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[PMID]: 29193920 [Au] Autor: Maldonado J; Lopez Candales A [Ti] Título: High Output Cardiac Failure in a Patient Presenting with Acute Myeloid Leukemia and Leukostasis. [So] Source: Bol Asoc Med P R;108(1):61-3, 2016. [Is] ISSN: 0004-4849 [Cp] País de publicação: Puerto Rico [La] Idioma: eng [Ab] Resumo: In this case report a patient presents with high-output cardiac failure in the clinical setting of acute leukemia and leukostasis. Case particulars are presented, literature is reviewed and a potential mechanistic explanation is proposed to describe presentation and clinical findings. [Mh] Termos MeSH primário: Débito Cardíaco Elevado/diagnóstico Insuficiência Cardíaca/diagnóstico Leucemia Mieloide Aguda/diagnóstico Leucostasia/diagnóstico [Mh] Termos MeSH secundário: Débito Cardíaco Elevado/fisiopatologia Insuficiência Cardíaca/fisiopatologia Seres Humanos Leucemia Mieloide Aguda/patologia Leucostasia/patologia Masculino Meia-Idade [Pt] Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE [Em] Mês de entrada: 1712 [Cu] Atualização por classe: 171214 [Lr] Data última revisão: 171214 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171202 [St] Status: MEDLINE

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[PMID]: 28980001 [Au] Autor: Qiu F; Matlock G; Chen Q; Zhou K; Du Y; Wang X; Ma JX [Ad] Endereço: Department of Physiology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States. [Ti] Título: Therapeutic Effects of PPARα Agonist on Ocular Neovascularization in Models Recapitulating Neovascular Age-Related Macular Degeneration. [So] Source: Invest Ophthalmol Vis Sci;58(12):5065-5075, 2017 Oct 01. [Is] ISSN: 1552-5783 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Purpose: This study was designed to evaluate effects of fenofibric acid (Feno-FA), a peroxisome proliferator-activated receptor-alpha (PPARα) agonist, on ocular neovascularization (NV) in models recapitulating neovascular age-related macular degeneration (AMD), and to explore whether the effects are PPARα dependent. Methods: Laser-induced choroidal NV (CNV) in rats and very low-density lipoprotein receptor knockout (Vldlr-/-) mice received daily intraperitoneal injections of Feno-FA or vehicle. Vascular leakage was examined by fundus fluorescein angiography and permeability assay using Evans blue as tracer. In CNV rats, severity of CNV was evaluated by CNV areas and CNV volume. In Vldlr-/- mice, subretinal NV (SRNV) and intraretinal NV (IRNV) were quantified in choroid flat mount and retina flat mount, respectively. Inflammatory factors were measured using Western blotting and retinal leukostasis assay. Further, Pparα-/- mice and age-matched wild-type (WT) mice were used for laser-induced CNV and treated with Feno-FA to explore the underlying mechanism. Results: Feno-FA significantly reduced vascular leakage in CNV rats and Vldlr-/- mice, reduced CNV volume in laser-induced CNV rats, and suppressed SRNV and IRNV in Vldlr-/- mice. In addition, Feno-FA downregulated the expression of inflammatory factors, including VEGF, TNF-α, and intercellular cell adhesion molecule-1 (ICAM-1), in the eyecups of CNV rats and decreased adherent retinal leukocytes in Vldlr-/- mice. Furthermore, Pparα-/- mice developed more severe CNV compared with WT mice, and PPARα knockout abolished the beneficial effects of Feno-FA on CNV. Conclusions: Feno-FA has therapeutic effects on ocular NV in models recapitulating neovascular AMD through a PPARα-dependent mechanism. [Mh] Termos MeSH primário: Neovascularização de Coroide/tratamento farmacológico Modelos Animais de Doenças Fenofibrato/análogos & derivados Hipolipemiantes/uso terapêutico PPAR alfa/agonistas Degeneração Macular Exsudativa/tratamento farmacológico [Mh] Termos MeSH secundário: Animais Western Blotting Permeabilidade Capilar Neovascularização de Coroide/metabolismo Neovascularização de Coroide/patologia Fenofibrato/uso terapêutico Angiofluoresceinografia Injeções Intraperitoneais Molécula 1 de Adesão Intercelular/metabolismo Leucostasia Masculino Camundongos Camundongos Endogâmicos C57BL Camundongos Knockout PPAR alfa/genética PPAR alfa/metabolismo Ratos Ratos Endogâmicos BN Receptores de LDL/genética Receptores de LDL/metabolismo Tomografia de Coerência Óptica Fator de Necrose Tumoral