Base de dados : MEDLINE
Pesquisa : C10.228.140.163.100.640 [Categoria DeCS]
Referências encontradas : 346 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 35 ir para página                         

  1 / 346 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29028801
[Au] Autor:Del Signore SJ; Biber SA; Lehmann KS; Heimler SR; Rosenfeld BH; Eskin TL; Sweeney ST; Rodal AA
[Ad] Endereço:Rosenstiel Basic Medical Sciences Research Center, Department of Biology, Brandeis University, Waltham, Massachusetts, United States of America.
[Ti] Título:dOCRL maintains immune cell quiescence by regulating endosomal traffic.
[So] Source:PLoS Genet;13(10):e1007052, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lowe Syndrome is a developmental disorder characterized by eye, kidney, and neurological pathologies, and is caused by mutations in the phosphatidylinositol-5-phosphatase OCRL. OCRL plays diverse roles in endocytic and endolysosomal trafficking, cytokinesis, and ciliogenesis, but it is unclear which of these cellular functions underlie specific patient symptoms. Here, we show that mutation of Drosophila OCRL causes cell-autonomous activation of hemocytes, which are macrophage-like cells of the innate immune system. Among many cell biological defects that we identified in docrl mutant hemocytes, we pinpointed the cause of innate immune cell activation to reduced Rab11-dependent recycling traffic and concomitantly increased Rab7-dependent late endosome traffic. Loss of docrl amplifies multiple immune-relevant signals, including Toll, Jun kinase, and STAT, and leads to Rab11-sensitive mis-sorting and excessive secretion of the Toll ligand Spåtzle. Thus, docrl regulation of endosomal traffic maintains hemocytes in a poised, but quiescent state, suggesting mechanisms by which endosomal misregulation of signaling may contribute to symptoms of Lowe syndrome.
[Mh] Termos MeSH primário: Citocinese/genética
Imunidade Inata/genética
Síndrome Oculocerebrorrenal/genética
Monoéster Fosfórico Hidrolases/genética
[Mh] Termos MeSH secundário: Animais
Drosophila
Endossomos/genética
Endossomos/patologia
Hemócitos/metabolismo
Hemócitos/patologia
Seres Humanos
Mutação
Síndrome Oculocerebrorrenal/patologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007052


  2 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28739877
[Au] Autor:Sun HM; Chen XL; Chen XJ; Liu J; Ma L; Wu HY; Huang QH; Xi XD; Yin T; Zhu J; Chen Z; Chen SJ
[Ad] Endereço:State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, RuiJin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
[Ti] Título:PALLD Regulates Phagocytosis by Enabling Timely Actin Polymerization and Depolymerization.
[So] Source:J Immunol;199(5):1817-1826, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PALLD is an actin cross-linker supporting cellular mechanical tension. However, its involvement in the regulation of phagocytosis, a cellular activity essential for innate immunity and physiological tissue turnover, is unclear. We report that is highly induced along with all- -retinoic acid-induced maturation of myeloid leukemia cells, to promote Ig- or complement-opsonized phagocytosis. PALLD mechanistically facilitates phagocytic receptor clustering by regulating actin polymerization and c-Src dynamic activation during particle binding and early phagosome formation. PALLD is also required at the nascent phagosome to recruit phosphatase oculocerebrorenal syndrome of Lowe, which regulates phosphatidylinositol-4,5-bisphosphate hydrolysis and actin depolymerization to complete phagosome closure. Collectively, our results show a new function for PALLD as a crucial regulator of the early phase of phagocytosis by elaborating dynamic actin polymerization and depolymerization.
[Mh] Termos MeSH primário: Actinas/metabolismo
Proteínas do Citoesqueleto/metabolismo
Células Dendríticas/imunologia
Leucemia Mieloide Aguda/imunologia
Células-Tronco Neoplásicas/fisiologia
Síndrome Oculocerebrorrenal/imunologia
Fagocitose
Fosfoproteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Linhagem Celular Tumoral
Autorrenovação Celular
Proteínas do Citoesqueleto/genética
Seres Humanos
Imunidade Inata
Camundongos
Camundongos Endogâmicos C57BL
Fagossomos/metabolismo
Fosfoproteínas/genética
Monoéster Fosfórico Hidrolases/metabolismo
Polimerização
Agregação de Receptores
Tretinoína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Cytoskeletal Proteins); 0 (Phosphoproteins); 0 (palladin protein, human); 5688UTC01R (Tretinoin); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (phosphoinositide 5-phosphatase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602018


