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1. Mechanotransduction-induced interplay between phospholamban and yes-activated protein induces smooth muscle cell hypertrophy

Author

Rawson, Renee, Duong, Loan, Tkachenko, Eugene, Chiang, Austin WT, Okamoto, Kevin, Dohil, Ranjan, Lewis, Nathan E, Kurten, Richard, Abud, Edsel M, and Aceves, Seema S

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Digestive Diseases, Food Allergies, 2.1 Biological and endogenous factors, Aetiology, Life on Land, Mechanotransduction, Cellular, Humans, Myocytes, Smooth Muscle, Hypertrophy, Calcium-Binding Proteins, YAP-Signaling Proteins, Animals, Adaptor Proteins, Signal Transducing, Transcription Factors, Mice, Biological Sciences, Medical and Health Sciences, Immunology
Abstract

The gastrointestinal system is a hollow organ affected by fibrostenotic diseases that cause volumetric compromise of the lumen via smooth muscle hypertrophy and fibrosis. Many of the driving mechanisms remain unclear. Yes-associated protein-1 (YAP) is a critical mechanosensory transcriptional regulator that mediates cell hypertrophy in response to elevated extracellular rigidity. In the type 2 inflammatory disorder, eosinophilic esophagitis (EoE), phospholamban (PLN) can induce smooth muscle cell hypertrophy. We used EoE as a disease model for understanding a mechanistic pathway in which PLN and YAP interact in response to rigid extracellular substrate to induce smooth muscle cell hypertrophy. PLN-induced YAP nuclear sequestration in a feed-forward loop caused increased cell size in response to a rigid substrate. This mechanism of rigidity sensing may have previously unappreciated clinical implications for PLN-expressing hollow systems such as the esophagus and heart.

Published
2024

3. Single-nuclei transcriptome analysis of Huntington disease iPSC and mouse astrocytes implicates maturation and functional deficits

Author

Reyes-Ortiz, Andrea M, Abud, Edsel M, Burns, Mara S, Wu, Jie, Hernandez, Sarah J, McClure, Nicolette, Wang, Keona Q, Schulz, Corey J, Miramontes, Ricardo, Lau, Alice, Michael, Neethu, Miyoshi, Emily, Van Vactor, David, Reidling, John C, Blurton-Jones, Mathew, Swarup, Vivek, Poon, Wayne W, Lim, Ryan G, and Thompson, Leslie M

Subjects
Biochemistry and Cell Biology, Genetics, Biological Sciences, Stem Cell Research - Induced Pluripotent Stem Cell, Neurosciences, Brain Disorders, Rare Diseases, Stem Cell Research - Nonembryonic - Human, Neurodegenerative, Huntington's Disease, Stem Cell Research, Regenerative Medicine, Underpinning research, 2.1 Biological and endogenous factors, Aetiology, 1.1 Normal biological development and functioning, Neurological, Neurology, Omics
Abstract

Huntington disease (HD) is a neurodegenerative disorder caused by expanded CAG repeats in the huntingtin gene that alters cellular homeostasis, particularly in the striatum and cortex. Astrocyte signaling that establishes and maintains neuronal functions are often altered under pathological conditions. We performed single-nuclei RNA-sequencing on human HD patient-induced pluripotent stem cell (iPSC)-derived astrocytes and on striatal and cortical tissue from R6/2 HD mice to investigate high-resolution HD astrocyte cell state transitions. We observed altered maturation and glutamate signaling in HD human and mouse astrocytes. Human HD astrocytes also showed upregulated actin-mediated signaling, suggesting that some states may be cell-autonomous and human specific. In both species, astrogliogenesis transcription factors may drive HD astrocyte maturation deficits, which are supported by rescued climbing deficits in HD drosophila with NFIA knockdown. Thus, dysregulated HD astrocyte states may induce dysfunctional astrocytic properties, in part due to maturation deficits influenced by astrogliogenesis transcription factor dysregulation.

Published
2023

4. Advances and ongoing challenges in eosinophilic gastrointestinal disorders presented at the CEGIR/TIGERs Symposium at the 2024 American Academy of Allergy, Asthma & Immunology meeting

Author

Wright, Benjamin L., Abonia, Juan Pablo, Abud, Edsel M., Aceves, Seema S., Ackerman, Steven J., Braskett, Melinda, Chang, Joy W., Chehade, Mirna, Constantine, Gregory M., Davis, Carla M., Dellon, Evan S., Doyle, Alfred D., Durban, Raquel, Hill, David A., Jensen, Elizabeth T., Kewalramani, Anupama, Khoury, Paneez, Klion, Amy D., Kottyan, Leah, Kuang, Fei Li, McGowan, Emily C., Ruffner, Melanie A., Spencer, Lisa A., Spergel, Jonathan M., Uchida, Amiko M., Wechsler, Joshua B., and Pesek, Robert D.

Published
2024
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5. Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes

Author

Novikova, Gloriia, Kapoor, Manav, TCW, Julia, Abud, Edsel M, Efthymiou, Anastasia G, Chen, Steven X, Cheng, Haoxiang, Fullard, John F, Bendl, Jaroslav, Liu, Yiyuan, Roussos, Panos, Björkegren, Johan LM, Liu, Yunlong, Poon, Wayne W, Hao, Ke, Marcora, Edoardo, and Goate, Alison M

Subjects
Biological Sciences, Genetics, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Neurodegenerative, Dementia, Alzheimer's Disease, Aging, Stem Cell Research, Human Genome, Biotechnology, Prevention, Brain Disorders, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Neurological, Alleles, Alzheimer Disease, Gene Expression Regulation, Genetic Predisposition to Disease, Genome-Wide Association Study, Genomics, Humans, Induced Pluripotent Stem Cells, Macrophages, Microglia, Myeloid Cells, Regulatory Sequences, Nucleic Acid, Transcriptome
Abstract

Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. Previously, we showed that AD risk alleles are enriched in myeloid-specific epigenomic annotations. Here, we show that they are specifically enriched in active enhancers of monocytes, macrophages and microglia. We integrated AD GWAS with myeloid epigenomic and transcriptomic datasets using analytical approaches to link myeloid enhancer activity to target gene expression regulation and AD risk modification. We identify AD risk enhancers and nominate candidate causal genes among their likely targets (including AP4E1, AP4M1, APBB3, BIN1, MS4A4A, MS4A6A, PILRA, RABEP1, SPI1, TP53INP1, and ZYX) in twenty loci. Fine-mapping of these enhancers nominates candidate functional variants that likely modify AD risk by regulating gene expression in myeloid cells. In the MS4A locus we identified a single candidate functional variant and validated it in human induced pluripotent stem cell (hiPSC)-derived microglia and brain. Taken together, this study integrates AD GWAS with multiple myeloid genomic datasets to investigate the mechanisms of AD risk alleles and nominates candidate functional variants, regulatory elements and genes that likely modulate disease susceptibility.

Published
2021

7. IgM response against amyloid-beta in aging: a potential peripheral protective mechanism

Author

Agrawal, Sudhanshu, Abud, Edsel M, Snigdha, Shikha, and Agrawal, Anshu

Subjects
Biomedical and Clinical Sciences, Immunology, Aging, Acquired Cognitive Impairment, Brain Disorders, Alzheimer's Disease, Dementia, Neurosciences, Neurodegenerative, Prevention, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Neurological, Inflammatory and immune system, Adult, Age Factors, Aged, Aged, 80 and over, Amyloid beta-Peptides, Cells, Cultured, Cytokines, Dendritic Cells, Female, Humans, Immunoglobulin M, Leukocytes, Mononuclear, Male, Peptide Fragments, Young Adult, tau Proteins, Dendritic cells, Amyloid beta, Human, IgM antibody, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundThe immune system plays a major role in the pathogenesis of age-related dementia, including Alzheimer's disease (AD). An insight into age-associated changes in the immune response to amyloid-beta (Aβ) in individuals without AD may be beneficial in identifying mechanisms preventing accumulation of Aβ.MethodsWe examined the response of human monocyte-derived dendritic cells (DCs), T cells, and peripheral blood mononuclear cells (PBMCs) from healthy aged and young subjects to Aβ peptide 1-42, Aβ fibrils, and recombinant, nonaggregated tau-4 protein with a view to understand the role of peripheral immunity in AD.ResultsOur studies revealed that DCs from healthy aged subjects display weak reactivity towards the Aβ peptide and no reactivity towards Aβ fibrils and tau compared with their young counterparts. An analysis of old and young PBMCs revealed that there is no significant T-cell memory against Aβ peptide, fibrils, or tau. Remarkably, the plasma levels of IgM antibodies specific to Aβ peptide 1-42 were significantly increased in aged subjects compared with young subjects, while IgG levels were comparable. Aβ peptide-specific IgM and IgG levels were also determined in the plasma of AD subjects compared with age-matched controls to demonstrate that the immune response against Aβ is stronger in AD patients. A decline in Aβ peptide-specific IgM antibodies was observed in AD patients compared with age-matched controls. In contrast, the levels of IgG as well as interleukin-21, the major cytokine involved in class switching, were increased in AD and patients with mild cognitive impairment, indicating a strong immune response against Aβ.ConclusionsCollectively, low immunogenicity of Aβ in healthy controls may prevent inflammation while the generation of specific IgM antibodies may help in the clearance of Aβ in healthy subjects.

