Search

Your search keyword '"Louis R."' showing total 373 results
Start Over Author "Louis R." Publisher elsevier
373 results on '"Louis R."'

1. Autophagy Contributes to Homeostasis in Esophageal Epithelium Where High Autophagic Vesicle Level Marks Basal Cells With Limited Proliferation and Enhanced Self-Renewal PotentialSummary

Author

Alena Klochkova, Adam L. Karami, Annie D. Fuller, Louis R. Parham, Surali R. Panchani, Shruthi Natarajan, Jazmyne L. Jackson, Anbin Mu, Yinfei Tan, Kathy Q. Cai, Andres J. Klein-Szanto, Amanda B. Muir, Marie-Pier Tétreault, Xavier Graña, Kathryn E. Hamilton, and Kelly A. Whelan

Subjects
Esophageal Epithelium, Autophagy, ATG7, Basal Cell Dynamics, Esophageal Progenitor Cells, Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Background & Aims: Autophagy plays roles in esophageal pathologies both benign and malignant. Here, we aim to define the role of autophagy in esophageal epithelial homeostasis. Methods: We generated tamoxifen-inducible, squamous epithelial-specific Atg7 (autophagy related 7) conditional knockout mice to evaluate effects on esophageal homeostasis and response to the carcinogen 4-nitroquinoline 1-oxide (4NQO) using histologic and biochemical analyses. We fluorescence-activated cell sorted esophageal basal cells based on fluorescence of the autophagic vesicle (AV)-identifying dye Cyto-ID and then subjected these cells to transmission electron microscopy, image flow cytometry, three-dimensional organoid assays, RNA sequencing, and cell cycle analysis. Three-dimensional organoids were subjected to passaging, single-cell RNA sequencing, cell cycle analysis, and immunostaining. Results: Genetic autophagy inhibition in squamous epithelium resulted in increased proliferation of esophageal basal cells under homeostatic conditions and also was associated with significant weight loss in mice treated with 4NQO that further displayed perturbed epithelial tissue architecture. Esophageal basal cells with high AV level (Cyto-IDHigh) displayed limited organoid formation capability on initial plating but passaged more efficiently than their counterparts with low AV level (Cyto-IDLow). RNA sequencing suggested increased autophagy in Cyto-IDHigh esophageal basal cells along with decreased cell cycle progression, the latter of which was confirmed by cell cycle analysis. Single-cell RNA sequencing of three-dimensional organoids generated by Cyto-IDLow and Cyto-IDHigh cells identified expansion of 3 cell populations and enrichment of G2/M-associated genes in the Cyto-IDHigh group. Ki67 expression was also increased in organoids generated by Cyto-IDHigh cells, including in basal cells localized beyond the outermost cell layer. Conclusions: Autophagy contributes to maintenance of the esophageal proliferation-differentiation gradient. Esophageal basal cells with high AV level exhibit limited proliferation and generate three-dimensional organoids with enhanced self-renewal capacity.

Published
2024
Full Text
View/download PDF

2. IGF2BP1/IMP1 Deletion Enhances a Facultative Stem Cell State via Regulation of MAP1LC3BSummary

Author

Louis R. Parham, Patrick A. Williams, Kay Katada, Shaneice K. Nettleford, Priya Chatterji, Kofi K. Acheampong, Charles H. Danan, Xianghui Ma, Lauren A. Simon, Kaitlyn E. Naughton, Rei Mizuno, Tatiana Karakasheva, Emily A. McMillan, Kelly A. Whelan, Donita C. Brady, Sydney M. Shaffer, and Kathryn E. Hamilton

Subjects
Autophagy, regeneration, post-transcriptional gene regulation, intestinal homeostasis, Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Background & Aims: The intestinal epithelium interfaces with a diverse milieu of luminal contents while maintaining robust digestive and barrier functions. Facultative intestinal stem cells are cells that survive tissue injury and divide to re-establish the epithelium. Prior studies have shown autophagic state as functional marker of facultative intestinal stem cells, but regulatory mechanisms are not known. The current study evaluated a post-transcriptional regulation of autophagy as an important factor for facultative stem cell state and tissue regeneration. Methods: We evaluated stem cell composition, autophagic vesicle content, organoid formation, and in vivo regeneration in mice with intestinal epithelial deletion of the RNA binding protein IGF2 messenger RNA binding protein 1 (IMP1). The contribution of autophagy to resulting in vitro and in vivo phenotypes was evaluated via genetic inactivation of Atg7. Molecular analyses of IMP1 modulation of autophagy at the protein and transcript localization levels were performed using IMP1 mutant studies and single-molecule fluorescent in situ hybridization. Results: Epithelial Imp1 deletion reduced leucine rich repeat containing G protein coupled receptor 5 cell frequency but enhanced both organoid formation efficiency and in vivo regeneration after irradiation. We confirmed prior studies showing increased autophagy with IMP1 deletion. Deletion of Atg7 reversed the enhanced regeneration observed with Imp1 deletion. IMP1 deletion or mutation of IMP1 phosphorylation sites enhanced expression of essential autophagy protein microtubule-associated protein 1 light chain 3β. Furthermore, immunofluorescence imaging coupled with single-molecule fluorescent in situ hybridization showed IMP1 colocalization with MAP1LC3B transcripts at homeostasis. Stress induction led to decreased colocalization. Conclusions: Depletion of IMP1 enhances autophagy, which promotes intestinal regeneration via expansion of facultative intestinal stem cells.

Published
2024
Full Text
View/download PDF

3. Association between Diabetes and Exfoliation Syndrome

Author

Megan Yu, BS, Hannah H. Hwang, BS, Janey L. Wiggs, MD, PhD, Louis R. Pasquale, MD, and Jae H. Kang, ScD

Subjects
Diabetes, Exfoliation, Glaucoma, Meta-analysis, Systematic review, Ophthalmology, RE1-994
Abstract

Topic: This systematic review and meta-analysis summarizes the existing evidence for the association of diabetes mellitus (DM) and exfoliation syndrome (XFS). Clinical Relevance: Understanding and quantifying these associations may aid clinical guidelines or treatment strategies and shed light on disease pathogenesis. The role of DM in determining XFS risk may also be of interest from an individual or public health perspective. Methods: The study protocol was preregistered on the International Prospective Register of Systematic Reviews with registration number CRD42023429771. We systematically searched PubMed and Embase from inception to June 15, 2023. Screening and full-text review were conducted by 2 independent reviewers. All observational studies reporting an age-adjusted odds ratio (OR) and 95% confidence interval (CI) for the association between DM and XFS among adults were included. Quantitative synthesis involved a random-effects meta-analysis using the DerSimonian-Laird method to generate a pooled OR. Risk of bias was evaluated using the Newcastle-Ottawa Scale. Results: Fourteen studies (9 cross-sectional and 5 case-control) comprising 47 853 participants were included in the systematic review and meta-analysis. Random-effects meta-analysis indicated no overall association between DM and XFS (OR 0.94; 95% CI, 0.73–1.21; I2 = 68.5%). However, subgroup analysis revealed a significant inverse association among individuals ≥ 65 years (OR 0.71; 95% CI, 0.54–0.93) versus individuals < 65 years (OR 1.22; 95% CI, 0.80–1.87; Peffect modification = 0.04). The relation between DM and XFS was also inverse in case-control studies (OR 0.75; 95% CI, 0.58–0.97) but was nonsignificant in cross-sectional studies (OR 1.17; 95% CI, 0.83–1.66; Peffect modification = 0.04). Overall risk of bias was low, with tests for publication bias showing P ≥ 0.06. Conclusion: This meta-analysis suggests no association between DM and XFS overall, with possible inverse associations of DM with XFS in older populations. However, given the substantial heterogeneity and borderline significance for publication bias, these findings should be interpreted with caution. Our results give insight into the unique etiology and clinical relevance of XFS while proposing the need for larger longitudinal and genetic biomarker studies. Financial Disclosure(s): Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Published
2024
Full Text
View/download PDF

4. Generative Artificial Intelligence Through ChatGPT and Other Large Language Models in Ophthalmology

Author

Ting Fang Tan, MBBS, Arun James Thirunavukarasu, BA MB, BChir (Cantab), J. Peter Campbell, MD, MPH, Pearse A. Keane, MD, FRCOphth, Louis R. Pasquale, MD, FARVO, Michael D. Abramoff, MD, PhD, Jayashree Kalpathy-Cramer, PhD, Flora Lum, MD, Judy E. Kim, MD, FARVO, Sally L. Baxter, MD, MSc, and Daniel Shu Wei Ting, MD, PhD

Subjects
Artificial intelligence, Chatbots, ChatGPT, Large language models, Ophthalmology, RE1-994
Abstract

The rapid progress of large language models (LLMs) driving generative artificial intelligence applications heralds the potential of opportunities in health care. We conducted a review up to April 2023 on Google Scholar, Embase, MEDLINE, and Scopus using the following terms: “large language models,” “generative artificial intelligence,” “ophthalmology,” “ChatGPT,” and “eye,” based on relevance to this review. From a clinical viewpoint specific to ophthalmologists, we explore from the different stakeholders’ perspectives—including patients, physicians, and policymakers—the potential LLM applications in education, research, and clinical domains specific to ophthalmology. We also highlight the foreseeable challenges of LLM implementation into clinical practice, including the concerns of accuracy, interpretability, perpetuating bias, and data security. As LLMs continue to mature, it is essential for stakeholders to jointly establish standards for best practices to safeguard patient safety. Financial Disclosure(s): Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Published
2023
Full Text
View/download PDF

5. Lipid droplets modulate proteostasis, SQST-1/SQSTM1 dynamics, and lifespan in C. elegans

Author

Anita V. Kumar, Joslyn Mills, Wesley M. Parker, Joshua A. Leitão, Diego I. Rodriguez, Sandrine E. Daigle, Celeste Ng, Rishi Patel, Joseph L. Aguilera, Joseph R. Johnson, Shi Quan Wong, and Louis R. Lapierre

Subjects
Biological sciences, Biochemistry, Science
Abstract

Summary: In several long-lived Caenorhabditis elegans strains, such as insulin/IGF-1 receptor daf-2 mutants, enhanced proteostatic mechanisms are accompanied by elevated intestinal lipid stores, but their role in longevity is unclear. Here, while determining the regulatory network of the selective autophagy receptor SQST-1/SQSTM1, we uncovered an important role for lipid droplets in proteostasis and longevity. Using genome-wide RNAi screening, we identified several SQST-1 modulators, including lipid droplets-associated and aggregation-prone proteins. Expansion of intestinal lipid droplets by silencing the conserved cytosolic triacylglycerol lipase gene atgl-1/ATGL enhanced autophagy, and extended lifespan. Notably, a substantial amount of ubiquitinated proteins were found on lipid droplets. Reducing lipid droplet levels exacerbated the proteostatic collapse when autophagy or proteasome function was compromised, and significantly reduced the lifespan of long-lived daf-2 animals. Altogether, our study uncovered a key role for lipid droplets in C. elegans as a proteostatic mediator that modulates ubiquitinated protein accumulation, facilitates autophagy, and promotes longevity.

Published
2023
Full Text
View/download PDF

6. Association between Heat Shock Protein-Specific T-Cell Counts and Retinal Nerve Fiber Layer Thickness in Patients with Primary Open-Angle Glaucoma

Author

Chhavi Saini, MD, Shuhong Jiang, MD, PhD, Julia Devlin, BS, Li Pan, PhD, Yizhen Tang, MD, PhD, Jing Tang, MD, PhD, Jessica A. Sun, BA, Maltish M. Lorenzo, MD, Qingyi Wang, MD, Louis R. Pasquale, MD, Kin-Sang Cho, PhD, Dong Feng Chen, MD, PhD, and Lucy Q. Shen, MD

Subjects
Glaucoma, Heat shock protein, Primary open-angle glaucoma, T-cell count, Retinal nerve fiber layer thickness, Ophthalmology, RE1-994
Abstract

Objective: Previous laboratory reports implicate heat shock protein (HSP)–specific T-cell responses in glaucoma pathogenesis; here, we aimed to provide direct clinical evidence by correlating systemic HSP-specific T-cell levels with glaucoma severity in patients with primary open-angle glaucoma (POAG). Design: Cross-sectional case-control study. Subjects: Thirty-two adult patients with POAG and 38 controls underwent blood draw and optic nerve imaging. Methods: Peripheral blood monocytes (PBMC) were stimulated in culture with HSP27, α-crystallin, a member of the small HSP family, or HSP60. Both interferon-γ (IFN-γ)+ CD4+ T helper type 1 cells (Th1) and transforming growth factor-β1 (TGF-β1)+ CD4+ regulatory T cells (Treg) were quantified by flow cytometry and presented as a percentage of total PBMC counts. Relevant cytokines were measured using enzyme-linked immunosorbent assays. Retinal nerve fiber layer thickness (RNFLT) was measured with OCT. Pearson’s correlation (r) was used to assess correlations. Main Outcome Measures: Correlations of HSP-specific T-cell counts, and serum levels of corresponding cytokine levels with RNFLT. Results: Patients with POAG (visual field mean deviation, –4.7 ± 4.0 dB) and controls were similar in age, gender, and body mass index. Moreover, 46.9% of POAG and 60.0% of control subjects had prior cataract surgery (P = 0.48). Although no significant difference in total nonstimulated CD4+ Th1 or Treg cells was detected, patients with POAG exhibited significantly higher frequencies of Th1 cells specific for HSP27, α-crystallin, or HSP60 than controls (7.3 ± 7.9% vs. 2.6 ± 2.0%, P = 0.004; 5.8 ± 2.7% vs. 1.8 ± 1.3%, P < 0.001; 13.2 ± 13.3 vs. 4.3 ± 5.2, P = 0.01; respectively), but similar Treg specific for the same HSPs compared with controls (P ≥ 0.10 for all). Concordantly, the serum levels of IFN-γ were higher in POAG than in controls (36.2 ± 12.1 pg/ml vs. 10.0 ± 4.3 pg/ml; P < 0.001), but TGF-β1 levels did not differ. Average RNFLT of both eyes negatively correlated with HSP27– and α-crystallin-specific Th1 cell counts, and IFN-γ levels in all subjects after adjusting for age (partial correlation coefficient r = –0.31, P = 0.03; r = –0.52, P = 0.002; r = –0.72, P < 0.001, respectively). Conclusions: Higher levels of HSP-specific Th1 cells are associated with thinner RNFLT in patients with POAG and control subjects. The significant inverse relationship between systemic HSP-specific Th1 cell count and RNFLT supports the role of these T cells in glaucomatous neurodegeneration. Financial Disclosure(s): Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Published
2023
Full Text
View/download PDF

