Background: The aim of this pilot study was to test whether diagnostic agreement of aggressive and chronic periodontitis amongst Board Certified Periodontists, is influenced by knowledge of a patient's age. In 1999 at the International World Workshop age was removed as a diagnostic criteria for aggressive periodontitis. The impact of this change on the diagnostic reliability amongst clinicians has not yet been assessed.
Methods: Nine periodontal case reports were twice presented to sixteen board certified periodontists, once with age withheld and again with patient age provided. Participants were instructed to choose a diagnosis of Chronic Periodontitis or Aggressive Periodontitis. Diagnostic agreement was calculated using the Fleiss Kappa test.
Results: Including the patients' age in case report information increased diagnostic agreement (the kappa statistic) from 0.49 (moderate agreement) to 0.61 (substantial agreement).
Conclusion: These results suggest that knowledge of a patients' age influenced clinical diagnosis, when distinguishing between aggressive periodontitis and chronic periodontitis, which may in turn impact treatment decision-making.
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http://dx.doi.org/10.1186/s12903-016-0258-0 | DOI Listing |
Alzheimers Dement (Amst)
January 2025
Weill Institute for Neurosciences, Department of Neurology, Memory and Aging Center University of California, San Francisco San Francisco California USA.
Introduction: Plasma amyloid beta/amyloid beta (Aβ/Aβ) and phosphorylated tau217 (p-tau217) identify individuals with primary Alzheimer's disease (AD). They may detect AD co-pathology in the setting of other primary neurodegenerative diseases, but this has not been systematically studied.
Methods: We compared the clinical, neuroimaging, and neuropathological associations of plasma Aβ/Aβ (mass spectrometry), p-tau217 (electrochemiluminescence), and neurofilament light ([NfL], single molecule array [Simoa]), as markers of AD co-pathology, in a sporadic frontotemporal dementia (FTD) cohort ( = 620).
Alzheimers Dement (Amst)
January 2025
Neurochemistry Laboratory Department of Laboratory Medicine Amsterdam UMC Amsterdam The Netherlands.
Introduction: Blood-based glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and phosphorylated tau (pTau) have shown promising prognostic potential in Alzheimer's disease (AD), but their applicability in clinical settings where comorbidities are prevalent remains uncertain.
Methods: Simoa assays quantified GFAP, NfL, and pTau181 in retrospectively retrieved prediagnostic serum samples from 102 AD patients and 21 non-AD controls.
Results: Higher serum GFAP levels predicted earlier clinical presentation and faster subsequent Mini-Mental State Examination decline in AD patients.
JACC Adv
February 2025
Barts Heart Centre, Department of Cardiac Diagnostics and The Inherited Cardiovascular Diseases Unit, St Bartholomew's Hospital, London, United Kingdom.
Front Cell Infect Microbiol
January 2025
Department of Clinical Laboratory, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Background: Though droplet digital PCR (ddPCR) has emerged as a promising tool for early pathogen detection in bloodstream infections (BSIs), more studies are needed to support its clinical application widely due to different ddPCR platforms with discrepant diagnostic performance. Additionally, there is still a lack of clinical data to reveal the association between pathogen loads detected by ddPCR and corresponding BSIs.
Methods: In this prospective study, 173 patients with suspected BSIs were enrolled.
Neural Regen Res
January 2025
Laboratorio de Neurofisiología, Departamento de Fisiología, Universidad de Concepción, Concepción, Chile.
For many decades, Alzheimer's disease research has primarily focused on impairments within cortical and hippocampal regions, which are thought to be related to cognitive dysfunctions such as memory and language deficits. The exact cause of Alzheimer's disease is still under debate, making it challenging to establish an effective therapy or early diagnosis. It is widely accepted that the accumulation of amyloid-beta peptide in the brain parenchyma leads to synaptic dysfunction, a critical step in Alzheimer's disease development.
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