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Probing spins in molecular structures on superconducting surfaces
Get PDFA quantum computer is considered to overtake classical computers from its ability of parallel information processing. However, qubits fabricated from quantum states are easily perturbed by their environment, leading to short decoherence time and limited gate operations. To extend decoherence time, qubits based on topological superconductivity are promising candidates thanks to their immunity against external perturbations. This dissertation aims on the fundamental understanding of condensed matter systems to realize topological superconductivity by targeting the observation of Majorana zero modes using low-temperature scanning probe microscopy. To accomplish this goal, we fabricate spin lattices via on-surface reactions on superconducting substrates (Nb and Pb). We first demonstrate the synthesis of atomically precise nanographenes on the superconducting Ag/Nb(110), and characterize their structures with atomic force microscopy at low temperatures. Our approach opens the route to couple π-magnetism to superconducting states. We then compare the spin signature of Fe atoms in the coordinated organometallic frameworks on Pb(111) and on Ag(111). On both substrates, we observe spin-flip excitations due to magnetocrystalline anisotropy. We last investigate an electron-spin superlattice fabricated by self-assembly of radical molecules on Pb(111). Using superconducting tips, we probe by tunneling spectroscopy Yu-Shiba-Rusinov states arising from the coupling of such spin-1/2 system with the superconductor. The observation of low-energy modes near boundaries of this two-dimensional magnetic island is consistent with the signature of Majorana zero modes
Vom deutschbaltischen Adel bis zum Fürsorgefall in der Schweiz - Fragmente einer europäischen Lebensgeschichte des 20. Jahrhunderts
No full textSpecialised paeditric palliative care: assessing economic outcomes in a multi-site context of various care settings (SPhAERA-E)
Get PDFOver the last decades, the prevalence of life limiting conditions (LLCs), conditions for which there is no reasonable hope of cure and where premature death is likely, in children has been increasing. As parenting a child with an LLC is an enormously challenging and demanding experience, parents of these children are at an increased risk of profound caregiver burden. Besides physical, psychological, emotional and social burdens, this also includes financial burden from out of pocket medical and non medical expenses and employment related income loss. However, there is an absence of literature on how illness related events, such as a child’s hospitalisation or even death, contribute to these costs. Moreover, inconsistencies in the outcome measures and methodological approaches used to quantify financial burden limit the interpretation and comparability of research findings, making it inherently difficult to draw conclusions about the magnitude of the financial burden experienced by affected families.
Nevertheless, robust evidence on the sources and determinants as well as the true magnitude of families’ financial burden is crucial for enabling care and support interventions, such as specialised paediatric palliative care (SPPC), to effectively address families’ financial support needs. SPPC is advocated as a standard of care for children with LLCs and their families. However, despite the acknowledged benefits of SPPC, funding constraints have emerged in Switzerland, which likely limit its accessibility and provision to families in need.
Therefore, this dissertation investigated existing measures of financial burden in families of children with LLCs, explored hospitalisation and death related financial and employment implications for these families and examined current funding structures, obstacles and priorities regarding the funding of SPPC programmes in Switzerland.
In conducting this dissertation, the published literature investigating financial costs incurred by families of children with LLCs was reviewed, economic data from the larger ‘Specialised Paediatric PAlliativE CaRe: Assessing family, healthcare professionals and health system outcomes in a multi-site context of various care settings (SPhAERA)’ study was analysed, and an expert panel on the provision and funding of SPPC in Switzerland was consulted.
Overall, this dissertation encompasses five chapters:
The first chapter of this dissertation provides an overview of the definition and prevalence of LLCs in children and embeds financial burden within the wider context of parental caregiving, including the multiple caregiver burdens experienced by parents. This sets the stage for an introduction of the conceptual framework guiding this research. This, in turn, is followed by a description of SPPC and a brief presentation of the SPhAERA study. A presentation of the rationale and aims concludes Chapter 1.