7. Disentangling the genetic overlap and causal relationships between primary open-angle glaucoma, brain morphology and four major neurodegenerative disordersResearch in context

Author

Santiago Diaz-Torres, Weixiong He, Jackson Thorp, Sahba Seddighi, Sean Mullany, Christopher J. Hammond, Pirro G. Hysi, Louis R. Pasquale, Anthony P. Khawaja, Alex W. Hewitt, Jamie E. Craig, David A. Mackey, Janey L. Wiggs, Cornelia van Duijn, Michelle K. Lupton, Jue-Sheng Ong, Stuart MacGregor, and Puya Gharahkhani

Subjects
Glaucoma, Brain morphology, Genetics, Neurodegenerative disorders, Dementia, MAPT, Medicine, Medicine (General), R5-920
Abstract

Summary: Background: Primary open-angle glaucoma (POAG) is an optic neuropathy characterized by progressive degeneration of the optic nerve that leads to irreversible visual impairment. Multiple epidemiological studies suggest an association between POAG and major neurodegenerative disorders (Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal dementia, and Parkinson's disease). However, the nature of the overlap between neurodegenerative disorders, brain morphology and glaucoma remains inconclusive. Method: In this study, we performed a comprehensive assessment of the genetic and causal relationship between POAG and neurodegenerative disorders, leveraging genome-wide association data from studies of magnetic resonance imaging of the brain, POAG, and four major neurodegenerative disorders. Findings: This study found a genetic overlap and causal relationship between POAG and its related phenotypes (i.e., intraocular pressure and optic nerve morphology traits) and brain morphology in 19 regions. We also identified 11 loci with a significant local genetic correlation and a high probability of sharing the same causal variant between neurodegenerative disorders and POAG or its related phenotypes. Of interest, a region on chromosome 17 corresponding to MAPT, a well-known risk locus for Alzheimer's and Parkinson's disease, was shared between POAG, optic nerve degeneration traits, and Alzheimer's and Parkinson's diseases. Despite these local genetic overlaps, we did not identify strong evidence of a causal association between these neurodegenerative disorders and glaucoma. Interpretation: Our findings indicate a distinctive and likely independent neurodegenerative process for POAG involving several brain regions although several POAG or optic nerve degeneration risk loci are shared with neurodegenerative disorders, consistent with a pleiotropic effect rather than a causal relationship between these traits. Funding: PG was supported by an NHMRC Investigator Grant (#1173390), SM by an NHMRC Senior Research Fellowship and an NHMRC Program Grant (APP1150144), DM by an NHMRC Fellowship, LP is funded by the NEI EY015473 and EY032559 grants, SS is supported by an NIH-Oxford Cambridge Fellowship and NIH T32 grant (GM136577), APK is supported by a UK Research and Innovation Future Leaders Fellowship, an Alcon Research Institute Young Investigator Award and a Lister Institute for Preventive Medicine Award.

Published
2023
Full Text
View/download PDF

8. The poly(C)-binding protein Pcbp2 is essential for CD4+ T cell activation and proliferation

Author

Massimo Martinelli, Gabrielle Aguilar, David S.M. Lee, Andrew Kromer, Nhu Nguyen, Benjamin J. Wilkins, Tatiana Akimova, Ulf H. Beier, and Louis R. Ghanem

Subjects
Molecular biology, Immunology, Cell biology, Science
Abstract

Summary: The RNA-binding protein Pcbp2 is widely expressed in the innate and adaptive immune systems and is essential for mouse development. To determine whether Pcbp2 is required for CD4+ T cell development and function, we derived mice with conditional Pcbp2 deletion in CD4+ T cells and assessed their overall phenotype and proliferative responses to activating stimuli. We found that Pcbp2 is essential for T conventional cell (Tconv) proliferation, working through regulation of co-stimulatory signaling. Pcbp2 deficiency in the CD4+ lineage did not impact Treg abundance in vivo or function in vitro. In addition, our data demonstrate a clear association between Pcbp2 control of Runx1 exon 6 splicing in CD4+ T cells and a specific role for Pcbp2 in the maintenance of peripheral CD4+ lymphocyte population size. Last, we show that Pcbp2 function is required for optimal in vivo Tconv cell activation in a T cell adoptive transfer colitis model system.

Published
2023
Full Text
View/download PDF

9. The diagnostic challenge of aortic intimal sarcomas, from vasculitis-like syndrome to mesenteric ischemia: Report of two cases and individual patient data literature review

Author

Mohammed I. Messihad, Anass Benomar, Nassim-Albert Merrachi, Louis R. Bégin, Guillaume Febrer, and Michel Philie

Subjects
Aortic intimal sarcoma, Angiosarcoma, Delayed diagnosis, Vasculitis, Mesenteric ischemia, Diseases of the circulatory (Cardiovascular) system, RC666-701, Surgery, RD1-811
Abstract

Primary aortic intimal sarcomas (AIS) are rare but often fatal. They are highly malignant and often recur despite aggressive therapy. We report two cases of AIS presenting with nonspecific clinical symptomatology leading to initial delayed diagnosis and poor prognosis. The first patient, a 79-year-old female, presented with vasculitis-like symptoms and tumoral peripheral emboli, while the second, a 63-year-old male, with new-onset hypertension and mesenteric ischemia. Both recurred after radical resection and died 16 months after surgery. 140 additional cases were identified in the literature, and their demographic and clinical characteristics individually reviewed, further reaffirming the wide clinical spectrum dilemma leading to AIS poor outcome. Radical resection seemed beneficial and associated with increased patient survival. Extending the initial aortic resection should be favored over choosing the smallest graft to avoid early recurrence.

Published
2022
Full Text
View/download PDF

10. Assessing Surface Shapes of the Optic Nerve Head and Peripapillary Retinal Nerve Fiber Layer in Glaucoma with Artificial Intelligence

Author

Chhavi Saini, MD, Lucy Q. Shen, MD, Louis R. Pasquale, MD, Michael V. Boland, MD, PhD, David S. Friedman, MD, PhD, Nazlee Zebardast, MD, MSc, Mojtaba Fazli, PhD, Yangjiani Li, MD, Mohammad Eslami, PhD, Tobias Elze, PhD, and Mengyu Wang, PhD

Subjects
Glaucoma, OCT, Structure–function relationship, Unsupervised artificial intelligence, Visual field loss rate prediction, Ophthalmology, RE1-994
Abstract

Purpose: To assess 3-dimensional surface shape patterns of the optic nerve head (ONH) and peripapillary retinal nerve fiber layer (RNFL) in glaucoma with unsupervised artificial intelligence (AI). Design: Retrospective study. Participants: Patients with OCT scans obtained between 2016 and 2020 from Massachusetts Eye and Ear. Methods: The first reliable Cirrus (Carl Zeiss Meditec, Inc) ONH OCT scans from each eye were selected. The ONH and RNFL surface shape was represented by the vertical positions of the inner limiting membrane (ILM) relative to the lowest ILM vertical position in each eye. Nonnegative matrix factorization was applied to determine the ONH and RNFL surface shape patterns, which then were correlated with OCT and visual field (VF) loss parameters and subsequent VF loss rate. We tested whether using ONH and RNFL surface shape patterns improved the prediction accuracy for associated VF loss and subsequent VF loss rates measured by adjusted r2 and Bayesian information criterion (BIC) difference compared with using established OCT parameters alone. Main Outcome Measures: Optic nerve head and RNFL surface shape patterns and prediction of the associated VF loss and subsequent VF loss rates. Results: We determined 14 ONH and RNFL surface shape patterns using 9854 OCT scans from 5912 participants. Worse mean deviation (MD) was most correlated (r = 0.29 and r = 0.24, Pearson correlation; each P < 0.001) with lower coefficients of patterns 10 and 12 representing inferior and superior para-ONH nerve thinning, respectively. Worse MD was associated most with higher coefficients of patterns 5, 4, and 9 (r = –0.16, r = –0.13, and r = –0.13, respectively), representing higher peripheral ONH and RNFL surfaces. In addition to established ONH summary parameters and 12–clock-hour RNFL thickness, using ONH and RNFL surface patterns improved (BIC decrease: 182, 144, and 101, respectively; BIC decrease ≥ 6; strong model improvement) the prediction of accompanied MD (r2 from 0.32 to 0.37), superior (r2 from 0.27 to 0.31), and inferior (r2 from 0.17 to 0.21) paracentral loss and improved (BIC decrease: 8 and 8, respectively) the prediction of subsequent VF MD loss rates (r2 from 0 to 0.13) and inferior paracentral loss rates (r2 from 0 to 0.16). Conclusions: The ONH and RNFL surface shape patterns quantified by unsupervised AI techniques improved the structure–function relationship and subsequent VF loss rate prediction.

Published
2022
Full Text
View/download PDF

11. Variant-to-Gene-Mapping Analyses Reveal a Role for the Hypothalamus in Genetic Susceptibility to Inflammatory Bowel DiseaseSummary

Author

Chiara Lasconi, Matthew C. Pahl, Diana L. Cousminer, Claudia A. Doege, Alessandra Chesi, Kenyaita M. Hodge, Michelle E. Leonard, Sumei Lu, Matthew E. Johnson, Chun Su, Reza K. Hammond, James A. Pippin, Natalie A. Terry, Louis R. Ghanem, Rudolph L. Leibel, Andrew D. Wells, and Struan F.A. Grant

Subjects
HPA, Stress, Colonoids, hESC, Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Background & Aims: Inflammatory bowel disease (IBD) is a polygenic disorder characterized principally by dysregulated inflammation impacting the gastrointestinal tract. However, there also is increasing evidence for a clinical association with stress and depression. Given the role of the hypothalamus in stress responses and in the pathogenesis of depression, useful insights could be gleaned from understanding its genetic role in IBD. Methods: We conducted genetic correlation analyses on publicly available genome-wide association study summary statistics for depression and IBD traits to identify genetic commonalities. We used partitioned linkage disequilibrium score regression, leveraging our ATAC sequencing and promoter-focused Capture C data, to measure enrichment of IBD single-nucleotide polymorphisms within promoter-interacting open chromatin regions of human embryonic stem cell-derived hypothalamic-like neurons (HNs). Using the same data sets, we performed variant-to-gene mapping to implicate putative IBD effector genes in HNs. To contrast these results, we similarly analyzed 3-dimensional genomic data generated in epithelium-derived colonoids from rectal biopsy specimens from donors without pathologic disease noted at the time of colonoscopy. Finally, we conducted enrichment pathway analyses on the implicated genes to identify putative IBD dysfunctional pathways. Results: We found significant genetic correlations (rg) of 0.122 with an adjusted P (Padj) = 1.4 × 10-4 for IBD: rg = 0.122; Padj = 2.5 × 10-3 for ulcerative colitis and genetic correlation (rg) = 0.094; Padj = 2.5 × 10-3 for Crohn’s disease, and significant approximately 4-fold (P = .005) and approximately 7-fold (P = .03) enrichment of IBD single-nucleotide polymorphisms in HNs and colonoids, respectively. We implicated 25 associated genes in HNs, among which CREM, CNTF, and RHOA encode key regulators of stress. Seven genes also additionally were implicated in the colonoids. We observed an overall enrichment for immune and hormonal signaling pathways, and a colonoid-specific enrichment for microbiota-relevant terms. Conclusions: Our results suggest that the hypothalamus warrants further study in the context of IBD pathogenesis.

Published
2021
Full Text
View/download PDF

12. First report of the mcr-1 colistin resistance gene identified in two Escherichia coli isolates from clinical samples, Philippines, 2018

Author

John Mark S. Velasco, Ma. Theresa G. Valderama, Katie R. Margulieux, Paula Corazon S. Diones, Angeli Mae B. Reyes, Susie G. Leonardia, Cynthia P. Liao, Domingo A. Chua, Jr, Fatima Claire S. Navarro, Sirigade Ruekit, Stefan Fernandez, Louis R. Macareo, John M. Crawford, and Brett E. Swierczewski

Subjects
mcr-1, Colistin, Antimicrobial resistance, Multidrug resistance, Microbiology, QR1-502
Abstract

Objectives: The first report of a plasmid-borne colistin resistance gene (mcr-1) detected in an Escherichia coli isolate from China heralded the emergence of pandrug-resistant bacteria. Since then, the mcr-1 gene has been detected worldwide, but to date it has not been reported in the Philippines. Methods: In this study, 123 antimicrobial-resistant isolates collected from January–June 2018 from patients admitted to a tertiary hospital in Manila, Philippines, were characterised. Biochemical identification and antimicrobial susceptibility testing were performed using a BD Phoenix™ M50 system with NMIC/ID-95 panel. Conventional PCR was performed to detect the genes mcr-1 to mcr-5, and short- and long-read whole-genome sequencing was performed. Results: Two mcr-1-positive E. coli clinical isolates from separate patients harboured mcr-1 on an IncI2 plasmid. One isolate was shown to carry 12 antimicrobial resistance genes (ARGs) in addition to mcr-1, including the extended-spectrum β-lactamase blaCTX-M-55, whilst the other E. coli isolate carried 6 ARGs in addition to mcr-1. Conclusion: Both patients had no prior colistin treatment recorded in their medical history and no travel history outside of the country within the past 6 months from the date of hospital admission, indicating local transmission and acquisition of the colistin-resistant strain from either community or hospital settings within the Philippines. This report should serve as a signal to local public-health officials of the need to intensify surveillance efforts and to increase vigilance and implementation of antimicrobial stewardship programmes to contain and slow the spread of antimicrobial resistance.

