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3. Mutations of EXOSC3/Rrp40p associated with neurological diseases impact ribosomal RNA processing functions of the exosome in S. cerevisiae

Author

Gillespie, Abby, Gabunilas, Jason, Jen, Joanna C, and Chanfreau, Guillaume F

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Genetics, Neurodegenerative, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Underpinning research, Aetiology, Neurological, Generic health relevance, Amino Acid Sequence, Amino Acid Substitution, Binding Sites, Conserved Sequence, Exosome Multienzyme Ribonuclease Complex, Gene Expression Regulation, Fungal, Humans, Mutation, Olivopontocerebellar Atrophies, Protein Binding, Protein Conformation, alpha-Helical, Protein Conformation, beta-Strand, Protein Interaction Domains and Motifs, RNA Precursors, RNA Processing, Post-Transcriptional, RNA, Fungal, RNA, Ribosomal, RNA-Binding Proteins, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Sequence Alignment, Sequence Homology, Amino Acid, pontocerebellar hypoplasia, exosome, EXOSC3, Rrp40, ribosomal RNA processing, Biochemistry and Cell Biology, Developmental Biology, Biochemistry and cell biology
Abstract

The RNA exosome is a conserved multiprotein complex that achieves a large number of processive and degradative functions in eukaryotic cells. Recently, mutations have been mapped to the gene encoding one of the subunits of the exosome, EXOSC3 (yeast Rrp40p), which results in pontocerebellar hypoplasia with motor neuron degeneration in human patients. However, the molecular impact of these mutations in the pathology of these diseases is not well understood. To investigate the molecular consequences of mutations in EXOSC3 that lead to neurological diseases, we analyzed the effect of three of the mutations that affect conserved residues of EXOSC3/Rrp40p (G31A, G191C, and W238R; G8A, G148C, and W195R, respectively, in human and yeast) in S. cerevisiae We show that the severity of the phenotypes of these mutations in yeast correlate with that of the disease in human patients, with the W195R mutant showing the strongest growth and RNA processing phenotypes. Furthermore, we show that these mutations affect more severely pre-ribosomal RNA processing functions of the exosome rather than other nuclear processing or surveillance functions. These results suggest that delayed or defective pre-rRNA processing might be the primary defect responsible for the pathologies detected in patients with mutations affecting EXOSC3 function in residues conserved throughout eukaryotes.

Published
2017

4. Rapid degradation of mutant SLC25A46 by the ubiquitin-proteasome system results in MFN1/2-mediated hyperfusion of mitochondria.

Author

Steffen, Janos, Vashisht, Ajay A, Wan, Jijun, Jen, Joanna C, Claypool, Steven M, Wohlschlegel, James A, and Koehler, Carla M

Subjects
Hela Cells, Mitochondria, Humans, Proteasome Endopeptidase Complex, GTP Phosphohydrolases, Ubiquitin-Protein Ligases, Phosphate Transport Proteins, Mitochondrial Membrane Transport Proteins, Mitochondrial Proteins, Ubiquitin, Apoptosis, Autophagy, Mitochondrial Membranes, Ubiquitination, HEK293 Cells, Proteolysis, Mitochondrial Dynamics, HeLa Cells, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

SCL25A46 is a mitochondrial carrier protein that surprisingly localizes to the outer membrane and is distantly related to Ugo1. Here we show that a subset of SLC25A46 interacts with mitochondrial dynamics components and the MICOS complex. Decreased expression of SLC25A46 results in increased stability and oligomerization of MFN1 and MFN2 on mitochondria, promoting mitochondrial hyperfusion. A mutation at L341P causes rapid degradation of SLC25A46, which manifests as a rare disease, pontocerebellar hypoplasia. The E3 ubiquitin ligases MULAN and MARCH5 coordinate ubiquitylation of SLC25A46 L341P, leading to degradation by organized activities of P97 and the proteasome. Whereas outer mitochondrial membrane-associated degradation is typically associated with apoptosis or a specialized type of autophagy termed mitophagy, SLC25A46 degradation operates independently of activation of outer membrane stress pathways. Thus SLC25A46 is a new component in mitochondrial dynamics that serves as a regulator for MFN1/2 oligomerization. Moreover, SLC25A46 is selectively degraded from the outer membrane independently of mitophagy and apoptosis, providing a framework for mechanistic studies in the proteolysis of outer membrane proteins.

Published
2017

5. Loss of function of SLC25A46 causes lethal congenital pontocerebellar hypoplasia.

Author

Wan, Jijun, Steffen, Janos, Yourshaw, Michael, Mamsa, Hafsa, Andersen, Erik, Rudnik-Schöneborn, Sabine, Pope, Kate, Howell, Katherine B, McLean, Catriona A, Kornberg, Andrew J, Joseph, Jörg, Lockhart, Paul J, Zerres, Klaus, Ryan, Monique M, Nelson, Stanley F, Koehler, Carla M, and Jen, Joanna C

Subjects
Biomedical and Clinical Sciences, Neurosciences, Genetics, Pediatric, Orphan Drug, Neurodegenerative, Rare Diseases, Brain Disorders, Congenital Structural Anomalies, Aetiology, 2.1 Biological and endogenous factors, Neurological, Amino Acids, Animals, Animals, Genetically Modified, Brain, Cell Line, Transformed, Cells, Cultured, Cerebellar Diseases, Cohort Studies, Embryo, Nonmammalian, Female, Genetic Predisposition to Disease, Humans, Infant, Magnetic Resonance Imaging, Male, Mitochondria, Mitochondrial Dynamics, Mitochondrial Proteins, Models, Molecular, Mutation, Phosphate Transport Proteins, Polymorphism, Single Nucleotide, Zebrafish, pontocerebellar hypoplasia, SLC25A46, mitochondria, optic atrophy spectrum disorder, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences, Psychology
Abstract

Disturbed mitochondrial fusion and fission have been linked to various neurodegenerative disorders. In siblings from two unrelated families who died soon after birth with a profound neurodevelopmental disorder characterized by pontocerebellar hypoplasia and apnoea, we discovered a missense mutation and an exonic deletion in the SLC25A46 gene encoding a mitochondrial protein recently implicated in optic atrophy spectrum disorder. We performed functional studies that confirmed the mitochondrial localization and pro-fission properties of SLC25A46. Knockdown of slc24a46 expression in zebrafish embryos caused brain malformation, spinal motor neuron loss, and poor motility. At the cellular level, we observed abnormally elongated mitochondria, which was rescued by co-injection of the wild-type but not the mutant slc25a46 mRNA. Conversely, overexpression of the wild-type protein led to mitochondrial fragmentation and disruption of the mitochondrial network. In contrast to mutations causing non-lethal optic atrophy, missense mutations causing lethal congenital pontocerebellar hypoplasia markedly destabilize the protein. Indeed, the clinical severity appears inversely correlated with the relative stability of the mutant protein. This genotype-phenotype correlation underscores the importance of SLC25A46 and fine tuning of mitochondrial fission and fusion in pontocerebellar hypoplasia and central neurodevelopment in addition to optic and peripheral neuropathy across the life span.

