Database : MEDLINE
Search on : Hypersensitivity [Words]
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[PMID]: 29524659
[Au] Autor:Wang S; Shi L; Hu Y; Liu R; Ren A; Zhu J; Zhao M
[Ad] Address:Key Laboratory of Agricultural Environmental Microbiology, Ministry of Agriculture, Microbiology Department, College of Life Sciences, Nanjing; Agricultural University, Nanjing 210095, Jiangsu, P.R. China.
[Ti] Title:Roles of the Skn7 response regulator in stress resistance, cell wall integrity and GA biosynthesis in Ganoderma lucidum.
[So] Source:Fungal Genet Biol;, 2018 Mar 07.
[Is] ISSN:1096-0937
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The transcription factor Skn7 is a highly conserved fungal protein that participates in a variety of processes, including oxidative stress adaptation, fungicide sensitivity, cell wall biosynthesis, cell cycle, and sporulation. In this study, a homologous gene of Saccharomyces cerevisiae Skn7 was cloned from Ganoderma lucidum. RNA interference (RNAi) was used to study the functions of Skn7, and the two knockdown strains Skn7i-5 and Skn7i-7 were obtained in G. lucidum. The knockdown of GlSkn7 resulted in hypersensitivity to oxidative and cell wall stresses. The concentrations of chitin and ß-1,3-glucan distinctly decreased in the GlSkn7 knockdown strains compared with those of the wild type (WT). In addition, the expression of cell wall biosynthesis related genes was also significantly down-regulated and the thickness of the cell wall also significantly reduced in the GlSkn7 knockdown strains. The intracellular reactive oxygen species (ROS) content and ganoderic acids biosynthesis increased significantly in the GlSkn7 knockdown strains. Interestingly, the level of intracellular ROS and the content of ganoderic acids decreased after N-acetyl-L-cysteine (NAC), an ROS scavenger, was added, indicating that GlSkn7 might regulate ganoderic acids biosynthesis via the intracellular ROS level. The transcript level of GlSkn7 were up-regulated in osmotic stress, heat stress and fungicide condition. At the same time, the content of ganoderic acids in the GlSkn7 knockdown strains also changed distinctly in these conditions. Overall, GlSkn7 is involved in stress resistance, cell wall integrity and ganoderic acid biosynthesis in G. lucidum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 155811 MEDLINE  
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[PMID]: 29515281
[Au] Autor:Pai S; Munshi R; Nayak C
[Ad] Address:Department of Clinical Pharmacology, TN Medical College and BYL Nair Charitable Hospital, Mumbai, Maharashtra, India.
[Ti] Title:Fatal dapsone hypersensitivity syndrome with hypothyroidism and steroid-induced diabetes mellitus.
[So] Source:Indian J Pharmacol;49(5):396-398, 2017 Sep-Oct.
[Is] ISSN:1998-3751
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Dapsone has been part of the World Health Organization multidrug therapy for the treatment of leprosy. While it has been efficacious in the management of leprosy, there are many patients who develop adverse drug reactions to the drug including life-threatening reactions such as dapsone hypersensitivity syndrome (DHS). We report a case of a patient who was prescribed dapsone as part of multidrug therapy for leprosy following which she developed DHS. Her condition worsened after tapering the oral steroids given to manage the DHS, and she was detected to have hypothyroidism. She developed diabetes mellitus and succumbed to septic shock.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.4103/ijp.IJP_764_16

  3 / 155811 MEDLINE  
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[PMID]: 29511567
[Au] Autor:Reinhart JM; Rose W; Panyard DJ; Newton MA; Liebenstein TK; Yee J; Trepanier LA
[Ad] Address:Department of Medical SciencesSchool of Veterinary MedicineUniversity of Wisconsin-MadisonMadisonWIUSA.
[Ti] Title:RNA expression profiling in sulfamethoxazole-treated patients with a range of in vitro lymphocyte cytotoxicity phenotypes.
[So] Source:Pharmacol Res Perspect;6(2):e00388, 2018 Apr.