  3 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28669993
[Au] Autor:De Matteis MA; Staiano L; Emma F; Devuyst O
[Ad] Endereço:Telethon Institute of Genetics and Medicine, Via Campi Flegrei 34, 80078, Pozzuoli, Italy.
[Ti] Título:The 5-phosphatase OCRL in Lowe syndrome and Dent disease 2.
[So] Source:Nat Rev Nephrol;13(8):455-470, 2017 Aug.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lowe syndrome is an X-linked disease that is characterized by congenital cataracts, central hypotonia, intellectual disability and renal Fanconi syndrome. The disease is caused by mutations in OCRL, which encodes an inositol polyphosphate 5-phosphatase (OCRL) that acts on phosphoinositides - quantitatively minor constituents of cell membranes that are nonetheless pivotal regulators of intracellular trafficking. In this Review we summarize the considerable progress made over the past decade in understanding the cellular roles of OCRL in regulating phosphoinositide balance along the endolysosomal pathway, a fundamental system for the reabsorption of proteins and solutes by proximal tubular cells. We discuss how studies of OCRL have led to important discoveries about the basic mechanisms of membrane trafficking and describe the key features and limitations of the currently available animal models of Lowe syndrome. Mutations in OCRL can also give rise to a milder pathology, Dent disease 2, which is characterized by renal Fanconi syndrome in the absence of extrarenal pathologies. Understanding how mutations in OCRL give rise to two clinical entities with differing extrarenal manifestations represents an opportunity to identify molecular pathways that could be targeted to develop treatments for these conditions.
[Mh] Termos MeSH primário: Doenças Genéticas Ligadas ao Cromossomo X/genética
Mutação
Nefrolitíase/genética
Síndrome Oculocerebrorrenal/genética
Monoéster Fosfórico Hidrolases/genética
[Mh] Termos MeSH secundário: Animais
Vesículas Revestidas por Clatrina
Modelos Animais de Doenças
Endocitose
Seres Humanos
Inositol Polifosfato 5-Fosfatases/genética
Túbulos Renais Proximais/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.83


  4 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28397227
[Au] Autor:Zhu X; Li J; Ru T; Zhu R; Dai C; Wang W; Hu Y
[Ad] Endereço:Prenatal Diagnosis Center of Jiangsu Province, Drum Tower Hospital Affiliated to Nanjing University Medical School, Nanjing, Jiangsu 210008, China. glyyhuyali@163.com.
[Ti] Título:[Prenatal diagnosis and follow-up of a case with Lowe syndrome caused by interstitial deletion of Xq25-26].
[So] Source:Zhonghua Yi Xue Yi Chuan Xue Za Zhi;34(2):236-239, 2017 Apr 10.
[Is] ISSN:1003-9406
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To report on a sporadic case of Lowe syndrome diagnosed prenatally with ultrasound examination and genetic testing. METHODS: Detailed sonographic fetal screening was performed by an experienced sonographer at 32 weeks of gestation. Fetal cranial magnetic resonance imaging (MRI) was applied to detect potential brain abnormality. Chromosomal microarray analysis (CMA) was conducted on amniotic fluid sample from the fetus and peripheral blood sample from the mother. RESULTS: Congenital cataract and enlarged posterior fossa were detected by fetal ultrasound screening. Fetal cranial MRI found hypoplasia of the gyrus. CMA revealed that the fetus has carried a 633 kb deletion at Xq25-26.1 which encompassed the OCRL gene. The mother was a carrier of the same deletion. Clinical examination after birth confirmed that the neonate was affected with Lowe syndrome in addition with an atrial septal defect. CONCLUSION: Prenatal diagnosis of Lowe syndrome without a family history largely depends on fetal imaging. Should cataract be found by ultrasound screening, fetal MRI may be considered to rule out central nervous system anomalies. CMA assay should also be considered to facilitate the diagnosis.
[Mh] Termos MeSH primário: Doenças Fetais/genética
Síndrome Oculocerebrorrenal/genética
[Mh] Termos MeSH secundário: Adulto
Criança
Pré-Escolar
Deleção Cromossômica
Cromossomos Humanos X/genética
Feminino
Doenças Fetais/diagnóstico
Seres Humanos
Lactente
Masculino
Análise em Microsséries
Síndrome Oculocerebrorrenal/diagnóstico
Síndrome Oculocerebrorrenal/embriologia
Monoéster Fosfórico Hidrolases/genética
Gravidez
Diagnóstico Pré-Natal
Ultrassonografia Pré-Natal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1003-9406.2017.02.019


