The i.v. administration of radiographic contrast media decreases cerebrospinal fluid (CSF) production as measured by negative pressure collection from the lateral ventricles of anesthetized dogs. Evidence suggests that adrenergic-mediated adenylate cyclase (AC) activity controls CSF production. AC activity was measured in membrane fractions of bovine and canine choroid plexus and rat heart and lung in the presence of various concentrations of the contrast agent sodium diatrizoate. A concentration-dependent inhibition of isoproterenol-stimulated AC activity by the contrast agent was observed in vitro. Specific binding of [3H]dihydroalprenolol to membrane fractions of bovine choroid plexus was also inhibited by sodium diatrizoate. An indication that the inhibition of choroidal AC activity by contrast media is significant in vivo was obtained by measuring CSF production in dogs. The inhibition of CSF production by sodium diatrizoate was reduced 50% when the contrast agent was administered during an i.v. infusion of isoproterenol (100 ng/kg/min). These results indicate that the mechanism of decreased CSF production by contrast media may involve inhibition of beta adrenergic-stimulated AC activity.
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Fish Shellfish Immunol
January 2025
Laboratory of Pathology and Immunology of Aquatic Animals, KLMME, Ocean University of China, 5 Yushan Road, Qingdao, 266003, PR China; Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao Marine Science and Technology Center, Qingdao, Shandong 266237, PR China. Electronic address:
Granulocyte colony stimulating factor (G-CSF) has been shown in mammalia to activate a series of signal transduction systems and exert various biological effects, such as controlling the differentiation, proliferation, and survival of granulocytes, promoting the movement of hematopoietic stem cells from the bone marrow to the bloodstream, and triggering the development of T cells, dendritic cells, and immune tolerance in transplants. In this study, the mRNA of flounder G-CSF (PoG-CSF) and its receptor (PoGCSFR) were detected and widely expressed in all examined tissues with the highest expression in peritoneal cells. G-CSF and GCSFR cells were observed to be abundantly distributed in the leukocytes from the peritoneal cavity, followed by head kidney.
View Article and Find Full Text PDFBrain
January 2025
Department of Neurology, National Taiwan University Hospital, Taipei, 100225, Taiwan.
Hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN) is a neurodegenerative disease caused by mutations in the gene encoding transthyretin (TTR). Despite amyloid deposition being pathognomonic for diagnosis, this pathology in nervous tissues cannot fully account for nerve degeneration, implying additional pathophysiology for neurodegeneration, which, however, has not yet been fully elucidated. In this study, neuroinflammation in ATTRv-PN was investigated by examining nerve morphometry, the blood-nerve barrier, and macrophage infiltration in the sural nerves of ATTRv-PN patients and the sciatic nerves of a complementary mouse system, i.
View Article and Find Full Text PDFMol Immunol
January 2025
Chinese Medicine Research and Development Center, China Medical University Hospital, Taichung, Taiwan; Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan; Master Program of Pharmaceutical Manufacture, College of Pharmacy, China Medical University, Taichung, Taiwan; Department of Medical Laboratory Science and Biotechnology, College of Medical and Health Science, Asia University, Taichung, Taiwan. Electronic address:
The immunoglobulin E (IgE) receptor FcεRI (Fc epsilon RI) plays a crucial role in allergic reactions. Recent studies have indicated that the interaction between FcεRIβ and the downstream protein phospholipase C beta 3 (PLCβ3) leads to the production of inflammatory cytokines. The aim of this study was to develop small molecules that inhibit the protein-protein interactions between FcεRIβ and PLCβ3 to treat allergic inflammation.
View Article and Find Full Text PDFAnn Clin Transl Neurol
January 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
Defining the CSF cytokine/chemokine and injury biomarker signature of glial fibrillary acidic protein (GFAP) autoimmunity can inform immunopathogenesis. CSF GFAP-IgG-positive samples (N = 98) were tested for 17 cytokines/chemokines, neurofilament light chain (NfL), and GFAP (ELLA, Bio-Techne). Controls included non-inflammatory (N = 42), AQP4-IgG-positive (N = 83), CNS infections (N = 13), and neurosarcoidosis (N = 32).
View Article and Find Full Text PDFJ Cell Immunol
January 2024
Department of Medicine, University of Washington, Seattle, Washington, U.S.A.
Neutrophil elastase () mutations are the most common cause of cyclic (CyN) and congenital neutropenia (SCN), two autosomal dominant disorders causing recurrent infections due to impaired neutrophil production. Granulocyte colony-stimulating factor (G-CSF) corrects neutropenia but has adverse effects, including bone pain and in some cases, an increased risk of myelodysplasia (MDS) and acute myeloid leukemia (AML). Hematopoietic stem cell transplantation is an alternative but is limited by its complications and donor availability.
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