Terry J. Smith
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View article: Comorbidities Are Associated With Unfavorable Outcome in Aquaporin‐4 Antibody Positive Neuromyelitis Optica Spectrum Disorders and Myelin Oligodendrocyte Glycoprotein Antibody‐Associated Disease: Exploratory Study From the <scp>CROCTINO</scp> Cohort
Comorbidities Are Associated With Unfavorable Outcome in Aquaporin‐4 Antibody Positive Neuromyelitis Optica Spectrum Disorders and Myelin Oligodendrocyte Glycoprotein Antibody‐Associated Disease: Exploratory Study From the <span>CROCTINO</span> Cohort Open
Background Comorbidities occur in aquaporin‐4 antibody‐positive neuromyelitis optica spectrum disorder (AQP4‐NMOSD), myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD), and double seronegative NMOSD (DN‐NMOSD), potenti…
View article: Virtual consultation in kidney care: a mixed-methods study on a model for safe and effective integration into routine clinical care
Virtual consultation in kidney care: a mixed-methods study on a model for safe and effective integration into routine clinical care Open
Rationale and Objective Globally, the COVID-19 pandemic necessitated a rapid introduction of virtual care delivery via telephone or videoconference. The rapid advancements in e-health technology facilitated options for virtual care, includ…
View article: Investigating factors influencing quality of life in thyroid eye disease: insight from machine learning approaches
Investigating factors influencing quality of life in thyroid eye disease: insight from machine learning approaches Open
Aims Thyroid eye disease (TED) is an autoimmune orbital disorder that diminishes the quality of life (QOL) in affected individuals. Graves’ ophthalmopathy (GO)-QOL questionnaire effectively assesses TED’s effect on patients. This study aim…
View article: Aquaporin-4 Immunoglobulin G–seropositive Neuromyelitis Optica Spectrum Disorder MRI Characteristics: Data Analysis from the International Real-World PAMRINO Study Cohort
Aquaporin-4 Immunoglobulin G–seropositive Neuromyelitis Optica Spectrum Disorder MRI Characteristics: Data Analysis from the International Real-World PAMRINO Study Cohort Open
Large, international, real-world MRI assessments showed high heterogeneity in the data collected from patients with aquaporin-4 immunoglobulin G–seropositive neuromyelitis optica spectrum disorder and frequent cerebral and lower spinal cor…
View article: 6814 Durability of Teprotumumab for the Treatment of Thyroid Eye Disease (TED) in Clinical Trials
6814 Durability of Teprotumumab for the Treatment of Thyroid Eye Disease (TED) in Clinical Trials Open
Disclosure: G.J. Kahaly: Consulting Fee; Self; Amgen Inc. Research Investigator; Self; Amgen Inc. P.S. Subramanian: Consulting Fee; Self; Amgen Inc. Research Investigator; Self; Amgen Inc. E. Conrad: Employee; Self; Amgen Inc. Stock Owner;…
View article: 8518 Prevalence of Hearing Dysfunction in Patients with Autoimmune Thyroid Disorders, Thyroid Eye Disease and the General US population: A Claims Database Analysis
8518 Prevalence of Hearing Dysfunction in Patients with Autoimmune Thyroid Disorders, Thyroid Eye Disease and the General US population: A Claims Database Analysis Open
Disclosure: T.J. Smith: Consulting Fee; Self; Amgen Inc, Viridian, Minghui, Lassen, Lundbeck. Other; Self; US patents covering the use of IGF-1 receptor inhibitors in TED which are held by UCLA and the Lundquist Institute. A. Meyers: Emplo…
View article: Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin isoform imbalance on survival of patients with metastatic melanoma.
View article: Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of combination treatment on p53-activation in skin melanoma malignant phenotype in in vitro 3D models
View article: Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of combination treatment on p53-activation in skin melanoma malignant phenotype in in vitro 3D models
View article: Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Rescue-validation of β-arrestin imbalance effects on MDM2-dependent IGF1R expression.
View article: Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Specificity of β-arrestin1/2 siRNA effectson MDM2 localization.
View article: Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Table S1. Cell lines used in this study.
View article: Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on IGF1R expression
View article: Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Rescue-validation of β-arrestin imbalance effects on MDM2-dependent IGF1R expression.
View article: Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on response to dacarbazine (DTIC)
View article: Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin isoform imbalance on survival of patients with metastatic melanoma.
View article: Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Specificity of β-arrestin1/2 siRNA effectson MDM2 localization.
View article: Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on MDM2 localization
View article: Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Table S2. Antibodies used in this study.
View article: Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on IGF1R expression
View article: Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on MDM2 localization
View article: Supplementary Figure 1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin isoform imbalance on melanoma cell viability
View article: Supplementary Figure 1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin isoform imbalance on melanoma cell viability
View article: Data from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Data from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Constraints on the p53 tumour suppressor pathway have long been associated with the progression, therapeutic resistance, and poor prognosis of melanoma, the most aggressive form of skin cancer. Likewise, the insulin-like growth factor type…
View article: Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Effect of β-arrestin imbalance on response to dacarbazine (DTIC)
View article: Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Table S1. Cell lines used in this study.
View article: Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness Open
Table S2. Antibodies used in this study.
View article: Diagnostic Value of Inter-Eye Difference Metrics on OCT for Myelin Oligodendrocyte Glycoprotein Antibody-Associated Optic Neuritis
Diagnostic Value of Inter-Eye Difference Metrics on OCT for Myelin Oligodendrocyte Glycoprotein Antibody-Associated Optic Neuritis Open
This study provides Class III evidence that the intereye difference on OCT can distinguish between those with MOG and normal controls.