Published
2016

6. Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export.

Author

Legati, Andrea, Giovannini, Donatella, Nicolas, Gaël, López-Sánchez, Uriel, Quintáns, Beatriz, Oliveira, João RM, Sears, Renee L, Ramos, Eliana Marisa, Spiteri, Elizabeth, Sobrido, María-Jesús, Carracedo, Ángel, Castro-Fernández, Cristina, Cubizolle, Stéphanie, Fogel, Brent L, Goizet, Cyril, Jen, Joanna C, Kirdlarp, Suppachok, Lang, Anthony E, Miedzybrodzka, Zosia, Mitarnun, Witoon, Paucar, Martin, Paulson, Henry, Pariente, Jérémie, Richard, Anne-Claire, Salins, Naomi S, Simpson, Sheila A, Striano, Pasquale, Svenningsson, Per, Tison, François, Unni, Vivek K, Vanakker, Olivier, Wessels, Marja W, Wetchaphanphesat, Suppachok, Yang, Michele, Boller, Francois, Campion, Dominique, Hannequin, Didier, Sitbon, Marc, Geschwind, Daniel H, Battini, Jean-Luc, and Coppola, Giovanni

Subjects
Humans, Brain Diseases, Metabolic, Inborn, Neurodegenerative Diseases, Calcinosis, Genetic Predisposition to Disease, Receptors, G-Protein-Coupled, Receptors, Virus, Pedigree, DNA Mutational Analysis, Lod Score, Mutation, Missense, Middle Aged, Female, Male, Genetic Association Studies, HEK293 Cells, Xenotropic and Polytropic Retrovirus Receptor, Neurosciences, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Primary familial brain calcification (PFBC) is a neurological disease characterized by calcium phosphate deposits in the basal ganglia and other brain regions and has thus far been associated with SLC20A2, PDGFB or PDGFRB mutations. We identified in multiple families with PFBC mutations in XPR1, a gene encoding a retroviral receptor with phosphate export function. These mutations alter phosphate export, implicating XPR1 and phosphate homeostasis in PFBC.

Published
2015

7. Neuropathology and Genetics of Cerebroretinal Vasculopathies

Author

Kolar, Grant R, Kothari, Parul H, Khanlou, Negar, Jen, Joanna C, Schmidt, Robert E, and Vinters, Harry V

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Cerebrovascular, Genetics, Aging, Stroke, Neurodegenerative, Peripheral Neuropathy, Rare Diseases, Brain Disorders, Neurosciences, Brain, Exodeoxyribonucleases, Frameshift Mutation, Hereditary Central Nervous System Demyelinating Diseases, Humans, Kidney, Phosphoproteins, Retinal Diseases, Vascular Diseases, cerebral microvascular disease, CRV, hereditary endotheliopathy with retinopathy, nephropathy, and stroke, hereditary vascular retinopathy, HERNS, ocular microvascular disease, Clinical Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

Cerebroretinal vasculopathy (CRV) and the related diseases hereditary endotheliopathy with retinopathy, neuropathy, and stroke (HERNS), hereditary vascular retinopathy (HVR) and hereditary systemic angiopathy (HSA) [subsequently combined as retinovasculopathy and cerebral leukodystrophy (RVCL)] are devastating autosomal-dominant disorders of early to middle-age onset presenting with a core constellation of neurologic and ophthalmologic findings. This family of diseases is linked by specific mutations targeting a core region of a gene. Frameshift mutations in the carboxyl-terminus of three prime exonuclease-1 (TREX1), the major mammalian 3' to 5' DNA exonuclease on chromosome 3p21.1-p21.3, result in a systemic vasculopathy that follows an approximately 5-year course leading to death secondary to progressive neurologic decline, with sometimes a more protracted course in HERNS. Neuropathological features include a fibrinoid vascular necrosis or thickened hyalinized vessels associated with white matter ischemia, necrosis and often striking dystrophic calcifications. Ultrastructural studies of the vessel walls often demonstrate unusual multilaminated basement membranes.

Published
2014

8. Mutations in SLC20A2 are a major cause of familial idiopathic basal ganglia calcification

Author

Hsu, Sandy Chan, Sears, Renee L, Lemos, Roberta R, Quintáns, Beatriz, Huang, Alden, Spiteri, Elizabeth, Nevarez, Lisette, Mamah, Catherine, Zatz, Mayana, Pierce, Kerrie D, Fullerton, Janice M, Adair, John C, Berner, Jon E, Bower, Matthew, Brodaty, Henry, Carmona, Olga, Dobricić, Valerija, Fogel, Brent L, García-Estevez, Daniel, Goldman, Jill, Goudreau, John L, Hopfer, Suellen, Janković, Milena, Jaumà, Serge, Jen, Joanna C, Kirdlarp, Suppachok, Klepper, Joerg, Kostić, Vladimir, Lang, Anthony E, Linglart, Agnès, Maisenbacher, Melissa K, Manyam, Bala V, Mazzoni, Pietro, Miedzybrodzka, Zofia, Mitarnun, Witoon, Mitchell, Philip B, Mueller, Jennifer, Novaković, Ivana, Paucar, Martin, Paulson, Henry, Simpson, Sheila A, Svenningsson, Per, Tuite, Paul, Vitek, Jerrold, Wetchaphanphesat, Suppachok, Williams, Charles, Yang, Michele, Schofield, Peter R, de Oliveira, João RM, Sobrido, María-Jesús, Geschwind, Daniel H, and Coppola, Giovanni

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Neurodegenerative, Human Genome, Clinical Research, Neurosciences, Genetic Testing, Prevention, Aetiology, 2.1 Biological and endogenous factors, Neurological, Adult, Aged, Amino Acid Sequence, Basal Ganglia Diseases, Calcinosis, Cohort Studies, DNA Mutational Analysis, Family, Female, Humans, Linkage Disequilibrium, Male, Middle Aged, Models, Biological, Molecular Sequence Data, Mutation, Neurodegenerative Diseases, Retrospective Studies, Sodium-Phosphate Cotransporter Proteins, Type III, Basal ganglia calcification, Fahr's, Sequencing, Mutations, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