The scoping review presented in Chapter 2 provides an overview of cost indicators and outcome measures used to measure financial burden in families of children with LLCs. The retrieved cost indicators and outcome measures were categorised into three broad groups: direct costs, that is, out of pocket medical and non-medical expenses; indirect costs and financial support. The review suggests that not all key components of families’ financial burden were consistently measured across reviewed studies. To facilitate future investigations of financial burden, a framework for comprehensively measuring families’ out of pocket medical and non medical expenses was developed, and clear recommendations for assessing income loss, opportunity costs, and financial support were provided.
Chapter 3 reports the results of a cohort study that investigated hospitalisation and death related financial and employment implications experienced by parents of children with LLCs. Over care and bereavement follow up assessments of 330 and 300 days, respectively; a broad range of out of pocket non medical expenses and employment related outcomes were analysed using descriptive statistics and fixed effects regressions. The analysis included 59 mothers and 51 fathers of 61 children. The results showed that families incur higher travel and accommodation expenses during hospitalisation than during non hospitalised periods. In addition, during the first 120 days of bereavement, more than one fifth of grieving parents increased their work commitments.
In the research presented in Chapter 4, a four step conceptualisation process, including a document analysis was used to conceptualise the funding of hospital based consultative SPPC programmes in Switzerland. The results revealed that current funding structures are complex and fragmented, combining funding from public, private and charitable sources. In addition, in consultation with an expert panel, a wide range of obstacles to and priorities for funding these programmes sustainably were identified. Overall, 21 experts participated in the modified Delphi study and identified 23 obstacles and 29 priorities. The highest level of consensus (>90%) was achieved for three priorities: the development of financing solutions to ensure long term funding of SPPC programmes; the provision of funding and support for integrated palliative care; and the sufficient reimbursement of inpatient service costs in the context of high deficit palliative care patients.
Chapter 5 provides a synthesis and discussion of the findings of this dissertation. The chapter starts with a discussion of the sources and determinants of financial burden in families of children with LLCs. This is followed by a discussion of how SPPC programmes can detect and actively address families’ financial burdens. In this regard, the chapter also discusses potential implications of funding shortfalls on the provision of support aimed at addressing families’ financial support needs. This in turn is followed by a brief discussion of contextual factors. Furthermore, the strengths and limitations of this research are examined while also presenting implications for future research, policy and practice.
In conclusion, SPPC programmes can help to address the financial support needs of families of children with LLCs. To enable these programmes to provide proactive support, it is essential that they are equipped with sufficient financial and personnel resources. In Switzerland, where SPPC programmes face major funding challenges, policy makers should establish an adequate financial and regulatory framework that facilitates the widespread implementation and provision of SPPC
Aging, stress and neuroplasticity
No full textThe effort to understand brain aging and discover treatments to postpone aging-related cognitive decline has long intrigued society. However, one of the substantial obstacles in aging research is finding and employing appropriate model systems that can effectively replicate the natural aging process of the human brain. This doctoral thesis aimed to broaden our knowledge and comprehension of promising models for studying human neuronal aging. To accomplish this, the thesis is divided into two sections: I. The first section explored potential neuronal aging models in vitro. A. This involved comparing induced pluripotent stem cell (iPSC)-derived neurons (iPSCsNs) with directly converted neurons (iNs) from aged human fibroblasts (HFs) of the same aged individuals. B. Additionally, this thesis endeavored to create a stress-induced aging model. II. The second section focused on examining the effect of childhood adversities (CAs) on biological alteration in adulthood to detect an accelerated aging-associated phenotype. C. This thesis studied the correlation between cellular aging and biological stress, as well as D. the interplay between brain-derived neurotrophic factor (BDNF), stress, and sleep in a high-risk sample of young adults with a history of residential youth care placements.