Published
2020
Full Text
View/download PDF

13. Increased bioavailability of cyclic guanylate monophosphate prevents retinal ganglion cell degeneration

Author

Lauren K. Wareham, Ana C. Dordea, Grigorij Schleifer, Vincent Yao, Annabelle Batten, Fei Fei, Joseph Mertz, Meredith Gregory-Ksander, Louis R. Pasquale, Emmanuel S. Buys, and Rebecca M. Sappington

Subjects
cGMP, Retinal ganglion cell, Glaucoma, Nitric oxide, PDE5, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

The nitric oxide – guanylyl cyclase-1 – cyclic guanylate monophosphate (NO-GC-1–cGMP) pathway has emerged as a potential pathogenic mechanism for glaucoma, a common intraocular pressure (IOP)-related optic neuropathy characterized by the degeneration of retinal ganglion cells (RGCs) and their axons in the optic nerve. NO activates GC-1 to increase cGMP levels, which are lowered by cGMP-specific phosphodiesterase (PDE) activity. This pathway appears to play a role in both the regulation of IOP, where reduced cGMP levels in mice leads to elevated IOP and subsequent RGC degeneration. Here, we investigated whether potentiation of cGMP signaling could protect RGCs from glaucomatous degeneration. We administered the PDE5 inhibitor tadalafil orally (10 mg/kg/day) in murine models of two forms of glaucoma – primary open angle glaucoma (POAG; GC-1−/− mice) and primary angle-closure glaucoma (PACG; Microbead Occlusion Model) - and measured RGC viability at both the soma and axon level. To determine the direct effect of increased cGMP on RGCs in vitro, we treated axotomized whole retina and primary RGC cultures with the cGMP analogue 8-Br-cGMP. Tadalafil treatment increased plasma cGMP levels in both models, but did not alter IOP or mean arterial pressure. Nonetheless, tadalafil treatment prevented degeneration of RGC soma and axons in both disease models. Treatment of whole, axotomized retina and primary RGC cultures with 8-Br-cGMP markedly attenuated both necrotic and apoptotic cell death pathways in RGCs. Our findings suggest that enhancement of the NO-GC-1-cGMP pathway protects the RGC body and axon in murine models of POAG and PACG, and that enhanced signaling through this pathway may serve as a novel glaucoma treatment, acting independently of IOP.

Published
2019
Full Text
View/download PDF

14. Lactate Limits T Cell Proliferation via the NAD(H) Redox State

Author

William J. Quinn, III, Jing Jiao, Tara TeSlaa, Jason Stadanlick, Zhonglin Wang, Liqing Wang, Tatiana Akimova, Alessia Angelin, Patrick M. Schäfer, Michelle D. Cully, Caroline Perry, Piotr K. Kopinski, Lili Guo, Ian A. Blair, Louis R. Ghanem, Michael S. Leibowitz, Wayne W. Hancock, Edmund K. Moon, Matthew H. Levine, Evgeniy B. Eruslanov, Douglas C. Wallace, Joseph A. Baur, and Ulf H. Beier

Subjects
T cell metabolism, glycolysis, immunometabolism, nicotinamide adenine dinucleotide, lactate metabolism, 3-phosphoglycerate, Biology (General), QH301-705.5
Abstract

Summary: Immune cell function is influenced by metabolic conditions. Low-glucose, high-lactate environments, such as the placenta, gastrointestinal tract, and the tumor microenvironment, are immunosuppressive, especially for glycolysis-dependent effector T cells. We report that nicotinamide adenine dinucleotide (NAD+), which is reduced to NADH by lactate dehydrogenase in lactate-rich conditions, is a key point of metabolic control in T cells. Reduced NADH is not available for NAD+-dependent enzymatic reactions involving glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and 3-phosphoglycerate dehydrogenase (PGDH). We show that increased lactate leads to a block at GAPDH and PGDH, leading to the depletion of post-GAPDH glycolytic intermediates, as well as the 3-phosphoglycerate derivative serine that is known to be important for T cell proliferation. Supplementing serine rescues the ability of T cells to proliferate in the presence of lactate-induced reductive stress. Directly targeting the redox state may be a useful approach for developing novel immunotherapies in cancer and therapeutic immunosuppression.

Published
2020
Full Text
View/download PDF

15. Primary renal Ewing Sarcoma masquerading as Wilms in an adolescent female

Author

Zachary M. Kozel, Jennifer E. Reifsnyder, Luke Griffiths, Jordan S. Gitlin, and Louis R. Kavoussi

Subjects
Pediatric, Renal cell carcinoma, Minimally invasive, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Primary renal Ewing's sarcoma (ES) of the kidney represents a rare oncologic entity belonging to the collection of small round cell tumors, which typically feature osseous presentations. Renal ES is an aggressive disease entity with high metastatic potential, either at time of presentation or following initial extirpative therapy. Herein, we report the case of a 14-year-old female who initially presented with intermittent gross painless hematuria and a large left renal mass identified on ultrasound and confirmed on follow up MRI. Following partial nephrectomy (PN), patient was diagnosed with primary renal ES and subsequently underwent completion nephrectomy and chemotherapy.

Published
2020
Full Text
View/download PDF

16. Persistent cough as a paraneoplastic presenting symptom in six patients with renal cell carcinoma

Author

Vinay R. Patel, Bradley A. Morganstern, and Louis R. Kavoussi

Subjects
Renal cell carcinoma, Paraneoplastic syndrome, Cough, Mass effect, Cytokines, Renin-angiotensin system, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Objective: With today's modern imaging modalities, patients diagnosed with renal cell carcinoma (RCC) rarely present symptomatically. In some cases, however, they can develop paraneoplastic syndromes with associated symptoms. To date, only three cases of RCC presenting with chronic dry cough have been reported. We describe six patients who presented with cough that improved following radical nephrectomy. Methods: A retrospective review of patients undergoing partial or radical nephrectomy for renal masses between January 2015 and March 2016 was performed, and patients presenting with a cough were examined. Results: Six patients presented with chronic cough and were discovered to have a large renal mass. Postoperative spontaneous resolution of cough was noted in all but one patient, in whom coughing was reduced and limited to the mornings. Cough duration ranged from 3 months to just over a year. All patients were treated with radical nephrectomy, which was cytoreductive in four patients. Average tumor size was 10.9 cm (SD = 2.2 cm). Five of the tumors had clear cell pathology, and every tumor was Fuhrman grade IV, unifocal, and demonstrated necrosis. Sarcomatoid features were reported in four of the tumors. Conclusion: Our study presents the largest series of patients with RCC who presented with a chronic cough that was significantly improved following radical nephrectomy. We believe the cause of cough is multifactorial and further investigation is needed to clearly elucidate the etiology.

Published
2017
Full Text
View/download PDF

17. Ureteropelvic Junction Obstruction Secondary to Metastatic Relapse of Breast Cancer

Author

Paras H. Shah, Alex T. Smith, David A. Leavitt, Oksana Yaskiv, and Louis R. Kavoussi

Subjects
Hydronephrosis, Ureteropelvic junction obstruction, Breast cancer metastasis, Diseases of the genitourinary system. Urology, RC870-923
Abstract

We describe the case of a 53-year-old woman with a history of localized breast cancer who presented with flank pain and was found to have new-onset obstruction of the left ureteropelvic junction. Although initially believed to be unrelated to her history of prior malignancy, intraoperative assessment of tissue from the ureteropelvic junction during planned laparoscopic pyeloplasty revealed urothelial infiltration by carcinoma of breast origin.

Published
2016
Full Text
View/download PDF

18. Polytopic vaccination with a live-attenuated dengue vaccine enhances B-cell and T-cell activation, but not neutralizing antibodies

Author

Taweewun Hunsawong, Sineewanlaya Wichit, Thipwipha Phonpakobsin, Yongyuth Poolpanichupatam, Chonticha Klungthong, Napaporn Latthiwongsakorn, Butsaya Thaisomboonsuk, Rawiwan Im-erbsin, In-Kyu Yoon, Damon W. Ellison, Louis R. Macareo, Anon Srikiatkhachorn, Robert V. Gibbons, and Stefan Fernandez

Subjects
Vaccine, Virology, Immunology, Health sciences, Science (General), Q1-390, Social sciences (General), H1-99
Abstract

Dengue, caused by dengue viruses (DENVs), is the most common arboviral disease of humans. Several dengue vaccine candidates are at different stages of clinical development and one has been licensed. Inoculation with live-attenuated DENV constructs is an approach that has been used by vaccine developers. Unfortunately, the simultaneous injection of all four attenuated DENV serotypes (DENV1-4) into a single injection site (monotopic vaccination) has been postulated to result in interference in the replication of some serotypes in favor of others, an important obstacle in obtaining a balanced immune response against all serotypes. Here, we demonstrate the virus replicative and immunostimulatory effects of polytopic monovalent dengue vaccination (PV) in which, each of the four components of the tetravalent vaccine is simultaneously delivered to four different sites versus the more traditional monotopic tetravalent vaccination (MV) in a non-human primate (NHP) model. With the exception of DENV-2, there was no significant difference in detectable viral RNA levels between PV and MV inoculation. Interestingly, longer periods of detection and higher viral RNA levels were seen in the lymph nodes of NHPs inoculated PV compared to MV. Induction of lymph node dendritic cell maturation and of blood T- and B-cell activation showed different kinetics in PV inoculated NHPs compared to MV. The MV inoculated group showed earlier maturation of dendritic cells and activation of B and T cells compared to PV inoculated NHPs. A similar kinetic difference was also observed in the cytokine response: MV induced earlier cytokine responses compared to PV. However, similar levels of DENV neutralizing antibodies were observed in PV and MV NHPs. These findings indicate that cellular immune response after vaccination may be affected by the location of inoculation. Design of vaccine delivery may need to take into account the effects of locations of vaccine delivery of multiples serotype live viral vaccine on the induction of immune response.

Published
2017
Full Text
View/download PDF

20. The AAA-ATPase p97 facilitates degradation of apolipoprotein B by the ubiquitin-proteasome pathways⃞

Author

Eric A. Fisher, Louis R. Lapierre, Robert D. Junkins, and Roger S. McLeod

Subjects
retrotranslocation, endoplasmic reticulum-associated degradation, ERAD, permeabilization, proteolysis, Biochemistry, QD415-436
Abstract

The ATPase associated with various cellular activities (AAA-ATPase) p97 (p97) has been implicated in the retrotranslocation of target proteins for delivery to the cytosolic proteasome during endoplasmic reticulum-associated degradation (ERAD). Apolipoprotein B-100 (apoB-100) is an ERAD substrate in liver cells, including the human hepatoma, HepG2. We studied the potential role of p97 in the ERAD of apoB-100 in HepG2 cells using cell permeabilization, coimmunoprecipitation, and gene silencing. Degradation was abolished when HepG2 cytosol was removed by digitonin permeabilization, and treatment of intact cells with the proteasome inhibitor MG132 caused accumulation of ubiquitinated apoB protein in the cytosol. Cross-linking of intact cells with the thiol-cleavable agent dithiobis(succinimidylpropionate) (DSP), as well as nondenaturing immunoprecipitation, demonstrated an interaction between p97 and intracellular apoB. Small interfering ribonucleic acid (siRNA)-mediated reduction of p97 protein increased the intracellular levels of newly synthesized apoB-100, predominantly because of a decrease in the turnover of newly synthesized apoB-100 protein. However, although the posttranslational degradation of newly synthesized apoB-100 was delayed by p97 knockdown, secretion of apoB-100 was not affected. Knockdown of p97 also impaired the release of apoB-100 and polyubiquitinated apoB into the cytosol. In summary, our results suggest that retrotranslocation and proteasomal degradation of apoB-100 can be dissociated in HepG2 cells, and that the AAA-ATPase p97 is involved in the removal of full-length apoB from the biosynthetic pathway to the cytosolic proteasome.

Published
2008
Full Text
View/download PDF

21. Amino acid sequences within the β1 domain of human apolipoprotein B can mediate rapid intracellular degradation

Author

Louis R. Lapierre, Deborah L. Currie, Zemin Yao, Jianjun Wang, and Roger S. McLeod

Subjects
endoplasmic reticulum-associated degradation, proteasome, translocation, Biochemistry, QD415-436
Abstract

Apolipoprotein B (apoB)-48 contains a region termed the β1 domain that is predicted to be composed of extensive amphipathic β-strands. Analysis of truncated apoB variants revealed that sequences between the carboxyl termini of apoB-37 and apoB-42 governed the secretion efficiency and intracellular stability of apoB. Although apoB-37, apoB-34, and apoB-29 were stable and secreted efficiently, apoB-42 and apoB-100 were secreted poorly and were degraded by an acetyl-leucyl-leucyl-norleucinal (ALLN)-sensitive pathway. Amino acid sequence analysis suggested that a segment between the carboxyl termini of apoB-38 and apoB-42 was 63% homologous to fatty acid binding proteins (FABPs), which contain orthogonal β-sheets. To test the hypothesis that sequences from the β1 domain are involved in apoB degradation, fusion proteins were created that contained apoB-29 linked to fragments derived from the β1 domain of apoB or to liver FABP. Fusion proteins containing the β1 domain segments apoB-34–42 or apoB-37–42 were degraded rapidly, whereas other fusion proteins were stable and secreted efficiently. Degradation was ALLN-sensitive, and the apoB-34–42 segment increased the association of the apoB protein with the cytosolic surface of the microsomal membrane.Our data suggest that the presence of specific sequences in the β1 domain of human apoB increases degradation by promoting the cytosolic exposure of the protein, although not all regions of the β1 domain are functionally equivalent.