alfa/metabolismo Fator A de Crescimento do Endotélio Vascular/metabolismo Degeneração Macular Exsudativa/metabolismo Degeneração Macular Exsudativa/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Hypolipidemic Agents); 0 (PPAR alpha); 0 (Receptors, LDL); 0 (Tumor Necrosis Factor-alpha); 0 (VLDL receptor); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, rat); 126547-89-5 (Intercellular Adhesion Molecule-1); BGF9MN2HU1 (fenofibric acid); U202363UOS (Fenofibrate) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171020 [Lr] Data última revisão: 171020 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171006 [St] Status: MEDLINE [do] DOI: 10.1167/iovs.17-22091

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[PMID]: 28979999 [Au] Autor: Deng G; Moran EP; Cheng R; Matlock G; Zhou K; Moran D; Chen D; Yu Q; Ma JX [Ad] Endereço: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China. [Ti] Título: Therapeutic Effects of a Novel Agonist of Peroxisome Proliferator-Activated Receptor Alpha for the Treatment of Diabetic Retinopathy. [So] Source: Invest Ophthalmol Vis Sci;58(12):5030-5042, 2017 Oct 01. [Is] ISSN: 1552-5783 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Purpose: Clinical studies have shown that peroxisome proliferator-activated receptor alpha (PPARα) agonist fenofibrate has therapeutic effects on diabetic retinopathy (DR). The purpose of this study was to identify a novel PPARα agonist and to evaluate its beneficial effects on DR. Methods: The transcriptional activity of PPARα was measured by a luciferase-based promoter assay. TUNEL was used to evaluate apoptosis in retinal precursor cells (R28). Diabetes was induced in rats by injection of streptozotocin. Retinal inflammation was examined using leukostasis assay, and retinal vascular leakage was measured using permeability assay. Retinal function was measured using electroretinogram (ERG) recording, and retinal apoptosis was quantified using the cell death ELISA. The anti-angiogenic effect was evaluated in the oxygen-induced retinopathy (OIR) model. Results: A compound, 7-chloro-8-methyl-2-phenylquinoline-4-carboxylic acid (Y-0452), with a chemical structure distinct from existing PPARα agonists, activated PPARα transcriptional activity and upregulated PPARα expression. Y-0452 significantly inhibited human retinal capillary endothelial cell migration and tube formation. The compound also protected R28 cells against apoptosis and inhibited NF-κB signaling in R28 cells exposed to palmitate. In diabetic rats, Y-0452 ameliorated leukostasis and vascular leakage in the retina. In addition, Y-0452 preserved the retinal function and reduced retinal cell death in diabetic rats. Y-0452 also alleviated retinal neovascularization in the OIR model. Conclusions: Y-0452 is a novel PPARα agonist and has therapeutic potential for DR. [Mh] Termos MeSH primário: Inibidores da Angiogênese/uso terapêutico Diabetes Mellitus Experimental/tratamento farmacológico Retinopatia Diabética/tratamento farmacológico Hidrocarbonetos Clorados/uso terapêutico PPAR alfa/agonistas Quinolinas/uso terapêutico Neovascularização Retiniana/tratamento farmacológico [Mh] Termos MeSH secundário: Animais Apoptose/efeitos dos fármacos Western Blotting Permeabilidade Capilar/efeitos dos fármacos Linhagem Celular Movimento Celular Diabetes Mellitus Experimental/genética Diabetes Mellitus Experimental/patologia Retinopatia Diabética/genética Retinopatia Diabética/patologia Modelos Animais de Doenças Eletrorretinografia Endotélio Vascular/efeitos dos fármacos Endotélio Vascular/patologia Ensaio de Imunoadsorção Enzimática Regulação da Expressão Gênica/fisiologia Marcação In Situ das Extremidades Cortadas Leucostasia Masculino Camundongos Camundongos Endogâmicos C57BL NF-kappa B/antagonistas & inibidores Oxigênio/toxicidade PPAR alfa/genética PPAR alfa/metabolismo Regiões Promotoras Genéticas Ratos Ratos Endogâmicos BN Neovascularização Retiniana/genética Neovascularização Retiniana/patologia Vasos Retinianos/patologia Estreptozocina Ativação Transcricional [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiogenesis Inhibitors); 0 (Hydrocarbons, Chlorinated); 0 (NF-kappa B); 0 (PPAR alpha); 0 (Quinolines); 0 (Y-0452); 5W494URQ81 (Streptozocin); S88TT14065 (Oxygen) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171020 [Lr] Data última revisão: 171020 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171006 [St] Status: MEDLINE [do] DOI: 10.1167/iovs.16-21402