I. In the first section, this thesis demonstrates that aged iPSCsNs exhibit an aging phenotype like that of aged iNs from the same donors in terms of mitochondrial functional properties, including a rise in mitochondrial reactive oxygen species (ROS), destabilizing of the respiratory chain, and dysfunction in the mitochondrial quality control system. However, aged iPSCsNs differed in terms of transcriptomic level and glycolytic activity compared to aged iNs. Based on these findings, aged iPSCsNs demonstrated rejuvenation in transcriptomic and glycolytic levels but unexpectedly maintained aging-associated impairment on mitochondrial properties linked to their cells of origin. Thereby contradicting the common assumption of a complete rejuvenation process. However, the aged iNs represent an overall model of neuronal aging to study other aging features beyond mitochondrial impairments. Although aged iNs exhibited promising results in studying aging, their poor efficiency in reprogramming and conversion impedes their usefulness. Given that stress has been identified as a significant contributor to aging, a stress approach to mimic an aging-associated phenotype in young iNs could be a potential approach to establish a fast and easy-to-use “aged” neuronal in vitro model. Our research presents those subjecting iNs obtained from young donors to rotenone exposure led to a more pronounced aging-associated phenotype on the mitochondrial level than exposure to the human stress hormone cortisol. However, we observed that neither of these acute stress approaches had any adverse impact on the morphology of the mitochondrial network. The thesis presented an innovative strategy for utilizing the sensitive iNs model system as a potential replacement model for in vivo aged iNs.
II. In that context, young people exposed to elevated stress levels may display an accelerated biological aging phenotype in early adulthood. It is essential to bridge the substantial gap in our understanding of the biological alteration on adversity's long-term effects, which still need to be overcome. The investigation of the association between biological stress responses and cellular aging has proven challenging due to the need for biological measures of chronic psychological stress in humans. This thesis represented that HCC (a parameter of chronic HPA activation) and LTL (an aging index) showed a strong negative correlation in a high-risk group with a history of placement in residential youth care. HCC as a tool could help us explore and understand the effects of chronic stress on biological changes related to aging. In our study in this high-risk population, we further discovered that each participant's sleep quality played an essential role in the relationship between CTQ (index of CAs) and BDNF concentration. Even though we did not find a direct correlation between various stress-related psychological factors (such as CTQ or well-being), biological indicators of stress (HCC), or sleep (PSQI) with BDNF concentration, our research did show that CTQ was associated with BDNF concentration levels in individuals who had healthy sleep patterns. However, this association was not observed in individuals who suffered from sleep disturbances. These findings highlight the importance of getting enough sleep to manage stress effectively.
The broad implication of the results of this thesis proposed that either aged iNs or iPSCsNs have their benefits and disadvantages, and depending on the application, one in vitro neuron model of human aging is more favorable than the other. Moreover, stress approaches on young iNs could be an alternative avenue to generate "aged" neurons. Exposure of rotenone on young iNs especially proposes a large-scale replacement model for in vivo aged iNs. In the second part of this thesis, our investigation suggested that HCC might be a valuable method for assessing chronic stress activation in the setting of cellular aging. Our discovery of a negative relationship between HCC and LTL supported this. Lastly, this thesis emphasized the matter of sleep in evaluating CAs on the long-term effect of BDNF
Insomnia disorder: characterization and evaluation of sleep architecture in adult and elderly individuals
No full textSleep is important for mental and physical well-being. Patients with chronic insomnia, a disorder characterized by difficulties in initiating or maintaining sleep, along with impaired daytime functioning for at least 3 months, often experience mood disturbances, reduced performance at work, absenteeism, and reduced quality of life. This condition continues to impact both day and night, suggesting a complex interplay between neurobiological and psychological factors. One of the leading hypotheses behind this disorder is that the disease is characterized by a persistent state of psychophysiological hyperarousal. However, research findings have been inconsistent. To shed some light into this and assess whether individuals diagnosed with insomnia show sleep architecture signatures consistent with hyperarousal, we utilized one of the largest insomnia PSG datasets to date, derived from the adult phase 2 and phase 3 clinical programs of daridorexant and two additional external datasets. It is important to note that this thesis focused on PSG-derived objective features. While hyperarousal also includes clinical effects like cognitive, emotional, and behavioral symptoms, these aspects were not the primary focus of this PSG-based analysis. Nevertheless, this research offers a comprehensive analysis of sleep architecture in these individuals addressing one of the biggest limitations of previous studies that