Published
2018

8. Tau Spread, Apolipoprotein E, Inflammation, and More Rapidly Evolving Basic Science in Alzheimer Disease

Author

Gonzalez, Bianca, Abud, Edsel M, Abud, Abigail M, Poon, Wayne W, and Gylys, Karen H

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Alzheimer's Disease, Brain Disorders, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Neurodegenerative, Acquired Cognitive Impairment, Neurological, Alzheimer Disease, Animals, Apolipoproteins E, Brain, Cholesterol, Humans, Inflammation, tau Proteins, Imaging flow cytometry, Oligomer, Synapse, Microglia, Neurology & Neurosurgery, Clinical sciences
Abstract

To date, Alzheimer disease drug candidates have produced negative results in human trials, and progress in moving new targets out of the laboratory and into trials has been slow. However, based on 3 decades of previous work, there is reason to hope that amyloid-based and other novel therapies will move at a faster pace toward successful clinical trials. This article highlights selected preclinical research topics that are rapidly advancing in the laboratory.

Published
2017

9. Activation of the STING-Dependent Type I Interferon Response Reduces Microglial Reactivity and Neuroinflammation

Author

Mathur, Vidhu, Burai, Ritwik, Vest, Ryan T, Bonanno, Liana N, Lehallier, Benoit, Zardeneta, Macy E, Mistry, Karishma N, Do, Danny, Marsh, Samuel E, Abud, Edsel M, Blurton-Jones, Mathew, Li, Lingyin, Lashuel, Hilal A, and Wyss-Coray, Tony

Subjects
Neurosciences, HIV/AIDS, Biotechnology, Animals, Animals, Newborn, Antiviral Agents, Cells, Cultured, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Female, Freund's Adjuvant, Ganciclovir, Gene Expression Regulation, Humans, Interferon Type I, Male, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microglia, Monocytes, Myelin-Oligodendrocyte Glycoprotein, Peptide Fragments, Pertussis Toxin, Signal Transduction, STING, experimental autoimmune encephalomyelitis, ganciclovir, microglia, neuroinflammation, type I interferon response, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

Brain aging and neurodegeneration are associated with prominent microglial reactivity and activation of innate immune response pathways, commonly referred to as neuroinflammation. One such pathway, the type I interferon response, recognizes viral or mitochondrial DNA in the cytoplasm via activation of the recently discovered cyclic dinucleotide synthetase cGAS and the cyclic dinucleotide receptor STING. Here we show that the FDA-approved antiviral drug ganciclovir (GCV) induces a type I interferon response independent of its canonical thymidine kinase target. Inhibition of components of the STING pathway, including STING, IRF3, Tbk1, extracellular IFNβ, and the Jak-Stat pathway resulted in reduced activity of GCV and its derivatives. Importantly, functional STING was necessary for GCV to inhibit inflammation in cultured myeloid cells and in a mouse model of multiple sclerosis. Collectively, our findings uncover an unexpected new activity of GCV and identify the STING pathway as a regulator of microglial reactivity and neuroinflammation.

Published
2017

11. iPSC-Derived Human Microglia-like Cells to Study Neurological Diseases

Author

Abud, Edsel M, Ramirez, Ricardo N, Martinez, Eric S, Healy, Luke M, Nguyen, Cecilia HH, Newman, Sean A, Yeromin, Andriy V, Scarfone, Vanessa M, Marsh, Samuel E, Fimbres, Cristhian, Caraway, Chad A, Fote, Gianna M, Madany, Abdullah M, Agrawal, Anshu, Kayed, Rakez, Gylys, Karen H, Cahalan, Michael D, Cummings, Brian J, Antel, Jack P, Mortazavi, Ali, Carson, Monica J, Poon, Wayne W, and Blurton-Jones, Mathew

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Stem Cell Research, Alzheimer's Disease, Aging, Stem Cell Research - Induced Pluripotent Stem Cell, Acquired Cognitive Impairment, Neurodegenerative, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Genetics, Brain Disorders, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Neurological, Alzheimer Disease, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Brain, Cells, Cultured, Cytokines, Disease Models, Animal, Humans, Induced Pluripotent Stem Cells, Mice, Microglia, Peptide Fragments, 3D organoids, AD-GWAS, Alzheimer’s disease, Beta-amyloid, Tau, cell models of disease, induced pluripotent stem cells, microglia, mouse transplantation, neurodegenerative diseases, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Microglia play critical roles in brain development, homeostasis, and neurological disorders. Here, we report that human microglial-like cells (iMGLs) can be differentiated from iPSCs to study their function in neurological diseases, like Alzheimer's disease (AD). We find that iMGLs develop in vitro similarly to microglia in vivo, and whole-transcriptome analysis demonstrates that they are highly similar to cultured adult and fetal human microglia. Functional assessment of iMGLs reveals that they secrete cytokines in response to inflammatory stimuli, migrate and undergo calcium transients, and robustly phagocytose CNS substrates. iMGLs were used to examine the effects of Aβ fibrils and brain-derived tau oligomers on AD-related gene expression and to interrogate mechanisms involved in synaptic pruning. Furthermore, iMGLs transplanted into transgenic mice and human brain organoids resemble microglia in vivo. Together, these findings demonstrate that iMGLs can be used to study microglial function, providing important new insight into human neurological disease.

Published
2017

13. The adaptive immune system restrains Alzheimer’s disease pathogenesis by modulating microglial function

Author

Marsh, Samuel E, Abud, Edsel M, Lakatos, Anita, Karimzadeh, Alborz, Yeung, Stephen T, Davtyan, Hayk, Fote, Gianna M, Lau, Lydia, Weinger, Jason G, Lane, Thomas E, Inlay, Matthew A, Poon, Wayne W, and Blurton-Jones, Mathew

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Immunology, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Alzheimer's Disease, Dementia, Aging, Neurosciences, Neurodegenerative, Acquired Cognitive Impairment, Brain Disorders, 2.1 Biological and endogenous factors, Inflammatory and immune system, Neurological, Adaptation, Physiological, Alzheimer Disease, Amyloid beta-Peptides, Animals, Humans, Immunoglobulin G, Mice, Microglia, Phagocytosis, Alzheimer's, amyloid, inflammation, microglia, IgG, Alzheimer’s
Abstract

The innate immune system is strongly implicated in the pathogenesis of Alzheimer's disease (AD). In contrast, the role of adaptive immunity in AD remains largely unknown. However, numerous clinical trials are testing vaccination strategies for AD, suggesting that T and B cells play a pivotal role in this disease. To test the hypothesis that adaptive immunity influences AD pathogenesis, we generated an immune-deficient AD mouse model that lacks T, B, and natural killer (NK) cells. The resulting "Rag-5xfAD" mice exhibit a greater than twofold increase in β-amyloid (Aβ) pathology. Gene expression analysis of the brain implicates altered innate and adaptive immune pathways, including changes in cytokine/chemokine signaling and decreased Ig-mediated processes. Neuroinflammation is also greatly exacerbated in Rag-5xfAD mice as indicated by a shift in microglial phenotype, increased cytokine production, and reduced phagocytic capacity. In contrast, immune-intact 5xfAD mice exhibit elevated levels of nonamyloid reactive IgGs in association with microglia, and treatment of Rag-5xfAD mice or microglial cells with preimmune IgG enhances Aβ clearance. Last, we performed bone marrow transplantation studies in Rag-5xfAD mice, revealing that replacement of these missing adaptive immune populations can dramatically reduce AD pathology. Taken together, these data strongly suggest that adaptive immune cell populations play an important role in restraining AD pathology. In contrast, depletion of B cells and their appropriate activation by T cells leads to a loss of adaptive-innate immunity cross talk and accelerated disease progression.