Familial idiopathic basal ganglia calcification (IBGC) or Fahr's disease is a rare neurodegenerative disorder characterized by calcium deposits in the basal ganglia and other brain regions, which is associated with neuropsychiatric and motor symptoms. Familial IBGC is genetically heterogeneous and typically transmitted in an autosomal dominant fashion. We performed a mutational analysis of SLC20A2, the first gene found to cause IBGC, to assess its genetic contribution to familial IBGC. We recruited 218 subjects from 29 IBGC-affected families of varied ancestry and collected medical history, neurological exam, and head CT scans to characterize each patient's disease status. We screened our patient cohort for mutations in SLC20A2. Twelve novel (nonsense, deletions, missense, and splice site) potentially pathogenic variants, one synonymous variant, and one previously reported mutation were identified in 13 families. Variants predicted to be deleterious cosegregated with disease in five families. Three families showed nonsegregation with clinical disease of such variants, but retrospective review of clinical and neuroimaging data strongly suggested previous misclassification. Overall, mutations in SLC20A2 account for as many as 41% of our familial IBGC cases. Our screen in a large series expands the catalog of SLC20A2 mutations identified to date and demonstrates that mutations in SLC20A2 are a major cause of familial IBGC. Non-perfect segregation patterns of predicted deleterious variants highlight the challenges of phenotypic assessment in this condition with highly variable clinical presentation.

Published
2013

9. Mutations in the RNA exosome component gene EXOSC3 cause pontocerebellar hypoplasia and spinal motor neuron degeneration

Author

Wan, Jijun, Yourshaw, Michael, Mamsa, Hafsa, Rudnik-Schöneborn, Sabine, Menezes, Manoj P, Hong, Ji Eun, Leong, Derek W, Senderek, Jan, Salman, Michael S, Chitayat, David, Seeman, Pavel, von Moers, Arpad, Graul-Neumann, Luitgard, Kornberg, Andrew J, Castro-Gago, Manuel, Sobrido, María-Jesús, Sanefuji, Masafumi, Shieh, Perry B, Salamon, Noriko, Kim, Ronald C, Vinters, Harry V, Chen, Zugen, Zerres, Klaus, Ryan, Monique M, Nelson, Stanley F, and Jen, Joanna C

Subjects
Biological Sciences, Genetics, Clinical Research, Pediatric, Neurosciences, Neurodegenerative, Neurological, Animals, Cerebellum, Exosome Multienzyme Ribonuclease Complex, Exosomes, Gene Knockdown Techniques, Humans, Motor Neurons, Nerve Degeneration, Olivopontocerebellar Atrophies, Pons, RNA, RNA-Binding Proteins, Spinal Nerves, Zebrafish, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

RNA exosomes are multi-subunit complexes conserved throughout evolution and are emerging as the major cellular machinery for processing, surveillance and turnover of a diverse spectrum of coding and noncoding RNA substrates essential for viability. By exome sequencing, we discovered recessive mutations in EXOSC3 (encoding exosome component 3) in four siblings with infantile spinal motor neuron disease, cerebellar atrophy, progressive microcephaly and profound global developmental delay, consistent with pontocerebellar hypoplasia type 1 (PCH1; MIM 607596). We identified mutations in EXOSC3 in an additional 8 of 12 families with PCH1. Morpholino knockdown of exosc3 in zebrafish embryos caused embryonic maldevelopment, resulting in small brain size and poor motility, reminiscent of human clinical features, and these defects were largely rescued by co-injection with wild-type but not mutant exosc3 mRNA. These findings represent the first example of an RNA exosome core component gene that is responsible for a human disease and further implicate dysregulation of RNA processing in cerebellar and spinal motor neuron maldevelopment and degeneration.

Published
2012

10. Large Genomic Deletions in CACNA1A Cause Episodic Ataxia Type 2.

Author

Wan, Jijun, Mamsa, Hafsa, Johnston, Janine L, Spriggs, Elizabeth L, Singer, Harvey S, Zee, David S, Al-Bayati, Alhamza R, Baloh, Robert W, Jen, Joanna C, and CINCH Investigators

Subjects
CINCH Investigators, CACNA1A, EA2, episodic ataxia, genomic rearrangement, mutation, Clinical Sciences, Neurosciences, Psychology
Abstract

Episodic ataxia (EA) syndromes are heritable diseases characterized by dramatic episodes of imbalance and incoordination. EA type 2 (EA2), the most common and the best characterized subtype, is caused by mostly nonsense, splice site, small indel, and sometimes missense mutations in CACNA1A. Direct sequencing of CACNA1A fails to identify mutations in some patients with EA2-like features, possibly due to incomplete interrogation of CACNA1A or defects in other EA genes not yet defined. Previous reports described genomic deletions between 4 and 40 kb in EA2. In 47 subjects with EA (26 with EA2-like features) who tested negative for mutations in the known EA genes, we used multiplex ligation-dependent probe amplification to analyze CACNA1A for exonic copy number variations. Breakpoints were further defined by long-range PCR. We identified distinct multi-exonic deletions in three probands with classic EA2-like features: episodes of prolonged vertigo and ataxia triggered by stress and fatigue, interictal nystagmus, with onset during infancy or early childhood. The breakpoints in all three probands are located in Alu sequences, indicating errors in homologous recombination of Alu sequences as the underlying mechanism. The smallest deletion spanned exons 39 and 40, while the largest deletion spanned 200 kb, missing all but the first three exons. One deletion involving exons 39 through 47 arose spontaneously. The search for mutations in CACNA1A appears most fruitful in EA patients with interictal nystagmus and onset early in life. The finding of large heterozygous deletions suggests haploinsufficiency as a possible pathomechanism of EA2.

Published
2011

11. Mutations in a Human ROBO Gene Disrupt Hindbrain Axon Pathway Crossing and Morphogenesis

Author

Jen, Joanna C., Chan, Wai-Man, Bosley, Thomas M., Wan, Jijun, Carr, Janai R., Rüb, Udo, Shattuck, David, Salamon, Georges, Kudo, Lili C., Ou, Jing, Kansu, Tülay, al Dhalaan, Hesham, al Zayed, Zayed, MacDonald, David B., Stigsby, Bent, Plaitakis, Andreas, Dretakis, Emmanuel K., Gottlob, Irene, Pieh, Christina, Traboulsi, Elias I., Wang, Qing, Wang, Lejin, Andrews, Caroline, Yamada, Koki, Demer, Joseph L., Karim, Shaheen, Alger, Jeffry R., Geschwind, Daniel H., Deller, Thomas, Sicotte, Nancy L., Nelson, Stanley F., Baloh, Robert W., and Engle, Elizabeth C.

