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[PMID]:29357290
[Au] Autor:Fujimoto N; Kitamura S; Uramaru N; Miyagawa S; Iguchi T
[Ad] Endereço:Institute for Radiation Biology and Medicine (RIRBM), Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. Electronic address: nfjm@hiroshima-u.ac.jp.
[Ti] Título:Identification of hepatic thyroid hormone-responsive genes in neonatal rats: Potential targets for thyroid hormone-disrupting chemicals.
[So] Source:Toxicol Lett;286:48-53, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:There have been many concerns about the possible adverse effects of thyroid hormone-disrupting chemicals in the environment. Because thyroid hormones are essential for regulating the growth and differentiation of many tissues, disruption of thyroid hormones during the neonatal period of an organism might lead to permanent effects on that organism. We postulated that there are target genes that are sensitive to thyroid hormones particularly during the neonatal period and that would thus be susceptible to thyroid hormone-disrupting chemicals. Global gene expression analysis was used to identify these genes in the liver of rat neonates. The changes in hepatic gene expression were examined 24 h after administering 1.0, 10, and 100 ng/g body weight (bw) triiodothyronine (T3) to male rats on postnatal day 3. Thirteen upregulated and four downregulated genes were identified in the neonatal liver. Among these, Pdp2 and Slc25a25 were found to be upregulated and more sensitive to T3 than the others, whereas Cyp7b1 and Hdc were found to be downregulated even at the lowest dose of 1.0 ng/g bw T3. Interestingly, when the responses of gene expression to T3 were examined in adult rats (8-week old), one-third of them did not respond to T3. The environmental chemicals with thyroid hormone-like activity, hydroxylated polybrominated diphenyl ethers, were then administered to neonatal rats to examine the effects on expression of the identified genes. The results showed that these chemicals were indeed capable of changing the expression of Slc25a25 and Hdc. Our results demonstrated a series of hepatic T3-responsive genes that are more sensitive to hormones during the neonatal period than during adulthood. These genes might be the potential targets of thyroid hormone-disrupting chemicals in newborns.
[Mh] Termos MeSH primário: Disruptores Endócrinos/toxicidade
Regulação da Expressão Gênica/efeitos dos fármacos
Fígado/efeitos dos fármacos
Tri-Iodotironina/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Família 7 do Citocromo P450/genética
Família 7 do Citocromo P450/metabolismo
Relação Dose-Resposta a Droga
Perfilação da Expressão Gênica/métodos
Histidina Descarboxilase/genética
Histidina Descarboxilase/metabolismo
Fígado/metabolismo
Masculino
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Piruvato Desidrogenase (Lipoamida)-Fosfatase/genética
Piruvato Desidrogenase (Lipoamida)-Fosfatase/metabolismo
Ratos Endogâmicos F344
Medição de Risco
Esteroide Hidroxilases/genética
Esteroide Hidroxilases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocrine Disruptors); 0 (Mitochondrial Membrane Transport Proteins); 0 (Slc25a25 protein, rat); 06LU7C9H1V (Triiodothyronine); EC 1.14.- (Steroid Hydroxylases); EC 1.14.13.100 (Cyp7b1 protein, rat); EC 1.14.14.23 (Cytochrome P450 Family 7); EC 3.1.3.43 (Pyruvate Dehydrogenase (Lipoamide)-Phosphatase); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


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[PMID]:28917668
[Au] Autor:Gao C; Ganesh BP; Shi Z; Shah RR; Fultz R; Major A; Venable S; Lugo M; Hoch K; Chen X; Haag A; Wang TC; Versalovic J
[Ad] Endereço:Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas; Department of Pathology, Texas Children's Hospital, Houston, Texas.
[Ti] Título:Gut Microbe-Mediated Suppression of Inflammation-Associated Colon Carcinogenesis by Luminal Histamine Production.
