Publications by authors named "Gerstner J"

Fatty acid binding protein 7 (FABP7) is a multifunctional chaperone involved in lipid metabolism and signaling. It is primarily expressed in astrocytes and neural stem cells (NSCs), as well as their derived malignant glioma cells within the central nervous system. Despite growing evidence for FABP7's tumor-intrinsic onco-metabolic functions, its mechanistic role in regulating the brain tumor immune microenvironment (TIME) and its impact on prognosis at the molecular level remain incompletely understood.

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  • * An online questionnaire was distributed to German physicians and rescue service personnel to gather their perspectives on trauma care and the use of blood products, showing a consensus on the need for improvement in this area.
  • * Results indicated that a significant majority of participants supported the prehospital use of certain blood products, particularly red blood cell concentrates and fibrinogen, to improve patient survival rates during trauma situations.
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  • Disruption of sleep and circadian rhythms is linked to various health issues, including neurodegenerative diseases, metabolic disorders, cancer, and neurological conditions.
  • Research typically focuses on genetic mutations, but the role of Alternative Polyadenylation (APA) in sleep and circadian disturbances is underexplored.
  • The study identified specific APA patterns in rat brains related to time of day and sleep deprivation, and analyzed these patterns in connection with human brain disorder susceptibility genes.
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Background: Digitalization in disaster medicine holds significant potential to accelerate rescue operations and ultimately save lives. Mass casualty incidents demand rapid and accurate information management to coordinate effective responses. Currently, first responders manually record triage results on patient cards, and brief information is communicated to the command post via radio communication.

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Disruption of sleep and circadian rhythms are a comorbid feature of many pathologies, and can negatively influence many health conditions, including neurodegenerative disease, metabolic illness, cancer, and various neurological disorders. Genetic association studies linking sleep and circadian disturbances with disease susceptibility have mainly focused on changes in gene expression due to mutations, such as single-nucleotide polymorphisms. The interaction between sleep and/or circadian rhythms with the use of Alternative Polyadenylation (APA) has been largely undescribed, particularly in the context of other disorders.

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Sleep and circadian rhythm disruptions are comorbid features of many pathologies and can negatively influence numerous health conditions, including degenerative diseases, metabolic illnesses, cancer, and various neurological disorders. Genetic association studies linking sleep and circadian disturbances with disease susceptibility have mainly focused on changes in gene expression due to mutations, such as single-nucleotide polymorphisms. Thus, associations between sleep and/or circadian rhythm and alternative polyadenylation (APA), particularly in the context of other health challenges, are largely undescribed.

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Sleep and circadian rhythms are observed broadly throughout animal phyla and influence neural plasticity and cognitive function. However, the few phylogenetically conserved cellular and molecular pathways that are implicated in these processes are largely focused on neuronal cells. Research on these topics has traditionally segregated sleep homeostatic behavior from circadian rest-activity rhythms.

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Humans with post-traumatic stress disorder (PTSD) exhibit sleep disturbances that include insomnia, nightmares, and enhanced daytime sleepiness. Sleep disturbances are considered a hallmark feature of PTSD; however, little is known about the cellular and molecular mechanisms regulating trauma-induced sleep disorders. Using a rodent model of PTSD called "Single Prolonged Stress" (SPS) we examined the requirement of the brain-type fatty acid binding protein Fabp7, an astrocyte expressed lipid-signaling molecule, in mediating trauma-induced sleep disturbances.

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Fatty acid binding proteins (FABPs) are a family of intracellular lipid chaperone proteins known to play critical roles in the regulation of fatty acid uptake and transport as well as gene expression. Brain-type fatty acid binding protein (FABP7) is enriched in astrocytes and has been implicated in sleep/wake regulation and neurodegenerative diseases; however, the precise mechanisms underlying the role of FABP7 in these biological processes remain unclear. FABP7 binds to both arachidonic acid (AA) and docosahexaenoic acid (DHA), resulting in discrete physiological responses.

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Background: Disaster medicine is a component of the German medical education since 2003. Nevertheless, studies have shown some inconsistencies within the implementation of the national curriculum, and limits in the number of students trained over the years. Recently, the SARS-CoV-2 pandemic and other disasters have called attention to the importance of training medical students in disaster medicine on a coordinated basis.

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Parkinson's Disease (PD) is the most common movement disorder, and the strongest genetic risk factor for PD is mutations in the glucocerebrosidase gene (). Mutations in also lead to the development of Gaucher Disease (GD), the most common type of lysosomal storage disorder. Current therapeutic approaches fail to address neurological GD symptoms.

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The astrocyte brain-type fatty-acid binding protein (Fabp7) circadian gene expression is synchronized in the same temporal phase throughout mammalian brain. Cellular and molecular mechanisms that contribute to this coordinated expression are not completely understood, but likely involve the nuclear receptor Rev-erbα (NR1D1), a transcriptional repressor. We performed ChIP-seq on ventral tegmental area (VTA) and identified gene targets of Rev-erbα, including .