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[PMID]: 28780307 [Au] Autor: Wang K; Zhu X; Zhang K; Zhou F; Zhu L [Ad] Endereço: Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi 214063, Jiangsu Province, China. Electronic address: wangke@jsinm.org. [Ti] Título: Neuroprotective effect of tetramethylpyrazine against all-trans-retinal toxicity in the differentiated Y-79 cells via upregulation of IRBP expression. [So] Source: Exp Cell Res;359(1):120-128, 2017 Oct 01. [Is] ISSN: 1090-2422 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: It is estimated that abnormal accumulation of all-trans-retinal (atRAL) is a leading cause of photoreceptor degeneration in retinal degenerative diseases. Deficiency of interphotoreceptor retinoid-binding protein (IRBP), a retinoid transporter in the visual cycle, is responsible for the impaired clearance of atRAL and results in atRAL toxicity in retina. Therefore, IRBP has been proposed to be a potent target in preventing atRAL-induced photoreceptor degeneration. In this study, the neuroprotective effect of tetramethylpyrazine (TMP) against atRAL toxicity in the differentiated Y-79 cells, a in vitro model of photoreceptor, was first investigated. Our findings showed that atRAL could induce cytotoxicity, oxidative/nitrosative stresses, apoptosis and leukostasis in the differentiated Y-79 cells; however, the pre-treatment of TMP significantly attenuated such effects in a dose-dependent manner. Furthermore, our results indicated that TMP exerted its neuroprotective effect mainly through upregulating IRBP expression. The present study significantly contributes to better understanding the important role of IRBP in retinal degenerative diseases and forms the basis of the therapeutic development of TMP in such diseases in the future. [Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos Proteínas do Olho/metabolismo Fármacos Neuroprotetores/farmacologia Pirazinas/farmacologia Retinaldeído/toxicidade Proteínas de Ligação ao Retinol/metabolismo Regulação para Cima/efeitos dos fármacos [Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos Morte Celular/efeitos dos fármacos Linhagem Celular Tumoral Seres Humanos Molécula 1 de Adesão Intercelular/metabolismo Leucostasia/patologia Mitocôndrias/efeitos dos fármacos Mitocôndrias/metabolismo Neurônios/efeitos dos fármacos Neurônios/metabolismo Neurônios/patologia Neuroproteção/efeitos dos fármacos Nitrosação Estresse Oxidativo/efeitos dos fármacos Molécula 1 de Adesão de Célula Vascular/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Eye Proteins); 0 (Neuroprotective Agents); 0 (Pyrazines); 0 (Retinol-Binding Proteins); 0 (Vascular Cell Adhesion Molecule-1); 0 (interstitial retinol-binding protein); 126547-89-5 (Intercellular Adhesion Molecule-1); RR725D715M (Retinaldehyde); V80F4IA5XG (tetramethylpyrazine) [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: 170807 [St] Status: MEDLINE

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[PMID]: 28724696 [Au] Autor: van der Wijk AE; Hughes JM; Klaassen I; Van Noorden CJF; Schlingemann RO [Ad] Endereço: Department of Ophthalmology, Ocular Angiogenesis Group, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. [Ti] Título: Is leukostasis a crucial step or epiphenomenon in the pathogenesis of diabetic retinopathy? [So] Source: J Leukoc Biol;102(4):993-1001, 2017 Oct. [Is] ISSN: 1938-3673 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Leukostasis in the retinal microvasculature in animal model studies of diabetes is associated with the development of diabetes-like retinopathy. Therefore, it is generally assumed that adhesion of leukocytes is a central event inciting a chronic, low-grade form of inflammation that causes the vascular abnormalities that are specific for the early stages of diabetic retinopathy (DR), which culminate in diabetic macular edema, proliferative DR, and vision loss in humans. Here, we review the literature critically with respect to leukostasis and assess its pathologic consequences in the human diabetic retina. First, we review the pathologic processes that are known to be involved in the development of human DR. Then, we