[So] Source:Am J Pathol;187(10):2323-2336, 2017 Oct.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microbiome-mediated suppression of carcinogenesis may open new avenues for identification of therapeutic targets and prevention strategies in oncology. Histidine decarboxylase (HDC) deficiency has been shown to promote inflammation-associated colorectal cancer by accumulation of CD11b Gr-1 immature myeloid cells, indicating a potential antitumorigenic effect of histamine. Here, we demonstrate that administration of hdc Lactobacillus reuteri in the gut resulted in luminal hdc gene expression and histamine production in the intestines of Hdc mice. This histamine-producing probiotic decreased the number and size of colon tumors and colonic uptake of [ F]-fluorodeoxyglucose by positron emission tomography in Hdc mice. Administration of L. reuteri suppressed keratinocyte chemoattractant (KC), Il22, Il6, Tnf, and IL1α gene expression in the colonic mucosa and reduced the amounts of proinflammatory, cancer-associated cytokines, keratinocyte chemoattractant, IL-22, and IL-6, in plasma. Histamine-generating L. reuteri also decreased the relative numbers of splenic CD11b Gr-1 immature myeloid cells. Furthermore, an isogenic HDC-deficient L. reuteri mutant that was unable to generate histamine did not suppress carcinogenesis, indicating a significant role of the cometabolite, histamine, in suppression of chronic intestinal inflammation and colorectal tumorigenesis. These findings link luminal conversion of amino acids to biogenic amines by gut microbes and probiotic-mediated suppression of colorectal neoplasia.
[Mh] Termos MeSH primário: Carcinogênese/patologia
Neoplasias Colorretais/patologia
Microbioma Gastrointestinal
Histamina/biossíntese
Inflamação/patologia
[Mh] Termos MeSH secundário: Animais
Carcinogênese/genética
Neoplasias Colorretais/sangue
Neoplasias Colorretais/diagnóstico por imagem
Neoplasias Colorretais/genética
Citocinas/sangue
Regulação Neoplásica da Expressão Gênica
Histidina Descarboxilase/genética
Histidina Descarboxilase/metabolismo
Seres Humanos
Inflamação/sangue
Inflamação/genética
Mucosa Intestinal/patologia
Lactobacillus reuteri/metabolismo
Camundongos Endogâmicos BALB C
Modelos Biológicos
Células Mieloides/metabolismo
Tomografia por Emissão de Pósitrons
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores Histamínicos H2/genética
Receptores Histamínicos H2/metabolismo
Baço/patologia
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (RNA, Messenger); 0 (Receptors, Histamine H2); 820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE


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[PMID]:28696146
[Au] Autor:Bjornsdottir-Butler K; Bencsath FA; McCarthy S; Benner RA
[Ad] Endereço:U.S. Food and Drug Administration, Division of Seafood Science and Technology, Gulf Coast Seafood Laboratory, 1 Iberville Drive, Dauphin Island, Alabama 36528, USA.
[Ti] Título:Heat Resistance of Histidine Decarboxylase from Gram-Negative Histamine-Producing Bacteria in Seafood.
[So] Source:J Food Prot;80(8):1273-1279, 2017 Aug.
[Is] ISSN:1944-9097
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Precooking of tuna is a potential critical control point (CCP) in the commercial manufacturing of canned tuna. To assess the efficacy of precooking as a CCP, an understanding of the thermal properties of histamine-producing bacteria (HPB) and their histidine decarboxylase (HDC) enzymes is required. The thermal properties of many HPB have been determined, but the thermal resistances of the HDC enzymes are unknown. The purpose of this study was to determine the D- and z-values of selected HDC enzymes to evaluate the CCP of precooking during the canning process and provide scientific data to support U.S. Food and Drug Administration guidelines. HDC (hdc) genes from three strains each of Morganella morganii, Enterobacter aerogenes, Raoultella planticola, and Photobacterium damselae were cloned, expressed, and purified using the Champion pET Directional TOPO Expression System, pET100 cloning vector, and HisPur Cobalt resin. The heat resistances of all enzymes were compared at 50°C, and the D- and z-values from one strain of each HPB were determined at 50 to 60°C. To evaluate the heat inactivation of HDC enzymes during canned tuna processing, tuna tissue was inoculated with HDCs and heated to 60°C in a water bath set at 65 and 100°C. The D-values for the HDC enzymes from M. morganii, E. aerogenes, R. planticola, and P. damselae ranged from 1.6 to 4.1, 1.6 to 6.3, 1.9 to 4.3, and 1.6 to 2.9 min, respectively, at 50 to 60°C. The z-values for M. morganii, E. aerogenes, R. planticola, and P. damselae were 19.2, 18.0, 22.0, and 13.3°C, respectively. The HDCs from all HPB except E. aerogenes showed no significant activity after being heated to 60°C. The data generated in this study will help refine current guidelines for the thermal destruction of the HDC enzymes.