relied on small sample sizes. The studies conducted revealed that adult and elderly individuals with insomnia are more likely to experience fragmented sleep and long bouts of waking (> 6 minutes) during the night. Additionally, we observed that sleep spindles, more precisely spindle density are reduced in individuals with insomnia compared to non-insomnia controls. This suggests that insomnia is characterized by a vulnerability of NREM sleep making individuals more likely to experience sleep disruptions. With further examination of the spectral composition of sleep, this analysis highlights significant differences in the electroencephalography signatures of insomnia, especially in the alpha and delta bands during night-time wake periods. Contrary to expectations, the study did not find a significant increase in relative beta power in individuals with insomnia compared to non-insomnia controls, suggesting that the faster brain frequencies such as beta bands are not an inherent characteristic of insomnia, instead it might be specific for some insomnia subtypes, and comorbidities associated with it. To assess whether the same set of sleep features were modulated after pharmacological treatment, namely daridorexant and zolpidem, we investigated their effect on sleep architecture for up to 3 months of continuous treatment. Daridorexant selectively reduced the overall number and the duration of long night-time awakenings, showing a greater effect than zolpidem when compared to placebo, with results remaining significant towards the end of the night. Notably, the tested medications (daridorexant and zolpidem) had only a limited effect in reducing shorter night-time awakenings (≤ 6 minutes). This reduction of time spent in long awakenings correlated with all daytime functioning domains of the IDSIQ questionnaire, showing an association between reducing long wake bouts and improving daytime functioning. Additionally, daridorexant dose-dependently increased the likelihood of transitioning into sleep and modulated spectral features during night-time waking without altering the proportion of sleep stages. This suggests a novel therapeutic approach targeting sleep features associated with hyperarousal such as fragmented sleep, long awakenings, and cortical arousal, without disrupting sleep architecture, making the orexinergic system particularly interesting for chronic insomnia.
In conclusion, this thesis describes novel PSG signatures of insomnia supportive of the hyperarousal model and offers insights into how a new class of treatment like daridorexant can selectively modulate these features, advancing our understanding of the disorder
Identifying pre-surgical risk factors of longitudinal changes in cancer-related cognitive impairment in patients with breast cancer
Get PDFBackground
Cancer-related cognitive impairment (CRCI) is a common symptom in patients with breast cancer. Approximately 75% of breast cancer patients experience cancer related cognitive impairment (CRCI) prior to, during, or after treatment. CRCI remains a significant long-term problem for about 35% of cancer survivors. CRCI may interfere with patients’ self-care activities, such as ability to adhere to treatment, manage side effects, and re-integrate into the workforce, which can have a negative impact on their quality of life. The Attentional Function Index (AFI) is a subjective measurement commonly used to assess attentional function and includes three subscales, namely effective action, attentional lapses, and interpersonal effectiveness. In our previous study of 397 women with breast cancer, three groups of patients with distinct CRCI profiles (i.e., High, Moderate, and Low-moderate attentional function) were identified. While the three classes were significantly different in demographic and clinical characteristics using the total AFI scores, little is known about how other pre-surgical psychological and physical symptom and genetic biomarker characteristics are associated with the distinct profiles of CRCI.
Aims
The overall aims of this dissertation were threefold: 1) to expand on our previous work and evaluate for the differences among the three latent classes in the severity of psychological (ie, anxiety, depression) and physical (ie, fatigue, decrements in energy, sleep disturbance, and pain) symptoms prior to surgery. 2) to identify distinct cognitive profiles for each of the AFI subscales, and then to determine the differences in demographic, clinical, and pre-surgical psychological and physical symptoms among the subgroups. 3) to evaluate for associations between CRCI subgroup membership and single nucleotide polymorphisms among 15 genes involved in catecholaminergic and serotonergic neurotransmission.
Methods
This PhD dissertation is based on the B-CaSS study. This descriptive, prospective, longitudinal study observational study included 398 female breast cancer patients, who were screened for the aforementioned risk factors prior to surgery. Longitudinal changes of CRCI were measured with the Attentional Function Index (AFI) from prior to surgery through 6 months after surgery (ie, baseline, 1, 2, 3, 4, 5, and 6 month). Growth mixture modeling (GMM) and Latent Class Growth Analyses (LCGA) were used to identify distinct CRCI profiles. Parametric and non-parametric statistics were used to determine differences of the aforementioned pre-surgical risk factors among the distinct profiles. Logistic regression analyses were used to identified significant differences between genotype frequencies and the extreme attentional function classes comprised of 296 patients (ie, High class [n=165] and Low-moderate class [n=131].
