Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5849876 | PMC |
| http://dx.doi.org/10.1016/j.eucr.2018.01.026 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Improving prognostic evaluations in patients with stage IIIb light chain cardiac amyloidosis: role of haemodynamic parameters.
Orphanet J Rare Dis
January 2025
Department of Cardiology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730, China.
Background: There is no unified prognostic scoring system for light chain cardiac amyloidosis (AL-CA), particularly stage IIIb AL-CA. This study aimed to use invasive haemodynamic information to investigate markers that can more accurately evaluate the prognosis of patients with stage IIIb AL-CA.
Methods: In this retrospective cohort study, we conducted invasive haemodynamic measurements concurrently with myocardial biopsies to diagnose AL-CA.
Molecular Stratification of Light-Chain Cardiac Amyloidosis With F-Florbetapir and Ga-FAPI-04 for Enhanced Prognostic Precision.
JACC Cardiovasc Imaging
January 2025
Department of Nuclear Medicine, Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Center for Rare Diseases Research, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Background: Cardiac involvement in amyloid light chain (AL) amyloidosis significantly influences prognosis, necessitating timely diagnosis and meticulous risk stratification.
Objectives: This prospective study aimed to delineate the molecular phenotypes of AL cardiac amyloidosis (AL-CA) by characterizing fibro-amyloid deposition using F-florbetapir and gallium-68-labeled fibroblast activation protein inhibitor-04 (Ga-FAPI-04) positron emission tomography (PET)/computed tomography (CT) imaging. The authors also proposed a novel molecular stratification methodology for prognosis.
Evaluation of the Anti-Amyloid and Anti-Inflammatory Properties of a Novel Vanadium(IV)-Curcumin Complex in Lipopolysaccharides-Stimulated Primary Rat Neuron-Microglia Mixed Cultures.
Int J Mol Sci
December 2024
Laboratory of Biochemistry, Department of Chemistry, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.
Lipopolysaccharides (LPS) are bacterial mediators of neuroinflammation that have been detected in close association with pathological protein aggregations of Alzheimer's disease. LPS induce the release of cytokines by microglia and mediate the upregulation of inducible nitric oxide synthase (iNOS)-a mechanism also associated with amyloidosis. Curcumin is a recognized natural medicine but has extremely low bioavailability.
View Article and Find Full Text PDFFrom Molecular to Radionuclide and Pharmacological Aspects in Transthyretin Cardiac Amyloidosis.
Int J Mol Sci
December 2024
Clinic of Nuclear Medicine Central University Emergency Military Hospital "Dr Carol Davila", 10825 Bucharest, Romania.
Amyloidosis is a rare pathology characterized by protein deposits in various organs and tissues. Cardiac amyloidosis (CA) can be caused by various protein deposits, but transthyretin amyloidosis (ATTR) and immunoglobulin light chain (AL) are the most frequent pathologies. Protein misfolding can be induced by several factors such as oxidative stress, genetic mutations, aging, chronic inflammation, and neoplastic disorders.
View Article and Find Full Text PDFLocalized light chain amyloidosis of the stomach that regressed after eradication of Helicobacter pylori over 15 years of follow-up: a case report and new hypothesis.
Clin J Gastroenterol
January 2025
Department of Gastroenterology, Saiseikai Kanazawa Hospital, Ni-13-6 Akatsuchimachi, Kanazawa, Ishikawa, 920-0353, Japan.
Localized light chain amyloidosis is considered to be a plasmacytic B-cell lymphoproliferative disorder caused by antigenic induction. A hypothesis has been proposed that antigen-induced local plasmacytic B cells produce amyloidogenic proteins that are processed into amyloid fibrils in giant cells leading to amyloid fibril deposition. However, the inciting antigen exposure or immune response that signals plasmacytic B-cell infiltration, activation, and selection, is unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!