[Mh] Termos MeSH primário: Histamina/análise
Histidina Descarboxilase/antagonistas & inibidores
Temperatura Alta
Alimentos Marinhos/microbiologia
[Mh] Termos MeSH secundário: Animais
Bactérias
Histamina/metabolismo
Histidina Descarboxilase/análise
Alimentos Marinhos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.4315/0362-028X.JFP-17-008


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[PMID]:28570646
[Au] Autor:McGregor R; Shan L; Wu MF; Siegel JM
[Ad] Endereço:Department of Psychiatry and Biobehavioral Sciences, University of California at Los Angeles, Los Angeles, California, United States of America.
[Ti] Título:Diurnal fluctuation in the number of hypocretin/orexin and histamine producing: Implication for understanding and treating neuronal loss.
[So] Source:PLoS One;12(6):e0178573, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The loss of specific neuronal phenotypes, as determined by immunohistochemistry, has become a powerful tool for identifying the nature and cause of neurological diseases. Here we show that the number of neurons identified and quantified using this method misses a substantial percentage of extant neurons in a phenotype specific manner. In mice, 24% more hypocretin/orexin (Hcrt) neurons are seen in the night compared to the day, and an additional 17% are seen after inhibiting microtubule polymerization with colchicine. We see no such difference between the number of MCH (melanin concentrating hormone) neurons in dark, light or colchicine conditions, despite MCH and Hcrt both being hypothalamic peptide transmitters. Although the size of Hcrt neurons did not differ between light and dark, the size of MCH neurons was increased by 15% in the light phase. The number of neurons containing histidine decarboxylase (HDC), the histamine synthesizing enzyme, was 34% greater in the dark than in the light, but, like Hcrt, cell size did not differ. We did not find a significant difference in the number or the size of neurons expressing choline acetyltransferase (ChAT), the acetylcholine synthesizing enzyme, in the horizontal diagonal band (HBD) during the dark and light conditions. As expected, colchicine treatment did not increase the number of these neurons. Understanding the function and dynamics of transmitter production within "non-visible" phenotypically defined cells has fundamental implications for our understanding of brain plasticity.
[Mh] Termos MeSH primário: Ritmo Circadiano
Histamina/biossíntese
Neurônios/metabolismo
Orexinas/biossíntese
[Mh] Termos MeSH secundário: Animais
Colina O-Acetiltransferase/metabolismo
Colchicina/administração & dosagem
Histidina Descarboxilase/metabolismo
Hormônios Hipotalâmicos/metabolismo
Masculino
Melaninas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Neurônios/citologia
Neurônios/enzimologia
Hormônios Hipofisários/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypothalamic Hormones); 0 (Melanins); 0 (Orexins); 0 (Pituitary Hormones); 67382-96-1 (melanin-concentrating hormone); 820484N8I3 (Histamine); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 4.1.1.22 (Histidine Decarboxylase); SML2Y3J35T (Colchicine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178573


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[PMID]:28275716
[Au] Autor:Chen A; Singh C; Oikonomou G; Prober DA
[Ad] Endereço:Division of Biology and Biological Engineering, California Institute of Technology , Pasadena, CA 91125.
[Ti] Título:Genetic Analysis of Histamine Signaling in Larval Zebrafish Sleep.