Published
2004
Full Text
View/download PDF

22. Strange Vibes – Novel Presentation of Prostatitis

Author

Wayland J. Wu, Jessica E. Kreshover, Robert Moldwin, and Louis R. Kavoussi

Subjects
CP/CPPS, Prostatitis, Buzz, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) has significant variability in its presentation. In this study, we present 2 novel cases of prostatitis in which “buzz” is described as the primary pain symptom. These cases describe patients with the primary complaint of “cell phone–like buzzing” within the perineum, with accompanying urinary symptoms consistent with prostatitis. CP/CPPS is a multifactorial disease within which psychological, inflammatory, neurologic, and neuromuscular etiologies are at play. As in other disease descriptions, a buzzing sensation represents the interaction of multiple pathways that have significant overlay with CP/CPPS. As such, we believe buzzing might represent a new symptom of CP/CPPS.

Published
2014
Full Text
View/download PDF

23. Contributors

Author

Abdulai-Saiku, Samira, primary, Appel, Stanley H., additional, Arnold, Arthur P., additional, Arnold, Lisa M., additional, Arnold, Robert M., additional, Bacha, Alexa, additional, Backonja, Miroslav “Misha”, additional, Bailey, Zinzi D., additional, Bateman, Lucinda, additional, Beers, David R., additional, Berti, Anna, additional, Bhatnagar, Mamta, additional, Binder, Devin K., additional, Boido, Marina, additional, Boldrini, Maura, additional, Borsook, David, additional, Breakefield, Xandra O., additional, Brown, Robert H., additional, Burstein, Rami, additional, Butelman, Eduardo R., additional, Caplan, Louis R., additional, Chen, S., additional, Chesselet, Marie-Françoise, additional, Clemens, Stefan, additional, Clemens, Paula R., additional, Coyle, Joseph T., additional, DeWitt, John C., additional, Dubal, Dena B., additional, Dubljević, Veljko, additional, Feldman, Eva L., additional, Fischer, Beth A., additional, Flux, M.C., additional, Fortin, J.S., additional, Frasca, Angelisa, additional, Garbarini, Francesca, additional, Gasser, Thomas, additional, Gillespie, Charles F., additional, Gold, Michael S., additional, Gold, Stefan M., additional, Hagerman, Randi, additional, Hamel, Regan, additional, Haney, Craig, additional, Harris, James C., additional, Hassani, Sara, additional, Haughey, Norman J., additional, Heng, Vibol, additional, Horn, J., additional, Ionescu, Rosana-Bristena, additional, Iorio, Raffaele, additional, Irwin, David J., additional, Kaminski, Henry J., additional, Khammash, Dalia, additional, Khurana, Vikram, additional, Kilstrup-Nielsen, Charlotte, additional, Kim, Bhumsoo, additional, Kim, Boram, additional, Klein, Marieke, additional, Koen, Nastassja, additional, Konopaske, Glenn T., additional, Korecka, Joanna A., additional, Kornum, Birgitte Rahbek, additional, Kreek, Mary Jeanne, additional, Kristensson, Krister, additional, Krzak, Grzegorz, additional, Kusner, Linda L., additional, Landsberger, Nicoletta, additional, Lee, Edward B., additional, Li, Tong, additional, Liberski, Paweł P., additional, Lochner, Christine, additional, Lowry, Christopher A., additional, Mann, J. John, additional, Marincowitz, Clara, additional, Mayer, E.A., additional, Mayer, E.D., additional, McCall, Iris Coates, additional, McCullough, Louise D., additional, Meaney, Michael J., additional, Melo de Gusmao, Claudio, additional, Menesgere, Abhishek L., additional, Mignot, Emmanuel, additional, Mobley, William C., additional, Montalvo, Mayra, additional, Moreland-Capuia, Alisha R., additional, Neppi-Modona, Marco, additional, Nicaise, Alexandra M., additional, Nishi, Rae, additional, O'Toole, Orna, additional, Overk, Cassia, additional, Ozelius, Laurie, additional, Parsons, Matthew P., additional, Penticoff, H.B., additional, Peruzzotti-Jametti, Luca, additional, Peters, Owen M., additional, Peterson, Allison, additional, Phan, Jessica M., additional, Pittock, Sean J., additional, Pluchino, Stefano, additional, Polk, Thad A., additional, Puwanant, Araya, additional, Rajagopal, Shreya K., additional, Ravindranath, Vijayalakshmi, additional, Raymond, Lynn A., additional, Reed, Brian, additional, Ressler, Kerry J., additional, Ritchie, Diane L., additional, Rubin, Leah H., additional, Sakowski, Stacey A., additional, Saporta, Mario A., additional, Savonenko, Alena V., additional, Scharfman, Helen E., additional, Shapiro, Bruce K., additional, Sharma, Nutan, additional, Shaw, Cayce K., additional, Shy, Michael E., additional, Sikorska, Beata, additional, Silverman, Ethan J., additional, Simon, Roger P., additional, Simonyan, Kristina, additional, Sims-Robinson, Catrina, additional, Smeyne, Richard Jay, additional, Smith, Clay, additional, Smith, Colin, additional, Srinivasan, Sharan R., additional, Stein, Dan J., additional, Stephen, Christopher D., additional, Subramanian, Indu, additional, Szabo, Edina, additional, Thomas, Alissa A., additional, Tovar-y-Romo, Luis B., additional, Vahabzadeh, Arshya, additional, Vercelli, Alessandro, additional, Viera-Ortiz, Ashley, additional, Wallin, Mitchell T., additional, Werling, Donna M., additional, Wichmann, Thomas, additional, Wiley, Clayton A., additional, Williams, David R., additional, Willis, Cory, additional, Wong, Philip C., additional, Yuferov, Vadim, additional, Zhao, Weihua, additional, Zigmond, Michael J., additional, and Živković, Saša A., additional

Published
2023
Full Text
View/download PDF

26. Contributors

Author

Adams, Harold P., primary, Adeoye, Opeolu, additional, Albers, Gregory W., additional, Alexandrov, Andrei V., additional, Amin-Hanjani, Sepideh, additional, An, Hongyu, additional, Anderson, Craig S., additional, Anrather, Josef, additional, Aparicio, Hugo J., additional, Arai, Ken, additional, Aronowski, Jaroslaw, additional, Atchaneeyasakul, Kunakorn, additional, Audebert, Heinrich, additional, Auer, Roland N., additional, Awad, Issam A., additional, Ay, Hakan, additional, Baltan, Selva, additional, Balu, Ramani, additional, Behbahani, Mandana, additional, Benavente, Oscar R., additional, Bershad, Eric M., additional, Berthaud, Jimmy V., additional, Blackburn, Spiros L., additional, Bonati, Leo H., additional, Bösel, Julian, additional, Bousser, Marie Germaine, additional, Broderick, Joseph P., additional, Brown, Martin M., additional, Brown, Wendy, additional, Brust, John C.M., additional, Bushnell, Cheryl, additional, Canhão, Patrícia, additional, Caplan, Louis R., additional, Carrión-Penagos, Julián, additional, Castellanos, Mar, additional, Caunca, Michelle R., additional, Chabriat, Hugues, additional, Chamorro, Angel, additional, Chen, Jieli, additional, Chen, Jun, additional, Chopp, Michael, additional, Christorforids, Greg, additional, Connolly, E. Sander, additional, Cramer, Steven C., additional, Cucchiara, Brett L., additional, Czap, Alexandra L., additional, Dannenbaum, Mark J., additional, Davis, Patricia H., additional, Dawson, Ted M., additional, Dawson, Valina L., additional, Day, Arthur L., additional, De Silva, T. Michael, additional, de Sousa, Diana Aguiar, additional, Del Brutto, Victor J., additional, del Zoppo, Gregory J., additional, Derdeyn, Colin P., additional, Di Tullio, Marco R., additional, Diener, Hans Christoph, additional, Diringer, Michael N., additional, Dobkin, Bruce H., additional, Dzialowski, Imanuel, additional, Elkind, Mitchell S.V., additional, Elm, Jordan, additional, Feigin, Valery L., additional, Ferro, José Manuel, additional, Field, Thalia S., additional, Fischer, Marlene, additional, Fornage, Myriam, additional, Furie, Karen L., additional, Garcia-Bonilla, Lidia, additional, Giannotta, Steven L., additional, Gobin, Y. Pierre, additional, Goldberg, Mark P., additional, Goldstein, Larry B., additional, Gonzales, Nicole R., additional, Greer, David M., additional, Grotta, James C., additional, Guo, Ruiming, additional, Gutierrez, Jose, additional, Harmel, Peter, additional, Howard, George, additional, Howard, Virginia J., additional, Hwang, Jee-Yeon, additional, Iadecola, Costantino, additional, Jahan, Reza, additional, Jickling, Glen C., additional, Joutel, Anne, additional, Kasner, Scott E., additional, Katan, Mira, additional, Kellner, Christopher P., additional, Khan, Muhib, additional, Kidwell, Chelsea S., additional, Kim, Helen, additional, Kim, Jong S., additional, Kircher, Charles E., additional, Krings, Timo, additional, Krishnamurthi, Rita V., additional, Kurth, Tobias, additional, Lansberg, Maarten G., additional, Levy, Elad I., additional, Liebeskind, David S., additional, Liew, Sook-Lei, additional, Lin, David J., additional, Lisle, Benjamin, additional, Lo, Eng H., additional, Lyden, Patrick D., additional, Maki, Takakuni, additional, Maragkos, Georgios A., additional, Marosfoi, Miklos, additional, McCullough, Louise D., additional, Meckler, Jason M., additional, Meschia, James Frederick, additional, Messé, Steven R., additional, Mocco, J, additional, Mokin, Maxim, additional, Mooney, Michael A., additional, Morgenstern, Lewis B., additional, Moskowitz, Michael A., additional, Mullen, Michael T., additional, Nägel, Steffen, additional, Nedergaard, Maiken, additional, Neira, Justin A., additional, Newman, Sarah, additional, Nicholson, Patrick J., additional, Norrving, Bo, additional, O’Donnell, Martin, additional, Ofengeim, Dimitry, additional, Ogata, Jun, additional, Ogilvy, Christopher S., additional, Orrù, Emanuele, additional, Ortega-Gutiérrez, Santiago, additional, Padrick, Matthew Maximillian, additional, Parsha, Kaushik, additional, Parsons, Mark, additional, Patel, Neil V., additional, Patel, Virendra I., additional, Pawlikowska, Ludmila, additional, Pérez, Adriana, additional, Perez-Pinzon, Miguel A., additional, Picard, John M., additional, Polster, Sean P., additional, Powers, William J., additional, Puetz, Volker, additional, Putaala, Jukka, additional, Rabinovich, Margarita, additional, Ransom, Bruce R., additional, Roa, Jorge A., additional, Rosenberg, Gary A., additional, Rossitto, Christina P., additional, Rundek, Tatjana, additional, Russin, Jonathan J., additional, Sacco, Ralph L., additional, Safouris, Apostolos, additional, Samaniego, Edgar A., additional, Sansing, Lauren H., additional, Satani, Nikunj, additional, Sattenberg, Ronald J., additional, Saver, Jeffrey L., additional, Savitz, Sean I., additional, Schmidt, Christian, additional, Seshadri, Sudha, additional, Sharma, Vijay K., additional, Sharp, Frank R., additional, Sheth, Kevin N., additional, Siddiqi, Omar K., additional, Singhal, Aneesh B., additional, Sobey, Christopher G., additional, Sommer, Clemens J., additional, Spetzler, Robert F., additional, Stapleton, Christopher J., additional, Strickland, Ben A., additional, Su, Hua, additional, Suarez, José I., additional, Takayama, Hiroo, additional, Tarsia, Joseph, additional, Tatlisumak, Turgut, additional, Thomas, Ajith J., additional, Thompson, John W., additional, Tsivgoulis, Georgios, additional, Tournier-Lasserve, Elizabeth, additional, Vidal, Gabriel, additional, Wakhloo, Ajay K., additional, Weksler, Babette B., additional, Willey, Joshua Z., additional, Wintermark, Max, additional, Wong, Lawrence K.S., additional, Xi, Guohua, additional, Xu, Jinchong, additional, Yaghi, Shadi, additional, Yamaguchi, Takenori, additional, Yang, Tuo, additional, Yasaka, Masahiro, additional, Zahuranec, Darin B., additional, Zhang, Feng, additional, Zhang, John H., additional, Zheng, Zhitong, additional, Zukin, R. Suzanne, additional, and Zweifler, Richard M., additional

