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  1. Article ; Online: Febrile children with breaches in the responses of innate immunity.

    Rigante, Donato

    Expert review of clinical immunology

    2023  Volume 19, Issue 11, Page(s) 1293–1298

    Language English
    Publishing date 2023-07-26
    Publishing country England
    Document type Editorial
    ZDB-ID 2274260-8
    ISSN 1744-8409 ; 1744-666X
    ISSN (online) 1744-8409
    ISSN 1744-666X
    DOI 10.1080/1744666X.2023.2240960
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6661: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Telemedicine and the risk of overshadowing children with Kawasaki disease in a worldwide coronavirus pandemic climate.

    Rigante, Donato

    Internal and emergency medicine

    2021  Volume 16, Issue 7, Page(s) 2027–2028

    MeSH term(s) COVID-19 ; Child ; Humans ; Mucocutaneous Lymph Node Syndrome/complications ; Mucocutaneous Lymph Node Syndrome/epidemiology ; Pandemics ; Telemedicine
    Language English
    Publishing date 2021-02-13
    Publishing country Italy
    Document type Letter ; Comment
    ZDB-ID 2454173-4
    ISSN 1970-9366 ; 1828-0447
    ISSN (online) 1970-9366
    ISSN 1828-0447
    DOI 10.1007/s11739-021-02662-7
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6673: Show issues Location:
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  3. Article ; Online: When, how, and why do fevers hold children hostage?

    Rigante, Donato

    Journal of evidence-based medicine

    2020  Volume 13, Issue 1, Page(s) 85–88

    MeSH term(s) Child ; Fever/diagnosis ; Fever/etiology ; Fever/therapy ; Humans
    Language English
    Publishing date 2020-02-22
    Publishing country England
    Document type Journal Article
    ISSN 1756-5391
    ISSN (online) 1756-5391
    DOI 10.1111/jebm.12377
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  4. Article: Kawasaki Disease as the Immune-Mediated Echo of a Viral Infection.

    Rigante, Donato

    Mediterranean journal of hematology and infectious diseases

    2020  Volume 12, Issue 1, Page(s) e2020039

    Abstract: Although the etiology of Kawasaki disease (KD) remains elusive, the available evidence indicates that the primum movens may be a dysregulated immune response to various microbial agents, leading to cytokine cascade and endothelial cell activation in ... ...

    Abstract Although the etiology of Kawasaki disease (KD) remains elusive, the available evidence indicates that the primum movens may be a dysregulated immune response to various microbial agents, leading to cytokine cascade and endothelial cell activation in patients with KD. Documented infections by different viruses in many individual cases have been largely reported and are discussed herein, but attempts to demonstrate their causative role in the distinctive KD scenario and KD epidemiological features have been disappointing. To date, no definite link has been irrefutably found between a single infection and KD.
    Keywords covid19
    Language English
    Publishing date 2020-07-01
    Publishing country Italy
    Document type Journal Article ; Review
    ZDB-ID 2674750-9
    ISSN 2035-3006
    ISSN 2035-3006
    DOI 10.4084/MJHID.2020.039
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  5. Article ; Online: Phenotype variability of autoinflammatory disorders in the pediatric patient: A pictorial overview.

    Rigante, Donato

    Journal of evidence-based medicine

    2020  Volume 13, Issue 3, Page(s) 227–245

    Abstract: Disruption of innate immunity leading to systemic inflammation and multi-organ dysfunction is the basilar footprint of autoinflammatory disorders (AIDs), ranging from rare hereditary monogenic diseases to a large number of common chronic inflammatory ... ...

    Abstract Disruption of innate immunity leading to systemic inflammation and multi-organ dysfunction is the basilar footprint of autoinflammatory disorders (AIDs), ranging from rare hereditary monogenic diseases to a large number of common chronic inflammatory conditions in which there is a simultaneous participation of multiple genetic components and environmental factors, sometimes combined with autoimmune phenomena and immunodeficiency. Whatever their molecular mechanism, hereditary AIDs are caused by mutations in regulatory molecules or sensors proteins leading to dysregulated production of proinflammatory cytokines or cytokine-inducing transcription factors, fever, elevation of acute phase reactants, and a portfolio of manifold inflammatory signs which might occur in a stereotyped manner, mostly with overactivity or misactivation of different inflammasomes. Symptoms might overlap in the pediatric patient, obscuring the final diagnosis of AIDs and delaying the most appropriate treatment. Actually, the fast-paced evolution of scientific knowledge has led to recognize or reclassify an overgrowing number of multifactorial diseases, which share the basic pathogenetic mechanisms with AIDs. The wide framework of classic hereditary periodic fevers, AIDs with prominent skin involvement, disorders of the ubiquitin-proteasome system, defects of actin cytoskeleton dynamics, and also idiopathic nonhereditary febrile syndromes occurring in children is herein presented. Interleukin-1 dependence of these diseases or involvement of other predominating molecules is also discussed.
    Language English
    Publishing date 2020-07-06
    Publishing country England
    Document type Journal Article ; Review
    ISSN 1756-5391
    ISSN (online) 1756-5391
    DOI 10.1111/jebm.12406
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  6. Article ; Online: New mosaic tiles in childhood hereditary autoinflammatory disorders.