summarize experimental evidence for the role of leukostasis in the development of DR and the mechanisms involved in leukostasis in the retina. Based on our critical review, we conclude that leukostasis may be an epiphenomenon of the diabetic retinal milieu, rather than a crucial, specific step in the development of human DR. [Mh] Termos MeSH primário: Retinopatia Diabética/imunologia Leucostasia/imunologia Edema Macular/imunologia Retina/imunologia [Mh] Termos MeSH secundário: Animais Retinopatia Diabética/patologia Seres Humanos Leucostasia/patologia Edema Macular/patologia Retina/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171009 [Lr] Data última revisão: 171009 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170721 [St] Status: MEDLINE [do] DOI: 10.1189/jlb.3RU0417-139

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[PMID]: 28351645 [Au] Autor: Ibrahim AS; Saleh H; El-Shafey M; Hussein KA; El-Masry K; Baban B; Sheibani N; Wang MH; Tawfik A; Al-Shabrawey M [Ad] Endereço: Department of Oral Biology and Anatomy, Dental College of Georgia, Augusta University, Augusta, GA, USA; Department of Ophthalmology and Culver Vision Discovery Institute, Medical College of Georgia (MCG), Augusta University, Augusta, GA, USA; Department of Biochemistry and Clinical Biochemistry, Fa [Ti] Título: Targeting of 12/15-Lipoxygenase in retinal endothelial cells, but not in monocytes/macrophages, attenuates high glucose-induced retinal leukostasis. [So] Source: Biochim Biophys Acta;1862(6):636-645, 2017 06. [Is] ISSN: 0006-3002 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: AIMS: Our previous studies have established a role for 12/15-lipoxygenase (LO) in mediating the inflammatory response in diabetic retinopathy (DR). However, the extent at which the local or systemic induction of 12/15-LO activity involved is unclear. Thus, the current study aimed to characterize the relative contribution of retinal endothelial versus monocytic/macrophagic 12/15-LO to inflammatory responses in DR. MATERIALS & METHODS: We first generated a clustered heat map for circulating bioactive lipid metabolites in the plasma of streptozotocin (STZ)-induced diabetic mice using liquid chromatography coupled with mass-spectrometry (LC-MS) to evaluate changes in circulating 12/15-LO activity. This was followed by comparing the in vitro mouse endothelium-leukocytes interaction between leukocytes isolated from 12/15-LO knockout (KO) versus those isolated from wild type (WT) mice using the myeloperoxidase (MPO) assay. Finally, we examined the effects of knocking down or inhibiting endothelial 12/15-LO on diabetes-induced endothelial cell activation and ICAM-1 expression. RESULTS: Analysis of plasma bioactive lipids' heat map revealed that the activity of circulating 12/15-LO was not altered by diabetes as evident by no significant changes in the plasma levels of major metabolites derived from 12/15-lipoxygenation of different PUFAs, including linoleic acid (13-HODE), arachidonic acid (12- and 15- HETEs), eicosapentaenoic acid (12- and 15- HEPEs), or docosahexaenoic acid (17-HDoHE). Moreover, leukocytes from 12/15-LO KO mice displayed a similar increase in adhesion to high glucose (HG)-activated endothelial cells as do leukocytes from WT mice. Furthermore, abundant proteins of 12-LO and 15-LO were detected in human retinal endothelial cells (HRECs), while it was undetected (15-LO) or hardly detectable (12-LO) in human monocyte-like U937 cells. Inhibition or knock down of endothelial 12/15-LO in HRECs blocked HG-induced expression of ICAM-1, a well-known identified important molecule for leukocyte adhesion in DR. CONCLUSION: Our data support that endothelial, rather than monocytic/macrophagic, 12/15-LO has a critical role in hyperglycemia-induced ICAM-1 expression, leukocyte adhesion, and subsequent local retinal barrier dysfunction. This may facilitate the development of more precisely targeted treatment strategies for DR. [Mh] Termos MeSH primário: Araquidonato 12-Lipoxigenase/metabolismo Araquidonato 15-Lipoxigenase/metabolismo Retinopatia Diabética/enzimologia Células Endoteliais/enzimologia Leucostasia/enzimologia Macrófagos/enzimologia Monócitos/enzimologia Retina/enzimologia [Mh] Termos MeSH secundário: Animais Araquidonato 12-Lipoxigenase/genética Araquidonato 