[Is] ISSN:2052-1707
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The lymphocyte toxicity assay (LTA) is a proposed surrogate marker of sulfonamide antibiotic hypersensitivity. In the LTA, peripheral blood mononuclear cells (PBMCs) undergo apoptosis more readily in hypersensitive versus tolerant patients when exposed to drug-hydroxylamine metabolites in vitro. The purpose of this study was to identify key gene transcripts associated with increased cytotoxicity from sulfamethoxazole-hydroxylamine in human PBMCs in the LTA. The LTA was performed on PBMCs of 10 patients hypersensitive to trimethoprim-sulfamethoxazole (HS) and 10 drug-tolerant controls (TOL), using two cytotoxicity assays: YO-PRO (n = 20) and MTT (n = 12). mRNA expression profiles of PBMCs, enriched for CD8 T cells, were compared between HS and TOL patients. Transcript expression was interrogated for correlation with % cytotoxicity from YO-PRO and MTT assays. Correlated transcripts of interest were validated by qPCR. LTA results were not significantly different between HS and TOL patients, and no transcripts were found to be differentially expressed between the two groups. 96 transcripts were correlated with cytotoxicity by YO-PRO ( = ±.63-.75, FDR 0.188). Transcripts were selected for validation based on mechanistic plausibility and three were significantly over-expressed by qPCR in high cytotoxicity patients: multi-specific organic anion transporter C ( ), mitoferrin-1 ( ), and Porimin ( ). These data identify novel transcripts that could contribute to sulfonamide-hydroxylamine induced cytotoxicity. These include , encoding a mitochondrial iron transporter, , encoding an arylamine drug transporter, and , encoding a transmembrane protein that mediates cell death.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1002/prp2.388

  4 / 155811 MEDLINE  
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[PMID]: 29511213
[Au] Autor:Hernández G; Ramírez MJ; Minguillón J; Quiles P; Ruiz de Garibay G; Aza-Carmona M; Bogliolo M; Pujol R; Prados-Carvajal R; Fernández J; García N; López A; Gutiérrez-Enríquez S; Diez O; Benítez J; Salinas M; Teulé A; Brunet J; Radice P; Peterlongo P; Schindler D; Huertas P; Puente XS; Lázaro C; Pujana MÀ; Surrallés J
[Ad] Address:Department of Genetics and Microbiology, Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain.
[Ti] Title:Decapping protein EDC4 regulates DNA repair and phenocopies BRCA1.
[So] Source:Nat Commun;9(1):967, 2018 Mar 06.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BRCA1 is a tumor suppressor that regulates DNA repair by homologous recombination. Germline mutations in BRCA1 are associated with increased risk of breast and ovarian cancer and BRCA1 deficient tumors are exquisitely sensitive to poly (ADP-ribose) polymerase (PARP) inhibitors. Therefore, uncovering additional components of this DNA repair pathway is of extreme importance for further understanding cancer development and therapeutic vulnerabilities. Here, we identify EDC4, a known component of processing-bodies and regulator of mRNA decapping, as a member of the BRCA1-BRIP1-TOPBP1 complex. EDC4 plays a key role in homologous recombination by stimulating end resection at double-strand breaks. EDC4 deficiency leads to genome instability and hypersensitivity to DNA interstrand cross-linking drugs and PARP inhibitors. Lack-of-function mutations in EDC4 were detected in BRCA1/2-mutation-negative breast cancer cases, suggesting a role in breast cancer susceptibility. Collectively, this study recognizes EDC4 with a dual role in decapping and DNA repair whose inactivation phenocopies BRCA1 deficiency.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41467-018-03433-3

  5 / 155811 MEDLINE  
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[PMID]: 29477696
[Au] Autor:Chen SX; Liao GJ; Yao PW; Wang SK; Li YY; Zeng WA; Liu XG; Zang Y
[Ad] Address:Pain Research Center and Department of Physiology, Zhongshan Medical School of Sun Yat-Sen University, 74 Zhongshan Rd. 2, Guangzhou 510080, PR China; Department of Anesthesiology, Cancer Center, Sun Yat-Sen University, State Key Laboratory of Oncology in South China, Collaborative, Innovation Cente
[Ti] Title:Calpain-2 Regulates TNF-α Expression Associated with Neuropathic Pain Following Motor Nerve Injury.