Results
Our results found: 1) significant differences of the severity level of trait and state anxiety, depression, fatigue, and sleep disturbance among the three classes (i.e., High < Moderate< Low-moderate). 2) Three latent classes were identified for the effective action subscale. Four latent classes were identified for the attentional lapses subscale. Two latent classes were identified for the interpersonal effectiveness subscale. Across the three subscales, lower functional status, higher level of anxiety, depression, fatigue, and sleep disturbance, and worse decrements in energy were associated with worse cognitive performance. 3) Genotypes in 5 genes were associated with membership in the Low-moderate attentional class: alpha-1D adrenergic receptor (ADRA1D) rs2326478, beta-2 adrenergic receptor (ADRB2) rs1042718, solute like carrier family 6 member 2- noradrenaline transporter (SLC6A2) rs47958, 5-hydroxytryptamine receptor 3A (HTR3A) rs10160548, and solute like carrier family 6 member 4- serotonin transporter (SLC6A4) rs8076005.
Conclusions
Our findings suggest that women with clinically meaningful levels of persistent CRCI have a relatively high symptom burden prior to surgery. Pre-surgery symptoms (i.e., anxiety, depression, fatigue, sleep disturbance) and other modifiable characteristic (e.g., lower functional status) may be potential targets for personalized interventions. Additionally, variability in genes within the catecholaminergic and serotonergic pathways may explain variability in development and severity of CRCI in women with breast cancer
Role of Rpl39l in translation, and consequences for pluripotency and cancer
Get PDFRecent research increasingly demonstrates that ribosome composition can be adjusted to efficiently translate the transcriptome of specific cell types. In this study, we examined the expression pattern, structure within the ribosome, and the influence on protein synthesis of the ribosomal protein paralog RPL39L. Using a novel mass spectrometric technique, we discovered that RPL39L protein is expressed not only in mouse germ cells but also in human pluripotent cells, cancer cell lines, and tissue samples. We created RPL39L knock-out mouse embryonic stem cell (mESC) lines and found that RPL39L affects translation dynamics, supporting pluripotency and differentiation, both spontaneously and along the germ cell lineage. The differences in protein abundance between wild-type and RPL39L knockout lines were largely attributed to widespread autophagy. CryoEM analysis of purified ribosomes containing RPL39 and RPL39L revealed that, unlike RPL39, RPL39L adopts two distinct conformations in the exposed segment of the nascent peptide exit tunnel, forming a unique hydrophobic patch predicted to facilitate efficient co-translational folding of alpha helices. Our findings indicate that ribosomal protein paralogs serve as switchable modular components that can adapt translation to the specific protein production needs of different cell types
Lighting the way: Compelling open questions in photosynthesis research
No full textPhotosynthesis - the conversion of energy from sunlight into chemical energy - is essential for life on Earth. Yet there is much we do not understand about photosynthetic energy conversion on a fundamental level: how it evolved and the extent of its diversity, its dynamics, and all the components and connections involved in its regulation. In this commentary, researchers working on fundamental aspects of photosynthesis including the light-dependent reactions, photorespiration, and C4 photosynthetic metabolism pose and discuss what they view as the most compelling open questions in their areas of research
Investigating the role of PI3-Kinase α in endothelial cell rearrangements during vascular morphogenesis
Get PDFDas Blutkreislaufsystem ist ein hierarchisch organisiertes Netzwerk von spezialisierten Blutgefäßen, welches essenziell für den Transport und die Verteilung von Nährstoffen und Sauerstoff durch den Körper von Wirbeltieren ist. Während der Entwicklung des Blutkreislaufes müssen besondere morphogenetische Prozesse, wie Aussprossung, Gefäßfusionen, Gefäßwachstum und Remodellierung des Netzwerkes, streng reguliert werden, um ein weit verzweigtes und funktionelles Netzwerk an Blutgefäßen zu schaffen. Besonders die Entwicklung multizellulärer Gefäße und die damit einhergehenden Zellinterkalationen benötigen koordinierte Zellverhalten, damit das sich entwickelnde Blutgefäß nicht undicht wird, während sich die Gefäßzellen (Endothelzellen) bewegen. Hier halten Zellmotilität und Zelladhäsion eine empfindliche Balance, die innerhalb der Zellen durch endotheliale Adhäsionsproteine, das Zytoskelett sowie deren übergeschalteten Signalwegen reguliert wird (Betz et al., 2016; Yin et al., 2021; Phng und Belting, 2021).