Published
2004

17. Erratum to: Bilateral vestibulopathy: Diagnostic criteria Consensus document of the Classification Committee of the Bárány Society

Author

Strupp, Michael, Kim, Ji-Soo, Murofushi, Toshihisa, Straumann, Dominik, Jen, Joanna C, Rosengren, Sally M, Della Santina, Charles C, Kingma, Herman, Strupp, Michael, Kim, Ji-Soo, Murofushi, Toshihisa, Straumann, Dominik, Jen, Joanna C, Rosengren, Sally M, Della Santina, Charles C, and Kingma, Herman

Abstract

This paper describes the diagnostic criteria for bilateral vestibulopathy (BVP) by the Classification Committee of the Bárány Society. The diagnosis of BVP is based on the patient history, bedside examination and laboratory evaluation. Bilateral vestibulopathy is a chronic vestibular syndrome which is characterized by unsteadiness when walking or standing, which worsen in darkness and/or on uneven ground, or during head motion. Additionally, patients may describe head or body movement-induced blurred vision or oscillopsia. There are typically no symptoms while sitting or lying down under static conditions. The diagnosis of BVP requires bilaterally significantly impaired or absent function of the vestibulo-ocular reflex (VOR). This can be diagnosed for the high frequency range of the angular VOR by the head impulse test (HIT), the video-HIT (vHIT) and the scleral coil technique and for the low frequency range by caloric testing. The moderate range can be examined by the sinusoidal or step profile rotational chair test. For the diagnosis of BVP, the horizontal angular VOR gain on both sides should be <0.6 (angular velocity 150–300°/s) and/or the sum of the maximal peak velocities of the slow phase caloric-induced nystagmus for stimulation with warm and cold water on each side <6°/s and/or the horizontal angular VOR gain <0.1 upon sinusoidal stimulation on a rotatory chair (0.1 Hz, Vmax = 50°/sec) and/or a phase lead >68 degrees (time constant of <5 seconds). For the diagnosis of probable BVP the above mentioned symptoms and a bilaterally pathological bedside HIT are required. Complementary tests that may be used but are currently not included in the definition are: a) dynamic visual acuity (a decrease of ≥0.2 logMAR is considered pathological); b) Romberg (indicating a sensory deficit of the vestibular or somatosensory system and therefore not specific); and c) abnormal cervical and ocular vestibular-evoked myogenic potentials for otolith function. At present the scie

