Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1126/science.165.3896.862 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The spleen in ischaemic heart disease.
Nat Rev Cardiol
January 2025
Institute for Pathophysiology, West German Heart and Vascular Center, University of Duisburg-Essen, Essen, Germany.
Article Synopsis
- Ischaemic heart disease results from coronary atherosclerosis, which is linked to systemic inflammation involving various immune cells released by the spleen.
- Prolonged inflammation can lead to ischaemic heart failure, while the spleen's interaction with the nervous system can modulate immune responses and protect the heart from damage.
- Splenectomy, which removes the spleen, increases mortality risk from ischaemic heart disease, highlighting the spleen's crucial role in immune responses and cardiovascular protection.
Exploration of bioactive molecules from Sesbania grandiflora (L.): identification of squalene as an effective compound against the two-spotted spider mite, Tetranychus urticae Koch, through molecular docking.
Exp Appl Acarol
December 2024
Department of Agricultural Entomology, Tamil Nadu Agricultural University, Coimbatore, Tamil Nadu, 641003, India.
Two-spotted spider mite (TSSM), Tetranychus urticae Koch is a devastating polyphagous mite causing considerable economic loss. Acaricides are showered in crops to manage this pest. The pest is known for developing resistance to several classical acaricides.
View Article and Find Full Text PDFInvestigating the Mechanisms Involved in Scopolamine-induced Memory Degradation.
Arch Razi Inst
June 2024
Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
In the present study, the mechanisms involved in scopolamine-induced memory impairment have been investigated. The molecular events that take place during memory mostly include mechanisms that are seen in the acquisition phase. Results showed that one of the mechanisms of memory destruction caused by scopolamine, in addition to weakening the cholinergic system, is the indirect effect of scopolamine on other neurotransmitter systems, including the glutamatergic system.
View Article and Find Full Text PDFFirst line treatment with subcutaneous efgartigimod in impending myasthenic crisis: a case report.
Ther Adv Neurol Disord
December 2024
Department of Neurology, Faculty of Medicine, University of Augsburg, Stenglinstrasse 2, Augsburg 86156, Germany.
In acetylcholine receptor (AChR) antibody-positive generalized myasthenia gravis (gMG), neonatal Fc-receptor (FcRn) inhibition has broadened the therapeutic spectrum. Myasthenic crisis (MC), heralded by an impending myasthenic crisis (iMC), is a critical condition requiring treatments with rapid onset and sustained efficacy. Currently treatments used for iMC, including intravenous immunoglobulins and plasma exchange/immunoadsorption, have limitations, such as delayed onset of action and potential side effects.
View Article and Find Full Text PDFComplement inhibition in seropositive generalized myasthenia gravis as rescue therapy in impending and effective treatment in frequently recurring impending myasthenic crisis-a case series.
Ther Adv Neurol Disord
December 2024
Department of Neurology, Faculty of Medicine, University of Augsburg, Stenglinstrasse 2, Augsburg 86156, Germany.
In seropositive myasthenia gravis (MG), complement inhibition has been shown to be an effective and a fast-acting therapeutic option. Myasthenic crisis (MC), usually preceded by impending MC, is a life-threatening complication requiring highly effective treatments with rapid onset of action. Currently used treatment options of MC are limited, consisting mainly of symptomatic and immune therapies, that is, intravenous immunoglobulins and plasma exchange/immunoadsorption.
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!