Published
2022
Full Text
View/download PDF

29. Contributors

Author

Aliucci, John, primary, Aman, Andrew J., additional, Barresi, Michael J.F., additional, Barton, Carrie L., additional, Baumann, Diana P., additional, Braasch, Ingo, additional, Brockerhoff, Susan E., additional, Burgess, Shawn M., additional, Cartner, Samuel C., additional, Castranova, Daniel, additional, Chow, Dawnis M., additional, Cleghorn, Whitney M., additional, Cockington, Jason, additional, Coffin, Allison B., additional, Collymore, Chereen, additional, Cox, James D., additional, Crim, Marcus J., additional, Currie, Peter, additional, D'Abramo, Louis R., additional, Davidson, Alan J., additional, Diep, Cuong Q., additional, Draper, Bruce W., additional, Durboraw, Earle, additional, Eisen, Judith S., additional, Farmer, Susan C., additional, Fetcho, Joseph R., additional, Fischer, Kay, additional, Fowler, L. Adele, additional, Galanternik, Marina Venero, additional, Ganz, Julia, additional, Gorelick, Daniel A., additional, Guillemin, Karen J., additional, Habenicht, Lauren M., additional, Hammer, Hugh S., additional, Hudson, Alexandria M., additional, Jonz, Michael G., additional, Kaslin, Jan, additional, Kent, Michael L., additional, Kimelman, David, additional, Kwon, Ronald Y., additional, Lains, David, additional, Lawrence, Christian, additional, Ledin, Johan, additional, Lee, Carole J., additional, Li, Jianlong, additional, Lieggi, Christine, additional, Löhr, Christiana, additional, McArthur, Kimberly L., additional, McCluskey, Braedan M., additional, Mikeasky, Noriko, additional, Mulrooney, Donna, additional, Murray, Katrina N., additional, Nichols, James T., additional, Pandolfo, Lauren, additional, Parichy, David M., additional, Pathak, Narendra H., additional, Paull, Gregory C., additional, Peterson, Randall T., additional, Phillips, Jennifer B., additional, Postlethwait, John H., additional, Prochaska, Morgan, additional, Raible, David W., additional, Rissone, Alberto, additional, Sanders, Erik, additional, Sanders, George E., additional, Sanders, Justin L., additional, Siegfried, Kellee R., additional, Smith, Natalie L., additional, Spagnoli, Sean T., additional, Stratman, Amber N., additional, Thomas, Eric D., additional, Traver, David, additional, Tulenko, Frank J., additional, Tyler, Charles R., additional, Wallace, Kenneth N., additional, Wang, Chongmin, additional, Watson, Claire J., additional, Watts, Amanda, additional, Watts, Stephen A., additional, Weinstein, Brant M., additional, Westerfield, Monte, additional, Whipps, Christopher M., additional, Wiles, Travis J., additional, Williams, Michael B., additional, Yoder, Jeffrey A., additional, Zhang, Tejia, additional, and Zynda, Jeffrey R., additional

Published
2020
Full Text
View/download PDF

30. Contributors

Author

Samira Abdulai-Saiku, Stanley H. Appel, Arthur P. Arnold, Lisa M. Arnold, Robert M. Arnold, Alexa Bacha, Miroslav 'Misha' Backonja, Zinzi D. Bailey, Lucinda Bateman, David R. Beers, Anna Berti, Mamta Bhatnagar, Devin K. Binder, Marina Boido, Maura Boldrini, David Borsook, Xandra O. Breakefield, Robert H. Brown, Rami Burstein, Eduardo R. Butelman, Louis R. Caplan, S. Chen, Marie-Françoise Chesselet, Stefan Clemens, Paula R. Clemens, Joseph T. Coyle, John C. DeWitt, Dena B. Dubal, Veljko Dubljević, Eva L. Feldman, Beth A. Fischer, M.C. Flux, J.S. Fortin, Angelisa Frasca, Francesca Garbarini, Thomas Gasser, Charles F. Gillespie, Michael S. Gold, Stefan M. Gold, Randi Hagerman, Regan Hamel, Craig Haney, James C. Harris, Sara Hassani, Norman J. Haughey, Vibol Heng, J. Horn, Rosana-Bristena Ionescu, Raffaele Iorio, David J. Irwin, Henry J. Kaminski, Dalia Khammash, Vikram Khurana, Charlotte Kilstrup-Nielsen, Bhumsoo Kim, Boram Kim, Marieke Klein, Nastassja Koen, Glenn T. Konopaske, Joanna A. Korecka, Birgitte Rahbek Kornum, Mary Jeanne Kreek, Krister Kristensson, Grzegorz Krzak, Linda L. Kusner, Nicoletta Landsberger, Edward B. Lee, Tong Li, Paweł P. Liberski, Christine Lochner, Christopher A. Lowry, J. John Mann, Clara Marincowitz, E.A. Mayer, E.D. Mayer, Iris Coates McCall, Louise D. McCullough, Michael J. Meaney, Claudio Melo de Gusmao, Abhishek L. Menesgere, Emmanuel Mignot, William C. Mobley, Mayra Montalvo, Alisha R. Moreland-Capuia, Marco Neppi-Modona, Alexandra M. Nicaise, Rae Nishi, Orna O'Toole, Cassia Overk, Laurie Ozelius, Matthew P. Parsons, H.B. Penticoff, Luca Peruzzotti-Jametti, Owen M. Peters, Allison Peterson, Jessica M. Phan, Sean J. Pittock, Stefano Pluchino, Thad A. Polk, Araya Puwanant, Shreya K. Rajagopal, Vijayalakshmi Ravindranath, Lynn A. Raymond, Brian Reed, Kerry J. Ressler, Diane L. Ritchie, Leah H. Rubin, Stacey A. Sakowski, Mario A. Saporta, Alena V. Savonenko, Helen E. Scharfman, Bruce K. Shapiro, Nutan Sharma, Cayce K. Shaw, Michael E. Shy, Beata Sikorska, Ethan J. Silverman, Roger P. Simon, Kristina Simonyan, Catrina Sims-Robinson, Richard Jay Smeyne, Clay Smith, Colin Smith, Sharan R. Srinivasan, Dan J. Stein, Christopher D. Stephen, Indu Subramanian, Edina Szabo, Alissa A. Thomas, Luis B. Tovar-y-Romo, Arshya Vahabzadeh, Alessandro Vercelli, Ashley Viera-Ortiz, Mitchell T. Wallin, Donna M. Werling, Thomas Wichmann, Clayton A. Wiley, David R. Williams, Cory Willis, Philip C. Wong, Vadim Yuferov, Weihua Zhao, Michael J. Zigmond, and Saša A. Živković

Published
2023

32. The association between serum lipids and intraocular pressure in two large UK cohorts

Author

Madjedi, Kian M., Stuart, Kelsey V., Chua, Sharon Y.L., Luben, Robert N., Warwick, Alasdair, Pasquale, Louis R., Kang, Jae H., Wiggs, Janey L., Lentjes, Marleen A.H., Aschard, Hugues, Sattar, Naveed, Foster, Paul J., and Khawaja, Anthony P.

Abstract

Purpose: \ud Serum lipids are modifiable, routinely collected blood test features associated with cardiovascular health. We examined the association of commonly collected serum lipid measures (total cholesterol [TC], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], and triglycerides) with intraocular pressure (IOP).\ud \ud Design: \ud Cross-sectional study in the UK Biobank and European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohorts.\ud \ud Participants: \ud We included 94 323 participants from the UK Biobank (mean age, 57 years) and 6230 participants from the EPIC-Norfolk (mean age, 68 years) cohorts with data on TC, HDL-C, LDL-C, and triglycerides collected between 2006 and 2009.\ud \ud Methods: \ud Multivariate linear regression adjusting for demographic, lifestyle, anthropometric, medical, and ophthalmic covariables was used to examine the associations of serum lipids with corneal-compensated IOP (IOPcc).\ud \ud Main Outcome Measures: \ud Corneal-compensated IOP.\ud \ud Results: \ud Higher levels of TC, HDL-C, and LDL-C were associated independently with higher IOPcc in both cohorts after adjustment for key demographic, medical, and lifestyle factors. For each 1-standard deviation increase in TC, HDL-C, and LDL-C, IOPcc was higher by 0.09 mmHg (95% confidence interval [CI], 0.06–0.11 mmHg; P < 0.001), 0.11 mmHg (95% CI, 0.08–0.13 mmHg; P < 0.001), and 0.07 mmHg (95% CI, 0.05–0.09 mmHg; P < 0.001), respectively, in the UK Biobank cohort. In the EPIC-Norfolk cohort, each 1-standard deviation increase in TC, HDL-C, and LDL-C was associated with a higher IOPcc by 0.19 mmHg (95% CI, 0.07–0.31 mmHg; P = 0.001), 0.14 mmHg (95% CI, 0.03–0.25 mmHg; P = 0.016), and 0.17 mmHg (95% CI, 0.06–0.29 mmHg; P = 0.003). An inverse association between triglyceride levels and IOP in the UK Biobank (–0.05 mmHg; 95% CI, –0.08 to –0.03; P < 0.001) was not replicated in the EPIC-Norfolk cohort (P = 0.30).\ud \ud Conclusions: \ud Our findings suggest that serum TC, HDL-C, and LDL-C are associated positively with IOP in 2 United Kingdom cohorts and that triglyceride levels may be associated negatively. Future research is required to assess whether these associations are causal in nature.

Published
2022

33. Adressen der Autoren

Author

Adams, Mark C., primary, Albala, David M., additional, Anger, Jennifer T., additional, Anoia, Elizabeth, additional, Assimos, Dean G., additional, Auge, Brian K., additional, Bagley, Demetrius H., additional, Baker, Linda A., additional, Barocas, Daniel A., additional, Barry, John M., additional, Baskin, Laurence S., additional, Beck, Stephen, additional, Bella, Anthony J., additional, Bishoff, Jay T., additional, Bivalacqua, Trinity J., additional, Blaivas, Jerry G., additional, Blute, Michael L., additional, Boorjian, Stephen Anthony, additional, Borer, Joseph, additional, Borin, James F., additional, Brant, William O., additional, Brock, John W., additional, Broghammer, Joshua A., additional, Brugh, Victor M., additional, Buckley, Jill C., additional, Bullock, Travis L., additional, Burkhard, Fiona C., additional, Burnett, Arthur L., additional, Cadeddu, Jeffrey A., additional, Campbell, Jeffrey B., additional, Canes, David, additional, Cartwright, Patrick C., additional, Castle, Erik P., additional, Champagne, Bradley, additional, Chang, Sam S., additional, Chen, Tony Y., additional, Cheng, Earl Y., additional, Cherullo, Edward, additional, Christie, Alison M., additional, Clark, Peter E., additional, Clayman, Ralph V., additional, Cookson, Michael S., additional, Corbett, Sean T., additional, Costabile, Raymond A., additional, Davis, Rodney, additional, Deane, Leslie A., additional, Dechet, Christopher B., additional, DeLancey, John O.L., additional, DeMarco, Romano T., additional, Denstedt, John D., additional, Desai, Mahesh R., additional, Desai, Mihir M., additional, Desai, Rahul A., additional, Disick, Grant, additional, Dmochowski, Roger R., additional, Elder, Jack S., additional, Elliott, Sean P., additional, Elmajian, Donald A., additional, Fergany, Amr, additional, Flynn, Brian J., additional, Fossett, Lindsay, additional, Foster, Richard, additional, Ganpule, Arvind P., additional, Gargollo, Patricio, additional, Gill, Inderbir S., additional, Gjertson, Carl K., additional, Goldfarb, David A., additional, Goldstein, Marc, additional, Gonzalgo, Mark L., additional, Gormley, E. Ann, additional, Guralnick, Michael, additional, Haber, Georges-Pascal, additional, Haleblian, George E., additional, Hartke, David, additional, Hellstrom, Wayne J.G., additional, Herrell, S. Duke, additional, Hinman, Frank, additional, Holzbeierlein, Jeffrey M., additional, Horowitz, Andrew I., additional, Hulbert, William C., additional, Ihara, Hiroyuki, additional, Inman, Brant, additional, Jarrett, Thomas W., additional, Jordan, Gerald H., additional, Kaplan, Steven A., additional, Kaufman, Melissa R., additional, Kavoussi, Louis R., additional, Kesler, Stuart, additional, Kick, Phillip S., additional, Kirsch, Andrew J., additional, Klein, Frederick A., additional, Kobashi, Kathleen C., additional, Koenig, Philippe, additional, Koh, Chester J., additional, Kokorowski, Paul, additional, Krishnamurthi, Venkatesh, additional, Kropp, Bradley P., additional, Kuo, Ramsay L., additional, Landman, Jaime, additional, Larson, Kindra, additional, Latini, Jerilyn M., additional, Leach, Gary E., additional, Lee, David I., additional, Leng, Wendy W., additional, L’Esperance, James O., additional, Leveillee, Raymond J., additional, Levy, David A., additional, Lingeman, James E., additional, Lue, Tom F., additional, Makari, John H., additional, Marderstein, Eric L., additional, Marguet, Charles G., additional, Martin, Frances M., additional, McAninch, Jack W., additional, McClure, R. Dale, additional, McGuire, Edward J., additional, McVary, Kevin T., additional, Mevorach, Robert A., additional, Middleton, Richard G., additional, Milam, Douglas F., additional, Miller, Elizabeth A., additional, Miller, Nicole, additional, Modder, Joshua K., additional, Moinzadeh, Ali, additional, Monga, Manoj, additional, Montague, Drogo K., additional, Montie, James, additional, Moore, Charles R., additional, Morey, Allen F., additional, Morgan, Daniel M., additional, Morrisroe, Shelby N., additional, Mufarrij, Patrick W., additional, Munver, Ravi, additional, Ng, Christopher S., additional, Nisbet, Alan A., additional, Novick, Andrew C., additional, O’Connor, R. Corey, additional, Okeke, Zeph, additional, Pak, Raymond W., additional, Parekh, Dipen J., additional, Pearle, Margaret S., additional, Perer, Elise, additional, Peterson, Andrew C., additional, Phillips, Courtney K., additional, Pierre, Ketsia, additional, Polascik, Thomas J., additional, Ponsky, Lee, additional, Pope, John, additional, Preminger, Glenn M., additional, Prieto, Juan C., additional, Rabinowitz, Ronald, additional, Rapp, David E., additional, Raz, Shlomo, additional, Redman, John F., additional, Richstone, Lee, additional, Roberts, William W., additional, Rosen, Michael J., additional, Rosenblatt, Gregory S., additional, Rowland, Randall G., additional, Saini, Rajiv, additional, Sampaio, Francisco J.B., additional, Scarpero, Harriette M., additional, Scherr, Douglas S., additional, Schlegel, Peter N., additional, Sherman, Neil D., additional, Shields, John, additional, Shinohara, Katsuto, additional, Siegel, Steven W., additional, Skinner, Eila, additional, Skoog, Steven J., additional, Smith, Arthur D., additional, Smith, Joseph A., additional, Snodgrass, Warren T., additional, Soltanian, Hooman, additional, Sotelo, Rene, additional, Spirnak, J. Patrick, additional, Steers, William D., additional, Stein, John P., additional, Stifelman, Michael D., additional, Studer, Urs E., additional, Sundaram, Chandru P., additional, Sur, Roger L., additional, Sutherland, Richard W., additional, Suzuki, Kazuo, additional, Tan, Yeh Hong, additional, Tanrikut, Cigdem, additional, Thiel, David D., additional, Thomas, John C., additional, Thomas, Raju, additional, Triaca, Veronica, additional, Trunzo, Joseph A., additional, Tsuru, Nobuo, additional, Turek, Paul J., additional, Twiss, Christian O., additional, Vanderbrink, Brian A., additional, Vasavada, Sandip P., additional, Vaughan, E. Darracott, additional, Venable, Dennis D., additional, Vourganti, Srinivas, additional, Wagner, Kristofer R., additional, Walsh, Dena L., additional, Walsh, Thomas J., additional, Wan, Julian, additional, Waters, W. Bedford, additional, Webster, George D., additional, Wessells, Hunter, additional, White, Wesley M., additional, Wiener, John S., additional, Wignall, Geoffrey R., additional, Winfield, Howard N., additional, Wise, Paul E., additional, Wolf, J. Stuart, additional, Wolter, Christopher E., additional, Woods, Michael E., additional, and Zeltser, Ilia S., additional