  5 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27895154
[Au] Autor:Inoue K; Balkin DM; Liu L; Nandez R; Wu Y; Tian X; Wang T; Nussbaum R; De Camilli P; Ishibe S
[Ad] Endereço:Departments of Internal Medicine.
[Ti] Título:Kidney Tubular Ablation of / Phenocopies Lowe Syndrome Tubulopathy.
[So] Source:J Am Soc Nephrol;28(5):1399-1407, 2017 May.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lowe syndrome and Dent disease are two conditions that result from mutations of the inositol 5-phosphatase oculocerebrorenal syndrome of Lowe (OCRL) and share the feature of impaired kidney proximal tubule function. Genetic ablation of in mice failed to recapitulate the human phenotypes, possibly because of the redundant functions of OCRL and its paralog type 2 inositol polyphosphate-5-phosphatase (INPP5B). Germline knockout of both paralogs in mice results in early embryonic lethality. We report that kidney tubule-specific inactivation of on a global -knockout mouse background resulted in low molecular weight proteinuria, phosphaturia, and acidemia. At the cellular level, we observed a striking impairment of clathrin-dependent and -independent endocytosis in proximal tubules, phenocopying what has been reported for Dent disease caused by mutations in the gene encoding endosomal proton-chloride exchange transporter 5. These results suggest that the functions of OCRL/INPP5B and proton-chloride exchange transporter 5 converge on shared mechanisms, the impairment of which has a dramatic effect on proximal tubule endocytosis.
[Mh] Termos MeSH primário: Túbulos Renais Proximais
Mutação
Síndrome Oculocerebrorrenal/genética
Fenótipo
Monoéster Fosfórico Hidrolases/genética
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (Ocrl protein, mouse); EC 3.1.3.36 (phosphoinositide 5-phosphatase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016080913


  6 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27178641
[Au] Autor:Ikehara S; Utani A
[Ad] Endereço:Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
[Ti] Título:Multiple protrusive epidermal cysts on the scalp of a Lowe syndrome patient.
[So] Source:J Dermatol;44(1):105-107, 2017 Jan.
[Is] ISSN:1346-8138
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Encefalopatias/diagnóstico
Cisto Epidérmico/diagnóstico
Síndrome Oculocerebrorrenal/complicações
Monoéster Fosfórico Hidrolases/genética
Dermatoses do Couro Cabeludo/diagnóstico
[Mh] Termos MeSH secundário: Encefalopatias/diagnóstico por imagem
Encefalopatias/etiologia
Criança
Cisto Epidérmico/etiologia
Cisto Epidérmico/patologia
Cisto Epidérmico/cirurgia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Síndrome Oculocerebrorrenal/genética
Couro Cabeludo
Dermatoses do Couro Cabeludo/etiologia
Dermatoses do Couro Cabeludo/patologia
Dermatoses do Couro Cabeludo/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160515
[St] Status:MEDLINE
[do] DOI:10.1111/1346-8138.13444


  7 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27398910
[Au] Autor:De Leo MG; Staiano L; Vicinanza M; Luciani A; Carissimo A; Mutarelli M; Di Campli A; Polishchuk E; Di Tullio G; Morra V; Levtchenko E; Oltrabella F; Starborg T; Santoro M; Di Bernardo D; Devuyst O; Lowe M; Medina DL; Ballabio A; De Matteis MA
[Ad] Endereço:Telethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Naples, Italy.
[Ti] Título:Autophagosome-lysosome fusion triggers a lysosomal response mediated by TLR9 and controlled by OCRL.
[So] Source:Nat Cell Biol;18(8):839-850, 2016 Aug.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Phosphoinositides (PtdIns) control fundamental cell processes, and inherited defects of PtdIns kinases or phosphatases cause severe human diseases, including Lowe syndrome due to mutations in OCRL, which encodes a PtdIns(4,5)P2 5-phosphatase. Here we unveil a lysosomal response to the arrival of autophagosomal cargo in which OCRL plays a key part. We identify mitochondrial DNA and TLR9 as the cargo and the receptor that triggers and mediates, respectively, this response. This lysosome-cargo response is required to sustain the autophagic flux and involves a local increase in PtdIns(4,5)P2 that is confined in space and time by OCRL. Depleting or inhibiting OCRL leads to an accumulation of lysosomal PtdIns(4,5)P2, an inhibitor of the calcium channel mucolipin-1 that controls autophagosome-lysosome fusion. Hence, autophagosomes accumulate in OCRL-depleted cells and in the kidneys of Lowe syndrome patients. Importantly, boosting the activity of mucolipin-1 with selective agonists restores the autophagic flux in cells from Lowe syndrome patients.
[Mh] Termos MeSH primário: Autofagossomos/fisiologia
Autofagia/fisiologia
Lisossomos/metabolismo
Fosfatidilinositóis/genética
Monoéster Fosfórico Hidrolases/genética
Receptor Toll-Like 9/genética
[Mh] Termos MeSH secundário: Animais
Autofagia/genética
Linhagem Celular
Seres Humanos
Mutação/genética
Síndrome Oculocerebrorrenal/genética
Síndrome Oculocerebrorrenal/metabolismo
Fosfatidilinositol 4,5-Difosfato/metabolismo
Monoéster Fosfórico Hidrolases/metabolismo
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphatidylinositol 4,5-Diphosphate); 0 (Phosphatidylinositols); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 9); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human); EC 3.1.3.36 (phosphoinositide 5-phosphatase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160712
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3386