Published
2016

14. Spinal stimulation of the upper lumbar spinal cord modulates urethral sphincter activity in rats after spinal cord injury

Author

Abud, Edsel M, Ichiyama, Ronaldo M, Havton, Leif A, and Chang, Huiyi H

Subjects
Neurodegenerative, Spinal Cord Injury, Traumatic Head and Spine Injury, Neurosciences, Urologic Diseases, Physical Injury - Accidents and Adverse Effects, Neurological, Animals, Disease Models, Animal, Electric Stimulation Therapy, Electromyography, Female, Lumbar Vertebrae, Rats, Sprague-Dawley, Reflex, Serotonin 5-HT1 Receptor Agonists, Serotonin 5-HT1 Receptor Antagonists, Spinal Cord, Spinal Cord Injuries, Time Factors, Urethra, Urinary Bladder, Neurogenic, Urodynamics, electromyography, epidural stimulation, serotonergic receptors, urethral resistance, Physiology, Clinical Sciences, Medical Physiology, Urology & Nephrology
Abstract

After spinal cord injury (SCI), the neurogenic bladder is observed to develop asynchronous bladder and external urethral sphincter (EUS) contractions in a condition known as detrusor-sphincter dyssnergia (DSD). Activation of the EUS spinal controlling center located at the upper lumbar spinal cord may contribute to reduce EUS dyssynergic contractions and decrease urethral resistance during voiding. However, this mechanism has not been well studied. This study aimed at evaluating the effects of epidural stimulation (EpS) over the spinal EUS controlling center (L3) in combination with a serotonergic receptor agonist on EUS relaxation in naive rats and chronic (6-8 wk) T8 SCI rats. Cystometrogram and EUS electromyography (EMG) were obtained before and after the intravenous administration of 5HT-1A receptor agonist and antagonist. The latency, duration, frequency, amplitude, and area under curve of EpS-evoked EUS EMG responses were analyzed. EpS on L3 evoked an inhibition of EUS tonic contraction and an excitation of EUS intermittent bursting/relaxation correlating with urine expulsion in intact rats. Combined with a 5HT-1A receptor agonist, EpS on L3 evoked a similar effect in chronic T8 SCI rats to reduce urethral contraction (resistance). This study examined the effect of facilitating the EUS spinal controlling center to switch between urine storage and voiding phases by using EpS and a serotonergic receptor agonist. This novel approach of applying EpS on the EUS controlling center modulates EUS contraction and relaxation as well as reduces urethral resistance during voiding in chronic SCI rats with DSD.

Published
2015

15. Pretreatment with P2Y12 inhibitors and relationship with clinical outcomes in NSTEMI: Analysis of 2 Argentinian registries

Author

Sigal, A, primary, Rivero, M, additional, Mezza, M, additional, Kersten, S, additional, Boissonnet, C, additional, Filippa, G, additional, Procopio, G, additional, Abud, C M, additional, Ahuad Calvelo, S A, additional, Nani, S, additional, Perez, G E, additional, Odone, M, additional, Guardiani, F, additional, Duronto, E, additional, and Costabel, J P, additional

Published
2023
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16. Impacto del pretratamiento con inhibidores P2Y12 en pacientes con síndromes coronarios agudos sin elevación del ST. Análisis de dos registros multicéntricos

Author

Sigal, Alan R., primary, Rivero, Mirza, additional, Meza, Mayra, additional, Filippa, Gerardo, additional, Procopio, Gastón, additional, Abud, Camila M., additional, Nani, Sebastián, additional, Odone, Martín, additional, Duronto, Ernesto, additional, and Costabel, Juan P., additional

Published
2023
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18. Capacidad predictiva de diferentes puntajes de riesgo quirúrgico en la endocarditis infecciosa.

Author

CALVELO, SANTIAGO A. AHUAD, ZACARIAS, CONSTANZA B., ABUD, CAMILA M., MAIDANA, MARTIN I., CASABÉ, HORACIO, CORTES, CLAUDIA M., GIUNTA, GUSTAVO, and HERSHSON, ALEJANDRO R.

Subjects
DISEASE risk factors, SURGICAL indications, INFECTIVE endocarditis, SURGICAL emergencies, CARDIAC surgery
Abstract

Copyright of Revista Argentina de Cardiología is the property of Sociedad Argentina de Cardiologia 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
2023
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21. Using the correlation coefficient to study the effects of the atherosclerosis on blood flow/velocity by Doppler shift.

Author

Ali, Nabaa Q. and Abud, Mariam M.

Subjects
*DOPPLER effect, *BLOOD flow, *FLOW velocity, *STATISTICAL correlation, *DOPPLER ultrasonography, *PEARSON correlation (Statistics), *CAPILLARY flow
Abstract

Hypertension, smoking, age, and Diabetes are all factors that lead to Atherosclerosis in blood flow during disease can be observed by calculating Doppler through the strength of the scattered using ultrasound techniques on dorsalis pedis in the foot. The goal of this study is to use the correlation coefficient of average blood flow velocity and Doppler scattering to investigate factors that influence Atherosclerosis. A study of the effect on blood flow by Doppler shift was achieved in Ibn Al-Nafees Hospital for Heart Patients and, taking samples from patients with Atherosclerosis aged between 35-90 years and taking ultrasound examinations. This study used a blood flow rate for 50 healthy. Distinguish for 42 patients by Doppler ultrasound techniques at the foot and statistical satisfy for the effect of age and Diabetes according to Matlab program. Results showed that the Pearson r correlation coefficient between the average blood flow velocity and Doppler shift is (0.94) to healthy and value at (0.99) for patients. This paper has shown a strong linear correlation. The aging factor affects blood flow for atherosclerosis patients, with the increase in age causing a decrease in the average blood flow in the capillary arteries. [ABSTRACT FROM AUTHOR]

Published
2023
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22. Study the optical characterization of blood for anemia samples using He-Ne (632.8 nm) and diode (785 nm) lasers.

Author

Zidane, Mohammed and Abud, Mariam M.

Subjects
*BLOOD sampling, *LASERS, *DIODES, *BLOOD coagulation, *SEMICONDUCTOR lasers, *OPTICAL properties
Abstract

The penetration of laser light in the blood depends on the optical properties of blood used to different lasers at a wavelength (632.8, 785nm) for whole blood for different Anemia diseases and different ages can be used in biomedical optics. The Measurement of blood's visible infrared (IR) spect. Therefore, this study aims to find an accurate physical method for diagnosis through the optical characterization of blood and the optical characterization of normal blood and anemia disease samples by different lasers. All samples have prospered in the international laboratory for the Pathological Analysis of blood. The setup system consists of a laser source with a wavelength (632.8 nm). EDTA Tubes for storing blood samples throughout transportation from the hospital to the workplace, and Tube was used to help prevent blood clotting. The blood sample of a person suffering from Anemia and measuring the penetrating intensity of the sample according to spectrum. This study calculated the absorption coefficient (2.6342 mm-1) for healthy using He-Ne (632.8nm) and (2.188651mm -1) using diode laser 785 nm. In the case of Anemia, the absorption coefficient μa (mm-1) for the Ne-Ne laser was higher at (3.265 mm-1) than used diode laser with (2.4537 mm-1), and the scattering coefficients were (55.3002mm-1)and (57.59mm-1), at 632.8, 785 nm, respectively. The higher refractive index of whole blood compared to using He-Ne laser for different cases healthy and Anemia than diode laser. The He _Ne laser is more effective than the diode laser to distinguish between healthy and Anemia in calculating the optical properties of whole blood. [ABSTRACT FROM AUTHOR]

Published
2023
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23. Rapid genome sequencing identifies novel variants in complement factor I

Author

Rodriguez, Katherine M., primary, Vaught, Jordan, additional, Dilley, Michelle, additional, Ellsworth, Kataryzna, additional, Heinen, Alaina, additional, Abud, Edsel M., additional, Zhang, Yuzhou, additional, Smith, Richard J.H., additional, Sheets, Robert, additional, Geng, Bob, additional, Hoffman, Hal M., additional, Worthen, H. Michael, additional, Dimmock, David, additional, and Coufal, Nicole G., additional

Published
2022
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25. Integrated transcriptome analysis of Huntington’s disease iPSC-derived and mouse astrocytes implicates dysregulated synaptogenesis, actin, and astrocyte maturation

Author

Reyes-Ortiz, Andrea M., primary, Abud, Edsel M., additional, Burns, Mara S., additional, Wu, Jie, additional, Hernandez, Sarah J., additional, Geller, Nicolette, additional, Wang, Keona Q., additional, Schulz, Corey, additional, Miramontes, Ricardo, additional, Lau, Alice, additional, Michael, Neethu, additional, Miyoshi, Emily, additional, Blurton-Jones, Mathew, additional, Van Vactor, David, additional, Reidling, John C., additional, Swarup, Vivek, additional, Poon, Wayne W., additional, Lim, Ryan G., additional, and Thompson, Leslie M., additional

Published
2022
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26. Comparative effectiveness and safety of non-vitamin K antagonists for atrial fibrillation in clinical practice:: GLORIA-AF Registry