Es konnte bereits gezeigt werden, dass der Signalweg der PI3-Kinasen verschiedene Zellverhalten wie Migration, Proliferation, Polarisierung und die Regulation des Zellskeletts beeinflusst. In in vitro Systemen sowie in den Endothelzellen verschiedener Modellorganismen regulieren PI3-Kinasen nachweislich die Differenzierung zu Arterien und Venen sowie die Entstehung von Lymphgefäßen. Hier sticht besonders die α-Isoform der PI3-Kinasen, PI3-Kinase α, hervor, die essenziell für die korrekte Entwicklung des Blutkreislaufsystems ist. Der genetische Verlust von PI3-Kinase α führt zu schweren Defekten in der Angiogenese und der Remodellierung von Gefäßnetzwerken (Graupera et al., 2008), eine für den Embryo schon früh letale Situation. Neuere Studien vermuten eine Rolle der PI3-Kinase α in der Regulation von Zellbewegungen während der Entwicklung multizellulärer Gefäße, in dem sie die zytoskeletale Kontraktionsfähigkeit beeinflusst (Angulo-Urarte et al., 2018). Hier fehlt jedoch noch ein tieferes Verständnis dafür, wie genau der Signalweg der PI3-Kinase α die Bewegungen von Endothelzellen koordiniert und wie und wo die Funktion der Kinase in die mechanistischen Prozesse der Entwicklung multizellulärer Blutgefäße integriert wird.
Diese Studie untersucht die Rolle der PI3-Kinase α in der Entwicklung des Blutkreislaufsystems und, im Besonderen, während der Bewegung der Zellen in der Genese multizellulärer Gefäße. Sie analysiert dafür die kardiovaskuläre Entwicklung von Embryonen des Zebrabärblings, in denen das Gen für die katalytische Untereinheit der PI3-Kinase α, pik3ca, ausgeschaltet wurde. Dabei werden vielfältige und hochentwickelte Möglichkeiten der Live-Mikroskopieverfahren genutzt, die nur der Zebrabärbling bietet.
Ähnlich wie in der Maus zeigen Zebrabärbling-Embryos nach Verlust der beiden pik3ca Gene Defekte in der kardiovaskulären Entwicklung und Letalität nach 6-7 Tagen nach der Befruchtung. Interessanterweise weisen dabei unterschiedliche Teile des Blutkreislaufssystems unterschiedliche Effekte nach Verlust der PI3-Kianse α auf; eine Beobachtung, welche bereits in vorherigen Studien in der Maus und in menschlichen Patienten mit genetischen Erkrankungen gemacht wurde. So zeigt der kaudale Venenplexus der mutanten Fischembryonen ventrale Hyperlasie und erhöhte Sprossaktivität, während der Durchmesser der dorsalen Aorta abnimmt, was auf verminderte Zellzahl und verringerte Proliferationsaktivität der Zellen hindeutet. Zusätzlich zu diesen Beobachtungen zeigt auch der Transkriptionsfaktor FOXO unterschiedliche Relokalisationsverhalten in Endothelzellen unterschiedlichen Ursprungs bei akuter Inhibition der PI3-Kinase α.