[So] Source:eNeuro;4(1), 2017 Jan-Feb.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pharmacological studies in mammals and zebrafish suggest that histamine plays an important role in promoting arousal. However, genetic studies using rodents with disrupted histamine synthesis or signaling have revealed only subtle or no sleep/wake phenotypes. Studies of histamine function in mammalian arousal are complicated by its production in cells of the immune system and its roles in humoral and cellular immunity, which can have profound effects on sleep/wake states. To avoid this potential confound, we used genetics to explore the role of histamine in regulating sleep in zebrafish, a diurnal vertebrate in which histamine production is restricted to neurons in the brain. Similar to rodent genetic studies, we found that zebrafish that lack histamine due to mutation of histidine decarboxylase ( ) exhibit largely normal sleep/wake behaviors. Zebrafish containing predicted null mutations in several histamine receptors also lack robust sleep/wake phenotypes, although we are unable to verify that these mutants are completely nonfunctional. Consistent with some rodent studies, we found that arousal induced by overexpression of the neuropeptide hypocretin (Hcrt) or by stimulation of -expressing neurons is not blocked in or mutants. We also found that the number of -expressing or histaminergic neurons is unaffected in animals that lack histamine or Hcrt signaling, respectively. Thus, while acute pharmacological manipulation of histamine signaling has been shown to have profound effects on zebrafish and mammalian sleep, our results suggest that chronic loss of histamine signaling due to genetic mutations has only subtle effects on sleep in zebrafish, similar to rodents.
[Mh] Termos MeSH primário: Histamina/genética
Histamina/metabolismo
Receptores Histamínicos H1/genética
Receptores Histamínicos H1/metabolismo
Sono/genética
Sono/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Ensaio de Imunoadsorção Enzimática
Histidina Descarboxilase/deficiência
Histidina Descarboxilase/genética
Imuno-Histoquímica
Larva
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Optogenética
Orexinas/genética
Orexinas/metabolismo
Estimulação Física
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Vigília/fisiologia
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hcrt protein, zebrafish); 0 (Orexins); 0 (Receptors, Histamine H1); 0 (Zebrafish Proteins); 820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


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[PMID]:28233179
[Au] Autor:Pittenger C
[Ad] Endereço:Departments of Psychiatry and Psychology, Yale Child Study Center, and Interdepartmental Neuroscience Program, Yale University School of Medicine, 34 Park Street, W315, New Haven, CT, 06519, USA. Christopher.pittenger@yale.edu.
[Ti] Título:Histidine Decarboxylase Knockout Mice as a Model of the Pathophysiology of Tourette Syndrome and Related Conditions.
[So] Source:Handb Exp Pharmacol;241:189-215, 2017.
[Is] ISSN:0171-2004
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:While the normal functions of histamine (HA) in the central nervous system have gradually come into focus over the past 30 years, the relationship of abnormalities in neurotransmitter HA to human disease has been slower to emerge. New insight came with the 2010 description of a rare nonsense mutation in the biosynthetic enzyme histidine decarboxylase (Hdc) that was associated with Tourette syndrome (TS) and related conditions in a single family pedigree. Subsequent genetic work has provided further support for abnormalities of HA signaling in sporadic TS. As a result of this genetic work, Hdc knockout mice, which were generated more than 15 years ago, have been reexamined as a model of the pathophysiology of TS and related conditions. Parallel work in these KO mice and in human carriers of the Hdc mutation has revealed abnormalities in the basal ganglia system and its modulation by dopamine (DA) and has confirmed the etiologic, face, and predictive validity of the model. The Hdc-KO model thus serves as a unique platform to probe the pathophysiology of TS and related conditions, and to generate specific hypotheses for subsequent testing in humans. This chapter summarizes the development and validation of this model and recent and ongoing work using it to further investigate pathophysiological changes that may contribute to these disorders.
[Mh] Termos MeSH primário: Síndrome de Tourette/metabolismo
Síndrome de Tourette/patologia
[Mh] Termos MeSH secundário: Animais
Dopamina/metabolismo
Histamina/metabolismo
Histidina Descarboxilase/genética
Histidina Descarboxilase/metabolismo
Seres Humanos
Camundongos
Camundongos Knockout
Mutação/genética
Síndrome de Tourette/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1007/164_2016_127


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[PMID]:28233178
[Au] Autor:Shan L; Bao AM; Swaab DF
[Ad] Endereço:Department of Neurobiology, Key Laboratory of Medical Neurobiology of Ministry of Health of China, Zhejiang Province Key Laboratory of Neurobiology, Zhejiang University School of Medicine, Hangzhou, China.
