Publications by authors named "B Kaltwasser"
Article Synopsis
- Acid sphingomyelinase (ASM) inhibitors, like amitriptyline, aid in recovering from post-stroke depression and enhance neurological recovery through neurorestorative effects in stroke models.
- The study revealed that amitriptyline boosts the formation of mitochondrial reactive oxygen species (ROS) in both human endothelial cells and mice models, which plays a key role in its ability to promote angiogenesis.
- Furthermore, amitriptyline triggers a metabolic reprogramming in endothelial cells that reduces harmful stress while encouraging protective responses, with the antioxidant heme oxygenase-1 being crucial for mediating its angiogenic effects.
Article Synopsis
- * Researchers discovered that this drop in IgA happens because the immune system cells that make it are harmed after injury.
- * They also found that certain cells called neutrophils cause this problem, but if these cells are removed or their action is blocked, the levels of IgA can be preserved in both patients and mice.
Article Synopsis
- Scientists tested if special brain cells, called neural precursor cells (NPCs), could help mice with strokes, especially those with high cholesterol.
- They found that giving NPCs to the mice reduced damage in the brain right after the stroke but caused some bad side effects, like bleeding and more immune cells in mice with high cholesterol.
- In the long run, NPCs helped the mice recover a little at first but didn't have lasting benefits on their brain or health later on.
Astrocytic responses are critical for the maintenance of neuronal networks in health and disease. In stroke, reactive astrocytes undergo functional changes potentially contributing to secondary neurodegeneration, but the mechanisms of astrocyte-mediated neurotoxicity remain elusive. Here, we investigated metabolic reprogramming in astrocytes following ischemia-reperfusion in vitro, explored their role in synaptic degeneration, and verified the key findings in a mouse model of stroke.
View Article and Find Full Text PDFIschemic conditioning is defined as a transient and subcritical period of ischemia integrated in an experimental paradigm that involves a stimulus of injurious ischemia, activating endogenous tissue repair mechanisms that lead to cellular protection under pathological conditions like stroke. Whereas ischemic pre-conditioning is irrelevant for stroke treatment, ischemic post-conditioning, and especially non-invasive remote ischemic post-conditioning (rPostC) is an innovative and potential strategy for stroke treatment. Although rPostC has been shown to induce neuroprotection in stroke models before, resulting in some clinical trials on the way, fundamental questions with regard to its therapeutic time frame and its underlying mechanisms remain elusive.
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