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[PMID]: 29524743
[Au] Autor:Sant KE; Sinno PP; Jacobs HM; Timme-Laragy AR
[Ad] Address:Department of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, United States.
[Ti] Title:Nrf2a modulates the embryonic antioxidant response to perfluorooctanesulfonic acid (PFOS) in the zebrafish, Danio rerio.
[So] Source:Aquat Toxicol;198:92-102, 2018 Feb 20.
[Is] ISSN:1879-1514
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The glutathione redox system undergoes precise and dynamic changes during embryonic development, protecting against and mitigating oxidative insults. The antioxidant response is coordinately largely by the transcription factor Nuclear factor erythroid-2 (Nrf2), an endogenous sensor for cellular oxidative stress. We have previously demonstrated that impaired Nrf family signaling disrupts the glutathione redox system in the zebrafish embryo, and that impaired Nrf2 function increases embryonic sensitivity to environmental toxicants. Here, we investigated the persistent environmental toxicant and reported pro-oxidant perfluorooctanesulfonic acid (PFOS), and its impact on the embryonic glutathione-mediated redox environment. We further examined whether impaired Nrf2a function exacerbates PFOS-induced oxidative stress and embryotoxicity in the zebrafish, and the potential for Nrf2-PPAR crosstalk in the embryonic adaptive response. Wild-type and nrf2a mutant embryos were exposed daily to 0 (0.01% v/v DMSO), 16, 32, or 64 µM PFOS beginning at 3 h post fertilization (hpf). Embryonic glutathione and cysteine redox environments were examined at 72 hpf. Gross embryonic toxicity, antioxidant gene expression, and apoptosis were examined at 96 hpf. Mortality, pericardial edema, and yolk sac utilization were increased in wild-type embryos exposed to PFOS. Embryonic glutathione and cysteine redox couples and gene expression of Nrf2 pathway targets were modulated by both exposure and genotype. Apoptosis was increased in PFOS-exposed wild-type embryos, though not in nrf2a mutants. In silico examination of putative transcription factor binding site suggested potential crosstalk between Nrf2 and PPAR signaling, since expression of PPARs and gene targets was modulated by both PFOS exposure and Nrf2a genotype. Overall, this work demonstrates that nrf2a modulates the embryonic response to PFOS, and that PPAR signaling may play a role in the embryonic adaptive response to PFOS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 171680 MEDLINE  
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[PMID]: 29515292
[Au] Autor:Carr JM; Ashander LM; Calvert JK; Ma Y; Aloia A; Bracho GG; Chee SP; Appukuttan B; Smith JR
[Ad] Address:Microbiology & Infectious Diseases, Flinders University School of Medicine, Rm 5D-316, 1 Flinders Drive, Bedford Park, Adelaide, SA 5042, Australia.
[Ti] Title:Molecular Responses of Human Retinal Cells to Infection with Dengue Virus.
[So] Source:Mediators Inflamm;2017:3164375, 2017.
[Is] ISSN:1466-1861
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Recent clinical reports indicate that infection with dengue virus (DENV) commonly has ocular manifestations. The most serious threat to vision is dengue retinopathy, including retinal vasculopathy and macular edema. Mechanisms of retinopathy are unstudied, but observations in patients implicate retinal pigment epithelial cells and retinal endothelial cells. Human retinal cells were inoculated with DENV-2 and monitored for up to 72 hours. Epithelial and endothelial cells supported DENV replication and release, but epithelial cells alone demonstrated clear cytopathic effect, and infection was more productive in those cells. Infection induced type I interferon responses from both cells, but this was stronger in epithelial cells. Endothelial cells increased expression of adhesion molecules, with sustained overexpression of vascular adhesion molecule-1. Transcellular impedance decreased for epithelial monolayers, but not endothelial monolayers, coinciding with cytopathic effect. This reduction was accompanied by disorganization of intracellular filamentous-actin and decreased expression of junctional molecules, zonula occludens 1, and catenin- 1. Changes in endothelial expression of adhesion molecules are consistent with the retinal vasculopathy seen in patients infected with DENV; decreases in epithelial junctional protein expression, paralleling loss of integrity of the epithelium, provide a molecular basis for DENV-associated macular edema. These molecular processes present potential therapeutic targets for vision-threatening dengue retinopathy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2017/3164375

  3 / 171680 MEDLINE  
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[PMID]: 29515282
[Au] Autor:Prajapati H; Kansal D; Negi R
[Ad] Address:Department of Pharmacology, Dr. Rajendera Prasad Government Medical College, Kangra at Tanda, Himachal Pradesh, India.