    Rigante, Donato

    Immunology letters

    2018  Volume 193, Page(s) 67–76

    Abstract: The protean clinical phenotypes of hereditary autoinflammatory disorders (HAID) are caused by abnormal activation of innate immunity and consist of seemingly unprovoked inflammatory flares localized to multiple organs, such as the skin, joints, serosal ... ...

    Abstract The protean clinical phenotypes of hereditary autoinflammatory disorders (HAID) are caused by abnormal activation of innate immunity and consist of seemingly unprovoked inflammatory flares localized to multiple organs, such as the skin, joints, serosal membranes, gut, and central nervous system. Different mutations in genes implied in activation of the interleukin-1 (IL-1)-structured inflammasome, cytoskeletal signaling and apoptosis contribute to the pathogenesis of different HAID, which mostly start in childhood with self-limited flares unrelated to infectious agents, autoantibody production or autoreactive cells. Though IL-1 remains pivotal in many inflammasome-mediated diseases, other cytokinopathies involving IL-18, nuclear factorκ-B, interferons, and tumor necrosis factor have provided new horizons in the definition of HAID of children: the list of HAID has expanded as a consequence of a better understanding of their pathogenetic molecular mechanisms and also application of new genetic technologies. However, diagnosis of most HAID is clinical and focused on several evidence-based criteria sets: their discrimination remains challenging for unexperienced pediatricians as there are no universally accepted algorithms, and a still relevant number of patients may linger without any clarifying genetic analysis, whose interpretation combined with processing of treatment options should be discussed on a multidisciplinary basis.
    MeSH term(s) Child ; Diagnosis, Differential ; Hereditary Autoinflammatory Diseases/diagnosis ; Hereditary Autoinflammatory Diseases/immunology ; Humans ; Immunity, Innate ; Inflammasomes/metabolism ; Inflammation ; Interleukin-1/genetics ; Interleukin-1/metabolism ; Interleukin-18/metabolism ; Mutation/genetics ; NF-kappa B/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Inflammasomes ; Interleukin-1 ; Interleukin-18 ; NF-kappa B ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2018
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 445150-8
    ISSN 1879-0542 ; 0165-2478
    ISSN (online) 1879-0542
    ISSN 0165-2478
    DOI 10.1016/j.imlet.2017.11.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1512: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article: The Broad-Ranging Panorama of Systemic Autoinflammatory Disorders with Specific Focus on Acute Painful Symptoms and Hematologic Manifestations in Children.

    Rigante, Donato

    Mediterranean journal of hematology and infectious diseases

    2018  Volume 10, Issue 1, Page(s) e2018067

    Abstract: Systemic autoinflammatory disorders (SAIDs) are inherited defects of innate immunity characterized by recurrent sterile inflammatory attacks involving skin, joints, serosal membranes, gastrointestinal tube, and other tissues, which recur with variable ... ...

    Abstract Systemic autoinflammatory disorders (SAIDs) are inherited defects of innate immunity characterized by recurrent sterile inflammatory attacks involving skin, joints, serosal membranes, gastrointestinal tube, and other tissues, which recur with variable rhythmicity and display reactive amyloidosis as a potential long-term complication. Dysregulated inflammasome activity leading to overproduction of many proinflammatory cytokines, such as interleukin-1 (IL-1), and delayed shutdown of inflammation are considered crucial pathogenic keys in the vast majority of SAIDs. Progress of cellular biology has partially clarified the mechanisms behind monogenic SAIDs, such as familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome, cryopyrin-associated periodic syndrome, mevalonate kinase deficiency, hereditary pyogenic diseases, idiopathic granulomatous diseases and defects of the ubiquitin-proteasome pathway. Whereas, little is clarified for the polygenic SAIDs, such as periodic fever, aphthous stomatitis, pharyngitis, and cervical adenopathy (PFAPA) syndrome. The puzzle of symptomatic febrile attacks recurring over time in children requires evaluating the mixture of clinical data, inflammatory parameters in different disease phases, the therapeutic efficacy of specific drugs such as colchicine, corticosteroids or IL-1 antagonists, and genotype analysis in selected cases. The long-term history of periodic fevers should also need to rule out chronic infections and malignancies. This review is conceived as a practical template for proper classification of children with recurring fevers and includes tips useful for the diagnostic approach to SAIDs, focusing on the specific acute painful symptoms and hematologic manifestations encountered in childhood.
    Language English
    Publishing date 2018-11-01
    Publishing country Italy
    Document type Journal Article ; Review
    ZDB-ID 2674750-9
    ISSN 2035-3006
    ISSN 2035-3006
    DOI 10.4084/MJHID.2018.067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The Clinical Chameleon of Autoinflammatory Diseases in Children.

