com/read/28212542/two-stage-genome-wide-association-study-identifies-a-novel-susceptibility-locus-associated-with-melanoma
#12
Katherine J Ransohoff, Wenting Wu, Hyunje G Cho, Harvind C Chahal, Yuan Lin, Hong-Ji Dai, Christopher I Amos, Jeffrey E Lee, Jean Y Tang, David A Hinds, Jiali Han, Qingyi Wei, Kavita Y Sarin
Genome-wide association studies have identified 21 susceptibility loci associated with melanoma. These loci implicate genes affecting pigmentation, nevus count, telomere maintenance, and DNA repair in melanoma risk. Here, we report the results of a two-stage genome-wide association study of melanoma. The stage 1 discovery phase consisted of 4,842 self-reported melanoma cases and 286,565 controls of European ancestry from the 23andMe research cohort and the stage 2 replication phase consisted of 1,804 melanoma cases and 1,026 controls from the University of Texas M...
March 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/28177523/association-between-genetic-variation-within-vitamin-d-receptor-dna-binding-sites-and-risk-of-basal-cell-carcinoma
#13
Yuan Lin, Harvind S Chahal, Wenting Wu, Hyunje G Cho, Katherine J Ransohoff, Hongji Dai, Jean Y Tang, Kavita Y Sarin, Jiali Han
An increasing number of studies have reported a protective association between vitamin D and cancer risk. The vitamin D endocrine system regulates transcriptional programs involved in inflammation, cell growth and differentiation through the binding of vitamin D receptor (VDR) to specific VDR elements. However, limited attention has been given to the role of variation within VDR binding sites in the development of basal cell carcinoma (BCC). Across 2,776 previously identified VDR binding sites, we identified 2,540 independent single-nucleotide polymorphisms (SNPs) and examined their associations with BCC risk in a genome-wide association meta-analysis totaling 17,187 BCC cases and 287,054 controls from two data sets...
May 1, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28100745/disease-progression-dependent-effects-of-trem2-deficiency-in-a-mouse-model-of-alzheimer-s-disease
#14
Taylor R Jay, Anna M Hirsch, Margaret L Broihier, Crystal M Miller, Lee E Neilson, Richard M Ransohoff, Bruce T Lamb, Gary E Landreth
Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2). Understanding TREM2 function promises to provide important insights into how neuroinflammation contributes to AD pathology. However, studies so far have produced seemingly conflicting results, with reports that amyloid pathology can be both decreased and increased in TREM2-deficient AD mouse models...
January 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28018943/effects-of-neuromyelitis-optica-igg-at-the-blood-brain-barrier-in-vitro
#15
Yukio Takeshita, Birgit Obermeier, Anne C Cotleur, Simona F Spampinato, Fumitaka Shimizu, Erin Yamamoto, Yasuteru Sano, Thomas J Kryzer, Vanda A Lennon, Takashi Kanda, Richard M Ransohoff
OBJECTIVE: To address the hypothesis that physiologic interactions between astrocytes and endothelial cells (EC) at the blood-brain barrier (BBB) are afflicted by pathogenic inflammatory signaling when astrocytes are exposed to aquaporin-4 (AQP4) antibodies present in the immunoglobulin G (IgG) fraction of serum from patients with neuromyelitis optica (NMO), referred to as NMO-IgG. METHODS: We established static and flow-based in vitro BBB models incorporating co-cultures of conditionally immortalized human brain microvascular endothelial cells and human astrocyte cell lines with or without AQP4 expression...
January 2017: Neurology® Neuroimmunology & Neuroinflammation
https://www.readbyqxmd.com/read/27940990/disease-progression-dependent-effects-of-trem2-deficiency-in-a-mouse-model-of-alzheimer-s-disease
#16
Taylor R Jay, Anna M Hirsch, Margaret L Broihier, Crystal M Miller, Lee E Neilson, Richard M Ransohoff, Bruce T Lamb, Gary E Landreth
Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene triggering receptor expressed on myeloid cells 2 (TREM2). Understanding TREM2 function promises to provide important insights into how neuroinflammation contributes to AD pathology. However, studies so far have produced seemingly conflicting results, with reports that amyloid pathology can be both decreased and increased in TREM2 deficient AD mouse models...