Published
2023

22. Colaboradores

Author

Abrams, Charles S., Adler, Ronald S., Agarwal, Anupam, Akin, Cem, Aksamit, Allen J., Jr., Al-Awqati, Qais, Allen, Upton D., Allos, Ban Mishu, Angus, Derek C., Appelbaum, Frederick R., Armitage, James O., Armstrong, April W., Armstrong, Deborah K., Arnaout, M. Amin, Arnold, Robert M., Aronson, Louise, Atkinson, John P., Attia, Evelyn, Auerbach, Andrew D., Ayanian, John Z., Baddour, Larry M., Baden, Lindsey R., Bailey, Thomas C., Bain, Barbara J., Bajorin, Dean F., Baloh, Robert W., Bangham, Charles R.M., Barasch, Jonathan, Barrett, Bruce, Bartholomew, John R., Bartleson, J.D., Barton, Mary B., Basner, Robert C., Bass, Adam J., Bass, Anne R., Bauman, Julie E., Bausch, Daniel G., Bayer, Arnold S., Bazarian, Jeffrey J., Bearman, Gonzalo M., Becker, Richard C., Beckham, J. David, Beckman, Joshua A., Beigel, John H., Bel, Elisabeth H., Belda, Walter, Jr., Benarroch, Eduardo E., Berger, Joseph R., Berliner, Nancy, Bernat, James L., Bessesen, Daniel H., Bibbins-Domingo, Kirsten, Biesecker, Leslie G., Biundo, Joseph J., Blankson, Joel N., Bloch, Karen C., Blom, Henk J., Boden, William E., Boivin, Guy, Bolognia, Jean, Bonomo, Robert A., Booth, Sarah L., Bosaeus, Ingvar G., Brenner, David J., Bridges, S. Louis, Jr., Brochard, Laurent, Brodsky, Robert A., Brook, Itzhak, Brown, Jennifer R., Brunetti, Enrico, Bryant, Amy E., Budge, Philip J., Buffet, Pierre A., Bushinsky, David A., Bykerk, Vivian P., Calabresi, Peter A., Calello, Diane P., Calfee, David P., Callahan, S. Todd, Camilleri, Michael, Canoso, Juan J., Cappellini, Maria Domenica, Carabello, Blase A., Carucci, Laura R., Castells, Mariana, Catherino, William H., Cederholm, Tommy E., Chalasani, Naga P., Chambers, Henry F., Chang, Larry W., Chang, Lin, Chao, Nelson J., Chatterjee, Mitali, Chaturvedi, Seemant, Chen, Lin H., Chen, Sharon C-A, Chon, Susan Y., Christiani, David C., Chu, Edward, Cieslak, Theodore J., Cioffi, George A., Clancy, Carolyn M., Clauss, Heather, Clauw, Daniel J., Clemmons, David R., Coffman, Thomas M., Cohen, David, Cohen, Jeffrey, Cohen, Myron S., Cohen, Steven P., Connors, Joseph M., Cook, Deborah J., Cook, Lucy B.M., Cooney, Kathleen A., Craigen, William J., Crandall, Jill P., Croft, Simon L., Crow, Mary K., Crump, John A., Cudkowicz, Merit E., Cunningham-Rundles, Charlotte, Dahir, Kathryn M., Damon, Inger K., Daras, Michael, Dart, Richard C., Davidson, Nancy E., Deane, Kevin D., DeAngelis, Lisa M., DeCamp, Malcolm M., DeLoughery, Thomas G., del Rio, Carlos, De Luca, Gabriele C., Denning, David W., Deuster, Patricia A., DeZern, Amy E., Dhatariya, Ketan K., Diasio, Robert B., Diemert, David J., Digre, Kathleen B., Dilsizian, Vasken, Dionne, Jodie A., Di Paola, Jorge, Dispenzieri, Angela, Dogra, Sunil, Doroshow, James H., Douglas, John M., Jr., Drazen, Jeffrey M., Drekonja, Dimitri, Dubberke, Erik R., DuBeau, Catherine E., Dumler, J. Stephen, Duvic, Madeleine, Ebi, Kristie, Edwards, Kathryn M., Edwards, N. Lawrence, Eikelboom, John W., Einhorn, Lawrence H., Elliott, Perry M., Emanuel, Ezekiel J., Falagas, Matthew E., Falk, Gary W., Fang, James C., Farley, Monica M., Feder, Gene, Feller-Kopman, David J., File, Thomas McDonald, Jr., Fishman, Glenn I., Flack, John M., Fleckenstein, James M., Fleisher, Lee A., Flint, Paul W., Fogel, Evan L., Fontana, Robert J., Forsmark, Chris E., Fournier, Pierre-Edouard, Fowler, Vance G., Jr., Franco, Manuel A., Fraser, Victoria J., Freeman, Roy, Freund, Karen M., Froberg, Blake A., Gallagher, Patrick G., Gandhi, Monica, Gandhi, Rajesh T., Ganz, Leonard, Garan, Hasan, Garcia-Tsao, Guadalupe, Geisler, William M., Gelfand, Joel M., George, Tony P., Gepstein, Lior, Gertz, Morie A., Ghanem, Khalil G., Gharavi, Ali G., Ghossein, Cybele, Gill, Christopher J., Ginsburg, Geoffrey S., Glesby, Marshall J., Gnann, John W., Jr., Goldman, David L., Goldman, Lee, Goldstein, Larry B., Gordon, Anthony C., Gotlib, Jason, Gotuzzo, Eduardo, Grasemann, Hartmut, Green-McKenzie, Judith, Greenberg, Harry B., Greenberg, Steven A., Greer, David M., Greysen, S. Ryan, Griffin, Marie R., Griggs, Robert C., Grossman, Daniel, Guay-Woodford, Lisa M., Gulick, Roy M., Haake, David A., Hagman, Melissa M., Hagspiel, Klaus D., Harris, Raymond C., Havers, Fiona P., Heath, Elisabeth I., Hecht, Frederick M., Hensrud, Donald D., Hess, Jeremy, Hewlett, Erik L., Hift, Richard J., Hill, David R., Hill, Nicholas S., Hillyer, Christopher D., Hirsch, Hans H., Hoeper, Marius M., Hoit, Brian D., Holers, V. Michael, Holland, Steven M., Hollenberg, Anthony N., Hollenberg, Steven M., Howard, Jo, Hunter, David J., Hussain, Khalid, Iannuzzi, Michael C., Inman, Robert D., Inouye, Sharon K., Ison, Michael G., Jen, Joanna C., Jensen, Dennis M., Jensen, Michael D., Jensen, Robert T., Johnston, S. Claiborne, Jones, Robin L., Jordan, Richard C., Kahi, Charles J., Kaiser, Laurent, Kaminski, Henry J., Kamya, Moses R., Kao, Louise W., Kaplan, Steven A., Kastner, Daniel L., Katzka, David A., Katzman, Debra K., Kaushansky, Kenneth, Kaye, Keith S., Keating, Armand, Kelley, Robin K., Kennedy, Richard B., Khuri, Fadlo R., Kim, Rose, Kirchhoff, Louis V., Kirking, Hannah, Kirtane, Ajay J., Kishnani, Priya S., Klausner, Jeffrey D., Klion, Amy D., Klompas, Michael, Knopman, David S., Ko, Christine J., Kodali, Susheel, Kontoyiannis, Dimitrios P., Koppel, Barbara S., Korenblat, Kevin M., Korf, Bruce R., Kortepeter, Mark G., Koshy, Anita