    Sangiorgi, Eugenio / Rigante, Donato

    Cells

    2022  Volume 11, Issue 14

    Abstract: The very first line of defense in humans is innate immunity, serving as a critical strongpoint in the regulation of inflammation. Abnormalities of the innate immunity machinery make up a motley group of rare diseases, named 'autoinflammatory', which are ... ...

    Abstract The very first line of defense in humans is innate immunity, serving as a critical strongpoint in the regulation of inflammation. Abnormalities of the innate immunity machinery make up a motley group of rare diseases, named 'autoinflammatory', which are caused by mutations in genes involved in different immune pathways. Self-limited inflammatory bouts involving skin, serosal membranes, joints, gut and other districts of the human body burst and recur with variable periodicity in most autoinflammatory diseases (ADs), often leading to secondary amyloidosis as a long-term complication. Dysregulated inflammasome activity, overproduction of interleukin (IL)-1 or other IL-1-related cytokines and delayed shutdown of inflammation are pivotal keys in the majority of ADs. The recent progress of cellular biology has clarified many molecular mechanisms behind monogenic ADs, such as familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome (or 'autosomal dominant familial periodic fever'), cryopyrin-associated periodic syndrome, mevalonate kinase deficiency, hereditary pyogenic diseases, idiopathic granulomatous diseases and defects of the ubiquitin-proteasome pathway. A long-lasting history of recurrent fevers should require the ruling out of chronic infections and malignancies before considering ADs in children. Little is known about the potential origin of polygenic ADs, in which sterile cytokine-mediated inflammation results from the activation of the innate immunity network, without familial recurrency, such as periodic fever/aphthous stomatitis/pharyngitis/cervical adenopathy (PFAPA) syndrome. The puzzle of febrile attacks recurring over time with chameleonic multi-inflammatory symptoms in children demands the inspection of the mixture of clinical data, inflammation parameters in the different disease phases, assessment of therapeutic efficacy of a handful of drugs such as corticosteroids, colchicine or IL-1 antagonists, and genotype analysis to exclude or confirm a monogenic origin.
    MeSH term(s) Amyloidosis ; Child ; Fever ; Hereditary Autoinflammatory Diseases/diagnosis ; Hereditary Autoinflammatory Diseases/genetics ; Humans ; Immunity, Innate ; Inflammation ; Interleukin-1 ; Recurrence ; Syndrome
    Chemical Substances Interleukin-1
    Language English
    Publishing date 2022-07-18
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11142231
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Kawasaki disease as the immune-mediated echo of a viral infection

    Rigante, Donato

    Mediterr. J. Hematol. Infect. Dis.

    Abstract: Although the etiology of Kawasaki disease (KD) remains elusive, the available evidence indicates that the primum movens may be a dysregulated immune response to various microbial agents, leading to cytokine cascade and endothelial cell activation in ... ...

    Abstract Although the etiology of Kawasaki disease (KD) remains elusive, the available evidence indicates that the primum movens may be a dysregulated immune response to various microbial agents, leading to cytokine cascade and endothelial cell activation in patients with KD. Documented infections by different viruses in many individual cases have been largely reported and are discussed herein, but attempts to demonstrate their causative role in the distinctive KD scenario and KD epidemiological features have been disappointing. To date, no definite link has been irrefutably found between a single infection and KD.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #646871
    Database COVID19

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  10. Article ; Online: A Potential Partnership between Genetics and the Oral Microbiome in Children Displaying Periodic Fever/Aphthosis/Pharyngitis/Adenitis Syndrome.

    Rigante, Donato / Calò, Lea / Ciavarro, Alessandro / Galli, Jacopo

    International journal of molecular sciences

    2023  Volume 24, Issue 21

    Abstract: Periodic fever/aphthosis/pharyngitis/adenitis (PFAPA) syndrome was initially described in a small cohort of American children [ ... ]. ...

    Abstract Periodic fever/aphthosis/pharyngitis/adenitis (PFAPA) syndrome was initially described in a small cohort of American children [...].
    MeSH term(s) Child ; Humans ; Stomatitis, Aphthous/genetics ; Lymphadenitis/genetics ; Lymphadenopathy ; Microbiota ; Pharyngitis/genetics ; Syndrome
    Language English
    Publishing date 2023-10-24
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242115505
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