Publications by authors named "Dirk Hermann"

Background: Older adults often face challenges in medication management due to multimorbidity and complex medication regimens, which frequently go unreported. Unrecognized problems, however, may lead to a loss of drug efficacy and harmful side effects. This study aimed to quantify the prevalence of such problems by applying a novel video-based assessment procedure in a sample of elderly patients.

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The major aim of stroke therapy is to stimulate brain repair and improve behavioral recovery after cerebral ischemia. One option is to stimulate endogenous neurogenesis in the subventricular zone and direct the newly formed neurons to the damaged area. However, only a small percentage of these neurons survive, and many do not reach the damaged area, possibly because the corpus callosum impedes the migration of subventricular zone-derived stem cells into the lesioned cortex.

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In many medical settings, medications are typically administered in the morning or evening, aligning with patients' daily routines. This practice does not stem from chronotherapy, which involves scheduling drug administration to enhance its effectiveness, but rather from the way clinical operations are structured. The timing of drug administration can significantly affect a medication's effectiveness and side effects, with the impact varying by up to ten times based on circadian rhythms.

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Neutrophils are indispensable for defense against pathogens. Injured tissue-infiltrated neutrophils can establish a niche of chronic inflammation and promote degeneration. Studies investigated transcriptome of single-infiltrated neutrophils which could misinterpret molecular states of these post mitotic cells.

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Psychotropic drugs are vital in psychiatry, aiding in the management of mental health disorders. Their use requires an understanding of their pharmacological properties, therapeutic applications, and potential side effects. Ongoing research aims to improve their efficacy and safety.

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Sphingolipids comprise a class of lipids, which are composed of a sphingoid base backbone and are essential structural components of cell membranes. Beyond their role in maintaining cellular integrity, several sphingolipids are pivotally involved in signaling pathways controlling cell proliferation, differentiation, and death. The brain exhibits a particularly high concentration of sphingolipids and dysregulation of the sphingolipid metabolism due to ischemic injury is implicated in consecutive pathological events.

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Background: The discrepancy between experimental research and clinical trial outcomes is a persistent challenge in preclinical studies, particularly in stroke research. A possible factor contributing to this issue is the lack of standardization across experimental stroke models, leading to poor reproducibility in multicenter studies. This study addresses this gap by aiming to enhance reproducibility and the efficacy of multicenter studies through the harmonization of protocols and training of involved personnel.

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Ischemic stroke is followed by an increased susceptibility to bacterial infections, which exacerbate histological stroke outcome, neurological deficits and memory impairment due to increased neuroinflammation and neurotransmitter dysfunction. Pharmacological activation of nicotinic acetylcholine receptors was suggested to mitigate brain inflammatory responses in ischemic stroke. The functional responses associated with nicotinic acetylcholine receptor activation were unknown.

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Microglia are critically involved in post-stroke inflammation affecting neurological outcomes. Lipid droplet (LD) accumulation in microglia results in a dysfunctional and pro-inflammatory state in the aged brain and worsens the outcome of neuroinflammatory and neurodegenerative diseases. However, the role of LD-rich microglia (LDRM) under stroke conditions is unknown.

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Article Synopsis
  • Small extracellular vesicles (sEVs) from mesenchymal stromal cells (MSCs) show promise for stroke treatment by enhancing brain tissue survival and promoting angiogenesis, especially when the MSCs are cultured in hypoxic conditions.
  • In a study involving rats with permanent distal MCAO, sEVs from hypoxic MSCs improved motor-coordination recovery and reduced brain inflammation compared to untreated controls.
  • Although hypoxic MSC-sEVs did not affect infarct volume, they significantly increased proliferating endothelial cells, suggesting they have a positive impact on recovery and healing in stroke models.
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  • 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.
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  • * 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.
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  • Recent advances in light-sheet microscopy now allow for 3D analysis of microvascular networks in brain tissue without the need for histological sectioning, which was previously a barrier.
  • In a study involving mice after a stroke model, researchers observed significant changes in microvessels over time, including an initial loss followed by a reemergence and increased complexity of small microvessels within 56 days.
  • The administration of FTY720 (Fingolimod) after ischemia enhanced the growth and branching of small microvessels, highlighting its potential in improving microvascular architecture following a stroke.
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Activation of the kallikrein-kinin system promotes vascular leakage, inflammation, and neurodegeneration in ischemic stroke. Inhibition of plasma kallikrein (PK) - a key component of the KKS - in the acute phase of ischemic stroke has been reported to reduce thrombosis, inflammation, and damage to the blood-brain barrier. However, the role of PK during the recovery phase after cerebral ischemia is unknown.

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Anti-aging research has made significant strides in identifying treatments capable of extending lifespan across a range of organisms, from simple invertebrates to mammals. This review showcases the current state of anti-aging interventions, highlighting the lifespan extensions observed in animal models through various treatments and the challenges encountered in translating these findings to humans. Despite promising results in lower organisms, the translation of anti-aging treatments to human applications presents a considerable challenge.

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Background: The benefits and risks of tenecteplase (TNK) versus alteplase (ALT) have recently been assessed in acute ischemic stroke (AIS) patients undergoing mechanical thrombectomy (MT) with diverse results. Due to its high fibrin specificity and lack of excitotoxicity, TNK may have a higher efficacy and safety profile. This study aimed to evaluate the benefits and risks of TNK compared to ALT in AIS patients prior to thrombectomy.

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Each year, 15 million people worldwide suffer from strokes. Consequently, researchers face increasing pressure to develop reliable behavioural tests for assessing functional recovery after a stroke. Our aim was to establish a new motor performance index that can be used to evaluate post-stroke recovery in both young and aged animals.

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Due to worldwide demographic change, the number of older persons in the population is increasing. Aging is accompanied by changes of sleep structure, deposition of beta-amyloid (Aß) and tau proteins and vascular changes and can turn into mild cognitive impairment (MCI) as well as dementia. Sleep disorders are discussed both as a risk factor for and as a consequence of MCI/dementia.

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Cerebrovascular diseases are the second leading cause of death worldwide. Despite significant research investment, the only available therapeutic options are mechanical thrombectomy and tissue plasminogen activator thrombolysis. None of the more than a thousand drugs tested on animal models have proven successful in human clinical trials.

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