[Ti] Título:Changes in Histidine Decarboxylase, Histamine N-Methyltransferase and Histamine Receptors in Neuropsychiatric Disorders.
[So] Source:Handb Exp Pharmacol;241:259-276, 2017.
[Is] ISSN:0171-2004
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Compared to other monoamine neurotransmitters, information on the association between the histaminergic system and neuropsychiatric disorders is scarce, resulting in a lack of histamine-related treatment for these disorders. The current chapter tries to combine information obtained from genetic studies, neuroimaging, post-mortem human brain studies and cerebrospinal fluid measurements with data from recent clinical trials on histamine receptor agonists and antagonists, with a view to determining the possible role of the histaminergic system in neuropsychiatric disorders and to pave the way for novel histamine-related therapeutic strategies.
[Mh] Termos MeSH primário: Histamina N-Metiltransferase/metabolismo
Histidina Descarboxilase/metabolismo
Transtornos Mentais/metabolismo
Receptores Histamínicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Histamina/metabolismo
Seres Humanos
Neuropsiquiatria/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Histamine); 820484N8I3 (Histamine); EC 2.1.1.8 (Histamine N-Methyltransferase); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1007/164_2016_125


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[PMID]:27889172
[Au] Autor:Jeong DW; Heo S; Lee JH
[Ad] Endereço:Department of Bio and Fermentation Convergence Technology, Kookmin University, Seoul 02707, Republic of Korea.
[Ti] Título:Safety assessment of Tetragenococcus halophilus isolates from doenjang, a Korean high-salt-fermented soybean paste.
[So] Source:Food Microbiol;62:92-98, 2017 Apr.
[Is] ISSN:1095-9998
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We assessed the safety of 49 Tetragenococcus halophilus strains isolated from doenjang in Korea. Minimum inhibitory concentration assays showed that all strains can be considered as susceptible to ampicillin, erythromycin, penicillin G, tetracycline, and vancomycin, but resistant to ciprofloxacin based on the Enterococcus breakpoint values provided by the European Committee on Antimicrobial Susceptibility testing in 2015. Ciprofloxacin resistance was sufficiently high to consider the potential for acquisition of transmissible determinants. Two strains exhibiting potentially acquired resistance to chloramphenicol and gentamicin, and chloramphenicol alone, were identified. None of the strains exhibited α-hemolytic activity or biofilm formation; two strains exhibited weak ß-hemolytic activity. Doenjang isolates produced an average of 3338.6 ppm of tyramine in the laboratory, considerably higher than the levels produced by two reference strains. All of the test strains exhibited similar cadaverine, histamine, and putrescine production patterns. Most T. halophilus strains could grow at a NaCl concentration >18%, exhibited acid production at 15% NaCl, and expressed strain-specific protease and lipase activities. The potential acquisition of transmissible determinants for antibiotic resistance and tyramine production identified in this study necessitate the need for a thorough safety assessment of T. halophilus before it can be considered for use in food fermentation processes.
[Mh] Termos MeSH primário: Enterococcaceae/isolamento & purificação
Fermentação
Inocuidade dos Alimentos
Alimentos de Soja/microbiologia
Feijão de Soja/microbiologia
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Biofilmes/crescimento & desenvolvimento
Aminas Biogênicas/biossíntese
Reatores Biológicos
Ciprofloxacino/farmacologia
Resistência Microbiana a Medicamentos
Enterococcaceae/efeitos dos fármacos
Enterococcaceae/genética
Manipulação de Alimentos
Microbiologia de Alimentos
Histidina Descarboxilase/genética
Testes de Sensibilidade Microbiana
República da Coreia
Cloreto de Sódio na Dieta
Tirosina Descarboxilase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Biogenic Amines); 0 (Sodium Chloride, Dietary); 5E8K9I0O4U (Ciprofloxacin); EC 4.1.1.22 (Histidine Decarboxylase); EC 4.1.1.25 (Tyrosine Decarboxylase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161128
[St] Status:MEDLINE


  9 / 1446 MEDLINE  
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[PMID]:27787718
[Au] Autor:Ohtsu H; Seike M
[Ad] Endereço:Applied Quantum Medical Engineering, Graduate School of Engineering, Tohoku University, Sendai, Japan. hiroshi.ohtsu@gmail.com.
