41 research outputs found

    Immunology: the neuronal pathway to mucosal immunity

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    Type 2 immunity at mucosal surfaces is thought to be initiated by type 2 innate lymphoid cells. New studies report that these cells are themselves activated by the neuropeptide neuromedin U, produced by cholinergic neurons in the gut and in airways

    Innate lymphoid cells in helminth infections—obligatory or accessory?

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    ILCs burst onto the immunological scene with their roles in bacterial and helminth infections. As their influence has emerged, it has become clear that they play a fundamental role in regulating intestinal homeostasis and the immune response during inflammation. A subset of ILCs, ILC2s, has become the focus of attention for many helminth biologists - stepping into the limelight as both an initiator and amplifier of the elusive type-2 response. In many of the early reports, conclusions as to their function were based on experiments using unadapted parasites or immune-compromised hosts. In this review we re-examine the generation and function of type-2 ILCs in helminth infection and the extent to which their roles may be essential or redundant, in both primary and challenge infections. ILC2s will be discussed in terms of a broader innate network, which when in dialogue with adaptive immunity, allows the generation of the anti-parasite response. Finally, we will review how our understanding of how helminths manipulate ILC2 populations to benefit their survival, as well as dampen systemic inflammation in the host, can be used to improve strategies to control disease

    Innate Lymphoid Cells in Helminth Infections—Obligatory or Accessory?

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    ILCs burst onto the immunological scene with their involvement in bacterial and helminth infections. As their influence has emerged, it has become clear that they play a fundamental role in regulating barrier tissue homeostasis and the immune response during inflammation. A subset of ILCs, ILC2s, has become the focus of attention for many helminth biologists—stepping into the limelight as both the elusive initiator and amplifier of the type-2 response. In many of the early reports, conclusions as to their function were based on experiments using unadapted parasites or immune-compromised hosts. In this review we re-examine the generation and function of type-2 ILCs in helminth infection and the extent to which their roles may be essential or redundant, in both primary and challenge infections. ILC2s will be discussed in terms of a broader innate network, which when in dialogue with adaptive immunity, allows the generation of the anti-parasite response. Finally, we will review how helminths manipulate ILC2 populations to benefit their survival, as well as dampen systemic inflammation in the host, and how this understanding may be used to improve strategies to control disease

    ESPEN guideline on clinical nutrition in acute and chronic pancreatitis

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    Both acute and chronic pancreatitis are frequent diseases of the pancreas, which, despite being of benign nature, are related to a significant risk of malnutrition and may require nutritional support. Acute necrotizing pancreatitis is encountered in 20% of patients with acute pancreatitis, is associated with increased morbidity and mortality, and may require artificial nutrition by enteral or parenteral route, as well as additional endoscopic, radiological or surgical interventions. Chronic pancreatitis represents a chronic inflammation of the pancreatic gland with development of fibrosis. Abdominal pain leading to decreased oral intake, as well as exocrine and endocrine failure are frequent complications of the disease. All of the above represent risk factors related to malnutrition. Therefore, patients with chronic pancreatitis should be considered at risk, screened and supplemented accordingly. Moreover, osteoporosis and increased facture risk should be acknowledged in patients with chronic pancreatitis, and preventive measures should be considered

    German S3 guideline "actinic keratosis and cutaneous squamous cell carcinoma" – long version of the update 2023

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    Actinic keratosis (AK) are common lesions in light-skinned individuals that can potentially progress to cutaneous squamous cell carcinoma (cSCC). Both conditions may be associated with significant morbidity and constitute a major disease burden, especially among the elderly. To establish an evidence-based framework for clinical decision making, the guideline “actinic keratosis and cutaneous squamous cell carcinoma” was updated and expanded by the topics cutanepus squamous cell carcinoma in situ (Bowen’s disease) and actinic cheilitis. This guideline was developed at the highest evidence level (S3) and is aimed at dermatologists, general practitioners, ear nose and throat specialists, surgeons, oncologists, radiologists and radiation oncologists in hospitals and office-based settings, as well as other medical specialties, policy makers and insurance funds involved in the diagnosis and treatment of patients with AK and cSCC

    Low Resting Membrane Potential and Low Inward Rectifier Potassium Currents Are Not Inherent Features of hiPSC-Derived Cardiomyocytes

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    Human induced pluripotent stem cell (hiPSC) cardiomyocytes (CMs) show less negative resting membrane potential (RMP), which is attributed to small inward rectifier currents (IK1). Here, IK1 was measured in hiPSC-CMs (proprietary and commercial cell line) cultured as monolayer (ML) or 3D engineered heart tissue (EHT) and, for direct comparison, in CMs from human right atrial (RA) and left ventricular (LV) tissue. RMP was measured in isolated cells and intact tissues. IK1 density in ML- and EHT-CMs from the proprietary line was similar to LV and RA, respectively. IK1 density in EHT-CMs from the commercial line was 2-fold smaller than in the proprietary line. RMP in EHT of both lines was similar to RA and LV. Repolarization fraction and IK,ACh response discriminated best between RA and LV and indicated predominantly ventricular phenotype in hiPSC-CMs/EHT. The data indicate that IK1 is not necessarily low in hiPSC-CMs, and technical issues may underlie low RMP in hiPSC-CMs

    Growing Stem Cells: The Impact of Federal Funding Policy on the US Scientific Frontier

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    This paper articulates a citation-based approach to science policy evaluation and employs that approach to investigate the impact of the United States’ 2001 policy regarding the federal funding of human embryonic stem cell (hESC) research. We evaluate the impact of the policy on the level of U.S. hESC research, the U.S. position at the knowledge frontier, and the strategic response of U.S. scientists. Consistent with recent research on the science of science and innovation policy, we employ a difference-in-differences approach using bibliometric data with the aim of analyzing the causal impact of the policy on cumulative research. Our estimates suggest that in the aftermath of the 2001 policy, U.S. production of hESC research lagged 35 to 40 percent behind anticipated levels. However, this relative decline was largely concentrated in the years 2001 to 2003 and ameliorated over time. The rebound in U.S. hESC research after 2003 was driven by contributions by researchers at elite U.S. institutions and U.S. researchers who collaborated with international partners. The results suggest that scientists respond strategically to research funding restrictions and that modest science policy shifts can have a significant influence on the within-country composition of research and the pattern of global research collaboration.National Science Foundation (U.S.) (Grant Number: 0738394

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