Publications by authors named "Christin Herrmann"

Objectives: The hospital setting is often perceived as slow to change. While employee-driven approaches offer a promising alternative to traditional top-down methods, guidance is limited. This study provides a description and formative evaluation of an employee-driven working group (WG) approach to tailor ward-specific measures to improve care in the dying phase.

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Persistent viral infections are associated with long-term health issues and prolonged transmission. How external perturbations after initial exposure affect the duration of infection is unclear. Here we discovered that murine astrovirus, an enteric RNA virus, persists indefinitely when mice remain unperturbed but is cleared rapidly after cage change.

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Most patients dying in hospitals die outside of specialist palliative care, making healthcare professionals of all disciplines responsible for the care of the dying. This cross-sectional study assessed how burdened healthcare professionals on non-palliative care hospital wards are when caring for dying patients. Descriptive and inferential statistics (chi and tests) were used to analyze the data.

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Background: Digital patient portals (PPs) are platforms that enhance patient engagement and promote active involvement in health care by providing remote access to personal health data. Although many hospitals are legally required to offer these portals, adoption varies widely among patients, often influenced by sociodemographic and socioeconomic determinants. Evidence suggests that higher income, education, employment status, and specific age groups correlate with increased portal usage, highlighting a digital divide.

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The literature describes a plethora of different measures to support healthcare professionals in the care for the dying. The aim is the identification and assessment of measures for the care in the dying phase to give healthcare professionals of all disciplines an overview on such measures in form of a self-developed toolkit. Two databases were searched systematically and all measures found ( = 7368 publications, = 308 measures) were categorized into six categories and integrated into a toolkit.

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Inbred mice used for biomedical research display an underdeveloped immune system compared with adult humans, which is attributed in part to the artificial laboratory environment. Despite representing a central component of adaptive immunity, the impact of the laboratory environment on the B cell compartment has not been investigated in detail. Here, we performed an in-depth examination of B cells following rewilding, the controlled release of inbred laboratory mice into an outdoor enclosure.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely used medications for the management of chronic pain; however, they are associated with numerous gastrointestinal (GI) adverse events. Although many mechanisms have been suggested, NSAID-induced enteropathy has been thought to be primarily due to inhibition of both cyclooxygenases (COX) -1 and -2, which results in suppression of prostaglandin synthesis. Yet surprisingly, we found that concomitant postnatal deletion of and over 10 months failed to cause intestinal injury in mice unless they were treated with naproxen or its structural analog, phenylpropionic acid, which is not a COX inhibitor.

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Background: Guidelines recommend the identification of potential mental and/or cognitive disorders (MCD) in patients with coronary heart disease (CHD). However, compliance with these guidelines appears to be lacking in primary care. A minimal invasive intervention was tailored with experts for the primary care setting to increase the identification of this patient group and ensure proper treatment.

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Persistent viral infections are associated with long-term health issues and prolonged transmission. How external perturbations after initial exposure affect the duration of infection is unclear. We discovered that murine astrovirus, an enteric RNA virus, persists indefinitely when mice remain unperturbed but is cleared rapidly after cage change.

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Purpose: The European health data space promises an efficient environment for research and policy-making. However, this data space is dependent on high data quality. The implementation of electronic medical record systems has a positive impact on data quality, but improvements are not consistent across empirical studies.

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Article Synopsis
  • Severe COVID-19 patients frequently experience coinfections with bacterial and fungal pathogens, leading to higher mortality rates compared to infections with just one pathogen.
  • A study investigated blood and respiratory samples from hospitalized patients to analyze the relationship between SARS-CoV-2 and coinfections, finding no specific lineage associated with COVID-19 but noting trends in the virulence of bloodstream strains.
  • Research using a mouse model demonstrated that SARS-CoV-2 infection increases susceptibility to subsequent infections with low-cytotoxicity pathogens, highlighting the enhanced risk of severe outcomes from these coinfections.
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Background: German hospitals are legally obliged to implement digital patient portals within the next years. Systematic reviews show that the use of patient portals may be associated with improved patient-centeredness and workflows. However, mandatory digital healthcare innovations are sometimes not used by the target group as planned or even completely rejected.