15-Lipoxigenase/genética Adesão Celular/genética Retinopatia Diabética/genética Retinopatia Diabética/patologia Células Endoteliais/patologia Seres Humanos Molécula 1 de Adesão Intercelular/biossíntese Molécula 1 de Adesão Intercelular/genética Leucostasia/genética Leucostasia/patologia Macrófagos/patologia Camundongos Camundongos Knockout Monócitos/patologia Retina/patologia Células U937 [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (12-15-lipoxygenase); 0 (Icam1 protein, mouse); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 1.13.11.31 (Arachidonate 12-Lipoxygenase); EC 1.13.11.33 (Arachidonate 15-Lipoxygenase) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170814 [Lr] Data última revisão: 170814 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170330 [St] Status: MEDLINE

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[PMID]: 28274631 [Au] Autor: Cai Y; Li W; Tu H; Chen N; Zhong Z; Yan P; Dong J [Ad] Endereço: School of Pharmacy, Wenzhou Medical University, Wenzhou 325035, People's Republic of China. [Ti] Título: Curcumolide reduces diabetic retinal vascular leukostasis and leakage partly via inhibition of the p38MAPK/NF-κ B signaling. [So] Source: Bioorg Med Chem Lett;27(8):1835-1839, 2017 04 15. [Is] ISSN: 1464-3405 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Retinal inflammation in a hyperglycemic condition is believed to play a crucial role in the development of diabetic retinopathy, and targeting inflammatory mediators is a promising strategy for the control of diabetic retinopathy. Curcumolide, a novel sesquiterpenoid with a unique 5/6/5 tricyclic skeleton, was isolated from Curcuma wenyujin. In this study, we demonstrate that treatment with curcumolide alleviated retinal inflammatory activities both in vitro and in vivo in a STZ-induced diabetic rat model and in TNF-α-stimulated HUVECs. Curcumolide alleviated retinal vascular permeability and leukostasis and attenuated the overexpression of TNF-α and ICAM-1 in diabetic retinas. Moreover, curcumolide also inhibited inducible p38 MAPK and NF-κB activation and the subsequent induction of proinflammatory mediators. These data suggest potential treatment strategies against diabetic retinopathy, particularly in the early stages of the disease. [Mh] Termos MeSH primário: Anti-Inflamatórios/química Anti-Inflamatórios/uso terapêutico Retinopatia Diabética/tratamento farmacológico Leucostasia/tratamento farmacológico Sesquiterpenos/química Sesquiterpenos/uso terapêutico [Mh] Termos MeSH secundário: Animais Anti-Inflamatórios/isolamento & purificação Curcuma/química Diabetes Mellitus Experimental/complicações Diabetes Mellitus Experimental/tratamento farmacológico Diabetes Mellitus Experimental/imunologia Retinopatia Diabética/complicações Retinopatia Diabética/imunologia Células Endoteliais da Veia Umbilical Humana Leucostasia/complicações Leucostasia/imunologia Masculino NF-kappa B/antagonistas & inibidores NF-kappa B/imunologia Ratos Ratos Wistar Sesquiterpenos/isolamento & purificação Transdução de Sinais/efeitos dos fármacos Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores Proteínas Quinases p38 Ativadas por Mitógeno/imunologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Anti-Inflammatory Agents); 0 (NF-kappa B); 0 (Sesquiterpenes); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 171124 [Lr] Data última revisão: 171124 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170310 [St] Status: MEDLINE

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[PMID]: 27967252 [Au] Autor: Giammarco S; Chiusolo P; Piccirillo N; Di Giovanni A; Metafuni E; Laurenti L; Sica S; Pagano L [Ad] Endereço: a Department of Hematology , Universita' Cattolica del Sacro Cuore , Rome , Italy. [Ti] Título: Hyperleukocytosis and leukostasis: management of a medical emergency. [So] Source: Expert Rev Hematol;10(2):147-154, 2017 Feb. [Is] ISSN: 1747-4094 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: INTRODUCTION: Hyperleukocytosis is defined as a white blood cell count greater than 100,000/mL in patients affected by acute leukemia and often it is associated with increased morbidity and mortality, that can be up to 40% if unrecognized. Areas covered: Risk factors include younger age, myelomonocytic or monocytic/monoblastic morphology, microgranular variant of acute