Published
2017
Full Text
View/download PDF

34. Contributors

Author

Abboud, Steven F., primary, Agrawal, Vineet, additional, Ahlawat, Rajesh, additional, Ahmed, Haris S., additional, Allaf, Mohamad E., additional, Al-Tartir, Tareq, additional, Anderson, Kyle, additional, Andonian, Sero, additional, Aronsohn, Judith, additional, Atalla, Mohamed A., additional, Averch, Timothy D., additional, Bandari, Jathin, additional, Bhandari, Mahendra, additional, Bhayani, Sam B., additional, Bianchi, Giampaolo, additional, Bishoff, Jay T., additional, Brancato, Sam J., additional, Cadeddu, Jeffrey A., additional, Caputo, Peter A., additional, Chow, George K., additional, Colleselli, Daniela, additional, Dajani, Daoud, additional, Duty, Brian D., additional, Elsamra, Sammy E., additional, Friedlander, Justin I., additional, Gettman, Matthew, additional, Ghanaat, Mazyar, additional, Glickman, Leonard, additional, Guru, Khurshid A., additional, Haddad, Ashraf S., additional, Hemal, Ashok K., additional, Hussein, Ahmed A., additional, Hwong, James S., additional, Jackman, Stephen V., additional, Janetschek, Günter, additional, Jarrett, Thomas W., additional, Jeong, Wooju, additional, Johnson, Michael H., additional, Joseph, Jean V., additional, Jung, Jin, additional, Kaouk, Jihad H., additional, Kavoussi, Louis R., additional, Kavoussi, Nicholas, additional, Kim, Bohyun, additional, Kim, Dae Keun, additional, Landman, Jaime, additional, Lay, Aaron H., additional, Leavitt, David A., additional, Magdy, Ahmed, additional, Manny, Ted B., additional, McAdams, Sean, additional, Menon, Mani, additional, Micali, Salvatore, additional, Moore, Debora, additional, Moore, Robert, additional, Morgan, Monica S.C., additional, Munver, Ravi, additional, Nakada, Stephen Y., additional, Noureldin, Yasser A., additional, Ost, Michael C., additional, Palmer, Lane S., additional, Parihar, Jaspreet Singh, additional, Piacitelli, Jeffery E., additional, Pinto, Peter A., additional, Pirola, Giacomo Maria, additional, Porter, James, additional, Potretzke, Aaron M., additional, Pruthi, Raj, additional, Raza, Johar S., additional, Reese, Jeremy N., additional, Rha, Koon Ho, additional, Richstone, Lee, additional, Salari, Bijan W., additional, Sandberg, Jason M., additional, Schomburg, John, additional, Schwartz, Michael J., additional, Seideman, Casey A., additional, Shah, Paras H., additional, Siev, Michael, additional, Smith, Armine K., additional, Sood, Akshay, additional, Srinivasan, Arun, additional, Stifelman, Michael D., additional, Streeper, Necole M., additional, Su, Li Ming, additional, Taan, Hassan G., additional, Territo, Angelo, additional, Vira, Manish A., additional, Wagner, Andrew A., additional, Weld, Kyle J., additional, Westerman, Mary E., additional, Woods, Michael, additional, Yamaguchi, Yuka, additional, Yamamoto, Akira, additional, Youssef, Ramy, additional, Zhao, Lee C., additional, Zhao, Philip T., additional, and Ziegelmann, Matthew, additional

Published
2017
Full Text
View/download PDF

37. List of Contributors

Author

Adams, Harold P., primary, El Ahmadieh, Tarek Y., additional, Albers, Gregory W., additional, Alexandrov, Andrei V., additional, Anrather, Josef, additional, Arai, Ken, additional, Aronowski, Jaroslaw (Jarek), additional, Auer, Roland N., additional, Awad, Issam A., additional, Ay, Hakan, additional, Baltan, Selva, additional, Batjer, Hunt H., additional, Benavente, Oscar R., additional, Bendok, Bernard R., additional, Bershad, Eric M., additional, Bonati, Leo H., additional, Bookland, Markus J., additional, Bousser, Marie-Germaine, additional, Braca, John A., additional, Broderick, Joseph P., additional, Brown, Martin M., additional, Brown, Wendy E., additional, Brust, John C.M., additional, Bushnell, Cheryl, additional, Bösel, Julian, additional, Canhão, Patrícia, additional, Caplan, Louis R., additional, Castellanos, Mar, additional, Chamorro, Angel, additional, Chandler, James P., additional, Chen, Jun, additional, Chopp, Michael, additional, Chrissobolis, Sophocles, additional, Chabriat, Hugues, additional, Cramer, Steven C., additional, Cucchiara, Brett L., additional, Dannenbaum, Mark J., additional, Davis, Patricia H., additional, Dawson, Ted M., additional, Dawson, Valina L., additional, Day, Arthur L., additional, del Zoppo, Gregory J., additional, Diener, Hans-Christoph, additional, Di Tullio, Marco R., additional, Dobkin, Bruce H., additional, Dzialowski, Imanuel, additional, Economos, Alexis, additional, Eddleman, Christopher S., additional, Elkind, Mitchell S.V., additional, Feigin, Valery L., additional, Ferro, José M., additional, Findlay, J. Max, additional, Furie, Karen L., additional, Fusco, Matthew R., additional, Field, Thalia S., additional, Geibprasert, Sasikhan, additional, Gensic, Anna P., additional, Gobin, Y. Pierre, additional, Goldberg, Mark P., additional, Goldstein, Larry B., additional, Gonzales, Nicole R., additional, Gounis, Matthew J., additional, Greenberg, Steven M., additional, Gregson, Barbara A., additional, Grotta, James C., additional, Gutierrez, Jose, additional, Hacke, Werner, additional, Hallenbeck, John M., additional, Haršány, Michal, additional, Heiferman, Daniel M., additional, Homma, Shunichi, additional, Howard, George, additional, Howard, Virginia J., additional, Hwang, Jee-Yeon, additional, Iadecola, Costantino, additional, Jahan, Reza, additional, Joutel, Anne, additional, Jüttler, Eric, additional, Kase, Carlos S., additional, Kasner, Scott E., additional, Katan, Mira, additional, Khader Eliyas, Javed, additional, Khan, Muhib, additional, Kim, Helen, additional, Kidwell, Chelsea S., additional, Kim, Jong S., additional, Krings, Timo, additional, Krishnamurthi, Rita, additional, Kurth, Tobias, additional, Lamy, Catherine, additional, Lansberg, Maarten G., additional, Levy, Elad I., additional, Liebeskind, David S., additional, Lo, Eng H., additional, Loftus, Christopher M., additional, Lyden, Patrick D., additional, Mas, Jean-Louis, additional, Massari, Francesco, additional, Meckler, Jason M., additional, Mendelow, A. David, additional, Meschia, James F., additional, Messé, Steven R., additional, Mitchel, Patrick, additional, Morgenstern, Lewis B., additional, Mokin, Maxim, additional, Moskowitz, Michael A., additional, Mullen, Michael T., additional, Nedergaard, Maiken, additional, Neugebauer, Hermann, additional, Newell, David W., additional, Norrving, Bo, additional, O'Donnell, Martin, additional, Ofengeim, Dimitry, additional, Ogata, Jun, additional, Ogilvy, Christopher S., additional, Pancioli, Arthur M., additional, Parsha, Kaushik, additional, Parsons, Mark W., additional, Pawlikowska, Ludmila, additional, Pérez, Adriana, additional, Perez-Pinzon, Miguel A., additional, Powers, William J., additional, Puetz, Volker, additional, Puri, Ajit S., additional, Ransom, Bruce R., additional, Roine, Risto O., additional, Rundek, Tatjana, additional, Russin, Jonathan J., additional, Sacco, Ralph L., additional, Spetzler, Robert F., additional, Sattenberg, Ronald J., additional, Saver, Jeffrey L., additional, Savitz, Sean I., additional, Schönenberger, Silvia, additional, Seshadri, Sudha, additional, Sharma, Vijay K., additional, Shi, Yejie, additional, Shoamanesh, Ashkan, additional, Silverboard, Gerald, additional, Singhal, Aneesh B., additional, Sobey, Christopher G., additional, Stapf, Christian, additional, Su, Hua, additional, Suarez, Jose I., additional, Sykora, Marek, additional, Tatlisumak, Turgut, additional, El Tecle, Najib, additional, terBrugge, Karel G., additional, Thompson, John W., additional, Tilley, Barbara C., additional, Tournier-Lasserve, Elisabeth, additional, Tsivgoulis, Georgios, additional, Vilela, Marcelo D., additional, von Kummer, Rüdiger, additional, Wakhloo, Ajay K., additional, Wagner, Kenneth R., additional, Warach, Steven, additional, Weksler, Babette B., additional, Werring, David, additional, Willey, Joshua Z., additional, Wintermark, Max, additional, Wolf, Philip A., additional, Wong, Lawrence K.S., additional, Woo, Daniel, additional, Wright, Clinton, additional, Xi, Guohua, additional, Yamaguchi, Takenori, additional, Yasaka, Masahiro, additional, Young, William L., additional, Zammar, Samer G., additional, Zahuranec, Darin B., additional, Zhang, Feng, additional, Zhang, Haiyue, additional, Zhang, John H., additional, Zhang, Zheng Gang, additional, Zukin, R. Suzzane, additional, and Zweifler, Richard M., additional

Published
2016
Full Text
View/download PDF

39. Intracerebral Hemorrhage

Author

Kase, Carlos S., primary, Shoamanesh, Ashkan, additional, Greenberg, Steven M., additional, and Caplan, Louis R., additional

Published
2016
Full Text
View/download PDF

40. List of Contributors

Author

Abbosh, Philip H., primary, Abdollah, Firas, additional, Achary, Mohan P., additional, Alanee, Shaheen, additional, Albertsen, Peter C., additional, Al-Shraideh, Yousef, additional, Andriole, Gerald, additional, Baack Kukreja, Janet E., additional, Babayan, Richard K., additional, Baker, Brock R., additional, Bayne, Christopher E., additional, Bilusic, Marijo, additional, Bokhorst, Leonard P., additional, Cahn, David B., additional, Canter, Daniel J., additional, Chen, David Y.T., additional, Chen, Ronald C., additional, Chipollini, Juan, additional, Choyke, Peter L., additional, Cooperberg, Matthew R., additional, Costello, Anthony, additional, Crawford, E. David, additional, Deville, Curtiland, additional, Dulaimi, Essel, additional, Dynda, Danuta, additional, Eifler, John B., additional, Ercole, Cesar E., additional, Eun, Daniel D., additional, Everaerts, Wouter, additional, Faiena, Izak, additional, Ferragamo, Michael A., additional, Flack, Chandra K., additional, Garg, Tullika, additional, Gherezghihir, Awet, additional, Godec, Ciril J., additional, Gomella, Leonard G., additional, Greenberg, Richard E., additional, Grob, Baruch Mayer, additional, Guazzoni, Giorgio, additional, Guzzo, Thomas J., additional, Haddad, Ahmed, additional, Haider, Maahum, additional, Harbin, Andrew C., additional, Horwitz, Eric M., additional, Hussein, Ahmed A., additional, Ito, Timothy, additional, Jarrett, Thomas W., additional, Jenkins, Lawrence C., additional, Kaplan, Joshua R., additional, Katz, Mark H., additional, Kavoussi, Louis R., additional, Kiechle, Jonathan, additional, Kim, Simon P., additional, Klotz, Laurence, additional, Koch, Michael O., additional, Kundavaram, Chandan, additional, Kutikov, Alexander, additional, Lallas, Costas D., additional, Lange, Paul H., additional, Lazzeri, Massimo, additional, Lin, Daniel W., additional, Lotan, Yair, additional, Lythgoe, Casey, additional, Makarov, Danil V., additional, Mann, Mark, additional, Marcus, David M., additional, Master, Viraj A., additional, Meeks, Joshua J., additional, Mendhiratta, Neil, additional, Menon, Mani, additional, Messing, Edward M., additional, Miyamoto, Curtis T., additional, Modi, Parth K., additional, Mohiuddin, Jahan J., additional, Monn, M. Francesca, additional, Montorsi, Francesco, additional, Moon, Daniel, additional, Moses, Kelvin A., additional, Moul, Judd W., additional, Moyad, Mark A., additional, Mucksavage, Phillip, additional, Mulhall, John P., additional, Murphy, Declan G., additional, Mydlo, Jack H., additional, Nelson, Joel B., additional, Parihar, Jaspreet Singh, additional, Parker, Daniel C., additional, Parrillo, Lisa, additional, Patel, Neal, additional, Pavlovich, Christian P., additional, Petrossian, Albert, additional, Pietzak, Eugene, additional, Pinto, Peter, additional, Piotrowski, Zachary, additional, Pontari, Michel A., additional, Punnen, Sanoj, additional, Raman, Jay D., additional, Reese, Adam C., additional, Reeves, Fairleigh, additional, Rij, Simon Van, additional, Ristau, Benjamin T., additional, Roobol, Monique J., additional, Salami, Simpa S., additional, Salmasi, Amirali H., additional, Sankineni, Sandeep, additional, Scarpato, Kristen R., additional, Schade, George R., additional, Schaff, Matthew S., additional, Sejpal, Samir V., additional, Shore, Neal D., additional, Simhan, Jay, additional, Slovin, Susan F., additional, Smaldone, Marc C., additional, Smith, Joseph A., additional, Stephenson, Andrew J., additional, Steyerberg, Ewout W., additional, Stimson, C.J., additional, Sutcliffe, Siobhan, additional, Taneja, Samir S., additional, Tang, Vincent, additional, Tausch, Timothy J., additional, Thrasher, James Brantley, additional, Torre, Taryn G., additional, Trabulsi, Edouard J., additional, Turkbey, Baris, additional, Turner, Robert M., additional, Underwood, Willie, additional, Vemana, Goutham, additional, Venkatachalam, Shilpa, additional, Ventii, Karen H., additional, Wein, Alan, additional, Wright, Jonathan L., additional, Wyre, Hadley, additional, Yi Kim, Isaac, additional, Young, Melissa R., additional, Yu, James B., additional, and Zaorsky, Nicholas G., additional