Author

Lip G. Y. H., Kotalczyk A., Teutsch C., Diener H. -C., Dubner S. J., Halperin J. L., Ma C. -S., Rothman K. J., Marler S., Gurusamy V. K., Huisman M. V., Abban D. W., Aziz E., Kalan M. B., Abdul N., Backes L. M., Bradman D., Abud A. M., Badings E., Brautigam D., Adams F., Bagni E., Breton N., Addala S., Baker S. H., Brouwers P. J. A. M., Adragao P., Bala R., Browne K., Ageno W., Baldi A., Cortada J. B., Aggarwal R., Bando S., Bruni A., Agosti S., Banerjee S., Brunschwig C., Agostoni P., Bank A., Buathier H., Aguilar F., Esquivias G. B., Buhl A., Linares J. A., Barr C., Bullinga J., Aguinaga L., Bartlett M., Cabrera J. W., Ahmed J., Basic Kes V., Caccavo A., Aiello A., Baula G., Cai S., Ainsworth P., Behrens S., Caine S., Aiub J. R., Bell A., Calo L., Al-Dallow R., Benedetti R., Calvi V., Alderson L., Mazuecos J. B., Sanchez M. C., Velasco J. A. A., Benhalima B., Candeias R., Alexopoulos D., Bergler-Klein J., Capuano V., Manterola F. A., Berneau J. -B., Capucci A., Aliyar P., Bernstein R. A., Caputo R., Alonso D., Berrospi P., Rizo T. C., da Costa F. A. A., Berti S., Cardona F., Amado J., Berz A., da Costa Darrieux F. C., Amara W., Best E., Vera Y. C. D., Amelot M., Bettencourt P., Carolei A., Amjadi N., Betzu R., Carreno S., Ammirati F., Bhagwat R., Carvalho P., Andrade M., Bhatta L., Cary S., Andrawis N., Biscione F., Casu G., Annoni G., Bisignani G., Cavallini C., Ansalone G., Black T., Cayla G., Ariani M. K., Bloch M. J., Celentano A., Arias J. C., Bloom S., Cha T. -J., Armero S., Blumberg E., Cha K. S., Arora C., Bo M., Chae J. K., Aslam M. S., Bohmer E., Chalamidas K., Asselman M., Bollmann A., Challappa K., Audouin P., Bongiorni M. G., Chand S. P., Augenbraun C., Boriani G., Chandrashekar H., Aydin S., Boswijk D. J., Chartier L., Bott J., Chatterjee K., Ayryanova I., Bottacchi E., Ayala C. A. C., Cheema A., Davis G., Evonich R., Davy J. -M., Evseeva O., Chen L., Dayer M., Ezhov A., Chen S. -A., De Biasio M., Fahmy R., Chen J. H., De Bonis S., Fang Q., Chiang F. -T., De Caterina R., Farsad R., Chiarella F., De Franceschi T., Fauchier L., Chih-Chan L., de Groot J. R., Favale S., Cho Y. K., De Horta J., Fayard M., Choi J. -I., De La Briolle A., Fedele J. L., Choi D. J., de la Pena Topete G., Fedele F., Chouinard G., de Paola A. A. V., Fedorishina O., Chow D. H. -F., de Souza W., Fera S. R., Chrysos D., de Veer A., Ferreira L. G. G., Chumakova G., De Wolf L., Ferreira J., Valenzuela E. J. J. R. C., Decoulx E., Ferri C., Nica N. C., Deepak S., Ferrier A., Cislowski D. J., Defaye P., Ferro H., Clay A., Munoz F. D. -C., Finsen A., Clifford P., Brkljacic D. D., First B., Cohen A., Deumite N. J., Fischer S., Cohen M., Di Legge S., Fonseca C., Cohen S., Diemberger I., Almeida L. 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L., Zizzo S., Xu Y., Zhang H., Zong W., Xu X., Zhang D., Zukerman L. S., Yamanoue H., Zhang X., Yamashita T., Cardiology, ACS - Heart failure & arrhythmias, Lip G.Y.H., Kotalczyk A., Teutsch C., Diener H.-C., Dubner S.J., Halperin J.L., Ma C.-S., Rothman K.J., Marler S., Gurusamy V.K., Huisman M.V., Abban D.W., Aziz E., Kalan M.B., Abdul N., Backes L.M., Bradman D., Abud A.M., Badings E., Brautigam D., Adams F., Bagni E., Breton N., Addala S., Baker S.H., Brouwers P.J.A.M., Adragao P., Bala R., Browne K., Ageno W., Baldi A., Cortada J.B., Aggarwal R., Bando S., Bruni A., Agosti S., Banerjee S., Brunschwig C., Agostoni P., Bank A., Buathier H., Aguilar F., Esquivias G.B., Buhl A., Linares J.A., Barr C., Bullinga J., Aguinaga L., Bartlett M., Cabrera J.W., Ahmed J., Basic Kes V., Caccavo A., Aiello A., Baula G., Cai S., Ainsworth P., Behrens S., Caine S., Aiub J.R., Bell A., Calo L., Al-Dallow R., Benedetti R., Calvi V., Alderson L., Mazuecos J.B., Sanchez M.C., Velasco J.A.A., Benhalima B., Candeias R., Alexopoulos D., Bergler-Klein J., Capuano V., Manterola F.A., Berneau J.-B., Capucci A., Aliyar P., Bernstein R.A., Caputo R., Alonso D., Berrospi P., Rizo T.C., da Costa F.A.A., Berti S., Cardona F., Amado J., Berz A., da Costa Darrieux F.C., Amara W., Best E., Vera Y.C.D., Amelot M., Bettencourt P., Carolei A., Amjadi N., Betzu R., Carreno S., Ammirati F., Bhagwat R., Carvalho P., Andrade M., Bhatta L., Cary S., Andrawis N., Biscione F., Casu G., Annoni G., Bisignani G., Cavallini C., Ansalone G., Black T., Cayla G., Ariani M.K., Bloch M.J., Celentano A., Arias J.C., Bloom S., Cha T.-J., Armero S., Blumberg E., Cha K.S., Arora C., Bo M., Chae J.K., Aslam M.S., Bohmer E., Chalamidas K., Asselman M., Bollmann A., Challappa K., Audouin P., Bongiorni M.G., Chand S.P., Augenbraun C., Boriani G., Chandrashekar H., Aydin S., Boswijk D.J., Chartier L., Bott J., Chatterjee K., Ayryanova I., Bottacchi E., Ayala C.A.C., Cheema A., Davis G., Evonich R., Davy J.-M., Evseeva O., Chen L., Dayer M., Ezhov A., Chen S.-A., De Biasio M., Fahmy R., 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J., Leschke M., Maurer T., Moschini L., Ley N., Mauro C., Moschos N., Li Z., May E., Mugge A., Mayer N., Mulhearn T.J., Muresan C., Jose E.P., Precoma D.B., Muriago M., Padilla F.G.P., Prelle A., Musial W., Rios V.P., Prodafikas J., Musser C.W., Pajes G., Protasov K., Musumeci F., Pandey A.S., Pye M., Nageh T., Paparella G., Qiu Z., Nakagawa H., Paris F., Quedillac J.-M., Nakamura Y., Park H.W., Raev D., Nakayama T., Park J.S., Grado C.A.R., Nam G.-B., Parthenakis F., Rahimi S., Nanna M., Passamonti E., Raisaro A., Natarajan I., Patel R.J., Rama B., Nayak H.M., Patel J., Ramos R., Naydenov S., Patel M., Ranieri M., Nazlic J., Patrick J., Raposo N., Nechita A.C., Jimenez R.P., Rashba E., Nechvatal L., Paz A., Rauch-Kroehnert U., Negron S.A., Pengo V., Reddy R., Neiman J., Pentz W., Renda G., Neuenschwander F.C., Perez B., Reza S., Neves D., Rios A.M.P., Ria L., Neykova A., Perez-Cabezas A., Richter D., Miguel R.N., Perlman R., Rickli H., Nijmeh G., Persic V., Rieker W., Nizov A., Perticone F., Vera T.R., Campos R.N., Peters T.K., Ritt L.E., Nossan J., Petkar S., Roberts D., Novikova T., Pezo L.F., Briones I.R., Nowalany-Kozielska E., Pflucke C., Escudero A.E.R., Nsah E., Pham D.N., Pascual C.R., Fragoso J.C.N., Phillips R.T., Roman M., Nurgalieva S., Phlaum S., Romeo F., Nuyens D., Pieters D., Ronner E., Nyvad O., Pineau J., Roux J.-F., de Los Rios Ibarra M.O., Pinter A., Rozkova N., O'Donnell P., Pinto F., Rubacek M., O'Donnell M., Pisters R., Rubalcava F., Oh S., Pivac N., Russo A.M., Oh Y.S., Pocanic D., Rutgers M.P., Oh D., Podoleanu C., Rybak K., O'Hara G., Politano A., Said S., Oikonomou K., Poljakovic Z., Sakamoto T., Olivares C., Pollock S., Salacata A., Oliver R., Garcea J.P., Salem A., Ruiz R.O., Poppert H., Bodes R.S., Olympios C., Porcu M., Saltzman M.A., Omaszuk-Kazberuk A., Reino A.P., Salvioni A., Asensi J.O., Prasad N., Vallejo G.S., Fernandez M.S., Sokal A., Tu T.M., Saporito W.F., Yan Y.S.O., Tuininga Y., Sarikonda K., Sotolongo R., Turakhia M., Sasaoka T., de Souza O.F., Turk S., Sati H., Sparby J.A., Turner W., Savelieva I., Spinar J., Tveit A., Scala P.-J., Sprigings D., Tytus R., Schellinger P., Spyropoulos A.C., Valadao C., Scherr C., Stakos D., van Bergen P.F.M.M., Schmitz L., Steinwender C., van de Borne P., Schmitz K.-H., Stergiou G., van den Berg B.J., Schmitz B., Stiell I., van der Zwaan C., Schnabel T., Stoddard M., Van Eck M., Schnupp S., Stoikov A., Vanacker P., Schoeniger P., Streb W., Vasilev D., Schon N., Styliadis I., Vasilikos V., Schwimmbeck P., Su G., Vasilyev M., Seamark C., Su X., Veerareddy S., Searles G., Sudnik W., Mino M.V., Seidl K.-H., Sukles K., Venkataraman A., Seidman B., Sun X., Verdecchia P., Sek J., Swart H., Versaci F., Sekaran L., Szavits-Nossan J., Vester E.G., Serrati C., Taggeselle J., Vial H., Shah N., Takagi Y., Victory J., Shah V., Takhar A.P.S., Villamil A., Shah A., Tamm A., Vincent M., Shah S., Tanaka K., Vlastaris A., Sharma V.K., Tanawuttiwat T., Dahl J., Shaw L., Tang S., Vora K., Sheikh K.H., Tang A., Vranian R.B., Shimizu N., Tarsi G., Wakefield P., Shimomura H., Tassinari T., Wang N., Shin D.-G., Tayal A., Wang M., Shin E.-S., Tayebjee M., Wang X., Shite J., Berg J.M., Wang F., Sibilio G., Tesloianu D., Wang T., Silver F., The S.H.K., Warner A.L., Sime I., Thomas D., Watanabe K., Simmers T.A., Timsit S., Wei J., Singh N., Tobaru T., Weimar C., Siostrzonek P., Tomasik A.R., Weiner S., Smadja D., Torosoff M., Weinrich R., Smith D.W., Touze E., Wen M.-S., Snitman M., Trendafilova E., Wiemer M., Filho D.S., Tsai W.K., Wiggers P., Soda H., Tse H.F., Wilke A., Sofley C., Tsutsui H., Williams D., Williams M.L., Yan P.Y.B., Zhang P., Witzenbichler B., Yang T., Zhang J., Wong B., Yao J., Zhao S.P., Wong K.S.L., Yeh K.-H., Zhao Y., Wozakowska-Kaplon B., Yin W.H., Zhao Z., Wu S., Yotov Y., Zheng Y., Wu R.C., Zahn R., Zhou J., Wunderlich S., Zarich S., Zimmermann S., Wyatt N., Zenin S., Zini A., Wylie J., Zeuthen E.L., Zizzo S., Xu Y., Zhang H., Zong W., Xu X., Zhang D., Zukerman L.S., Yamanoue H., Zhang X., and Yamashita T.