[So] Source:Neuroscience;376:142-151, 2018 Feb 23.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Both calpain-2 (CALP2) and tumor necrosis factor-α (TNF-α) contribute to persistent bilateral hypersensitivity in animals subjected to L5 ventral root transection (L5-VRT), a model of selective motor fiber injury without sensory nerve damage. However, specific upstream mechanisms regulating TNF-α overexpression and possible relationships linking CALP2 and TNF-α have not yet been investigated in this model. We examined changes in CALP2 and TNF-α protein levels and alterations in bilateral mechanical threshold within 24 h following L5-VRT model injury. We observed robust elevation of CALP2 and TNF-α in bilateral dorsal root ganglias (DRGs) and bilateral spinal cord neurons. CALP2 and TNF-α protein induction by L5-VRT were significantly inhibited by pretreatment using the calpain inhibitor MDL28170. Administration of CALP2 to rats without nerve injury further supported a role of CALP2 in the regulation of TNF-α expression. Although clinical trials of calpain inhibition therapy for alleviation of neuropathic pain induced by motor nerve injury have not yet shown success, our observations linking CALP2 and TNF-α provide a framework of a systems' approach based perspective for treating neuropathic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 155811 MEDLINE  
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[PMID]: 29409836
[Au] Autor:Shah A; Dobrovolskaia MA
[Ad] Address:Nanotechnology Characterization Laboratory, Cancer Research Technology Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD.
[Ti] Title:Immunological effects of iron oxide nanoparticles and iron-based complex drug formulations: Therapeutic benefits, toxicity, mechanistic insights, and translational considerations.
[So] Source:Nanomedicine;14(3):977-990, 2018 Feb 02.
[Is] ISSN:1549-9642
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nanotechnology offers several advantages for drug delivery. However, there is the need for addressing potential safety concerns regarding the adverse health effects of these unique materials. Some such effects may occur due to undesirable interactions between nanoparticles and the immune system, and they may include hypersensitivity reactions, immunosuppression, and immunostimulation. While strategies, models, and approaches for studying the immunological safety of various engineered nanoparticles, including metal oxides, have been covered in the current literature, little attention has been given to the interactions between iron oxide-based nanomaterials and various components of the immune system. Here we provide a comprehensive review of studies investigating the effects of iron oxides and iron-based nanoparticles on various types of immune cells, highlight current gaps in the understanding of the structure-activity relationships of these materials, and propose a framework for capturing their immunotoxicity to streamline comparative studies between various types of iron-based formulations.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 155811 MEDLINE  
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[PMID]: 29524258
[Au] Autor:Diczig B; Németh I; Pónyai G; Sárdy M
[Ad] Address:Department of Dermatology, Venereology and Dermatooncology, Semmelweis University Budapest.
[Ti] Title:Contact hypersensitivity in rosacea - a report on 143 cases.
[So] Source:J Eur Acad Dermatol Venereol;, 2018 Mar 10.
[Is] ISSN:1468-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Rosacea is a chronic skin disease characterized by inflammatory processes affecting mainly the center of the face. The pathophysiology is complex, environmental factors seem to play an important role in the exacerbation and worsening of the lesions. The barrier-dysfunction theory in atopic dermatitis has been well described in the literature. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/jdv.14922

  8 / 155811 MEDLINE  
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[PMID]: 29523399
[Au] Autor:Claeson AS; Palmquist E; Nordin S
[Ad] Address:Department of Psychology, Umeå University, Umeå, Sweden. Electronic address: Anna-Sara.Claeson@umu.se.
[Ti] Title:Physical and chemical trigger factors in environmental intolerance.
[So] Source:Int J Hyg Environ Health;, 2018 Mar 06.
[Is] ISSN:1618-131X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:BACKGROUND: Individuals with environmental intolerance (EI) react to exposure from different environmental sources at levels tolerated by most people and that are below established toxicological and hazardous thresholds. The main aim of this study was to determine the prevalence of attributing symptoms to chemical and physical sources in the environment among individuals with different forms of self-reported EI and in referents. METHODS: Cross-sectional data from a population-based study, the Västerbotten Environmental Health Study (n = 3406), were used and individuals with self-reported EI to chemicals, buildings, electromagnetic fields and sounds as well as a group with multiple EIs were identified. The Environmental-Symptom Attribution Scale was used to quantify degree to which health symptoms are attributed to 40 specific environmental exposures and sources, with subscales referring to the four types of EI. RESULTS: All EI groups, except the group with building related intolerance (BRI), reported more symptoms from the expected sources compared to the referents. In addition, individuals with chemical and sound intolerance reported symptoms from building related trigger factors, and individuals with electromagnetic hypersensitivity reported symptoms from chemical trigger factors. CONCLUSIONS: The study suggests that individuals with BRI react to fewer and more specific trigger factors than do individuals with other EIs, and that it is important to ask about different sources since three of the EI groups attribute their symptoms to a wide variety of sources in addition to the sources to which their EI implicates.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 155811 MEDLINE  
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[PMID]: 29522876
[Au] Autor:Rai ZL; Fowles HE; Wright C; Joseph H; Morice AH
[Ad] Address:Castle Hill Hospital, Clinical Trials Unit, Castle Hill Hospital Cottingham, Cottingham, HU16 5JQ, UK. Electronic address: Zainab.rai@nhs.net.