Published
2016
Full Text
View/download PDF

42. Vertebrobasilar Disease

Author

Louis R. Caplan and Jong S. Kim

Subjects
medicine.medical_specialty, business.industry, Internal medicine, Vertebrobasilar disease, medicine, Cardiology, business
Published
2022

43. Contributors

Author

Harold P. Adams, Opeolu Adeoye, Gregory W. Albers, Andrei V. Alexandrov, Sepideh Amin-Hanjani, Hongyu An, Craig S. Anderson, Josef Anrather, Hugo J. Aparicio, Ken Arai, Jaroslaw Aronowski, Kunakorn Atchaneeyasakul, Heinrich Audebert, Roland N. Auer, Issam A. Awad, Hakan Ay, Selva Baltan, Ramani Balu, Mandana Behbahani, Oscar R. Benavente, Eric M. Bershad, Jimmy V. Berthaud, Spiros L. Blackburn, Leo H. Bonati, Julian Bösel, Marie Germaine Bousser, Joseph P. Broderick, Martin M. Brown, Wendy Brown, John C.M. Brust, Cheryl Bushnell, Patrícia Canhão, Louis R. Caplan, Julián Carrión-Penagos, Mar Castellanos, Michelle R. Caunca, Hugues Chabriat, Angel Chamorro, Jieli Chen, Jun Chen, Michael Chopp, Greg Christorforids, E. Sander Connolly, Steven C. Cramer, Brett L. Cucchiara, Alexandra L. Czap, Mark J. Dannenbaum, Patricia H. Davis, Ted M. Dawson, Valina L. Dawson, Arthur L. Day, T. Michael De Silva, Diana Aguiar de Sousa, Victor J. Del Brutto, Gregory J. del Zoppo, Colin P. Derdeyn, Marco R. Di Tullio, Hans Christoph Diener, Michael N. Diringer, Bruce H. Dobkin, Imanuel Dzialowski, Mitchell S.V. Elkind, Jordan Elm, Valery L. Feigin, José Manuel Ferro, Thalia S. Field, Marlene Fischer, Myriam Fornage, Karen L. Furie, Lidia Garcia-Bonilla, Steven L. Giannotta, Y. Pierre Gobin, Mark P. Goldberg, Larry B. Goldstein, Nicole R. Gonzales, David M. Greer, James C. Grotta, Ruiming Guo, Jose Gutierrez, Peter Harmel, George Howard, Virginia J. Howard, Jee-Yeon Hwang, Costantino Iadecola, Reza Jahan, Glen C. Jickling, Anne Joutel, Scott E. Kasner, Mira Katan, Christopher P. Kellner, Muhib Khan, Chelsea S. Kidwell, Helen Kim, Jong S. Kim, Charles E. Kircher, Timo Krings, Rita V. Krishnamurthi, Tobias Kurth, Maarten G. Lansberg, Elad I. Levy, David S. Liebeskind, Sook-Lei Liew, David J. Lin, Benjamin Lisle, Eng H. Lo, Patrick D. Lyden, Takakuni Maki, Georgios A. Maragkos, Miklos Marosfoi, Louise D. McCullough, Jason M. Meckler, James Frederick Meschia, Steven R. Messé, J Mocco, Maxim Mokin, Michael A. Mooney, Lewis B. Morgenstern, Michael A. Moskowitz, Michael T. Mullen, Steffen Nägel, Maiken Nedergaard, Justin A. Neira, Sarah Newman, Patrick J. Nicholson, Bo Norrving, Martin O’Donnell, Dimitry Ofengeim, Jun Ogata, Christopher S. Ogilvy, Emanuele Orrù, Santiago Ortega-Gutiérrez, Matthew Maximillian Padrick, Kaushik Parsha, Mark Parsons, Neil V. Patel, Virendra I. Patel, Ludmila Pawlikowska, Adriana Pérez, Miguel A. Perez-Pinzon, John M. Picard, Sean P. Polster, William J. Powers, Volker Puetz, Jukka Putaala, Margarita Rabinovich, Bruce R. Ransom, Jorge A. Roa, Gary A. Rosenberg, Christina P. Rossitto, Tatjana Rundek, Jonathan J. Russin, Ralph L. Sacco, Apostolos Safouris, Edgar A. Samaniego, Lauren H. Sansing, Nikunj Satani, Ronald J. Sattenberg, Jeffrey L. Saver, Sean I. Savitz, Christian Schmidt, Sudha Seshadri, Vijay K. Sharma, Frank R. Sharp, Kevin N. Sheth, Omar K. Siddiqi, Aneesh B. Singhal, Christopher G. Sobey, Clemens J. Sommer, Robert F. Spetzler, Christopher J. Stapleton, Ben A. Strickland, Hua Su, José I. Suarez, Hiroo Takayama, Joseph Tarsia, Turgut Tatlisumak, Ajith J. Thomas, John W. Thompson, Georgios Tsivgoulis, Elizabeth Tournier-Lasserve, Gabriel Vidal, Ajay K. Wakhloo, Babette B. Weksler, Joshua Z. Willey, Max Wintermark, Lawrence K.S. Wong, Guohua Xi, Jinchong Xu, Shadi Yaghi, Takenori Yamaguchi, Tuo Yang, Masahiro Yasaka, Darin B. Zahuranec, Feng Zhang, John H. Zhang, Zhitong Zheng, R. Suzanne Zukin, and Richard M. Zweifler

Published
2022

44. List of Contributors

Author

Abrams-Tobe, Leslie, primary, Abuswider, Samer A, additional, Acosta, Jorge, additional, Agrawal, Pavi, additional, Albis-Donado, Oscar, additional, Alencar, Luciana M, additional, Allingham, R Rand, additional, Amireskandari, Annahita, additional, Anand, Nitin, additional, Aptel, Florent, additional, Araie, Makoto, additional, Arcieri, Enyr S, additional, Assia, Ehud I, additional, Aung, Tin, additional, Baerveldt, George, additional, Baig, Nafees, additional, Baik, Annie K, additional, Bansal, Rajendra K, additional, Babic, Mirko, additional, Barikian, Anita, additional, Barnebey, Howard, additional, Barton, Keith, additional, Baudouin, Christophe, additional, Beck, Allen, additional, Bennett, Sonya L, additional, Berke, Stanley J, additional, Bevin, Tui H, additional, Bhartiya, Shibal, additional, Bloom, Philip A, additional, Blumberg, Dana M, additional, Bollinger, Kathryn, additional, Bowd, Christopher, additional, Boyle, John W, additional, Brandt, James D, additional, Broadway, David C, additional, Brocchini, Stephen, additional, Bron, Alain M, additional, Budenz, Donald L, additional, Bunce, Catey, additional, Burgoyne, Claude F, additional, Burr, Jennifer, additional, Buys, Yvonne M, additional, Cantor, Louis B, additional, Caprioli, Joseph, additional, Carassa, Roberto G, additional, Casper, Daniel S, additional, Catoira-Boyle, Yara Paula, additional, Ceruti, Piero, additional, Chakrabarti, Debasis, additional, Chakrabarti, Raka, additional, Challa, Pratap, additional, Chan, Errol, additional, Chang, Peter T, additional, Chang, Robert T, additional, Chauhan, Balwantray C, additional, Chen, Aiyin, additional, Cheng, Jason, additional, Chew, Paul TK, additional, Chiang, Mark, additional, Chihara, Etsuo, additional, Choplin, Neil T, additional, Cioffi, George A, additional, Clement, Colin I, additional, Coleman, Anne L, additional, Congdon, Nathan G, additional, Coote, Michael A, additional, Costa, Vital P, additional, Crabb, David P, additional, Crandall, Alan S, additional, Craven, E Randy, additional, Crawley, Laura, additional, Crowston, Jonathan G, additional, Cunningham, Emmett T, additional, Dahan, Elie, additional, Dahlmann-Noor, Annegret H, additional, Damji, Karim F, additional, Day, Alexander, additional, Day, Me'Ja, additional, Denis, Philippe, additional, Dorairaj, Syril, additional, Downs, J Crawford, additional, Dutton, Gordon N, additional, Eldaly, Hassan, additional, El Sayyad, Fathi F, additional, Falsini, Benedetto, additional, Fantes, Francisco, additional, Fechter, Herbert P, additional, Fechtner, Robert D, additional, Fellman, Ronald L, additional, Fenwick, Eva, additional, Fernando, Arosha, additional, Fisher, Ann Caroline, additional, Fitzke, Frederick W, additional, Fortune, Brad, additional, Foster, Paul, additional, Founti, Panayiota, additional, Freedman, Jeffrey, additional, Gandolfi, Stefano A, additional, García-Feijoó, Julián, additional, Garway-Heath, David, additional, Gazzard, Gus, additional, Gedde, Steven J, additional, Geffen, Noa, additional, Georgoulas, Stelios, additional, Giangiacomo, Annette, additional, Gill, Katie, additional, Gkatzioufas, Zisis, additional, Goldberg, Ivan, additional, Gouws, Pieter, additional, Graham, Stuart L, additional, Grajewski, Alana L, additional, Greenfield, David S, additional, Grehn, Franz, additional, Grigera, Daniel E, additional, Gross, Ronald L, additional, Grover, Davinder S, additional, Grytz, Rafael, additional, Gupta, Meenakashi, additional, Gupta, Neeru, additional, de Moraes, Carlos Gustavo, additional, Hafez, Ali S, additional, Hafezi, Farhad, additional, Hamanaka, Teruhiko, additional, Harris, Alon, additional, Hatanaka, Marcelo, additional, Hawker, Matthew J, additional, Healey, Paul R, additional, Heatley, The late Catherine J, additional, Heuer, Dale K, additional, Higginbotham, Eve J, additional, Hirn, Cornelia, additional, Hitchings, Roger A, additional, Holló, Gábor, additional, Hoste, Ann M, additional, Huck, Andrew, additional, Hutnik, Cindy ML, additional, Hylton, Camille, additional, Ittoop, Sabita M, additional, Ja'afar, Farrah, additional, Jampel, Henry, additional, Johnson, Thomas V, additional, Jonas, Jost B, additional, Kahook, Malik Y, additional, Kass, Michael A, additional, Katsanos, Andreas, additional, Katz, L Jay, additional, Keeffe, Jill E, additional, Kersey, Thomas, additional, Khachatryan, Naira, additional, Khaw, Sir Peng Tee, additional, Khouri, Albert S, additional, Kiage, Dan, additional, Kiang, Lee, additional, Kim, Danny, additional, Kiuchi, Yoshiaki, additional, Klink, Thomas, additional, Koenigsman, Helen, additional, Konstas, Anastasios GP, additional, Kotecha, Aachal, additional, Kulkarni, Avinash, additional, Kuroyedov, Alexander V, additional, Labbé, Antoine, additional, Lacey, Alan, additional, Lam, Dennis SC, additional, Lamourex, Ecosse L, additional, Lee, Graham, additional, Lee, Paul, additional, Lemij, Hans G, additional, Leoncavallo, Anthony, additional, Lesk, Mark R, additional, Leung, Christopher KS, additional, Leung, Dexter YL, additional, Levin, Leonard A, additional, Lewis, Richard A, additional, Lim, K Sheng, additional, Lim, Ridia, additional, Lima, Ricardo de, additional, Liu, Yutao, additional, Lockwood, Alastair, additional, Low, Sancy, additional, Mabuchi, Fumihiko, additional, Mackey, David A, additional, Malik, Rizwan, additional, Mandal, Anil K, additional, Mansberger, Steven L, additional, Mansouri, Kaweh, additional, Marchini, Giorgio, additional, Marella, Manjula, additional, Martin, Keith R, additional, McGlynn, Robert H, additional, McKinley, Steven H, additional, McKinnon, Stuart J, additional, McManus, J Ryan, additional, Medeiros, Felipe A, additional, Mermoud, André, additional, Migdal, Clive S, additional, Minckler, Don, additional, Molteno, Anthony CB, additional, Mora, Paolo, additional, Moreno-Montañés, Javier, additional, Morgan, James E, additional, Mosaed, Sameh, additional, Moschos, Marilita M, additional, Muir, Kelly W, additional, Muñoz, Gonzalo, additional, Muñoz-Negrete, Francisco J, additional, Neelakantan, Arvind, additional, Negi, Anil K, additional, Netland, Peter A, additional, Newman-Casey, Paula Anne, additional, Nicolela, Marcelo T, additional, Niyadurupola, Nuwan, additional, Nofal, Magdy A, additional, Nolan, Winnie, additional, Nongpiur, Monisha E, additional, Noureddin, Baha'a N, additional, Novack, Gary D, additional, Nuyen, Brenda, additional, Palaniswamy, Krishnamurthy, additional, Palma, Camille, additional, Park, Ki Ho, additional, Parrish, Richard K, additional, Papadopoulos, Maria, additional, Parikh, Rajul S, additional, Pasquale, Louis R, additional, Pébay, Alice, additional, Petrov, Sergey, additional, Piltz-Seymour, Jody, additional, Pinto, Luís Abegão, additional, Pitha, Ian F, additional, Pfeiffer, Norbert, additional, Quaranta, Luciano, additional, Ramulu, Pradeep Y, additional, Ravinet, Emilie, additional, Realini, Tony, additional, Rebolleda, Gema, additional, Reus, Nic J, additional, Reynolds, Adam C, additional, Rhee, Douglas J, additional, Riss, Isabelle, additional, Ritch, Robert, additional, Riva, Charles E, additional, Roberti, Gloria, additional, Roberts, Cynthia J, additional, Robin, Alan L, additional, Rojanapongpun, Prin, additional, Roy, Sylvain, additional, Salmon, John F, additional, Sampaolesi, Juan Roberto, additional, Sangermani, Chiara, additional, Sarodia, Usman A, additional, Schaefer, Jamie Lea, additional, Schloetzer-Schrehardt, Ursula, additional, Schultz, Gregory S, additional, Schuman, Joel S, additional, Seibold, Leonard K, additional, Shaarawy, Tarek M, additional, Shah, Peter, additional, Sherwood, Mark B, additional, Shiroma, Lineu Oto, additional, Siesky, Brent, additional, Silva, Sergio Estrela, additional, Singh, Annapurna, additional, Singh, Arun D, additional, Singh, Kuldev, additional, Sng, Chelvin CA, additional, Song, Brian J, additional, Spaeth, George L, additional, Spratt, Alexander, additional, Stalmans, Ingeborg, additional, Stamper, Robert L, additional, Sugiyama, Kazuhisa, additional, Susanna, Remo, additional, Suwanpimolkul, Orathai, additional, Swanson, William H, additional, Tamm, Ernst R, additional, Tania Tai, Tak Yee, additional, Tanna, Angelo P, additional, Teekhasaenee, Chaiwat, additional, Tham, Clement CY, additional, Thieme, Hagen, additional, Thomas, Ravi, additional, Thompson, Andrew M, additional, Thulasiraj, Ravilla D, additional, Thygesen, John, additional, Tomey, Karim, additional, Ton, Yokrat, additional, Topouzis, Fotis, additional, Toris, Carol B, additional, Tosi, Roberto, additional, Tsai, James C, additional, Tuli, Sonal S, additional, Tuulonen, Anja, additional, Ungaro, Nicola, additional, Vale, Luke, additional, van Koolwijk, Leonieke ME, additional, Vaswani, Reena S, additional, Venkatesh, Rengaraj, additional, Venturini, Cristina, additional, Vernon, Stephen A, additional, Vithana, Eranga N, additional, Vijaya, Lingam, additional, Viswanathan, Ananth C, additional, Vizzari, Gabriele, additional, Voudouragkaki, Irini C, additional, Waisbourd, Michael, additional, Walland, Mark J, additional, Weinreb, Robert N, additional, Werner, Mark, additional, Wells, Anthony, additional, Wiafe, Boateng, additional, Wilensky, Jacob, additional, Wong, Tina T, additional, WuDunn, Darrell, additional, Yip, Jennifer LY, additional, Yucel, Yeni, additional, Zangwill, Linda M, additional, Zanutigh, Virginia E, additional, Zelefsky, Joseph R, additional, and Zeyen, Thierry, additional