Subjects
Apixaban, Atrial fibrillation, Dabigatran, Non-vitamin K antagonists, Rivaroxaban, Pyridones, Medizin, Myocardial Infarction, Administration, Oral, Anticoagulants, Hemorrhage, General Medicine, Non-vitamin K antagonist, Stroke, Clinical Trials, Phase III as Topic, Humans, Prospective Studies, Registries, Cardiology and Cardiovascular Medicine
Abstract

Background and purpose Prospectively collected data comparing the safety and effectiveness of individual non-vitamin K antagonists (NOACs) are lacking. Our objective was to directly compare the effectiveness and safety of NOACs in patients with newly diagnosed atrial fibrillation (AF). Methods In GLORIA-AF, a large, prospective, global registry program, consecutive patients with newly diagnosed AF were followed for 3 years. The comparative analyses for (1) dabigatran vs rivaroxaban or apixaban and (2) rivaroxaban vs apixaban were performed on propensity score (PS)-matched patient sets. Proportional hazards regression was used to estimate hazard ratios (HRs) for outcomes of interest. Results The GLORIA-AF Phase III registry enrolled 21,300 patients between January 2014 and December 2016. Of these, 3839 were prescribed dabigatran, 4015 rivaroxaban and 4505 apixaban, with median ages of 71.0, 71.0, and 73.0 years, respectively. In the PS-matched set, the adjusted HRs and 95% confidence intervals (CIs) for dabigatran vs rivaroxaban were, for stroke: 1.27 (0.79–2.03), major bleeding 0.59 (0.40–0.88), myocardial infarction 0.68 (0.40–1.16), and all-cause death 0.86 (0.67–1.10). For the comparison of dabigatran vs apixaban, in the PS-matched set, the adjusted HRs were, for stroke 1.16 (0.76–1.78), myocardial infarction 0.84 (0.48–1.46), major bleeding 0.98 (0.63–1.52) and all-cause death 1.01 (0.79–1.29). For the comparison of rivaroxaban vs apixaban, in the PS-matched set, the adjusted HRs were, for stroke 0.78 (0.52–1.19), myocardial infarction 0.96 (0.63–1.45), major bleeding 1.54 (1.14–2.08), and all-cause death 0.97 (0.80–1.19). Conclusions Patients treated with dabigatran had a 41% lower risk of major bleeding compared with rivaroxaban, but similar risks of stroke, MI, and death. Relative to apixaban, patients treated with dabigatran had similar risks of stroke, major bleeding, MI, and death. Rivaroxaban relative to apixaban had increased risk for major bleeding, but similar risks for stroke, MI, and death. Registration URL: https://www.clinicaltrials.gov. Unique identifiers: NCT01468701, NCT01671007. Date of registration: September 2013. Graphical abstract

Published
2022

28. Anticoagulant selection in relation to the SAMe-TT2R2 score in patients with atrial fibrillation: The GLORIA-AF registry

