Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Staphylococcal toxic shock syndrome (TSS) and staphylococcal scalded skin syndrome (SSSS) are two distinct toxin-mediated syndromes with prominent cutaneous features. The exanthematous presentation of these syndromes places them in the broad category of childhood exanthems, and the ability to recognize these potentially devastating illnesses is essential for pediatricians and dermatologists who may encounter children with fever and rash. Recent advances in the understanding of the pathogenesis of these entities has helped to explain the distinctive clinical presentations of TSS and SSSS. Toxic shock syndrome toxin-1 (TSST-1) and enterotoxins are the secretory products of Staphylococcus aureus that lead to TSS. Many of the clinical features of TSS (fever, shock, multiple organ dysfunction) can be explained by the effects of cytokines (especially interleukin-1 and tumor necrosis factor) induced by TSST-1. TSS is not an exclusively menstrual event associated with tampon use. Nonmenstrual pediatric TSS may be associated with a wide variety of staphylococcal infections. Infected burn wounds in hospitalized children and bacterial tracheitis (in some cases following influenza B infection) are relatively high-risk settings for pediatric TSS. The epidermolytic toxins (A and B) directly produce subgranular epidermolysis leading to SSSS. SSSS encompasses a clinical spectrum from bullous impetigo to the widespread exfoliation of the Ritter disease variant of SSSS. This entity usually occurs in children under 5 years of age, and is primarily explained by lack of immunity to the toxins as well as renal immaturity leading to poor clearance of toxin. The newborn nursery is an important setting where epidemics of SSSS have occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Staphylococcal toxin-mediated syndromes in childhood. 155 Jul 11

T cell blasts resulting from stimulating human cord blood (CB) mononuclear cells (MC) and adult peripheral blood (APB) MC with a bacterial superantigen, toxic shock syndrome toxin-1 (TSST-1), and then with human rIL-2 were investigated for their reactions to restimulation with TSST-1. Expression of TCR V beta 2, which determines the potential reactivity to TSST-1 and of CD45RO, was increased in both TSST-1-induced CB and APB T cell blasts. Most preparations of the TSST-1-induced CB T cell blasts exhibited low or no production of IL-2 and IL-4 in response to restimulation with TSST-1, while the APB T cell blasts showed high responses. TSST-1-induced T cell blasts derived from APB T cells depleted of both CD45RO+ T cells and HLA class II+ T cells showed high IL-2 production in response to restimulation with TSST-1. TSST-1-induced CB T cell blasts generated in the presence of DR+ L cells with high accessory cell activity still showed a low response to restimulation with TSST-1. These results indicate that CB T cells are inherently highly susceptible to tolerance induction by bacterial superantigens, suggesting the immunologic immaturity of CB T cells.
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PMID:Evidence for immunologic immaturity of cord blood T cells. Cord blood T cells are susceptible to tolerance induction to in vitro stimulation with a superantigen. 759 32

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non-sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increases with development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia, which is a stimulator of the immune response while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock - a feature of SIDS.
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PMID:Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens. 1045 40

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non- sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increase wtih development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia which is a stimulator of the immune response, while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock--a feature of SIDS.
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PMID:Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens. 1079 Jul 32