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Article Synopsis
  • - The study investigates how genetics and environment together affect immune responses in mice, focusing on three different inbred strains (C57BL/6, 129S1, PWK/PhJ) in an outdoor setting and infected with a specific parasite.
  • - It finds that while the overall structure of immune cells is influenced by both genetics and the environment, the variation in certain immune responses, like cytokine levels, is mainly determined by genetics, affecting how many parasites the mice carry.
  • - Additionally, the expression of immune markers like CD44 shows different influences: on T cells, it’s mostly genetic, while on B cells, it’s more environmental; and importantly, the impact of genetics appears to lessen when the mice
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The relative and synergistic contributions of genetics and environment to inter-individual immune response variation remain unclear, despite its implications for understanding both evolutionary biology and medicine. Here, we quantify interactive effects of genotype and environment on immune traits by investigating three inbred mouse strains rewilded in an outdoor enclosure and infected with the parasite, . Whereas cytokine response heterogeneity was primarily driven by genotype, cellular composition heterogeneity was shaped by interactions between genotype and environment.

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Eukaryotic cells recognize intracellular pathogens through pattern recognition receptors, including sensors of aberrant nucleic acid structures. Sensors of double-stranded RNA (dsRNA) are known to detect replication intermediates of RNA viruses. It has long been suggested that annealing of mRNA from symmetrical transcription of both top and bottom strands of DNA virus genomes can produce dsRNA during infection.

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Article Synopsis
  • The study investigates how viruses in the gut microbiome (the virome) affect both innate and adaptive immune responses in mice.
  • Most viral infections were asymptomatic, with immune response strength and duration influenced by the mouse's existing gut microbiota.
  • Researchers found both general immune adaptations (like changes in lymphocyte behavior) and unique responses to specific viral strains, highlighting the virome's role in shaping immune responses similar to certain bacteria.
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Viruses promote infection by hijacking the ubiquitin machinery of the host to counteract or redirect cellular processes. Adenovirus encodes two early proteins, E1B55K and E4orf6, that together co-opt a cellular ubiquitin ligase complex to overcome host defences and promote virus production. Adenovirus mutants lacking E1B55K or E4orf6 display defects in viral RNA processing and protein production, but previously identified substrates of the redirected ligase do not explain these phenotypes.

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Adenoviruses represent ubiquitous and clinically significant human pathogens, gene-delivery vectors, and oncolytic agents. The study of adenovirus-infected cells has long been used as an excellent model to investigate fundamental aspects of both DNA virus infection and cellular biology. While many key details supporting a well-established model of adenovirus replication have been elucidated over a period spanning several decades, more recent findings suggest that we have only started to appreciate the complex interplay between viral genome replication and cellular processes.

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Viruses exploit cellular ubiquitination machinery to shape the host proteome and promote productive infection. Among the cellular processes influenced by viral manipulation of ubiquitination is the DNA damage response (DDR), a network of cellular signaling pathways that sense and respond to genomic damage. This host-pathogen interaction is particularly important during virus replication and transformation by DNA tumor viruses.

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Nucleosomes are the core units of cellular chromatin and are comprised of 147 base pairs (bp) of DNA wrapped around an octamer of histone proteins. Proteins such as chromatin remodelers, transcription factors, and DNA repair proteins interact dynamically with chromatin to regulate access to DNA, control gene transcription, and maintain genome integrity. The extent of association with chromatin changes rapidly in response to stresses, such as immune activation, oxidative stress, or viral infection, resulting in downstream effects on chromatin conformation and transcription of target genes.

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Viral manipulation of cellular proteins allows viruses to suppress host defenses and generate infectious progeny. Due to the linear double-stranded DNA nature of the adenovirus genome, the cellular DNA damage response (DDR) is considered a barrier to successful infection. The adenovirus genome is packaged with protein VII, a virally encoded histone-like core protein that is suggested to protect incoming viral genomes from detection by the cellular DNA damage machinery.

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Herpes simplex virus (HSV-1) lytic infection results in global changes to the host cell proteome and the proteins associated with host chromatin. We present a system level characterization of proteome dynamics during infection by performing a multi-dimensional analysis during HSV-1 lytic infection of human foreskin fibroblast (HFF) cells. Our study includes identification and quantification of the host and viral proteomes, phosphoproteomes, chromatin bound proteomes and post-translational modifications (PTMs) on cellular histones during infection.

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Viral proteins mimic host protein structure and function to redirect cellular processes and subvert innate defenses. Small basic proteins compact and regulate both viral and cellular DNA genomes. Nucleosomes are the repeating units of cellular chromatin and play an important part in innate immune responses.

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Dendritic cells can capture and transfer retroviruses in vitro across synaptic cell-cell contacts to uninfected cells, a process called trans-infection. Whether trans-infection contributes to retroviral spread in vivo remains unknown. Here, we visualize how retroviruses disseminate in secondary lymphoid tissues of living mice.

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