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In response to the urgent need for safe aircrew respiratory protection due to the COVID-19 pandemic, three small descriptive evaluations were conducted with aircrew and air traffic controllers (ATC) that assessed the impact of mask use on safety and performance onboard rotary wing aircraft. A series of evaluations assessed aircrew performance using the 3M Model 1860 N95 respiratory protection mask, two aviation-specific cloth mask prototypes, and a commercial off-the-shelf aviation-specific cloth mask. The series of evaluations included different sets of subjects consisting of up to five Black Hawk helicopter aircrew members, air traffic control (ATC), and 12 CH-47 aircrew members.

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Sleep is intimately linked to cognitive performance and exposure to traumatic stress that leads to post-traumatic stress disorder (PTSD) impairs both sleep and cognitive function. However, the contribution of pre-trauma sleep loss to subsequent trauma-dependent fear-associated memory impairment remains unstudied. We hypothesized that sleep deprivation (SD) prior to trauma exposure may increase the severity of a PTSD-like phenotype in rats exposed to single prolonged stress (SPS), a rodent model of PTSD.

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Seizure patterns observed in patients with epilepsy suggest that circadian rhythms and sleep/wake mechanisms play some role in the disease. This review addresses key topics in the relationship between circadian rhythms and seizures in epilepsy. We present basic information on circadian biology, but focus on research studying the influence of both the time of day and the sleep/wake cycle as independent but related factors on the expression of seizures in epilepsy.

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The astrocyte brain-type fatty acid binding protein (Fabp7) gene expression cycles globally throughout mammalian brain, and is known to regulate sleep in multiple species, including humans. The mechanisms that control circadian Fabp7 gene expression are not completely understood and may include core circadian clock components. Here we examined the circadian expression of Fabp7 mRNA in the hypothalamus of core clock gene Bmal1 knock-out (KO) mice.

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Sleep is a behavior that exists broadly across animal phyla, from flies to humans, and is necessary for normal brain function. Recent studies in both vertebrates and invertebrates have suggested a role for glial cells in sleep regulatory processes. Changes in neural-glial interactions have been shown to be critical for synaptic plasticity and circuit function.

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Introduction: Crises, wars, and disasters are remarkably increasing across the world. Responders are frequently tackled with an ever-greater number of challenges, and undoubtedly, they are physically and mentally affected during and after their missions, during which posttraumatic stress disorder (PTSD) is considered high-risk. To the authors' knowledge, no studies have addressed which type of incident has the greatest influence to trigger stress, and consequently, to cause PTSD for the responders after their missions.

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Sleep contributes to cognitive functioning and is sufficient to alter brain morphology and function. However, mechanisms underlying sleep regulation remain poorly understood. In mammals, tumor necrosis factor-alpha (TNFα) is known to regulate sleep, and cytokine expression may represent an evolutionarily ancient mechanism in sleep regulation.

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Sleep-wake abnormalities are common in patients with Alzheimer's disease, and can be a major reason for institutionalization. However, an emerging concept is that these sleep-wake disturbances are part of the causal pathway accelerating the neurodegenerative process. Recently, new findings have provided intriguing evidence for a positive feedback loop between sleep-wake dysfunction and β-amyloid (Aβ) aggregation.

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Sleep is found widely in the animal kingdom. Despite this, few conserved molecular pathways that govern sleep across phyla have been described. The mammalian brain-type fatty acid binding protein (Fabp7) is expressed in astrocytes, and its mRNA oscillates in tandem with the sleep-wake cycle.

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Article Synopsis
  • Sleep is essential for brain function, but the molecular processes behind sleep need and recovery are not well understood.
  • Researchers analyzed gene expression changes in mice after sleep deprivation and recovery, using a novel method to improve accuracy in detecting these changes.
  • Findings indicate that most genes affected by sleep deprivation take about 6 hours of recovery sleep to return to normal levels, while others can normalize within 1-3 hours, suggesting distinct waves of gene regulation during recovery sleep.
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Discussions surrounding concussion have made their way into the public sphere over the previous decade with media attention and coverage of the injury fueling public debate. These conversations have devolved into discussions on banning contact and collision sports and raised legal questions surrounding injury management. Questions raised about concussion eclipse what science can answer, but the University of Michigan Injury Center (MI, USA) hosted a Concussion Summit in September 2015 as a means to condense, solidify and disseminate what is currently known on the topic.

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Disruption of sleep/wake activity in Alzheimer's disease (AD) patients significantly affects their quality of life and that of their caretakers and is a major contributing factor for institutionalization. Levels of amyloid-β (Aβ) have been shown to be regulated by neuronal activity and to correlate with the sleep/wake cycle. Whether consolidated sleep can be disrupted by Aβ alone is not well understood.

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