Author

Ntaios, G., Huisman, M. V., Diener, H. -C., Halperin, J. L., Teutsch, C., Marler, S., Gurusamy, V. K., Thompson, M., Lip, G. Y. H., Olshansky, B., Abban, D. W., Abdul, N., Abud, A. M., Adams, F., Addala, S., Adragao, P., Ageno, W., Aggarwal, R., Agosti, S., Agostoni, P., Aguilar, F., Linares, J. A., Aguinaga, L., Ahmed, J., Aiello, A., Ainsworth, P., Aiub, J. R., Al-Dallow, R., Alderson, L., Aldrete Velasco, J. A., Alexopoulos, D., Manterola, F. A., Aliyar, P., Alonso, D., Alves da Costa, F. A., Amado, J., Amara, W., Amelot, M., Amjadi, N., Ammirati, F., Andrade, M., Andrawis, N., Annoni, G., Ansalone, G., Ariani, M. K., Arias, J. C., Armero, S., Arora, C., Aslam, M. S., Asselman, M., Audouin, P., Augenbraun, C., Aydin, S., Ayryanova, I., Aziz, E., Backes, L. M., Badings, E., Bagni, E., Baker, S. H., Bala, R., Baldi, A., Bando, S., Banerjee, S., Bank, A., Esquivias, G. B., Barr, C., Bartlett, M., Kes, V. B., Baula, G., Behrens, S., Bell, A., Benedetti, R., Mazuecos, J. B., Benhalima, B., Bergler-Klein, J., Berneau, J. -B., Bernstein, R. A., Berrospi, P., Berti, S., Berz, A., Best, E., Bettencourt, P., Betzu, R., Bhagwat, R., Bhatta, L., Biscione, F., Bisignani, G., Black, T., Bloch, M. J., Bloom, S., Blumberg, E., Bo, M., Bohmer, E., Bollmann, A., Bongiorni, M. G., Boriani, G., Boswijk, D. J., Bott, J., Bottacchi, E., Kalan, M. B., Bradman, D., Brautigam, D., Breton, N., Brouwers, P. J. A. M., Browne, K., Cortada, J. B., Bruni, A., Brunschwig, C., Buathier, H., Buhl, A., Bullinga, J., Cabrera, J. W., Caccavo, A., Cai, S., Caine, S., Calo, L., Calvi, V., Sanchez, M. C., Candeias, R., Capuano, V., Capucci, A., Caputo, R., Rizo, T. C., Cardona, F., Carlos da Costa Darrieux, F., Duarte Vera, Y. C., Carolei, A., Carreno, S., Carvalho, P., Cary, S., Casu, G., Cavallini, C., Cayla, G., Celentano, A., Cha, T. -J., Cha, K. S., Chae, J. K., Chalamidas, K., Challappa, K., Chand, S. P., Chandrashekar, H., Chartier, L., Chatterjee, K., Chavez Ayala, C. A., Cheema, A., Chen, L., Chen, S. -A., Chen, J. H., Chiang, F. -T., Chiarella, F., Chih-Chan, L., Cho, Y. K., Choi, J. -I., Choi, D. J., Chouinard, G., Hoi-Fan Chow, D., Chrysos, D., Chumakova, G., Jose Roberto Chuquiure Valenzuela, E. J., Nica, N. C., Cislowski, D. J., Clay, A., Clifford, P., Cohen, A., Cohen, M., Cohen, S., Colivicchi, F., Collins, R., Colonna, P., Compton, S., Connolly, D., Conti, A., Buenostro, G. C., Coodley, G., Cooper, M., Coronel, J., Corso, G., Sales, J. C., Cottin, Y., Covalesky, J., Cracan, A., Crea, Filippo, Crean, P., Crenshaw, J., Cullen, T., Darius, H., Dary, P., Dascotte, O., Dauber, I., Davalos, V., Davies, R., Davis, G., Davy, J. -M., Dayer, M., De Biasio, M., De Bonis, S., De Caterina, R., De Franceschi, T., de Groot, J. R., De Horta, J., De La Briolle, A., Topete, G. D. L. P., Vicenzo de Paola, A. A., de Souza, W., de Veer, A., De Wolf, L., Decoulx, E., Deepak, S., Defaye, P., Del-Carpio Munoz, F., Brkljacic, D. D., Deumite, N. 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E., Higashino, Y., Hill, M., Hisadome, T., Hishida, E., Hoffer, E., Hoghton, M., Hong, K., Hong, S. K., Horbach, S., Horiuchi, M., Hou, Y., Hsing, J., Huang, C. -H., Huckins, D., Kathy, Hughe, Huizinga, A., Hulsman, E. L., Hung, K. -C., Hwang, G. -S., Ikpoh, M., Imberti, D., Ince, H., Indolfi, C., Inoue, S., Irles, D., Iseki, H., Israel, C. N., Iteld, B., Iyer, V., Jackson-Voyzey, E., Jaffrani, N., Jager, F., James, M., Jang, S. -W., Jaramillo, N., Jarmukli, N., Jeanfreau, R. J., Jenkins, R. D., Sanchez, C. J., Jimenez, J., Jobe, R., Joen-Jakobsen, T., Jones, N., Moura Jorge, J. C., Jouve, B., Jung, B. C., Jung, K. T., Jung, W., Kachkovskiy, M., Kafkala, K., Kalinina, L., Kallmunzer, B., Kamali, F., Kamo, T., Kampus, P., Kashou, H., Kastrup, A., Katsivas, A., Kaufman, E., Kawai, K., Kawajiri, K., Kazmierski, J. F., Keeling, P., Kerr Saraiva, J. F., Ketova, G., Khaira, A. S., Khripun, A., Kim, D. -I., Kim, Y. H., Kim, N. H., Kim, D. K., Kim, J. S., Kim, K. S., Kim, J. B., Kinova, E., Klein, A., Kmetzo, J. J., Kneller, G. L., Knezevic, A., Angela Koh, S. M., Koide, S., Kollias, A., Kooistra, J. A., Koons, J., Koschutnik, M., Kostis, W. J., Kovacic, D., Kowalczyk, J., Koziolova, N., Kraft, P., Kragten, J. A., Krantz, M., Krause, L., Krenning, B. J., Krikke, F., Kromhout, Z., Krysiak, W., Kumar, P., Kumler, T., Kuniss, M., Kuo, J. -Y., Kuppers, A., Kurrelmeyer, K., Kwak, C. H., Laboulle, B., Labovitz, A., Lai, W. T., Lam, A., Lam, Y. Y., Zanetti, F. L., Landau, C., Landini, G., Figueiredo, E. L., Larsen, T., Lavandier, K., Leblanc, J., Lee, M. H., Lee, C. -H., Lehman, J., Leitao, A., Lellouche, N., Lelonek, M., Lenarczyk, R., Lenderink, T., Gonzalez, S. L., Leong-Sit, P., Leschke, M., Ley, N., Li, Z., Li, X., Li, W., Lichy, C., Lieber, I., Limon Rodriguez, R. H., Lin, H., Liu, F., Liu, H., Esperon, G. L., Navarro, N. L., Lo, E., Lokshyn, S., Lopez, A., Lopez-Sendon, J. L., Lorga Filho, A. M., Lorraine, R. S., Luengas, C. A., Luke, R., Luo, M., Lupovitch, S., Lyrer, P., Ma, C., Ma, G., Madariaga, I., Maeno, K., Magnin, D., Maid, G., Mainigi, S. K., Makaritsis, K., Malhotra, R., Manning, R., Manolis, A., Manrique Hurtado, H. A., Mantas, I., Jattin, F. M., Maqueda, V., Marchionni, N., Ortuno, F. M., Santana, A. M., Martinez, J., Maskova, P., Hernandez, N. M., Matsuda, K., Maurer, T., Mauro, C., May, E., Mayer, N., Mcclure, J., Mccormack, T., Mcgarity, W., Mcintyre, H., Mclaurin, B., Medina Palomino, F. A., Melandri, F., Meno, H., Menzies, D., Mercader, M., Meyer, C., Meyer, B. J., Miarka, J., Mibach, F., Michalski, D., Michel, P., Chreih, R. M., Mikdadi, G., Mikus, M., Milicic, D., Militaru, C., Minaie, S., Minescu, B., Mintale, I., Mirault, T., Mirro, M. J., Mistry, D., Miu, N. V., Miyamoto, N., Moccetti, T., Mohammed, A., Nor, A. M., Mollerus, M., Molon, G., Mondillo, S., Moniz, P., Mont, L., Montagud, V., Montana, O., Monti, C., Moretti, L., Mori, K., Moriarty, A., Morka, J., Moschini, L., Moschos, N., Mugge, A., Mulhearn, T. J., Muresan, C., Muriago, M., Musial, W., Musser, C. W., Musumeci, F., Nageh, T., Nakagawa, H., Nakamura, Y., Nakayama, T., Nam, G. -B., Nanna, M., Natarajan, I., Nayak, H. M., Naydenov, S., Nazli, J., Nechita, A. C., Nechvatal, L., Negron, S. A., Neiman, J., Neuenschwander, F. C., Neves, D., Neykova, A., Miguel, R. N., Nijmeh, G., Nizov, A., Campos, R. N., Nossan, J., Novikova, T., Nowalany-Kozielska, E., Nsah, E., Nunez Fragoso, J. C., Nurgalieva, S., Nuyens, D., Nyvad, O., Odin de Los Rios Ibarra, M., O'Donnell, P., O'Donnell, M., Oh, S., Oh, Y. S., Oh, D., O'Hara, G., Oikonomou, K., Olivares, C., Oliver, R., Ruiz, R. O., Olympios, C., Anna, omaszuk-Kazberuk, Asensi, J. O., eena Padayattil, Jose, Padilla Padilla, F. G., Rios, V. P., Pajes, G., Pandey, A. S., Paparella, G., Paris, F., Park, H. W., Park, J. S., Parthenakis, F., Passamonti, E., Patel, R. J., Patel, J., Patel, M., Patrick, J., Jimenez, R. P., Paz, A., Pengo, V., Pentz, W., Perez, B., Perez Rios, A. M., Perez-Cabezas, A., Perlman, R., Persic, V., Perticone, F., Peters, T. K., Petkar, S., Pezo, L. F., Pflucke, C., Pham, D. N., Phillips, R. T., Phlaum, S., Pieters, D., Pineau, J., Pinter, A., Pinto, F., Pisters, R., Pivac, N., Pocanic, D., Podoleanu, C., Politano, A., Poljakovic, Z., Pollock, S., Garcea, J. P., Poppert, H., Porcu, M., Reino, A. P., Prasad, N., Precoma, D. B., Prelle, A., Prodafikas, J., Protasov, K., Pye, M., Qiu, Z., Quedillac, J. -M., Raev, D., Raffo Grado, C. A., Rahimi, S., Raisaro, A., Rama, B., Ramos, R., Ranieri, M., Raposo, N., Rashba, E., Rauch-Kroehnert, U., Reddy, R., Renda, G., Reza, S., Ria, L., Richter, D., Rickli, H., Rieker, W., Vera, T. R., Ritt, L. E., Roberts, D., Briones, I. R., Rodriguez Escudero, A. E., Pascual, C. R., Roman, M., Romeo, F., Ronner, E., Roux, J. -F., Rozkova, N., Rubacek, M., Rubalcava, F., Russo, A. M., Rutgers, M. P., Rybak, K., Said, S., Sakamoto, T., Salacata, A., Salem, A., Bodes, R. S., Saltzman, M. A., Salvioni, A., Vallejo, G. S., Fernandez, M. S., Saporito, W. F., Sarikonda, K., Sasaoka, T., Sati, H., Savelieva, I., Scala, P. -J., Schellinger, P., Scherr, C., Schmitz, L., Schmitz, K. -H., Schmitz, B., Schnabel, T., Schnupp, S., Schoeniger, P., Schon, N., Schwimmbeck, P., Seamark, C., Searles, G., Seidl, K. -H., Seidman, B., Sek, J., Sekaran, L., Serrati, C., Shah, N., Shah, V., Shah, A., Shah, S., Sharma, V. K., Shaw, L., Sheikh, K. H., Shimizu, N., Shimomura, H., Shin, D. -G., Shin, E. -S., Shite, J., Sibilio, G., Silver, F., Sime, I., Simmers, T. A., Singh, N., Siostrzonek, P., Smadja, D., Smith, D. W., Snitman, M., Filho, D. S., Soda, H., Sofley, C., Sokal, A., Oi Yan, Y. S., Sotolongo, R., Ferreira de Souza, O., Sparby, J. A., Spinar, J., Sprigings, D., Spyropoulos, A. C., Stakos, D., Steinwender, C., Stergiou, G., Stiell, I., Stoddard, M., Stoikov, A., Streb, W., Styliadis, I., Su, G., Su, X., Sudnik, W., Sukles, K., Sun, X., Swart, H., Szavits-Nossan, J., Taggeselle, J., Takagi, Y., Singh Takhar, A. P., Tamm, A., Tanaka, K., Tanawuttiwat, T., Tang, S., Tang, A., Tarsi, G., Tassinari, T., Tayal, A., Tayebjee, M., Berg, J. M. T., Tesloianu, D., The, S. H. K., Thomas, D., Timsit, S., Tobaru, T., Tomasik, A. R., Torosoff, M., Touze, E., Trendafilova, E., Tsai, W. K., Tse, H. F., Tsutsui, H., Tu, T. M., Tuininga, Y., Turakhia, M., Turk, S., Tcurner, W., Tveit, A., Tytus, R., Valadao, C., van Bergen, P. F. M. M., van de Borne, P., van den Berg, B. J., van der Zwaan, C., Van Eck, M., Vanacker, P., Vasilev, D., Vasilikos, V., Vasilyev, M., Veerareddy, S., Mino, M. V., Venkataraman, A., Verdecchia, P., Versaci, F., Vester, E. G., Vial, H., Victory, J., Villamil, A., Vincent, M., Vlastaris, A., Dahl, J. 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V., Vora, K., Vranian, R. B., Wakefield, P., Wang, N., Wang, M., Wang, X., Wang, F., Wang, T., Warner, A. L., Watanabe, K., Wei, J., Weimar, C., Weiner, S., Weinrich, R., Wen, M. -S., Wiemer, M., Wiggers, P., Wilke, A., Williams, D., Williams, M. L., Witzenbichler, B., Wong, B., Lawrence Wong, K. S., Wozakowska-Kaplon, B., Wu, S., Wu, R. C., Wunderlich, S., Wyatt, N., Wylie, J. J., Xu, Y., Xu, X., Yamanoue, H., Yamashita, T., Bryan Yan, P. Y., Yang, T., Yao, J., Yeh, K. -H., Yin, W. H., Yotov, Y., Zahn, R., Zarich, S., Zenin, S., Zeuthen, E. L., Zhang, H., Zhang, D., Zhang, X., Zhang, P., Zhang, J., Zhao, S. P., Zhao, Y., Zhao, Z., Zheng, Y., Zhou, J., Zimmermann, S., Zini, A., Zizzo, S., Zong, W., Zukerman, L. S., and Crea F. (ORCID:0000-0001-9404-8846)