A., Kottilil, Shyamasundaran, Kovacs, Joseph A., Kovacs, Thomas O., Kowdley, Kris V., Kraft, Monica, Kramer, Christopher M., Krasnewich, Donna M., Kraus, William E., Krause, Peter J., Kroger, Andrew T., Kroshinsky, Daniela, Kuemmerle, John F., Kuipers, Ernst J., Kutner, Jean S., Laheru, Daniel, Lampert, Rachel, Landefeld, C. Seth, Landovitz, Raphael J., Landry, Donald W., Lange, Richard A., Lee, Hochang B., Lee, Nelson, Levey, Andrew S., Levine, Stephanie M., Lichtenstein, Gary R., Liebmann, Jeffrey M., Liebschutz, Jane M., Lim, Henry W., Lima, Aldo A.M., Limaye, Ajit P., Limdi, Nita A., Link, Mark S., Liu, Catherine, Lloyd-Jones, Donald M., Lopez, Fred A., Louie, Arnold, Lyness, Jeffrey M., MacKenzie, C. Ronald, MacLennan, Calman A., MacMillan, Harriet L., Madoff, Robert D., Maher, Jacquelyn, Maier, Lisa A., Maldarelli, Frank, Malhotra, Atul, Manary, Mark J., Marcos, Luis A., Marelli, Ariane J., Marks, Andrew R., Marschall, Jonas, Martin, Paul, Martinez, Fernando J., Mason, Joel B., Masur, Henry, Mathers, Amy J., Matthay, Michael A., McCool, F. Dennis, McInnes, Iain B., McLaughlin, Vallerie, McMichael, Amy, McMurray, John J.V., McQuaid, Kenneth R., Mead, Paul S., Means, Robert T., Jr., Melia, Michael T., Mellinghoff, Ingo K., Melton, Genevieve B., Merrick, Samuel T., Miceli, Marisa H., Michel, Marc, Mokdad, Ali H., Moy, Ernest, Mukherjee, Debabrata, Murr, Andrew H., Myerburg, Robert J., Nadeau, Kari C., Nath, Avindra, Neal-Perry, Genevieve, Neilson, Eric G., Nelson, Christina A., Nelson, David B., Nelson, Lewis S., Nestler, Eric J., Neuzil, Kathleen M., Nieman, Lynnette K., Niven, Alexander S., O’Connor, Christopher M., O’Connor, Francis G., O’Connor, Patrick G., O’Donnell, Anne E., O’Donnell, James S., Oh, Jae K., Okun, Michael S., O’Leary, Sean T., Olgin, Jeffrey E., Olivier, Kenneth N., Olivotto, Iacopo, Olsen, Nancy J., Orenstein, Walter A., Ortel, Thomas L., O’Shea, John J., Osmon, Douglas R., Ostrem, Jill L., Ostrosky-Zeichner, Luis, Otto, Catherine M., Ottolini, Martin G., Ovsyannikova, Inna G., Pappas, Peter G., Park, Ben Ho, Patel, Robin, Patterson, Thomas F., Pawlotsky, Jean-Michel, Payne, Thomas H., Pearce, Elizabeth N., Pearson, Richard D., Perl, Trish M., Petersen, Brett W., Petri, William A., Jr., Pfeffer, Marc A., Philips, Jennifer A., Pisetsky, David S., Pletcher, Steven D., Plumb, Ian D., Poland, Gregory A., Powell, Frank, Pyeritz, Reed E., Quinn, Thomas C., Racaniello, Vincent, Radhakrishnan, Jai, Radich, Jerald, Rafailidis, Petros I., Raghu, Ganesh, Ragni, Margaret V., Rahman, Proton, Rajkumar, S. Vincent, Ralston, Stuart H., Raoult, Didier, Reboli, Annette C., Reddy, K. Rajender, Redelmeier, Donald A., Redlich, Carrie A., Reilly, John, Reller, Megan E., Reno, Hilary E.L., Resnick, Neil M., Rice, Louis B., Roach, E. Steve, Robinson, Jennifer G., Rogatsky, Inez, Rogers, Joseph G., Rolain, Jean-Marc, Rollins, Barrett J., Romero, José R., Rosen, Jennifer B., Rosenthal, Philip J., Russell, James A., Rustgi, Anil K., Safer, Joshua D., Saini, Sarbjit S., Salmon, Jane E., Salvana, Edsel Maurice T., Santoro, Nanette, Santucci, Peter A., Sarnak, Mark J., Savage, Kerry J., Savard, Patrice, Sawka, Michael N., Scanlon, Paul D., Schafer, Andrew I., Schiff, Manuel, Schilsky, Michael L., Schneider, Thomas Rudolf, Schooley, Robert T., Schriger, David L., Schuchter, Lynn M., Schwartz, Lawrence B., Seas, Carlos, Seifert, Steven A., Seifter, Julian Lawrence, Selcen, Duygu, Selim, Magdy, Semrad, Carol E., Sepulveda, Jorge, Shaw, Pamela J., Shaz, Beth H., Sheridan, Robert L., Sherman, Stuart, Shojania, Kaveh G., Shopsin, Bo, Shy, Michael E., Sidransky, Ellen, Sifri, Costi D., Siliciano, Robert F., Simel, David L., Skorecki, Karl, Slawski, Barbara A., Slutsky, Arthur S., Smetana, Gerald W., Smith, A. Gordon, Smith, Stephen R., Southwick, Frederick S., Spiegel, Allen M., Spiera, Robert, Spinola, Stanley M., Spong, Catherine Y., Stabler, Sally P., Stark, Paul, Clair, E. William St., Steiner, Theodore S., Stephens, David S., Stevens, David A., Stevens, Dennis L., Stokes, M. Barry, Stoller, James K., Stone, John H., Stone, Richard M., Su, Edwin P., Swerdloff, Ronald S., Swygard, Heidi, Sykes, Megan, Talbot, H. Keipp, Tamimi, Rulla M., Tanofsky-Kraff, Marian, Tarlo, Susan M., Taylor, Stephanie N., Teirstein, Paul S., Telford, Sam R., III, Thakker, Rajesh V., Therrien, Judith, Thompson, George R., III, Tormoehlen, Laura, Tosti, Antonella, Trehan, Indi, Umpierrez, Guillermo E., Valeri, Anthony Michael, Varga, John, Vaughn, Bradley V., Venook, Alan P., Verbalis, Joseph G., Vose, Julie M., Wachter, Robert M., Walsh, B. Timothy, Walsh, Edward E., Walsh, Thomas J., Walston, Jeremy D., Walter, Roland B., Wang, Christina, Wang, Kenneth K., Ware, Lorraine B., Warren, Cirle A., Watkins, Paul B., Weber, Thomas J., Weimer, Louis H., Weinberg, Geoffrey A., Weinstein, Robert S., Weiss, Roger D., Weiss, Roy E., Weitz, Jeffrey I., Welt, Frederick G.P., Wenzel, Richard P., Werth, Victoria P., West, Sterling G., White, A. Clinton, Jr., White, Christopher J., White, Julian, White, Perrin C., Whitley, Richard J., Whyte, Michael P., Wiebe, Samuel, Wiener-Kronish, Jeanine P., Wilber, David J., Wilcox, Mark H., Winikoff, Beverly, Winter, Jane N., Wittink, Marsha N., Wolff, Tracy A., Wolin, Edward M., Wormser, Gary P., Yancy, Clyde W., Young, Neal S., Young, Vincent B., Young, William F., Jr., Yu, Alan S.L., Zimetbaum, Peter, and Zucker, Jane R.