promyelocitic leukemia and T-cell ALL, and some cytogenetic abnormalities. Poor prognosis due to high early death rate secondary to leukostasis. The mechanisms at the origin of leukostasis are still poorly understood. The management of acute hyperleukocytosis and leukostasis involves supportive measures and reducing the number of circulating leukemic blast cells, with careful monitoring of fluid balance, control of uric acid production and control of urine pH to prevent tumour lysis syndrome. Expert commentary: Several studies have been performed to ameliorate the outcome of this setting of patients. The high number of leukocytes may cause 3 main complications: disseminated intravascular coagulation (DIC), tumor lysis syndrome (TLS), and leukostasis. Although hyperleukocytosis and tumour lysis syndrome are still a challenge for clinicians, a better prognosis for these conditions is emerging in the last years. [Mh] Termos MeSH primário: Leucemia/diagnóstico Leucemia/terapia Contagem de Leucócitos Leucostasia/diagnóstico Leucostasia/terapia [Mh] Termos MeSH secundário: Doença Aguda Terapia Combinada Gerenciamento Clínico Serviços Médicos de Emergência Seres Humanos Leucemia/sangue Leucemia/etiologia Leucostasia/sangue Leucostasia/etiologia Fenótipo Fatores de Risco Índice de Gravidade de Doença Síndrome de Lise Tumoral/diagnóstico Síndrome de Lise Tumoral/etiologia [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Em] Mês de entrada: 1705 [Cu] Atualização por classe: 170518 [Lr] Data última revisão: 170518 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161215 [St] Status: MEDLINE [do] DOI: 10.1080/17474086.2017.1270754

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[PMID]: 27474370 [Au] Autor: Portillo JC; Lopez Corcino Y; Miao Y; Tang J; Sheibani N; Kern TS; Dubyak GR; Subauste CS [Ad] Endereço: Division of Infectious Diseases and HIV Medicine, Department of Medicine, Case Western Reserve University, Cleveland, OH. [Ti] Título: CD40 in Retinal Müller Cells Induces P2X7-Dependent Cytokine Expression in Macrophages/Microglia in Diabetic Mice and Development of Early Experimental Diabetic Retinopathy. [So] Source: Diabetes;66(2):483-493, 2017 Feb. [Is] ISSN: 1939-327X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Müller cells and macrophages/microglia are likely important for the development of diabetic retinopathy; however, the interplay between these cells in this disease is not well understood. An inflammatory process is linked to the onset of experimental diabetic retinopathy. CD40 deficiency impairs this process and prevents diabetic retinopathy. Using mice with CD40 expression restricted to Müller cells, we identified a mechanism by which Müller cells trigger proinflammatory cytokine expression in myeloid cells. During diabetes, mice with CD40 expressed in Müller cells upregulated retinal tumor necrosis factor-α (TNF-α), interleukin 1ß (IL-1ß), intracellular adhesion molecule 1 (ICAM-1), and nitric oxide synthase (NOS2), developed leukostasis and capillary degeneration. However, CD40 did not cause TNF-α or IL-1ß secretion in Müller cells. TNF-α was not detected in Müller cells from diabetic mice with CD40 Müller cells. Rather, TNF-α was upregulated in macrophages/microglia. CD40 ligation in Müller cells triggered phospholipase C-dependent ATP release that caused P2X -dependent production of TNF-α and IL-1ß by macrophages. P2X mice and mice treated with a P2X inhibitor were protected from diabetes-induced TNF-α, IL-1ß, ICAM-1, and NOS2 upregulation. Our studies indicate that CD40 in Müller cells is sufficient to upregulate retinal inflammatory markers and appears to promote experimental diabetic retinopathy and that Müller cells orchestrate inflammatory responses in myeloid cells through a CD40-ATP-P2X pathway. [Mh] Termos MeSH primário: Antígenos CD40/imunologia Citocinas/imunologia Diabetes Mellitus Experimental/imunologia Retinopatia Diabética/imunologia Células Ependimogliais/imunologia Macrófagos/imunologia Microglia/imunologia Receptores Purinérgicos P2X7/imunologia [Mh] Termos MeSH secundário: Animais Antígenos CD40/genética Capilares Diabetes Mellitus Experimental/complicações Retinopatia Diabética/etiologia Inflamação Molécula 1 de Adesão Intercelular/imunologia Interleucina-1beta/imunologia Leucostasia/imunologia Masculino Camundongos Camundongos Knockout Células Mieloides/imunologia Óxido Nítrico Sintase Tipo II/imunologia Antagonistas do Receptor Purinérgico P2X/farmacologia Fator de Necrose Tumoral alfa/imunologia Fosfolipases Tipo C/imunologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (CD40 Antigens); 0 (Cytokines); 0 (IL1B protein, mouse); 0 (Icam1 protein, mouse); 0 (Interleukin-1beta); 0 (Purinergic P2X Receptor Antagonists); 0 (Receptors, Purinergic P2X7); 0 (Tumor Necrosis Factor-alpha); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 3.1.4.