Abstract

Aim: The SAMe-TT2R2 score helps identify patients with atrial fibrillation (AF) likely to have poor anticoagulation control during anticoagulation with vitamin K antagonists (VKA) and those with scores >2 might be better managed with a target-specific oral anticoagulant (NOAC). We hypothesized that in clinical practice, VKAs may be prescribed less frequently to patients with AF and SAMe-TT2R2 scores >2 than to patients with lower scores. Methods and results: We analyzed the Phase III dataset of the Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation (GLORIA-AF), a large, global, prospective global registry of patients with newly diagnosed AF and ≥1 stroke risk factor. We compared baseline clinical characteristics and antithrombotic prescriptions to determine the probability of the VKA prescription among anticoagulated patients with the baseline SAMe-TT2R2 score >2 and ≤ 2. Among 17,465 anticoagulated patients with AF, 4,828 (27.6%) patients were prescribed VKA and 12,637 (72.4%) patients an NOAC: 11,884 (68.0%) patients had SAMe-TT2R2 scores 0-2 and 5,581 (32.0%) patients had scores >2. The proportion of patients prescribed VKA was 28.0% among patients with SAMe-TT2R2 scores >2 and 27.5% in those with scores ≤2. Conclusions: The lack of a clear association between the SAMe-TT2R2 score and anticoagulant selection may be attributed to the relative efficacy and safety profiles between NOACs and VKAs as well as to the absence of trial evidence that an SAMe-TT2R2-guided strategy for the selection of the type of anticoagulation in NVAF patients has an impact on clinical outcomes of efficacy and safety. The latter hypothesis is currently being tested in a randomized controlled trial. Clinical trial registration: URL: https://www.clinicaltrials.gov//Unique identifier: NCT01937377, NCT01468701, and NCT01671007.

Published
2021

32. Genetic studies of Alzheimer's disease risk implicate clearance of lipid rich debris in myeloid cells

Author

Novikova, Gloriia, primary, T.C.W., Julia, additional, Marcora, Edoardo, additional, Kapoor, Manav, additional, Renton, Alan E., additional, Efthymiou, Anastasia M., additional, Abud, Edsel M., additional, Bendl, Jaroslav M., additional, Cheng, Haoxiang M., additional, Fullard, John F., additional, Roussos, Panos, additional, Poon, Wayne W., additional, Hao, Ke, additional, and Goate, Alison M., additional

Published
2020
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33. Integration of Alzheimer’s disease genetics and myeloid genomics reveals novel disease risk mechanisms

Author

Novikova, Gloriia, primary, Marcora, Edoardo, additional, Kapoor, Manav, additional, TCW, Julia, additional, Renton, Alan E., additional, Efthymiou, Anastasia M., additional, Abud, Edsel M., additional, Bendl, Jaroslav M., additional, Cheng, Haoxiang M., additional, Fullard, John F., additional, Roussos, Panos, additional, Poon, Wayne W., additional, Hao, Ke, additional, and Goate, Alison M., additional

Published
2020
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35. Tau spread, apoE, inflammation, and more: Rapidly evolving basic science in AD

Author

Gonzalez, Bianca, Abud, Edsel M., Abud, Abigail M., Poon, Wayne W., and Gylys, Karen H.

Subjects
Inflammation, Apolipoproteins E, Cholesterol, Alzheimer Disease, Animals, Brain, Humans, tau Proteins, Article
Abstract

To date, Alzheimer's disease (AD) drug candidates have produced negative results in human trials and progress moving new targets out of the laboratory and into trials has been slow. However, based on three decades of previous work, there is reason to hope that amyloid-based and other novel therapies will move at a faster pace towards successful clinical trials. Here we highlight selected preclinical research topics that are rapidly advancing in the laboratory.

