Publications by authors named "Steinbach K"

There is a wide gap between what research evidence identifies as effective reading intervention and what is currently offered in schools. This effectiveness study reports the results of a long-term research/school system partnership that is implementing reading intervention for children with reading difficulties in Canadian community schools. In Study 1, growth-curve analyses revealed significant long-term shifts in the reading trajectories of children ( = 731) from Kindergarten to Grade 5 as a function of receiving the Empower™ Reading: Decoding and Spelling intervention.

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Background: Video consultation is a possibility for physician-patient communication independent of the location; however, only limited information is available for the possibility of sole use since 2018.

Methods: After the implementation of video consultation (Viomedi) in lipid consultations at the Medical University Mainz, the patients in the first quarter of 2022 were assessed depending on the possibility, suitability and readiness to participate. Included were patients under lipid management and long COVID patients.

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Individual differences in reading ability are associated with characteristics of white matter microstructure in the brain. However, previous studies have largely measured reading as a single construct, resulting in difficulty characterizing the role of structural connectivity in discrete subskills of reading. The present study used diffusion tensor imaging to examine how white matter microstructure, measured by fractional anisotropy (FA), relates to individual differences in reading subskills in children aged 8 to 14 (n = 65).

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Background: Predicting complications associated with pulmonary hypertension (PH) after cardiac transplantation is an important factor when considering cardiac transplantation. The transpulmonary gradient (TPG) is recommended to quantify PH in transplant candidates. Nonetheless, PH remains a common driver of mortality.

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Thermal adaptation is an extensively used intervention for enhancing or suppressing thermogenic and mitochondrial activity in adipose tissues. As such, it has been suggested as a potential lifestyle intervention for body weight maintenance. While the metabolic consequences of thermal acclimation are not limited to the adipose tissues, the impact on the rest of the tissues in context of their gene expression profile remains unclear.

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In chronic inflammatory diseases of the central nervous system (CNS), immune cells persisting behind the blood-brain barrier are supposed to promulgate local tissue destruction. The drivers of such compartmentalized inflammation remain unclear, but tissue-resident memory T cells (T) represent a potentially important cellular player in this process. Here, we investigated whether resting CD8 T persisting after cleared infection with attenuated lymphocytic choriomeningitis virus (LCMV) can initiate immune responses directed against cognate self-antigen in the CNS.

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Autoimmunity is energetically costly, but the impact of a metabolically active state on immunity and immune-mediated diseases is unclear. Ly6C monocytes are key effectors in CNS autoimmunity with an elusive role in priming naive autoreactive T cells. Here, we provide unbiased analysis of the immune changes in various compartments during cold exposure and show that this energetically costly stimulus markedly ameliorates active experimental autoimmune encephalomyelitis (EAE).

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Individual differences in reading ability have been linked to characteristics of functional connectivity in the brain in both children and adults. However, many previous studies have used single or composite measures of reading, leading to difficulty characterizing the role of functional connectivity in discrete subskills of reading. The present study addresses this issue using resting-state fMRI to examine how resting-state functional connectivity (RSFC) related to individual differences in children's reading subskills, including decoding, sight word reading, reading comprehension, and rapid automatized naming (RAN).

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Article Synopsis
  • * Researchers found that early-life viral infections led to changes in the brain's immune environment, specifically the buildup of memory T cells that produce a signaling molecule called CCL5.
  • * Blocking CCL5 signaling in mice prevented brain damage related to autoimmune diseases, suggesting that early viral infections could create long-lasting changes in the immune system, making it more prone to autoimmune reactions.
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Tissue-resident-memory CD8+ T cells (T) have been described as a non-circulating memory T cell subset that persists at sites of previous infection. While T in all non-lymphoid organs probably share a core signature differentiation pathway, certain aspects of their maintenance and effector functions may vary. It is well-established that T provide long-lived protective immunity through immediate effector function and accelerated recruitment of circulating immune cells.

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Inflammatory disorders of the CNS are frequently accompanied by synaptic loss, which is thought to involve phagocytic microglia and complement components. However, the mechanisms accounting for aberrant synaptic connectivity in the context of CD8 T cell-driven neuronal damage are poorly understood. Here, we profiled the neuronal translatome in a murine model of encephalitis caused by CD8 T cells targeting antigenic neurons.