- (Type C Phospholipases) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 160731 [St] Status: MEDLINE [do] DOI: 10.2337/db16-0051

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[PMID]: 27442082 [Au] Autor: Hossain A; Tauhid L; Davenport I; Huckaba T; Graves R; Mandal T; Muniruzzaman S; Ahmed SA; Bhattacharjee PS [Ad] Endereço: a Department of Biology , Xavier University of Louisiana , New Orleans , LA , USA. [Ti] Título: LRP-1 Pathway Targeted Inhibition of Vascular Abnormalities in the Retina of Diabetic Mice. [So] Source: Curr Eye Res;42(4):640-647, 2017 Apr. [Is] ISSN: 1460-2202 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: PURPOSE: The cell surface LDL (low-density lipoprotein) receptor-related protein-1 (LRP-1) is important for lipid transport and several cell signaling processes. Human apolipoprotein E (apoE) is a ligand of LRP-1. We previously reported that a short peptide (apoEdp) mimicking the LRP-1 binding region of apoE prevents hyperglycemia-induced retinal endothelial cell dysfunction in vitro. The in-vivo outcome of apoE-based peptidomimetic inhibition of LRP-1 in the treatment of diabetic retinopathy is unknown. METHODS: Six months after streptozotocin induction of diabetes, male C57Bl/6 mice were intravitreally inoculated with apoEdp in a controlled release formulation. On the 15th day post-apoEdp treatment, mouse retinas were harvested to examine (1) blood-retinal-barrier (BRB) permeability by Evans blue dye, inflammatory leukostasis by concanavalin staining of leukocytes and LRP-1 pathway-related protein expression by Western blot analysis and gelatin zymography. RESULTS: Intravitreal apoEdp treatment of diabetic mice significantly reduced Evans blue extravasation and the number of adherent leukocytes in the diabetic mouse retinas. ApoEdp treatment inhibited the expression of extracellular matrix (ECM) degrading proteases heparanase and MMP-2, and restores the BRB tight junction proteins occludin and ZO-1. ApoEdp treatment also inhibited Wnt/ß-catenin-related expression of pro-inflammatory molecules ICAM-1, HIF-1α, and VEGF through negative regulation by LRP-1. CONCLUSION: Intravitreal apoEdp treatment of diabetic mice resulted a significant decrease in retinal vascular abnormalities through downregulation of LRP-1-related ECM protein degradation and Wnt/ß-catenin-related pro-angiogenic molecules. [Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia Apolipoproteínas E/farmacologia Retinopatia Diabética/tratamento farmacológico Fragmentos de Peptídeos/farmacologia Receptores de LDL/antagonistas & inibidores Neovascularização Retiniana/prevenção & controle Proteínas Supressoras de Tumor/antagonistas & inibidores [Mh] Termos MeSH secundário: Animais Glicemia/metabolismo Barreira Hematorretiniana/fisiologia Western Blotting Permeabilidade Capilar Diabetes Mellitus Experimental/tratamento farmacológico Diabetes Mellitus Experimental/metabolismo Diabetes Mellitus Experimental/fisiopatologia Retinopatia Diabética/metabolismo Retinopatia Diabética/fisiopatologia Proteínas da Matriz Extracelular/metabolismo Injeções Intravítreas Leucostasia Masculino Camundongos Camundongos Endogâmicos C57BL Neovascularização Retiniana/metabolismo Neovascularização Retiniana/fisiopatologia Vasos Retinianos/fisiologia Via de Sinalização Wnt/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiogenesis Inhibitors); 0 (ApoEdpL-W peptide, human); 0 (Apolipoproteins E); 0 (Blood Glucose); 0 (Extracellular Matrix Proteins); 0 (Lrp1 protein, mouse); 0 (Peptide Fragments); 0 (Receptors, LDL); 0 (Tumor Suppressor Proteins) [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: 160722 [St] Status: MEDLINE [do] DOI: 10.1080/02713683.2016.1203441

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