[Ti] Title:The Effect of pH on Citric Acid Cough Challenge: A Randomised Control Trial in Chronic Cough and Healthy Volunteers.
[So] Source:Respir Physiol Neurobiol;, 2018 Mar 06.
[Is] ISSN:1878-1519
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Citric acid has been used for over six decades to induce cough; however the mechanism of its pro-tussive effect is still not fully understood. We assessed the response to inhalation of citric acid at varying levels of acidity to determine if the pH of the solution plays a role in the induction of cough. Data was collected from both healthy volunteers and patients with chronic cough. METHODS: 20 chronic cough patients and 20 healthy volunteers were recruited and underwent three cough challenges on separate days. Each visit involved 5 repeated one second inhalations of 300 mM citric acid solution. The concentration of the citrate cation remained constant, but the pH of the solution altered by the addition of sodium bicarbonate to 3, 5 and 6, representing the pK values of the individual acid moieties. The total number of coughs elicited was recorded for each inhalation. RESULTS: Two subjects withdrew and were not included in the analysis. Participants were gender matched, each group consisting of 12 females. 74% of chronic coughers coughed at pH 3 (mean coughs 16), 89% coughed at pH 5 (18) and 63% coughed at pH 6 (7). In healthy volunteers, 60% of subjects coughed at pH 3 (9), 30% of subjects coughed at pH 5 (3), and 10% of subjects coughed at pH 6 (0). Thus chronic cough patients coughed more than healthy volunteers and did not exhibit a clear pH concentration response. There was also a greater variability in their response to individual challenges.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 155811 MEDLINE  
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[PMID]: 29522843
[Au] Autor:Suto H; Nambu A; Morita H; Yamaguchi S; Numata T; Yoshizaki T; Shimura E; Arae K; Asada Y; Motomura K; Kaneko M; Abe T; Matsuda A; Iwakura Y; Okumura K; Saito H; Matsumoto K; Sudo K; Nakae S
[Ad] Address:Atopy Research Center, Juntendo University, Tokyo.
[Ti] Title:IL-25 enhances Th17 cell-mediated contact dermatitis by promoting IL-1ß production by dermal dendritic cells.
[So] Source:J Allergy Clin Immunol;, 2018 Mar 06.
[Is] ISSN:1097-6825
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: As well as thymic stromal lymphopoietin (TSLP) and IL-33, IL-25 is known to induce Th2 cytokine production by various cell types-including Th2 cells, Th9 cells, invariant NKT cells and group 2 innate lymphoid cells-involved in Th2-type immune responses. Since both Th2-type and Th17-type cells/cytokines are crucial for contact hypersensitivity (CHS), IL-25 may contribute to this by enhancing Th2-type immune responses. However, the precise role of IL-25 in the pathogenesis of FITC-induced CHS is poorly understood. OBJECTIVE: We investigated the contribution of IL-25 to CHS using Il25 mice. METHODS: CHS was evaluated by measurement of ear skin thickness in mice after FITC-painting. Skin dendritic cell (DC) migration, hapten-specific Th cell differentiation and detection of IL-1ß-producing cells were determined by flow cytometry, ELISA and immunohistochemistry, respectively. RESULTS: In contrast to TSLP, we found that IL-25 was not essential for skin DC migration or hapten-specific Th cell differentiation in the sensitization phase of CHS. Unexpectedly, mast cell- and non-immune cell-derived IL-25 was important for hapten-specific Th17 cell-, rather than Th2 cell-, mediated inflammation in the elicitation phase of CHS by enhancing Th17-related, but not Th2-related, cytokines in the skin. In particular, IL-1ß produced by dermal DCs in response to IL-25 was crucial for hapten-specific Th17 cell activation, contributing to induction of local inflammation in the elicitation phase of CHS. CONCLUSION: Our results identify a novel IL-25 inflammatory pathway involved in induction of Th17, but not Th2, cell-mediated CHS. IL-25 neutralization may be a potential approach for treatment of CHS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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