Monoclonal antibodies were used in competitive binding assays to investigate the arrangement of three epitopes on the protein p19 of avian myeloblastosis virus (AMV). It was reasoned that if the epitopes recognized by two monoclonal antibodies are physically close, the binding of one antibody will sterically block the binding of the second; conversely no blocking will occur if the epitopes are sufficiently distant. The results of these competitive binding assays demonstrated the presence of two distinct antigenic sites on the protein p19. Monoclonal antibodies against the protein p19 of AMV were tested also in gel double immunodiffusion. Since the p19 protein has strong tendency to aggregate, it was not surprising, that clear precipitin lines with these monoclonal antibodies were obtained.
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BMC Med Res Methodol
January 2025
Clifton Insight, Bristol, UK.
Background: Population-adjusted indirect comparison using parametric Simulated Treatment Comparison (STC) has had limited application to survival outcomes in unanchored settings. Matching-Adjusted Indirect Comparison (MAIC) is commonly used but does not account for violation of proportional hazards or enable extrapolations of survival. We developed and applied a novel methodology for STC in unanchored settings.
View Article and Find Full Text PDFSci Rep
January 2025
Key Laboratory of Cancer Immunotherapy of Guangdong Tertiary Education, Guangdong CAR-T Treatment Related Adverse Reaction Key Laboratory, The First Affiliated Hospital/Clinical Medical School, Guangdong Pharmaceutical University, Guangzhou, 510080, China.
Previously, we demonstrated that natural host-defence peptide caerin 1.1/caerin 1.9 (F1/F3) increases the efficacy of anti-PD-1 and therapeutic vaccine, in a HPV16 + TC-1 tumour model, but the anti-tumor mechanism of F1/F3 is still unclear.
View Article and Find Full Text PDFExpert Rev Neurother
January 2025
Headache Centre, Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy.
Introduction: When a first anti-CGRP monoclonal antibody (anti-CGRP mAb) fails, switching to a different anti-CGRP mAb is an option often considered, despite this approach is not yet systemically studied.
Methods: We present the findings of a systematic review conducted according to the PRISMA recommendations on published studies - of any design - investigating the clinical outcomes after switching for any reason to different anti-CGRP mAbs.
Results: The literature search retrieved 76 records, while 19 papers were eventually reviewed.
ACS Sens
January 2025
Centre for Advanced Imaging (CAI) and Australian Institute for Bioengineering and Nanotechnology, ARC Training Centre for Innovation in Biomedical Imaging Technology, The University of Queensland, St. Lucia, Queensland 4072, Australia.
Recent examples of immune responses directed against the synthetic polymer poly(ethylene glycol) (PEG) have led to the development of biocompatible polymers, which are viewed as promising candidates to act as surrogate materials for use in biological applications, such as hydrophilic poly(2-oxazoline)s (POx). Despite this, the characterization of critical aspects of the immune response against these emerging materials is sparse, in part because no known monoclonal antibodies (mAbs) against this family of synthetic material have been reported. To advance the understanding of such responses, we report the successful isolation and characterization of hybridoma-derived mAbs with excellent specificity for different POx species and notable selectivity for highly branched polymer architectures over linear systems.
View Article and Find Full Text PDFCytokine Growth Factor Rev
January 2025
Faculty of Pharmacy, University of Ljubljana, Slovenia. Electronic address:
A cytokine storm is marked by excessive pro-inflammatory cytokine release, and has emerged as a key factor in severe COVID-19 cases - making it a critical therapeutic target. However, its pathophysiology was poorly understood, which hindered effective treatment. SARS-CoV-2 initially disrupts angiotensin signalling, promoting inflammation through ACE-2 downregulation.
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