Published
2017

36. Integration of Alzheimer’s disease genetics and myeloid genomics reveals novel disease risk mechanisms

Author

Novikova, Gloriia, primary, Kapoor, Manav, additional, TCW, Julia, additional, Abud, Edsel M., additional, Efthymiou, Anastasia G., additional, Cheng, Haoxiang, additional, Fullard, John F., additional, Bendl, Jaroslav, additional, Roussos, Panos, additional, Poon, Wayne W., additional, Hao, Ke, additional, Marcora, Edoardo, additional, and Goate, Alison M., additional

Published
2019
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37. Activation of the STING-Dependent Type I Interferon Response Reduces Microglial Reactivity and Neuroinflammation

Author

Mathus, Vidhu, Burai, Ritwik, Vest, Ryan, Bonanno, Liana, Lehallier, Benoit, Zardeneta, Macy, Mistry, Karishma, Do, Danny, Marsh, Samuel, Abud, Edsel M, Blurton-Jones, Mathew, Li, Lingyin, Lashuel, Hilal A, and Wyss-Coray, Tony

Subjects
Male, type I interferon response, ganciclovir, viruses, Cells, Freund's Adjuvant, experimental autoimmune encephalomyelitis, microglia, Inbred C57BL, Antiviral Agents, Monocytes, Transgenic, neuroinflammation, Mice, Experimental, Neuroinflammation, Animals, Humans, Psychology, Encephalomyelitis, Ganciclovir, Cultured, Neurology & Neurosurgery, Animal, Neurosciences, Membrane Proteins, Newborn, eye diseases, Neuroprotection, Peptide Fragments, Microglial, Pertussis Toxin, Gene Expression Regulation, Disease Models, Interferon Type I, HIV/AIDS, Female, Myelin-Oligodendrocyte Glycoprotein, Cognitive Sciences, Autoimmune, Signal Transduction, STING, Biotechnology
Abstract

Brain aging and neurodegeneration are associated with prominent microglial reactivity and activation of innate immune response pathways, commonly referred to as neuroinflammation. One such pathway, the type I interferon response, recognizes viral or mitochondrial DNA in the cytoplasm via activation of the recently discovered cyclic dinucleotide synthetase cGAS and the cyclic dinucleotide receptor STING. Here we show that the FDA-approved antiviral drug ganciclovir (GCV) induces a type I interferon response independent of its canonical thymidine kinase target. Inhibition of components of the STING pathway, including STING, IRF3, Tbk1, extracellular IFN beta, and the Jak-Stat pathway resulted in reduced activity of GCV and its derivatives. Importantly, functional STING was necessary for GCV to inhibit inflammation in cultured myeloid cells and in a mouse model of multiple sclerosis. Collectively, our findings uncover an unexpected new activity of GCV and identify the STING pathway as a regulator of microglial reactivity and neuroinflammation.

Published
2017

40. DIVERSIDAD, ABUNDANCIA Y ESTACIONALIDAD DEL POLEN ALERGÉNICO EN LA ATMÓSFERA DE MAR DEL PLATA (ARGENTINA).

Author

Abud Sierra, M. Laura and Latorre, Fabiana

Subjects
*POLLEN, *AIR pollutants, *AIR quality, *POLLINATION, *GRASSES, *MORACEAE, *GRAIN
Abstract

Background and aims: Pollen grains represent one of the main biological pollutants in the air causing allergies in the population. To know the biological quality of the air and how it varies throughout the year, is essential to implement therapeutic and preventive measures. It was proposed: 1) to determine the allergenic potential of the atmospheric pollen spectrum of the city of Mar del Plata, 2) to elaborate a pollen calendar with the most allergenic taxa, and 3) to establish pollen stations that allow to identify the periods with greater incidence of pollen, recognizing the main allergenic contributors. M&M: Aerobiological monitoring was carried out for one year with a volumetric and continuous aerobiological sampler. Results: The average daily concentrations totaled 12742 grains. Fifty pollen types were recorded; 30 were allergenic (21 arboreal and 9 herbaceous). The taxa with a moderate or high allergenicity were: Cupressaceae, Poaceae, Cedrus and Platanus with more than 5% per year, and Acer, Urticaceae, Moraceae, Myrtaceae, Populus, Ulmus and Fraxinus with values between 2 and 5%. Also Ambrosia and Artemisia that are highly allergenic, all were included in a pollen calendar to visualize the duration, intensity and seasonality of each individual pollination period. Five main pollen stations were defined by the abundase of taxa with high levels of allergenicity: February-March, April, August, September-October, November-December. Conclusions: Ninety-five percent of airborne pollen grains along the year are allergenic or potentially allergenic. Aerobiological monitoring continues to incorporate interannual variations. [ABSTRACT FROM AUTHOR]

Published
2020
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43. Fibrilación auricular en situaciones especiales

Author

González Zuelgaray, Jorge, Abud, Atilio M, Abud, Marcelo, Picolini, Agustín, and Szyszko, Ariel E

Subjects
HYPERTHYROIDISM, MYOCARDIAL INFARCTION, WOLFF-PARKINSON-WHITE SYNDROME, COMPLICACIONES CARDIOVASCULARES DEL EMBARAZO, EMBARAZO, PREGNANCY COMPLICATIONS, CARDIOVASCULAR, INFARTO DEL MIOCARDIO, CIRUGÍA CARDÍACA, POSTOPERATIVE PERIOD, ATRIAL FIBRILLATION, CARDIAC SURGERY, PREGNANCY, INSUFICIENCIA CARDÍACA, HEART FAILURE, PERÍODO POSOPERATORIO, HIPERTIROIDISMO, FIBRILACIÓN AURICULAR, SÍNDROME DE WOLFF-PARKINSON-WHITE
Published
2016

45. P1-158: The Adaptive Immune System Critically Regulates Alzheimer’s Disease Pathogenesis by Modulating Microglial Function

Author

Marsh, Samuel E., primary, Karimzadeh, Alborz, additional, Abud, Edsel M., additional, Lakatos, Anita, additional, Yeung, Stephen T., additional, Davtyan, Hayk, additional, Fote, Gianna, additional, Lau, Lydia, additional, Weinger, Jason G., additional, Lane, Thomas E., additional, Poon, Wayne W., additional, Inlay, Matthew A., additional, and Blurton-Jones, Mathew, additional

Published
2016
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46. EXTRACCIÓN ENZIMÁTICA DEL ACEITE DE: Jatropha curcas L., Oecopetalum mexicanum Y Pistacia vera.

Author

Ovando-Chacón, S. L., Nolasco-Arroyo, B., Abud-Archila, M. A., and Ovando-Chacón, G.

Abstract

Copyright of Agro Productividad is the property of Colegio de Postgraduados 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
2018

48. Development of an image analysis methodology for following shrinkage and cracking of rice kernels during convective drying

Author

Abud-Archila, M., Catherine Bonazzi, Heyd, B., Bimbenet, J. J., Génie industriel alimentaire (GENIAL), and Institut National de la Recherche Agronomique (INRA)-Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Institut National Agronomique Paris-Grignon (INA P-G)-Ecole Nationale Supérieure des Industries Agricoles et alimentaires

Subjects
[SDV]Life Sciences [q-bio], EFFET DE LA TEMPERATURE, ComputingMilieux_MISCELLANEOUS, RIZ
Abstract

International audience

Published
1999

49. Kinetics of mechanical degradation of paddy rice during drying: influence of process operation conditions and modelling for control design

Author

Abud Archila, M., Francis Courtois, Catherine Bonazzi, Jean-Jacques Bimbenet, Ecole Nationale Supérieure des Industries Agricoles et Alimentaires, Ingénierie Procédés Aliments (GENIAL), Institut National de la Recherche Agronomique (INRA)-AgroParisTech-Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA), Génie industriel alimentaire (GENIAL), Institut National de la Recherche Agronomique (INRA)-Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Institut National Agronomique Paris-Grignon (INA P-G)-Ecole Nationale Supérieure des Industries Agricoles et alimentaires, Institut National de la Recherche Agronomique (INRA)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)-AgroParisTech-Conservatoire National des Arts et Métiers [CNAM] (CNAM), Institut National de la Recherche Agronomique (INRA)-AgroParisTech-Conservatoire National des Arts et Métiers [CNAM] (CNAM), and HESAM Université (HESAM)-HESAM Université (HESAM)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)

Subjects
rice, [SDV]Life Sciences [q-bio], kinetic model, yield, ComputingMilieux_MISCELLANEOUS, RIZ
Abstract

Editor : Mujumdar, A.S. Akritidis, C.B. ; Marinos-Kouris, D. ; Saravacos, G.D.; Kinetics of mechanical degradation of paddy rice during drying: influence of process operation conditions and modelling for control design. 11. International Drying Symposium - IDS '98

Published
1998

50. Modelling of drying kinetics and processing quality degradation of rough rice for CAD and control design

Author

Catherine Bonazzi, Francis Courtois, Abud Archila, M., Jean-Jacques Bimbenet, Ingénierie Procédés Aliments (GENIAL), Institut National de la Recherche Agronomique (INRA)-AgroParisTech-Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA), Ecole Nationale Supérieure des Industries Agricoles et Alimentaires, Institut National de la Recherche Agronomique (INRA)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)-AgroParisTech-Conservatoire National des Arts et Métiers [CNAM] (CNAM), Institut National de la Recherche Agronomique (INRA)-AgroParisTech-Conservatoire National des Arts et Métiers [CNAM] (CNAM), and HESAM Université (HESAM)-HESAM Université (HESAM)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)

Subjects
drying kinetics, head rice, [SDV]Life Sciences [q-bio], paddy rice, comportmental model, yield
Abstract

Modelling of drying kinetics and processing quality degradation of rough rice for CAD and control design. 1. European Congress of chemical Engineering (ECCE 1)

Published
1997

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