In den Gefäßen des Rumpfes beeinträchtigt der Verlust von PI3-Kinase α die Umlagerungen und Bewegungen der Endothelzellen innerhalb der Gefäße. Die genauere Analyse der Zellverhalten während der Umlagerungsphase der Entstehung multizellulärer Gefäße in den pik3ca mutanten Embryonen offenbart eingeschränkte Interkalationsfähigkeiten, verschlechterte Zell-Zell-paarung und eine Destabilisierung trizellulärer Kontakte. Des Weiteren enthüllt die spatiotemporale Analyse der PI3-Kinase α-Aktivität durch einen Lipid-Biosensor lokale und periodisch wiederkehrende Aktivität an den distalen Polen der endothelialen Zell-Zell-Grenzen. Diese Oszillationen überlappen sowohl in der Lokalisierung als auch in der Periodizität mit Junction-based lamellipodia (JBL), dem steuernden Mechanismus der Zellgrenzbewegung im Wirbeltierendothel (Paatero et al., 2018). Dies lässt auf einen funktionalen oder regulatorischen Zusammenhang zwischen PI3-Kinase α und JBL schließen.
Zusammengenommen zeigen meine Ergebnisse eine kritische Rolle der PI3-Kinase α in den Bewegungen der Endothelzellen während der Entwicklung multizellulärer Gefäße, potenziell durch die lokale Regulation der zytoskeletalen Kontraktion an den Zell-Zell-Grenzen. Ich konnte zeigen, dass PI3-Kinase α Funktionen in verschiedenen Teilen des Blutgefäßsystems hat, indem sie mit jeweils anderen Signalwegen interagiert. Schlussendlich zeigt eine genaue räumliche und zeitliche Auflösung die hochlokalisierte und oszillierende Aktivität der PI3-Kinase α an den distalen Grenzen der Endothelzellen, wo sie als eine treibende Kraft in der Formation und Funktion von JBL in der Entwicklung multizellulärer Blutgefäße anzusiedeln ist
Cognitive Disengagement Syndrome bei Kindern und Jugendlichen: Vorläufige Auswertung der Validierungsstudie zum Deutschen Child and Adolescent Behavior Inventory (CABI)
No full textHintergrund: Kinder und Jugendliche mit Cognitive Disengagement Syndrom (CDS) und Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung-unaufmerksamer Subtyp (ADHS-IN) weisen besondere Muster hinsichtlich Schlafproblemen und Tagesschläfrigkeit auf. Regelmässige körperliche Aktivität kann in diesem Zusammenhang ein relevanter Faktor bei der Betrachtung dieser Störungen sein. Studien zeigen, dass körperliche Aktivität positive Auswirkungen auf das Schlafverhalten und die Symptomatik bei ADHS-IN hat. Es ist daher naheliegend, dass bei CDS ähnliche positive Zusammenhänge zwischen regelmässiger körperlicher Aktivität, verbesserter Schlafqualität und einer Abnahme der Symptome bestehen.
Methoden: In dieser Studie wurden 43 Kinder und Jugendliche im Alter zwischen 7 und 19 Jahren in Bezug auf CDS, ADHS-IN, Schlafqualität und körperlicher Aktivität untersucht. Die Daten wurden durch Elternberichte anhand eines Online-Fragebogens erhoben. Zur Analyse der Daten wurden Korrelations- und Regressionsanalysen eingesetzt, um die Beziehungen zwischen CDS, ADHS-IN, Schlaf- und Bewegungsverhalten zu erforschen.
Ergebnisse: Die Ergebnisse zeigen signifikante Korrelationen zwischen CDS und erhöhter Tagesschläfrigkeit sowie zwischen ADHS-IN und Schlafproblemen. Darüber hinaus wurden negative Zusammenhänge zwischen CDS und ADHS-IN sowie der Dauer intensiver körperlicher Aktivität identifiziert. Viele dieser Zusammenhänge blieben unter Kontrolle von konfundierenden Variablen jedoch nicht signifikant. Daher ist es wichtig, die Stichprobe zu erweitern, um die komplexen Beziehungen weiter zu erforschen.
Schlussfolgerungen: Zusammenfassend betont die vorliegende Studie die Bedeutung der Berücksichtigung des Schlafverhaltens und der körperlichen Aktivität von Kindern und Jugendlichen mit CDS und ADHS-IN