Biology subjects

Maurer, S.

Publications and source records attributed to Maurer, S..

6 recordsLinked to original sources

bioRxiv2026

Balancing Lucidity: Muscle and Vestibular Stimulation for Lucid Dream Induction

Lucid dream (LD) induction using external sensory stimulation has most commonly relied on distal cues such as lights or auditory signals, with mixed success rates. In this study, we investigated whether more direct bodily stimulation targeting the muscle and vestibular systems could influence LD induction. We compared electrical muscle stimulation (EMS) and galvanic vestibular stimulation (GVS), each combined with a two-week cognitive training protocol including dream journaling, reality checks, and association training. Twenty-eight participants (14 per group) completed two counterbalanced morning naps: one with stimulation (STIM) during REM sleep and with one sham-stimulation control (SHAM). EMS and GVS stimulation did not lead to increased incorporation of the stimulus. Lucidity rates were high in both EMS conditions, highlighting the substantial role of elevated baseline lucidity in induction studies, cognitive training, and expectation effects. In contrast, GVS stimulation significantly increased externally rated lucidity and DLQ questionnaire scores compared to control. Overall, the findings indicate that galvanic vestibular stimulation can increase dream lucidity. Future work should further examine the mechanisms by which vestibular stimulation influences dream awareness and its potential role in lucid dream induction. O_FIG O_LINKSMALLFIG WIDTH=191 HEIGHT=200 SRC="FIGDIR/small/711028v1_ufig1.gif" ALT="Figure 1"> View larger version (86K): org.highwire.dtl.DTLVardef@7de78forg.highwire.dtl.DTLVardef@1ed7628org.highwire.dtl.DTLVardef@e84964org.highwire.dtl.DTLVardef@2a5f5e_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2026

Waking Up in the Dream Lab: A Lab-Based Lucid Dream Induction Paradigm Using Virtual Reality and Sensory Stimulation

Lucid dreaming (LD), during which the dreamer is aware that they are dreaming, is frequently induced in laboratory settings by delivering sensory cues during rapid eye movement (REM) sleep. These cues should be incorporated into ongoing dreams and can trigger reflective awareness. This approach relies on the continuity between waking experiences and dream content. In sleep laboratories, participants often dream of the experimental setting itself (lab dreaming), providing a predictable context in which lucidity may emerge. The present studies leveraged this phenomenon by explicitly training participants to associate the sleep laboratory with reflective awareness prior to sleep. Across three studies (total N = 101), participants completed a morning nap following verbal LD instructions and presleep audio designed to prime recognition of the laboratory context in dreams. In addition, conditions included immersive virtual reality (VR) rehearsal of the laboratory environment, VR combined with haptic stimulation (HS) during REM sleep, or VR containing subtle fake system errors intended to prompt reflective checking. LD frequency was assessed through external ratings of signal-verified LD (SVLD) dream reports. Lucidity rates were high across all conditions, with approximately 40-45% of dreams externally rated as lucid and 11%-32% SVLDs occurring in every group. However, neither VR rehearsal, haptic stimulation, nor implicit VR errors increased lucidity relative to the baseline laboratory induction procedure. Exploratory analyses investigated the overlap between laboratory dreaming, false awakenings (FAs), and lucidity. These findings suggest that explicit training focused on the predictable context of the sleep laboratory may already provide a powerful pathway to lucidity, with additional technological manipulations offering limited benefit under a single-nap protocol. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=140 SRC="FIGDIR/small/711049v2_ufig1.gif" ALT="Figure 1"> View larger version (47K): org.highwire.dtl.DTLVardef@8f2327org.highwire.dtl.DTLVardef@14cfbaeorg.highwire.dtl.DTLVardef@11f9bbforg.highwire.dtl.DTLVardef@2a57bf_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2024

Visitor effect on the behavior of chimpanzees (pan troglodyte) at a primate rescue center

1.The objective of this study was to examine the impact of visitors on the behavior of chimpanzees at a sanctuary. We hypothesized there wouldnt be an increase in abnormal, agnostic, or self-directed behaviors during visits, nor a decrease in affiliative behaviors when visitors are present. The study examined the effects of visitor presence on chimpanzee behavior at Fundacio MONA, a rescue center. Key findings includeO_LINo significant changes in abnormal or self-directed behaviors or agonistic behaviors were observed with visitor presence. C_LIO_LIAffiliative behaviors (excluding grooming) showed a slight decrease during visits. C_LI These results indicate that guided visitor interactions do not adversely affect chimpanzee behavior and may even enhance their welfare. The study supports the implementation of structured visitor programs for public education and funding, without compromising animal well-being. This contrasts with some previous research in zoo settings, suggesting that controlled visits can be beneficial in primate sanctuaries.

animal behavior and cognition↗

bioRxiv2024

p53-induced GDF-15 expression promotes a pro-regenerative response in human chondrocytes upon cartilage injury