Published
2015
Full Text
View/download PDF

46. List of Contributors

Author

Appel, Stanley H., primary, Backonja, Miroslav “Misha”, additional, Bailey, Zinzi D., additional, Beers, David R., additional, Begay, Tommy K., additional, Berti, Anna, additional, Boido, Marina, additional, Boldrini, Maura, additional, Borsook, David, additional, Brown, R.H., additional, Burstein, Rami, additional, Burton, Vera Joanna, additional, Butelman, Eduardo R., additional, Caplan, Louis R., additional, Castellanos, F. Xavier, additional, Cattaneo, Elena, additional, Clemens, Paula R., additional, Cortese, Samuele, additional, Cossetti, Chiara, additional, Coyle, Joseph T., additional, Daneshvar, Daniel H., additional, DeLong, Mahlon R., additional, Feldman, Eva L., additional, Garbarini, Francesca, additional, Gasser, Thomas, additional, Gold, Michael S., additional, Grunze, Heinz, additional, Hagerman, Randi, additional, Harris, James C., additional, Haughey, Norman J., additional, Illes, Judy, additional, Iorio, Raffaele, additional, Ironside, James W., additional, Kaminski, Henry J., additional, Kim, Bhumsoo, additional, Koen, Nastassja, additional, Konopaske, Glenn T., additional, Kornum, Birgitte Rahbek, additional, Kreek, Mary Jeanne, additional, Kristensson, Krister, additional, Kurtzke, John F., additional, Kusner, Linda L., additional, Landsberger, Nicoletta, additional, Li, Tong, additional, Liberski, Paweł P., additional, Lyons, Jennifer L., additional, Maleki, Nasim, additional, Mallucci, Giulia, additional, McArthur, Justin C., additional, McEwen, Bruce S., additional, McKee, Ann C., additional, McKhann, Guy, additional, Melnikova, Tatiana, additional, Mignot, Emmanuel, additional, Miller, Andrew H., additional, Mobley, William C., additional, Neppi-Modona, Marco, additional, O’Toole, Orna, additional, Parsons, Matthew P., additional, Peters, O.M., additional, Picetti, Roberto, additional, Pittock, Sean J., additional, Pluchino, Stefano, additional, Pressman, Peter, additional, Price, Donald L., additional, Raison, Charles L., additional, Raymond, Lynn A., additional, Reed, Brian, additional, Reiner, Peter B., additional, Ressler, Kerry J., additional, Rook, Graham W., additional, Rosen, Howard J., additional, Rowland, Lewis P., additional, Ruparelia, Aarti, additional, Saporta, Mario A., additional, Savonenko, Alena V., additional, Schaeffer, Julia, additional, Scharfman, Helen E., additional, Shapiro, Bruce K., additional, Shy, Michael E., additional, Simon, Roger P., additional, Sims-Robinson, Catrina, additional, Stein, Dan J., additional, Summers, Scott M., additional, Thakur, Kiran T., additional, Tovar-y-Romo, Luis B., additional, Vahabzadeh, Arshya, additional, Vercelli, Alessandro, additional, Wallin, Mitchell T., additional, Wichmann, Thomas, additional, Wiley, Clayton A., additional, Williams, David R., additional, Wong, Philip C., additional, Yuferov, Vadim, additional, Zhao, Weihua, additional, Zigmond, Michael J., additional, and Živković, Saša A., additional

Published
2015
Full Text
View/download PDF

47. Advanced Amyloid Cardiomyopathy Unmasked Following Mitral Valve Replacement

Author

Maude Pagé, Chimène Zaïani, Tasheen Wissanji, Frédéric Poulin, Karim Serri, and Louis R. Bégin

Subjects
Global longitudinal strain, Mitral regurgitation, medicine.medical_specialty, business.industry, medicine.medical_treatment, Amyloidosis, Mitral valve replacement, General Medicine, medicine.disease, Diagnosing Diseases, Internal medicine, medicine, Cardiology, Amyloid cardiomyopathy, business, ComputingMethodologies_COMPUTERGRAPHICS
Abstract

Graphical abstract, Highlights • A case of amyloid light-chain amyloidosis with primarily severe MR is described. • Diagnosis was unrecognized preoperatively due to normal LV thickness and function. • Diagnosis was unrecognized preoperatively due to normal LV thickness and function. • Retrospective analysis of preoperative GLS was suggestive of amyloid cardiomyopathy.

Published
2020

48. First report of the mcr-1 colistin resistance gene identified in two Escherichia coli isolates from clinical samples, Philippines, 2018

Author

Paula Corazon Diones, John Crawford, Angeli Mae B. Reyes, Sirigade Ruekit, Louis R. Macareo, Susie Leonardia, Fatima Claire Navarro, Ma. Theresa G. Valderama, Cynthia Liao, Stefan Fernandez, John Mark Velasco, Domingo Chua, Brett E. Swierczewski, and Katie R. Margulieux

Subjects
0301 basic medicine, Microbiology (medical), China, Philippines, 030106 microbiology, Immunology, Biology, mcr-1, Multidrug resistance, medicine.disease_cause, Antimicrobial resistance, Microbiology, beta-Lactamases, 03 medical and health sciences, 0302 clinical medicine, Antibiotic resistance, Plasmid, Escherichia coli, medicine, Humans, Immunology and Allergy, Antimicrobial stewardship, 030212 general & internal medicine, Colistin, Escherichia coli Proteins, biology.organism_classification, QR1-502, Multiple drug resistance, MCR-1, Bacteria, hormones, hormone substitutes, and hormone antagonists, medicine.drug
Abstract

Objectives The first report of a plasmid-borne colistin resistance gene (mcr-1) detected in an Escherichia coli isolate from China heralded the emergence of pandrug-resistant bacteria. Since then, the mcr-1 gene has been detected worldwide, but to date it has not been reported in the Philippines. Methods In this study, 123 antimicrobial-resistant isolates collected from January–June 2018 from patients admitted to a tertiary hospital in Manila, Philippines, were characterised. Biochemical identification and antimicrobial susceptibility testing were performed using a BD Phoenix™ M50 system with NMIC/ID-95 panel. Conventional PCR was performed to detect the genes mcr-1 to mcr-5, and short- and long-read whole-genome sequencing was performed. Results Two mcr-1-positive E. coli clinical isolates from separate patients harboured mcr-1 on an IncI2 plasmid. One isolate was shown to carry 12 antimicrobial resistance genes (ARGs) in addition to mcr-1, including the extended-spectrum β-lactamase blaCTX-M-55, whilst the other E. coli isolate carried 6 ARGs in addition to mcr-1. Conclusion Both patients had no prior colistin treatment recorded in their medical history and no travel history outside of the country within the past 6 months from the date of hospital admission, indicating local transmission and acquisition of the colistin-resistant strain from either community or hospital settings within the Philippines. This report should serve as a signal to local public-health officials of the need to intensify surveillance efforts and to increase vigilance and implementation of antimicrobial stewardship programmes to contain and slow the spread of antimicrobial resistance.

Published
2020

49. Increased bioavailability of cyclic guanylate monophosphate prevents retinal ganglion cell degeneration

Author

Fei Fei, Ana C. Dordea, Grigorij Schleifer, Lauren K. Wareham, Meredith S Gregory-Ksander, Annabelle Batten, Emmanuel S. Buys, Rebecca M. Sappington, Joseph L. Mertz, Vincent Yao, and Louis R. Pasquale

Subjects
0301 basic medicine, Retinal Ganglion Cells, Intraocular pressure, genetic structures, Glaucoma, Apoptosis, Pharmacology, Retinal ganglion, Article, Tadalafil, lcsh:RC321-571, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Retinal ganglion cell, Axon, Cyclic GMP, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Cells, Cultured, Mice, Knockout, Retina, Chemistry, Retinal Degeneration, Phosphodiesterase, Nitric oxide, Phosphodiesterase 5 Inhibitors, medicine.disease, eye diseases, cGMP, Disease Models, Animal, 030104 developmental biology, medicine.anatomical_structure, Neurology, Guanylate Cyclase, Optic nerve, Female, sense organs, PDE5, 030217 neurology & neurosurgery, Signal Transduction
Abstract

The nitric oxide – guanylyl cyclase-1 – cyclic guanylate monophosphate (NO-GC-1–cGMP) pathway has emerged as a potential pathogenic mechanism for glaucoma, a common intraocular pressure (IOP)-related optic neuropathy characterized by the degeneration of retinal ganglion cells (RGCs) and their axons in the optic nerve. NO activates GC-1 to increase cGMP levels, which are lowered by cGMP-specific phosphodiesterase (PDE) activity. This pathway appears to play a role in both the regulation of IOP, where reduced cGMP levels in mice leads to elevated IOP and subsequent RGC degeneration. Here, we investigated whether potentiation of cGMP signaling could protect RGCs from glaucomatous degeneration. We administered the PDE5 inhibitor tadalafil orally (10 mg/kg/day) in murine models of two forms of glaucoma – primary open angle glaucoma (POAG; GC-1−/− mice) and primary angle-closure glaucoma (PACG; Microbead Occlusion Model) - and measured RGC viability at both the soma and axon level. To determine the direct effect of increased cGMP on RGCs in vitro, we treated axotomized whole retina and primary RGC cultures with the cGMP analogue 8-Br-cGMP. Tadalafil treatment increased plasma cGMP levels in both models, but did not alter IOP or mean arterial pressure. Nonetheless, tadalafil treatment prevented degeneration of RGC soma and axons in both disease models. Treatment of whole, axotomized retina and primary RGC cultures with 8-Br-cGMP markedly attenuated both necrotic and apoptotic cell death pathways in RGCs. Our findings suggest that enhancement of the NO-GC-1-cGMP pathway protects the RGC body and axon in murine models of POAG and PACG, and that enhanced signaling through this pathway may serve as a novel glaucoma treatment, acting independently of IOP.

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results