[Ti] Title:Magnesium valproate-induced pedal edema on chronic therapy: A rare adverse drug reaction.
[So] Source:Indian J Pharmacol;49(5):399-400, 2017 Sep-Oct.
[Is] ISSN:1998-3751
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Valproate-related pedal edema is usually regarded as a problem occurring after long-term administration of valproate. Valproate has been a drug of choice for the treatment of generalized or partial seizures as monotherapy or adjunctive therapy, bipolar disorder, for the prophylaxis of migraine headache in adults. This case report described patient-acquiring bilateral pedal edema after long-term use of magnesium valproate. Discontinuing valproate resulted in rapid improvement of the condition. This adverse reaction to the best of our knowledge is first reported a case of bilateral pedal edema cause by magnesium valproate in low dose. The dose of magnesium valproate was 1200 mg/day. No previous case as reported with the same dose.
[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_239_17

  4 / 171680 MEDLINE  
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[PMID]: 29452194
[Au] Autor:Hou Z; Tian R; Han F; Hao S; Wu W; Mao X; Tao X; Lu T; Dong J; Zhen Y; Liu B
[Ad] Address:Department of Neurosurgery, Beijing Tian Tan Hospital, Capital Medical University, Beijing, 100050, PR China; China National Clinical Research Center for Neurological Diseases, Beijing, 100050, PR China; Beijing Key Laboratory of Central Nervous System Injury, Beijing, 100050, PR China.
[Ti] Title:Decompressive craniectomy protects against hippocampal edema and behavioral deficits at an early stage of a moderately controlled cortical impact brain injury model in adult male rats.
[So] Source:Behav Brain Res;345:1-8, 2018 Feb 13.
[Is] ISSN:1872-7549
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:A decompressive craniectomy (DC) has been shown to be a life-saving therapeutic treatment for traumatic brain injury (TBI) patients, which also might result in post-operative behavioral dysfunction. However, there is still no definite conclusion about whether the behavioral dysfunction already existed at an early stage after the DC operation or is just a long-term post-operation complication. Therefore, the aim of the present study was to analyze whether DC treatment was beneficial to behavioral function at an early stage post TBI. In this study, we established a controlled cortical impact injury rat model to evaluate the therapeutic effect of DC treatment on behavioral deficits at 1 d, 2 d, 3 d and 7 d after TBI. Our results showed that rats suffered significant behavioral and mood deficits after TBI compared to the control group, while decompressive craniectomy treatment could normalize MMP-9 expression levels and reduce hippocampal edema formation, stabilize the expression of Synapsin I, which was a potential indicator of maintaining the hippocampal synaptic function, thus counteracting behavioral but not mood decay in rats subjected to TBI. In conclusion, decompressive craniectomy, excepting for its life-saving effect, could also play a potential beneficial neuroprotective role on behavioral but not mood deficits at an early stage of moderate traumatic brain injury in rats.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 171680 MEDLINE  
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[PMID]: 29432911
[Au] Autor:Yang J; Tian H; Huang X
[Ad] Address:Emergency Department, Guizhou Provincial People's Hospital, Guiyang, Guizhou, 550002, China.
[Ti] Title:Tephrosin attenuates sepsis induced acute lung injury in rats by impeding expression of ICAM-1 and MIP-2.