[Ti] Título:Histamine and Histamine Receptors in Allergic Dermatitis.
[So] Source:Handb Exp Pharmacol;241:333-345, 2017.
[Is] ISSN:0171-2004
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:In this chapter we will first introduce the pathophysiological process of several skin diseases including allergic dermatitis, a common skin disease, including chronic allergic contact dermatitis (CACD), and atopic dermatitis (AD). In CACD and AD patients, repeated skin exposure to antigens contributes to the development of chronic eczematous lesions. Repeated application of haptens on mice allows emulation of the development of CACD in humans. Further, we will focus on H1, H2, and H4 histamine receptors and their effects on CACD and AD. Histamine-deficient mice, with a knockout histidine decarboxylase (HDC) gene, were used to investigate the role of histamine in CACD and AD. Histamine induces infiltration of inflammatory cells, including mast cells and eosinophils, and elevates Th2 cytokine levels in CACD. Histamine promotes the development of eczematous lesions, elevates IgE serum levels, and induces scratching behavior in CACD. The administration of H1 or H4 receptor antagonists was effective to ameliorate these symptoms in murine CACD models. The combination of H1 and H4 receptor antagonists is a potential therapeutic target for chronic inflammatory skin diseases such as CACD and AD, since combined therapy proved to be more effective than monotherapy.
[Mh] Termos MeSH primário: Dermatite Alérgica de Contato/metabolismo
Dermatite Atópica/metabolismo
Histamina/metabolismo
Receptores Histamínicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Dermatite Alérgica de Contato/sangue
Dermatite Atópica/sangue
Histidina Descarboxilase/metabolismo
Seres Humanos
Imunoglobulina E/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Histamine); 37341-29-0 (Immunoglobulin E); 820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE
[do] DOI:10.1007/164_2016_9


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[PMID]:27752845
[Au] Autor:Schirone M; Visciano P; Tofalo R; Suzzi G
[Ad] Endereço:Faculty of Bioscience and Technology for Food, Agriculture and Environment, University of Teramo, Teramo, Italy. mschirone@unite.it.
[Ti] Título:Histamine Food Poisoning.
[So] Source:Handb Exp Pharmacol;241:217-235, 2017.
[Is] ISSN:0171-2004
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The consumption of food containing high amounts of histamine and other biogenic amines can cause food poisoning with different symptoms linked to the individual sensitivity and the detoxification activity. Histamine is the only biogenic amine with regulatory limits set by the European Commission in fish and fishery products, because it can lead to a fatal outcome. However, also fermented foods can be involved in outbreaks and sporadic cases of intoxication. The factors affecting the presence of histamine in food are variable and product specific including the availability of the precursor amino acid, the presence of microorganisms producing decarboxylases, and the conditions allowing their growth and enzyme production. Generally, the good quality of raw material and hygienic practices during food processing as well as the use of histidine decarboxylase-negative starter cultures can minimize the occurrence of histamine. Further studies are necessary to estimate the human exposure and the relationship between the total amount of the biogenic amines ingested with food and health effects.
[Mh] Termos MeSH primário: Aminas Biogênicas/metabolismo
Doenças Transmitidas por Alimentos/etiologia
Histamina/efeitos adversos
Histamina/metabolismo
[Mh] Termos MeSH secundário: Animais
Aminas Biogênicas/efeitos adversos
Histidina Descarboxilase/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biogenic Amines); 820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161019
[St] Status:MEDLINE
[do] DOI:10.1007/164_2016_54



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