Posttraumatic osteoarthritis (PTOA) is a special form of OA, developing after joint injuries. Except for some minor differences between the clinical characteristics of patients suffering from idiopathic OA (IOA) and PTOA, no biologic marker has yet been identified to distinguish IOA from PTOA. In this study, we investigated the expression of the stress-responsive cytokine growth differentiation factor 15 (GDF-15) in clinical samples from the Ulm OA study cohort (PTOA: n =12; IOA: n=54) and in a human ex vivo cartilage trauma model. We found significantly higher GDF-15 levels in synovial fluid of end-stage PTOA patients as compared to IOA patients. Further, we confirmed that fibroblast-like synoviocytes secreted increased levels of GDF-15 after stimulation with medium of ex vivo-traumatized cartilage. GDF-15 and its receptor, GFRAL, were significantly elevated in highly degenerated OA cartilage. By means of a human cartilage trauma model, we discovered that chondrocytes produced GDF-15 upon tissue injury, while antioxidative treatment attenuated GDF-15 secretion. We confirmed that oxidative stress and subsequent activation of p53 resulted in GDF-15 expression. As a transcriptional target of p53, GDF-15 was associated with chondrosenescence. Although the cytokine might therefore represent a senescence-associated secretory phenotype (SASP) factor, stimulation with exogenous GDF-15 did not cause detrimental effects but induced a pro-regenerative response in chondrocytes, characterized by enhanced proliferation as well as chondro- and cell protection after cartilage trauma. Overall, this study first describes GDF-15 as a stress-responsive and potentially pro-regenerative cytokine in the context of human PTOA.

cell biology↗

bioRxiv2024

Senolytic therapy combining Dasatinib and Quercetin restores the chondrogenic phenotype of human osteoarthritic chondrocytes by promoting the release of pro-anabolic mediators

Cellular senescence is associated with various age-related disorders and is assumed to play a major role in the pathogenesis of osteoarthritis (OA). Based on this, we tested a senolytic combination therapy using Dasatinib (D) and Quercetin (Q) on aged isolated human articular chondrocytes (hACs), as well as in OA-affected cartilage tissue (OARSI grade 1-2). Stimulation with D+Q selectively eliminated senescent cells in both, cartilage explants and isolated hAC. Furthermore, the therapy significantly promoted chondroanabolism, as demonstrated by increased gene expression levels of COL2A1, ACAN, and SOX9, as well as elevated collagen type II and glycosaminoglycan biosynthesis. Additionally, D+Q treatment significantly reduced the release of SASP factors (IL6, CXCL1). RNA sequencing analysis revealed an upregulation of the anabolic factors, inter alia, FGF18, IGF1, and TGFB2, as well as inhibitory effects on cytokines and the YAP-1 signaling pathway, explaining the underlying mechanism of the chondroanabolic promotion upon senolytic treatment. Accordingly, stimulation of untreated hAC with conditioned medium of D+Q-treated cells similarly induced the expression of chondrogenic markers. Detailed analyses demonstrated that chondroanabolic effects could be mainly attributed to Dasatinib, while monotherapeutical application of Quercetin or Navitoclax did not promote the chondroanabolism. Overall, D+Q therapy restored the chondrogenic phenotype in OA hAC most likely by creating a pro-chondroanabolic environment through the reduction of SASP factors and upregulation of growth factors. This senolytic approach could therefore be a promising candidate for further testing as a disease-modifying osteoarthritis drug.

cell biology↗

bioRxiv2021

Susceptibility to diet induced obesity at thermoneutral conditions is independent of UCP1

ObjectiveActivation of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) upon cold stimulation leads to substantial increase in energy expenditure to defend body temperature. Increases in energy expenditure after a high caloric food intake, termed diet-induced thermogenesis, are also attributed to BAT. These properties render BAT a potential target to combat diet-induced obesity. However, studies investigating the role of UCP1 to protect against diet-induced obesity are controversial and rely on the phenotyping of a single constitutive UCP1-knockout model. To address this issue, we generated a novel UCP1-knockout model by Cre-mediated deletion of Exon 2 in the UCP1 gene. We studied the effect of constitutive UCP1 knockout on metabolism and the development of diet-induced obesity. MethodsUCP1 knockout and wildtype mice were housed at 30{degrees}C and fed a control diet for 4-weeks followed by 8-weeks of high-fat diet. Body weight and food intake were monitored continuously over the course of the study and indirect calorimetry was used to determine energy expenditure during both feeding periods. ResultsBased on Western blot analysis, thermal imaging and noradrenaline test, we confirmed the lack of functional UCP1 in knockout mice. However, body weight gain, food intake and energy expenditure were not affected by deletion of UCP1 gene function during both feeding periods. ConclusionConclusively, we show that UCP1 does not protect against diet-induced obesity at thermoneutrality. Further we introduce a novel UCP1-KO mouse enabling the generation of conditional UCP1-knockout mice to scrutinize the contribution of UCP1 to energy metabolism in different cell types or life stages.

physiology↗