[So] Source:Microb Pathog;117:93-99, 2018 Feb 09.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Acute lung injury (ALI), a devastating form of respiratory infections, is characterized by increased edema, release of cytokines, weakened arterial oxygenation and infiltration of neutrophils and lymphocytes. The objective of the research envisaged was to reveal protective effects of tephrosin (TP) in ALI. In the present investigation, sepsis was triggered in rats by cecal ligation and puncture (CLP) method, and TP was administered intraperitonially. Five groups - Group A (control), Group B (Sham group) Group C (infected and untreated), and Group D and E (infected and treated with 25 and 50 mg/kg TP respectively) - of ten rats each, were used for the investigation. Evaluation parameters included measurement of arterial oxygenation, lung water content, protein determination, cytokine determination, neutrophil and lymphocyte count in the bronchoalveolar lavage fluid (BALF). As indicated by histopathological examination, the lung injury score was maximum in group C, but indicated reduction in group D and E. Intracellular adhesion molecule (ICAM)-1 and macrophage inflammatory protein-2 (MIP-2) are known to be important mediators responsible for ALI. Reduction in the ICAM-1 and MIP-2 expression was found to reduce after treatment with TP. In comparison to group D, group E reflected higher magnitude of ICAM-1 and MIP-2 suppression due to administration of higher TP dose. Compared to Group A and B, Group E indicated slightly higher expression of ICAM-1 and MIP-2. The research envisaged thus supports that TP attenuates ICAM-1 and MIP-2 expression in sepsis induced ALI rat model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 171680 MEDLINE  
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[PMID]: 29427710
[Au] Autor:Khan A; Saleemi MK; Ali F; Abubakar M; Hussain R; Abbas RZ; Khan IA
[Ad] Address:Faculty of Veterinary Science, University of Agriculture, Faisalabad-38040, Pakistan. Electronic address: ahrar1122@uaf.edu.pk.
[Ti] Title:Pathophysiology of peste des petits ruminants in sheep (Dorper & Kajli) and goats (Boer & Beetal).
[So] Source:Microb Pathog;117:139-147, 2018 Feb 07.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Peste des petits ruminants (PPR), an economically important viral transboundary disease of small ruminants is not only prevalent in Pakistan but also in other countries where people rely on agriculture and animal products. The present study was aimed at describing the pathology and antigen localization in natural PPR infections in local (Kajli sheep; Beetal goats) as well as imported small ruminant breeds (Dorper sheep; Australian Boer goat). Morbidity and mortality rates were significantly (P < 0.001) higher in indigenous Kajli sheep (75.37 and 32.80%) and Beetal goats (81.10 and 37.24%) as compared to Dorper sheep (6.99 and 1.48%) and Australian Boer goat (5.01 and 2.23%). Affected animals exhibited high fever, severe diarrhea, abdominal pain, respiratory distress and nodular lesions on lips and nostrils. Thick mucous discharge was oozing out from nostrils. On necropsy, lungs were congested and pneumonic, with nodular and cystic appearance. Intestines were hemorrhagic with zebra stripping. Characteristic histopathological lesions of PPR were noted in intestines, lymphoid organs and lungs. In GI tract, stunting and blunting of villi, necrotic enteritis, and infiltration of mononuclear cells in duodenum, jejunum and ileum. Small intestines exhibited diffuse edema of the submucosa along with proliferation of fibrocytes leading to thickened submucosa which has not been reported previously. Lymphoid organs showed partial to complete destruction of lymphoid follicles. Lesions of the respiratory tract included depictive of bronchopneumonia, severe congestion of trachea and apical lobe of lungs with deposition of fibrinous materials. Histopathological lesions of respiratory tract were severe and characteristic of broncho-interstitial pneumonia, bronchopneumonia, interstitial pneumonia and fibrinous pneumonia. The alveoli were filled with edematous fluid mixed with fibrinous exudate, numerous alveolar macrophages, mononuclear cells along with thickened interalveolar septa and presence of intranuclear eosinophilic inclusion bodies. One-Step RT-PCR using NP3 and NP4 primers confirmed a PPR virus of 352 bp size in spleen, lungs and mesenteric and brachial lymph node samples. It was concluded that morbidity and mortality due to PPR were significantly higher in indigenous breeds of sheep and goat as compared to imported sheep and goat breeds. PPR has rendered various lesions in GI and respiratory tract which are characteristic in nature for the diagnosis of the disease under field condition.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 171680 MEDLINE  
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[PMID]: 29305272
[Au] Autor:Shah M; Birnbaum L; Rasmussen J; Sekar P; Moomaw CJ; Osborne J; Vashkevich A; Woo D
[Ad] Address:Department of Neurology, UT Health Houston, Houston, Texas.