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Article Synopsis
  • - Infection with the lymphocytic choriomeningitis virus (LCMV) can induce damaging immune responses in the central nervous system (CNS), potentially leading to autoimmunity, while infection with Listeria monocytogenes (Lm) does not have this effect.
  • - The DNA-binding factor TOX is crucial for the harmful properties of CD8 cytotoxic T lymphocytes (CTLs) during LCMV infection, while its expression is suppressed by interleukin-12 during Lm infection.
  • - TOX affects CTL behavior by repressing key transcription factors that promote their differentiation and by reducing the presence of inhibitory receptors, thus contributing to increased tissue damage in autoimmune conditions triggered by infections.
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Across multiple schools in three sites, the impact of grade-at-intervention was evaluated for children at risk or meeting criteria for reading disabilities. A multiple-component reading intervention with demonstrated efficacy was offered to small groups of children in 1, 2, or 3 grade. In a quasi-experimental design, 172 children received the Triple-Focus Program (PHAST + RAVE-O), and 47 were control participants.

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Tissue-resident memory T cells (TRM) persist at sites of prior infection and have been shown to enhance pathogen clearance by recruiting circulating immune cells and providing bystander activation. Here, we characterize the functioning of brain-resident memory T cells (bTRM) in an animal model of viral infection. bTRM were subject to spontaneous homeostatic proliferation and were largely refractory to systemic immune cell depletion.

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The macroautophagy machinery has been implicated in MHC class II restricted antigen presentation. Here, we report that this machinery assists in the internalization of MHC class I molecules. In the absence of the autophagy factors Atg5 and Atg7, MHC class I surface levels are elevated due to decreased endocytosis and degradation.

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Background: The aim of this report was to estimate the prevalence of meldonium use in athletes competing in the Baku 2015 European Games to contribute to the surveillance of substances on the 2015 World Anti-Doping Agency (WADA) Monitoring Program. Meldonium is reported to be used by athletes to potentially enhance personal performance and shorten the recovery period after physical activity.

Methods: Three sources of data were reviewed to determine the prevalence of meldonium use during the Games including: (1) athlete self-reported declarations of drug and supplement use; (2) declarations from National Olympic Committee medical teams of the list of medicines that they imported into Azerbaijan as part of their stock of drugs for administration; (3) results from the antidoping laboratories reporting the detection of meldonium.

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Recent association studies have linked numerous genetic variants with an increased risk for multiple sclerosis, although their functional relevance remains largely unknown. Here we investigated phenotypical and functional consequences of a genetic variant in the CD226 gene that, among other autoimmune diseases, predisposes to multiple sclerosis. Phenotypically, effector and regulatory CD4(+) memory T cells of healthy individuals carrying the predisposing CD226 genetic variant showed, in comparison to carriers of the protective variant, reduced surface expression of CD226 and an impaired induction of CD226 after stimulation.

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Plasmacytoid dendritic cells (pDCs) exhibit both innate and adaptive functions. In particular they are the main source of type I IFNs and directly impact T cell responses through antigen presentation. We have previously demonstrated that during experimental autoimmune encephalomyelitis (EAE) initiation, myelin-antigen presentation by pDCs is associated with suppressive Treg development and results in attenuated EAE.

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Neuropathological techniques such as conventional and immunohistochemical staining of paraffin-embedded tissue sections are instrumental for identification and characterization of aberrations of organ architecture during human inflammatory disorders of the central nervous system (CNS) as in their animal models. Here we describe step-by-step protocols for tissue processing, sectioning, and conventional and immunohistochemical stainings to display as well as quantify CNS inflammation, demyelination, and neuronal damage in experimental autoimmune encephalomyelitis (EAE), an animal model of Multiple Sclerosis (MS).

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The 2-lysophosphatidylcholine analog edelfosine induces apoptosis in highly proliferating cells, e.g. activated immune cells.

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Recent findings indicate a pathogenic involvement of IL-17-producing CD8(+) T cells in multiple sclerosis (MS). IL-17 production has been attributed to a subset of CD8(+) T cells that belong to the mucosal-associated invariant T (MAIT) cell population. Here, we report a reduction of CD8(+) MAIT cells in the blood of MS patients compared with healthy individuals, which significantly correlated with IL-18 serum levels in MS patients.

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Background: In human and animal prion diseases, pathological prion protein, PrPSc, as well as prion infectivity is mainly found in the central nervous system, but also in lymphoid organs and muscle. Pathophysiology of prion colonization of lymphoid organs has been studied intensively, yet how myositis influences prion accumulation in muscle is unknown.

Result: We have investigated the influence of myositis on PrPSc accumulation and prion infectivity in two distinct mouse models of experimental autoimmune myositis.

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Multiple sclerosis is considered to be initiated by a deregulated, myelin-specific T cell response. However, the formation of inflammatory CNS lesions and the contribution of different leukocyte subsets in setting up these lesions are still incompletely understood. In this study, we show that, in the mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis, neutrophil granulocytes are important contributors in preparing CNS inflammation.

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