Published
2025
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31. Two cases of rheumatoid meningitis

Author

Magaki, Shino, Chang, Edward, Hammond, Robert R., Yang, Isaac, Mackenzie, Ian R. A., Chou, Benedict T., Choi, Soo I., Jen, Joanna C., Pope, Whitney B., Bell, David A., and Vinters, Harry V.

Published
2016
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32. Contributors

Author

Abrams, Charles S., Adler, Ronald S., Agarwal, Anupam, Akin, Cem, Aksamit, Allen J., Jr., Al-Awqati, Qais, Allen, Upton D., Allos, Ban Mishu, Angus, Derek C., Appelbaum, Frederick R., Armitage, James O., Armstrong, April W., Armstrong, Deborah K., Arnaout, M. Amin, Arnold, Robert M., Aronson, Louise, Atkinson, John P., Attia, Evelyn, Auerbach, Andrew D., Ayanian, John Z., Baddour, Larry M., Baden, Lindsey R., Bailey, Thomas C., Bain, Barbara J., Bajorin, Dean F., Baloh, Robert W., Bangham, Charles R.M., Barasch, Jonathan, Barrett, Bruce, Bartholomew, John R., Bartleson, J.D., Barton, Mary B., Basner, Robert C., Bass, Adam J., Bass, Anne R., Bauman, Julie E., Bausch, Daniel G., Bayer, Arnold S., Bazarian, Jeffrey J., Bearman, Gonzalo M., Becker, Richard C., Beckham, J. David, Beckman, Joshua A., Beigel, John H., Bel, Elisabeth H., Belda, Walter, Jr., Benarroch, Eduardo E., Berger, Joseph R., Berliner, Nancy, Bernat, James L., Bessesen, Daniel H., Bibbins-Domingo, Kirsten, Biesecker, Leslie G., Biundo, Joseph J., Blankson, Joel N., Bloch, Karen C., Blom, Henk J., Boden, William E., Boivin, Guy, Bolognia, Jean, Bonomo, Robert A., Booth, Sarah L., Bosaeus, Ingvar G., Brenner, David J., Bridges, S. Louis, Jr., Brochard, Laurent, Brodsky, Robert A., Brook, Itzhak, Brown, Jennifer R., Brunetti, Enrico, Bryant, Amy E., Budge, Philip J., Buffet, Pierre A., Bushinsky, David A., Bykerk, Vivian P., Calabresi, Peter A., Calello, Diane P., Calfee, David P., Callahan, S. Todd, Camilleri, Michael, Canoso, Juan J., Cappellini, Maria Domenica, Carabello, Blase A., Carucci, Laura R., Castells, Mariana, Catherino, William H., Cederholm, Tommy E., Chalasani, Naga P., Chambers, Henry F., Chang, Larry W., Chang, Lin, Chao, Nelson J., Chatterjee, Mitali, Chaturvedi, Seemant, Chen, Lin H., C-A Chen, Sharon, Chon, Susan Y., Christiani, David C., Chu, Edward, Cieslak, Theodore J., Cioffi, George A., Clancy, Carolyn M., Clauss, Heather, Clauw, Daniel J., Clemmons, David R., Coffman, Thomas M., Cohen, David, Cohen, Jeffrey, Cohen, Myron S., Cohen, Steven P., Connors, Joseph M., Cook, Deborah J., Cook, Lucy B.M., Cooney, Kathleen A., Craigen, William J., Crandall, Jill P., Croft, Simon L., Crow, Mary K., Crump, John A., Cudkowicz, Merit E., Cunningham-Rundles, Charlotte, Dahir, Kathryn M., Damon, Inger K., Daras, Michael, Dart, Richard C., Davidson, Nancy E., Deane, Kevin D., DeAngelis, Lisa M., DeCamp, Malcolm M., DeLoughery, Thomas G., Rio, Carlos del, De Luca, Gabriele C., Denning, David W., Deuster, Patricia A., DeZern, Amy E., Dhatariya, Ketan K., Diasio, Robert B., Diemert, David J., Digre, Kathleen B., Dilsizian, Vasken, Dionne, Jodie A., Di Paola, Jorge, Dispenzieri, Angela, Dogra, Sunil, Doroshow, James H., Douglas, John M., Jr., Drazen, Jeffrey M., Drekonja, Dimitri, Dubberke, Erik R., DuBeau, Catherine E., Dumler, J. Stephen, Duvic, Madeleine, Ebi, Kristie, Edwards, Kathryn M., Edwards, N. Lawrence, Eikelboom, John W., Einhorn, Lawrence H., Elliott, Perry M., Emanuel, Ezekiel J., Falagas, Matthew E., Falk, Gary W., Fang, James C., Farley, Monica M., Feder, Gene, Feller-Kopman, David J., McDonald File, Thomas, Jr., Fishman, Glenn I., Flack, John M., Fleckenstein, James M., Fleisher, Lee A., Flint, Paul W., Fogel, Evan L., Fontana, Robert J., Forsmark, Chris E., Fournier, Pierre-Edouard, Fowler, Vance G., Jr., Franco, Manuel A., Fraser, Victoria J., Freeman, Roy, Freund, Karen M., Froberg, Blake A., Gallagher, Patrick G., Gandhi, Monica, Gandhi, Rajesh T., Ganz, Leonard, Garan, Hasan, Garcia-Tsao, Guadalupe, Geisler, William M., Gelfand, Joel M., George, Tony P., Gepstein, Lior, Gertz, Morie A., Ghanem, Khalil G., Gharavi, Ali G., Ghossein, Cybele, Gill, Christopher J., Ginsburg, Geoffrey S., Glesby, Marshall J., Gnann, John W., Jr., Goldman, David L., Goldman, Lee, Goldstein, Larry B., Gordon, Anthony C., Gotlib, Jason, Gotuzzo, Eduardo, Grasemann, Hartmut, Green-McKenzie, Judith, Greenberg, Harry B., Greenberg, Steven A., Greer, David M., Greysen, S. Ryan, Griffin, Marie R., Griggs, Robert C., Grossman, Daniel, Guay-Woodford, Lisa M., Gulick, Roy M., Haake, David A., Hagman, Melissa M., Hagspiel, Klaus D., Harris, Raymond C., Havers, Fiona P., Heath, Elisabeth I., Hecht, Frederick M., Hensrud, Donald D., Hess, Jeremy, Hewlett, Erik L., Hift, Richard J., Hill, David R., Hill, Nicholas S., Hillyer, Christopher D., Hirsch, Hans H., Hoeper, Marius M., Hoit, Brian D., Holers, V. Michael, Holland, Steven M., Hollenberg, Anthony N., Hollenberg, Steven M., Howard, Jo, Hunter, David J., Hussain, Khalid, Iannuzzi, Michael C., Inman, Robert D., Inouye, Sharon K., Ison, Michael G., Jen, Joanna C., Jensen, Dennis M., Jensen, Michael D., Jensen, Robert T., Johnston, S. Claiborne, Jones, Robin L., Jordan, Richard C., Kahi, Charles J., Kaiser, Laurent, Kaminski, Henry J., Kamya, Moses R., Kao, Louise W., Kaplan, Steven A., Kastner, Daniel L., Katzka, David A., Katzman, Debra K., Kaushansky, Kenneth, Kaye, Keith S., Keating, Armand, Kelley, Robin K., Kennedy, Richard B., Khuri, Fadlo R., Kim, Rose, Kirchhoff, Louis V., Kirking, Hannah, Kirtane, Ajay J., Kishnani, Priya S., Klausner, Jeffrey D., Klion, Amy D., Klompas, Michael, Knopman, David S., Ko, Christine