[Ti] Title:Effect of Hyperosmolar Therapy on Outcome Following Spontaneous Intracerebral Hemorrhage: Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) Study.
[So] Source:J Stroke Cerebrovasc Dis;27(4):1061-1067, 2018 Apr.
[Is] ISSN:1532-8511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: We aimed to identify the effect of hyperosmolar therapy (mannitol and hypertonic saline) on outcomes after intracerebral hemorrhage (ICH) in the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study. METHODS: Comparison of ICH cases treated with hyperosmolar therapy versus untreated cases was performed using a propensity score based on age, initial Glasgow Coma Scale, location of ICH (lobar, deep, brainstem, and cerebellar), log-transformed initial ICH volume, presence of intraventricular hemorrhage, and surgical interventions. ERICH subjects with a pre-ICH modified Rankin Scale (mRS) score of 3 or lower were included. Treated cases were matched 1:1 to untreated cases by the closest propensity score (difference ≤.15), gender, and race and ethnicity (non-Hispanic white, non-Hispanic black, or Hispanic). The McNemar and the Wilcoxon signed-rank tests were used to compare 3-month mRS outcomes between the 2 groups. Good outcome was defined as a 3-month mRS score of 3 or lower. RESULTS: As of December 31, 2013, the ERICH study enrolled 2279 cases, of which 304 hyperosmolar-treated cases were matched to 304 untreated cases. Treated cases had worse outcome at 3 months compared with untreated cases (McNemar, P = .0326), and the mean 3-month mRS score was lower in the untreated group (Wilcoxon, P = .0174). Post hoc analysis revealed more brain edema, herniation, and death at discharge for treated cases. CONCLUSIONS: Hyperosmolar therapy was not associated with better 3-month mRS outcomes for ICH cases in the ERICH study. This finding likely resulted from greater hyperosmolar therapy use in patients with edema and herniation rather than those agents leading to worse outcomes. Further studies should be performed to determine if hyperosmolar agents are effective in preventing poor outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  8 / 171680 MEDLINE  
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[PMID]: 29249729
[Au] Autor:Park S; Kim K; Kim Y; Seo K
[Ad] Address:Department of Veterinary Clinical Sciences, College of Veterinary Medicine and Research Institute for Veterinary Science, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea.
[Ti] Title:Bilateral anterior segment dysgenesis with the presumed Peters' anomaly in a cat.
[So] Source:J Vet Med Sci;80(2):297-301, 2018 Feb 20.
[Is] ISSN:1347-7439
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:A seven-month-old female domestic shorthaired cat was presented for buphthalmos in the right eye and corneal cloudiness in the left eye. Full ophthalmic examinations were performed for both eyes and enucleation was done for the right nonvisual eye. Congenital glaucoma caused by anterior segment dysgenesis was confirmed for the right eye. In the left eye, slit-lamp examination revealed focal corneal edema with several iris strands from iris collarette to the affected posterior corneal surfaces. Circular posterior corneal defect was suggested to be the cause of edema. Goniodysgenesis, additionally, was identified. Taken together, the diagnosis of Peters' anomaly which is a subtype of anterior segment dysgenesis was suggested in the left eye.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1292/jvms.17-0532

  9 / 171680 MEDLINE  
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[PMID]: 28456933
[Au] Autor:Tang X; Liu K; Hamblin MH; Xu Y; Yin KJ
[Ad] Address:Pittsburgh Institute of Brain Disorders & Recovery, Department of Neurology, University of Pittsburgh School of Medicine, S514 BST, 200 Lothrop Street, Pittsburgh, PA, 15213, USA.
[Ti] Title:Genetic Deletion of Krüppel-Like Factor 11 Aggravates Ischemic Brain Injury.
[So] Source:Mol Neurobiol;55(4):2911-2921, 2018 Apr.
