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Filename: controllers/Detail.php
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Lymphoma research has advanced thanks to introduction of [(18)F]fludarabine, a positron-emitting tool. This novel radiotracer has been shown to display a great specificity for lymphoid tissues. However, in a benign process such as inflammation, the uptake of this tracer has not been questioned. Indeed, in inflammatory zones, elevated glucose metabolism rate may result in false-positives with [(18)F]FDG-PET Imaging. In the present investigation, it has been argued that cells, involved in inflammation, might be less avid of [(18)F]fludarabine. To generate inflammation, Swiss mice were intramuscularly injected with 0.1 mL of turpentine oil into the right front paw. Imaging sessions with (18)F-labeled tracers named above were conducted on days 5 and 25 after inoculation. For each animal, volumes of interest (VOI), delineating the muscle of the inflamed (IP) and normal paws (NP), were determined on PET scans. For characterization of inflammation, muscle samples from IP and NP were stained with hematoxylin and eosin (H&E). In early (day 5) inflammation, [(18)F]FDG accumulation was 4.00 ± 1.65 times greater in the IP than in the contralateral NP; for [(18)F]fludarabine, this IP/NP ratio was 1.31 ± 0.28, resulting in a significant difference between radiotracer groups (p < 0.01). In late (day 25) inflammation, the IP/NP ratios were 2.07 ± 0.49 and 1.03 ± 0.07, for [(18)F]FDG and [(18)F]fludarabine, respectively (p < 0.001). [(18)F]Fludarabine showed significantly weaker uptake in inflammation when compared with [(18)F]FDG. This encouraging finding suggests that [(18)F]fludarabine-PET might well be a robust approach for distinguishing tumor from inflammatory tissue, avoiding false-positive PET results and thus enabling an accurate imaging of lymphoma.
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http://dx.doi.org/10.1021/acs.molpharmaceut.6b00050 | DOI Listing |
Redox Rep
December 2025
Department of Medical Biochemistry, Tanta Faculty of Medicine, Tanta University, Tanta, Egypt.
Background: The most prevalent endocrine disorder affecting women is PCOS. Programmed death of ovarian cells has yet to be elucidated. Ferroptosis is a kind of iron-dependent necrosis featured by significantly Fe-dependent lipid peroxidation.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA.
Background: Inclusion body myositis (IBM) is the most prevalent muscle disease in adults for which no current treatment exists. The pathogenesis of IBM remains poorly defined. In this study, we aimed to explore the interplay between inflammation and mitochondrial dysfunction in IBM.
View Article and Find Full Text PDFAntioxid Redox Signal
December 2024
National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease, and podocyte injury is one of the major contributors to DKD. As a crucial transcriptional factor that regulates cellular response to oxidative stress, nuclear factor erythroid 2-related factor 2 (Nrf2) is an attractive therapeutic target for DKD. In this study, we evaluated the therapeutic potential of DDO-1039, a novel small-molecule Nrf2 activator developed with protein-protein interaction strategy, on podocyte injury in DKD.
View Article and Find Full Text PDFAnn Med
December 2025
Department of Hebei Provincial Key Laboratory of Basic Medicine for Diabetes, The Shijiazhuang Second Hospital, Shijiazhuang, China.
Objectives: To explore the effect and the probable mechanisms of JLD in the treatment of type 2 diabetes mellitus (T2DM) - associated cognitive impairment (TDACI).
Methods: The effect of JLD in combating TDACI was assessed in T2DM model mice by conducting Morris water maze (MWM) behaviour testing. Active components and their putative targets, as well as TDACI-related targets, were collected from public databases.
Front Cardiovasc Med
December 2024
Seattle Children's Hospital, Seattle, WA, United States.
Introduction: The use of cardiopulmonary bypass (CPB) can induce sterile systemic inflammation that contributes to morbidity and mortality, especially in children. Patients have been found to have increased expression of cytokines and transmigration of leukocytes during and after CPB. Previous work has demonstrated that the supraphysiologic shear stresses existing during CPB are sufficient to induce proinflammatory behavior in non-adherent monocytes.
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