J., Kodali, Susheel, Kontoyiannis, Dimitrios P., Koppel, Barbara S., Korenblat, Kevin M., Korf, Bruce R., Kortepeter, Mark G., Koshy, Anita A., Kottilil, Shyamasundaran, Kovacs, Joseph A., Kovacs, Thomas O., Kowdley, Kris V., Kraft, Monica, Kramer, Christopher M., Krasnewich, Donna M., Kraus, William E., Krause, Peter J., Kroger, Andrew T., Kroshinsky, Daniela, Kuemmerle, John F., Kuipers, Ernst J., Kutner, Jean S., Laheru, Daniel, Lampert, Rachel, Landefeld, C. Seth, Landovitz, Raphael J., Landry, Donald W., Lange, Richard A., Lee, Hochang B., Lee, Nelson, Levey, Andrew S., Levine, Stephanie M., Lichtenstein, Gary R., Liebmann, Jeffrey M., Liebschutz, Jane M., Lim, Henry W., Lima, Aldo A.M., Limaye, Ajit P., Limdi, Nita A., Link, Mark S., Liu, Catherine, Lloyd-Jones, Donald M., Lopez, Fred A., Louie, Arnold, Lyness, Jeffrey M., MacKenzie, C. Ronald, MacLennan, Calman A., MacMillan, Harriet L., Madoff, Robert D., Maher, Jacquelyn, Maier, Lisa A., Maldarelli, Frank, Malhotra, Atul, Manary, Mark J., Marcos, Luis A., Marelli, Ariane J., Marks, Andrew R., Marschall, Jonas, Martin, Paul, Martinez, Fernando J., Mason, Joel B., Masur, Henry, Mathers, Amy J., Matthay, Michael A., McCool, F. Dennis, McInnes, Iain B., McLaughlin, Vallerie, McMichael, Amy, McMurray, John J.V., McQuaid, Kenneth R., Mead, Paul S., Means, Robert T., Jr., Melia, Michael T., Mellinghoff, Ingo K., Melton, Genevieve B., Merrick, Samuel T., Miceli, Marisa H., Michel, Marc, Mokdad, Ali H., Moy, Ernest, Mukherjee, Debabrata, Murr, Andrew H., Myerburg, Robert J., Nadeau, Kari C., Nath, Avindra, Neal-Perry, Genevieve, Neilson, Eric G., Nelson, Christina A., Nelson, David B., Nelson, Lewis S., Nestler, Eric J., Neuzil, Kathleen M., Nieman, Lynnette K., Niven, Alexander S., O’Connor, Christopher M., O’Connor, Francis G., O’Connor, Patrick G., O’Donnell, Anne E., O’Donnell, James S., Oh, Jae K., Okun, Michael S., O’Leary, Sean T., Olgin, Jeffrey E., Olivier, Kenneth N., Olivotto, Iacopo, Olsen, Nancy J., Orenstein, Walter A., Ortel, Thomas L., O’Shea, John J., Osmon, Douglas R., Ostrem, Jill L., Ostrosky-Zeichner, Luis, Otto, Catherine M., Ottolini, Martin G., Ovsyannikova, Inna G., Pappas, Peter G., Park, Ben Ho, Patel, Robin, Patterson, Thomas F., Pawlotsky, Jean-Michel, Payne, Thomas H., Pearce, Elizabeth N., Pearson, Richard D., Perl, Trish M., Petersen, Brett W., Petri, William A., Jr., Pfeffer, Marc A., Philips, Jennifer A., Pisetsky, David S., Pletcher, Steven D., Plumb, Ian D., Poland, Gregory A., Powell, Frank, Pyeritz, Reed E., Quinn, Thomas C., Racaniello, Vincent, Radhakrishnan, Jai, Radich, Jerald, Rafailidis, Petros I., Raghu, Ganesh, Ragni, Margaret V., Rahman, Proton, Rajkumar, S. Vincent, Ralston, Stuart H., Raoult, Didier, Reboli, Annette C., Reddy, K. Rajender, Redelmeier, Donald A., Redlich, Carrie A., Reilly, John, Reller, Megan E., Reno, Hilary E.L., Resnick, Neil M., Rice, Louis B., Roach, E. Steve, Robinson, Jennifer G., Rogatsky, Inez, Rogers, Joseph G., Rolain, Jean-Marc, Rollins, Barrett J., Romero, José R., Rosen, Jennifer B., Rosenthal, Philip J., Russell, James A., Rustgi, Anil K., Safer, Joshua D., Saini, Sarbjit S., Salmon, Jane E., Salvana, Edsel Maurice T., Santoro, Nanette, Santucci, Peter A., Sarnak, Mark J., Savage, Kerry J., Savard, Patrice, Sawka, Michael N., Scanlon, Paul D., Schafer, Andrew I., Schiff, Manuel, Schilsky, Michael L., Schneider, Thomas Rudolf, Schooley, Robert T., Schriger, David L., Schuchter, Lynn M., Schwartz, Lawrence B., Seas, Carlos, Seifert, Steven A., Seifter, Julian Lawrence, Selcen, Duygu, Selim, Magdy, Semrad, Carol E., Sepulveda, Jorge, Shaw, Pamela J., Shaz, Beth H., Sheridan, Robert L., Sherman, Stuart, Shojania, Kaveh G., Shopsin, Bo, Shy, Michael E., Sidransky, Ellen, Sifri, Costi D., Siliciano, Robert F., Simel, David L., Skorecki, Karl, Slawski, Barbara A., Slutsky, Arthur S., Smetana, Gerald W., Smith, A. Gordon, Smith, Stephen R., Southwick, Frederick S., Spiegel, Allen M., Spiera, Robert, Spinola, Stanley M., Spong, Catherine Y., Stabler, Sally P., Stark, Paul, St. Clair, E. William, Steiner, Theodore S., Stephens, David S., Stevens, David A., Stevens, Dennis L., Stokes, M. Barry, Stoller, James K., Stone, John H., Stone, Richard M., Su, Edwin P., Swerdloff, Ronald S., Swygard, Heidi, Sykes, Megan, Talbot, H. Keipp, Tamimi, Rulla M., Tanofsky-Kraff, Marian, Tarlo, Susan M., Taylor, Stephanie N., Teirstein, Paul S., Telford, Sam R., III, Thakker, Rajesh V., Therrien, Judith, Thompson, George R., III, Tormoehlen, Laura, Tosti, Antonella, Trehan, Indi, Umpierrez, Guillermo E., Valeri, Anthony Michael, Varga, John, Vaughn, Bradley V., Venook, Alan P., Verbalis, Joseph G., Vose, Julie M., Wachter, Robert M., Walsh, B. Timothy, Walsh, Edward E., Walsh, Thomas J., Walston, Jeremy D., Walter, Roland B., Wang, Christina, Wang, Kenneth K., Ware, Lorraine B., Warren, Cirle A., Watkins, Paul B., Weber, Thomas J., Weimer, Louis H., Weinberg, Geoffrey A., Weinstein, Robert S., Weiss, Roger D., Weiss, Roy E., Weitz, Jeffrey I., Welt, Frederick G.P., Wenzel, Richard P., Werth, Victoria P., West, Sterling G., White, A. Clinton, Jr., White, Christopher J., White, Julian, White, Perrin C., Whitley, Richard J., Whyte, Michael P., Wiebe, Samuel, Wiener-Kronish, Jeanine P., Wilber, David J., Wilcox, Mark H., Winikoff, Beverly, Winter, Jane N., Wittink, Marsha N., Wolff, Tracy A., Wolin, Edward M., Wormser, Gary P., Yancy, Clyde W., Young, Neal S., Young, Vincent B., Young, William F., Jr., Yu, Alan S.L., Zimetbaum, Peter, and Zucker, Jane R.

Published
2024
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