[Is] ISSN:1559-1182
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Krüppel-like factors (KLFs) belong to the zinc finger family of transcription factors, and their function in the CNS is largely unexplored. KLF11 is a member of the KLF family, and we have previously demonstrated that peroxisome proliferator-activated receptor gamma-mediated cerebral protection during ischemic insults needs recruitment of KLF11 as its critical coactivator. Here, we sought to determine the role of KLF11 itself in cerebrovascular function and the pathogenesis of ischemic stroke. Transient middle cerebral artery occlusion (MCAO) was performed in KLF11 knockout and wild-type control mice, and brain infarction was analyzed by TTC staining. BBB integrity was assessed by using Evans Blue and TMR-Dextran extravasation assays. KLF11 KO mice exhibited significantly larger brain infarction and poorer neurological outcomes in response to ischemic insults. Genetic deficiency of KLF11 in mice also significantly aggravated ischemia-induced BBB disruption by increasing cerebrovascular permeability and edema. Mechanistically, KLF11 was found to directly regulate IL-6 in the brains of ischemic mice. These findings suggest that KLF11 acts as a novel protective factor in ischemic stroke. Elucidating the functional importance of KLF11 in ischemia may lead us to discover novel pharmacological targets for the development of effective therapies against ischemic stroke.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s12035-017-0556-9

  10 / 171680 MEDLINE  
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[PMID]: 29524327
[Au] Autor:Lidén Å; Karlsen TV; Guss B; Reed RK; Rubin K
[Ad] Address:Department of Biomedicine, University of Bergen, Jonas Lies vei 91, N-5009, Bergen, Norway.
[Ti] Title:Integrin α ß can substitute for collagen-binding ß -integrins in vivo to maintain a homeostatic interstitial fluid pressure.
[So] Source:Exp Physiol;, 2018 Mar 10.
[Is] ISSN:1469-445X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:NEW FINDINGS: What is the central question of this study? Collagen-binding ß -integrins function physiologically in cellular control of dermal interstitial fluid pressure (P ) in vivo and thereby participate in control of extravascular fluid volume. During anaphylaxis, simulated by injection of Compound 48/80 integrin α ß takes over this physiological function. Here we addressed the question whether integrin α ß can replace collagen-binding ß -integrin to maintain a long-term homeostatic P . What is the main finding and its importance? Mice lacking the collagen-binding integrin α ß show a complex dermal phenotype with regard to the interstitial physiology apparent in the control of P . Notably dermal P is not lowered with Compound 48/80 in these animals. Our present data infer the integrin α ß to be the likely candidate that has taken over the role of collagen-binding ß -integrins for maintaining a steady-state homeostatic P . A better understanding of molecular processes involved in control of P is instrumental for establishing novel treatment regimens for control of edema formation in anaphylaxis and septic shock. ABSTRACT: Accumulated data indicate that cell-mediated contraction of reconstituted collagenous gels in vitro can serve as a model for cell-mediated control of interstitial fluid pressure (P ) in vivo. A central role for collagen-binding ß -integrins in both processes has been established. Furthermore, integrin α ß takes over the role of collagen-binding ß -integrins in mediating contraction after perturbations of collagen-binding ß -integrins in vitro. Integrin α ß is also instrumental for normalization of dermal P that has been lowered due to mast cell degranulation with Compound 48/80 (C48/80) in vivo. Here we demonstrate a role of integrin α ß in maintaining a long term homeostatic dermal P in mice lacking the collagen-binding integrin  α ß (α11 mice). Measurements of P were performed after circulatory arrest. Furthermore, cell-mediated integrin α ß -directed contraction of collagenous gels in vitro depends on free access of a collagen-site known to bind several ECM proteins that form substrates for α ß -directed cell attachment, such as fibronectin and fibrin. A streptococcal collagen-binding protein, CNE, specifically binds to and block this site on the collagen triple helix. Here we show that whereas CNE perturbed α ß -directed and PDGF-BB induced normalization of dermal P after C48/80 it did not affect α ß -dependent maintenance of a homeostatic dermal P . These data imply that dynamic modifications of the ECM structure is needed during acute patho-physiologic modulations of P but not for long-term maintenance of a homeostatic P . Our data thus show that collagen-binding ß -integrins, integrin α ß and ECM-structure are potential targets for novel therapy aimed to modulate edema formation and hypovolemic shock during anaphylaxis. 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:10.1113/EP086902


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