December 9, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27913649/identification-and-function-of-fibrocytes-in-skeletal-muscle-injury-repair-and-muscular-dystrophy
#17
Xingyu Wang, Wanming Zhao, Richard M Ransohoff, Lan Zhou
We identified and characterized the function of CD45(+)/collagen I(+) fibrocytes in acutely injured skeletal muscle of wild-type (WT) and Ccr2(-/-) mice, and in quadriceps and diaphragm muscles of mdx(5cv) mice, a mouse model for Duchenne muscular dystrophy. Fibrocytes were not detected in peripheral blood of WT mice after acute muscle injury or mdx(5cv) mice. Fibrocytes were detected in acutely injured muscles and in mdx(5cv) quadriceps and diaphragm muscles. These cells expressed F4/80 and CCR2, and they were mostly Ly6C(lo) They expressed a low level of collagens but a high level of profibrotic growth factors as compared with i...
December 15, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27902821/risk-factors-for-basal-cell-carcinoma-among-patients-with-basal-cell-nevus-syndrome-development-of-a-basal-cell-nevus-syndrome-patient-registry
#18
Daniel C Solis, Gina P Kwon, Katherine J Ransohoff, Shufeng Li, Harvind S Chahal, Mina S Ally, Marieke A D Peters, Kristi Schmitt-Burr, Joselyn Lindgren, Irene Bailey-Healy, Joyce M Teng, Ervin H Epstein, Jean Y Tang
Importance: Patients with basal cell nevus syndrome (BCNS) have a greater risk of developing numerous basal cell carcinomas (BCCs). Risk factors influencing the wide variation in tumor burden are poorly understood. Objective: To describe the burden of BCCs in patients with BCNS in the United States and identify potential risk factors for BCCs. Design, Setting, and Participants: Prospective clinical registry with data collected from September 2014 to March 2016...
November 30, 2016: JAMA Dermatology
https://www.readbyqxmd.com/read/27882502/institutional-responsibility-and-the-flawed-genomic-biomarkers-at-duke-university-a-missed-opportunity-for-transparency-and-accountability
#19
David L DeMets, Thomas R Fleming, Gail Geller, David F Ransohoff
When there have been substantial failures by institutional leadership in their oversight responsibility to protect research integrity, the public should demand that these be recognized and addressed by the institution itself, or the funding bodies. This commentary discusses a case of research failures in developing genomic predictors for cancer risk assessment and treatment at a leading university. In its review of this case, the Office of Research Integrity, an agency within the US Department of Health and Human Services, focused their report entirely on one individual faculty member and made no comment on the institution's responsibility and its failure to provide adequate oversight and investigation...
August 2017: Science and Engineering Ethics
https://www.readbyqxmd.com/read/27796746/a-neuroprotective-effect-of-the-glutamate-receptor-antagonist-mk801-on-long-term-cognitive-and-behavioral-outcomes-secondary-to-experimental-cerebral-malaria
#20
Aline Silva de Miranda, Fátima Brant, Luciene Bruno Vieira, Natália Pessoa Rocha, Érica Leandro Marciano Vieira, Gustavo Henrique Souza Rezende, Pollyana Maria de Oliveira Pimentel, Marcio F D Moraes, Fabíola Mara Ribeiro, Richard M Ransohoff, Mauro Martins Teixeira, Fabiana Simão Machado, Milene Alvarenga Rachid, Antônio Lúcio Teixeira
Cerebral malaria (CM) is a life-threatening complication of Plasmodium falciparum infection, which can result in long-term cognitive and behavioral deficits despite successful anti-malarial therapy. Due to the substantial social and economic burden of CM, the development of adjuvant therapies is a scientific goal of highest priority. Apart from vascular and immune responses, changes in glutamate system have been reported in CM pathogenesis suggesting a potential therapeutic target. Based on that, we hypothesized that interventions in the glutamatergic system induced by blockage of N-methyl-D-aspartate (NMDA) receptors could attenuate experimental CM long-term cognitive and behavioral outcomes...
October 28, 2016: Molecular Neurobiology
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