  8 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27229703
[Au] Autor:Mikhail M; Modabber M; Koenekoop RK; Braverman N; Khan A
[Ad] Endereço:Department of Ophthalmology, McGill University, Montreal, Quebec, Canada.
[Ti] Título:Delayed vitreous haemorrhage after paediatric cataract surgery in Lowe syndrome.
[So] Source:Eye (Lond);30(9):1272-3, 2016 Sep.
[Is] ISSN:1476-5454
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Extração de Catarata/efeitos adversos
Síndrome Oculocerebrorrenal/cirurgia
Hemorragia Vítrea/etiologia
[Mh] Termos MeSH secundário: Seres Humanos
Lactente
Masculino
Mutação/genética
Síndrome Oculocerebrorrenal/diagnóstico
Síndrome Oculocerebrorrenal/genética
Monoéster Fosfórico Hidrolases/genética
Sítios de Splice de RNA/genética
Hemorragia Vítrea/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA Splice Sites); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160528
[St] Status:MEDLINE
[do] DOI:10.1038/eye.2016.100


  9 / 346 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26928805
[Au] Autor:Roksnoer LC; Heijnen BF; Nakano D; Peti-Peterdi J; Walsh SB; Garrelds IM; van Gool JM; Zietse R; Struijker-Boudier HA; Hoorn EJ; Danser AH
[Ad] Endereço:From the Division of Pharmacology and Vascular Medicine (L.C.W.R, I.M.G., J.M.G.v.G., A.H.J.D.), Division of Nephrology and Transplantation (L.C.W.R., R.Z., E.J.H.), Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands; Department of Pharmacology, Cardiovascular Research Institute
[Ti] Título:On the Origin of Urinary Renin: A Translational Approach.
[So] Source:Hypertension;67(5):927-33, 2016 May.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Urinary angiotensinogen excretion parallels albumin excretion, which is not the case for renin, while renin's precursor, prorenin, is undetectable in urine. We hypothesized that renin and prorenin, given their smaller size, are filtered through the glomerulus in larger amounts than albumin and angiotensinogen, and that differences in excretion rate are because of a difference in reabsorption in the proximal tubule. To address this, we determined the glomerular sieving coefficient of renin and prorenin and measured urinary renin/prorenin 1) after inducing prorenin in Cyp1a1-Ren2 rats and 2) in patients with Dent disease or Lowe syndrome, disorders characterized by defective proximal tubular reabsorption. Glomerular sieving coefficients followed molecular size (renin>prorenin>albumin). The induction of prorenin in rats resulted in a >300-fold increase in plasma prorenin and doubling of blood pressure but did not lead to the appearance of prorenin in urine. It did cause parallel rises in urinary renin and albumin, which losartan but not hydralazine prevented. Defective proximal tubular reabsorption increased urinary renin and albumin 20- to 40-fold, and allowed prorenin detection in urine, at ≈50% of its levels in plasma. Taken together, these data indicate that circulating renin and prorenin are filtered into urine in larger amounts than albumin. All 3 proteins are subsequently reabsorbed in the proximal tubule. For prorenin, such reabsorption is ≈100%. Minimal variation in tubular reabsorption (in the order of a few %) is sufficient to explain why urinary renin and albumin excretion do not correlate. Urinary renin does not reflect prorenin that is converted to renin in tubular fluid.
[Mh] Termos MeSH primário: Albuminas/metabolismo
Angiotensinogênio/metabolismo
Doença de Dent/urina
Síndrome Oculocerebrorrenal/urina
Renina/metabolismo
Pesquisa Médica Translacional/métodos
[Mh] Termos MeSH secundário: Animais
Doença de Dent/fisiopatologia
Modelos Animais de Doenças
Taxa de Filtração Glomerular
Seres Humanos
Glomérulos Renais/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Síndrome Oculocerebrorrenal/fisiopatologia
Ratos
Sistema Renina-Angiotensina/fisiologia
Amostragem
Urinálise
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Albumins); 11002-13-4 (Angiotensinogen); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.115.07012


  10 / 346 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26813509
[Au] Autor:Sekine T
[Ad] Endereço:Department of Pediatrics, Toho University Ohashi Hospital, Japan.
[Ti] Título:[Renal hypophosphatemia:pathophysiology and treatment].
[So] Source:Clin Calcium;26(2):284-94, 2016 Feb.
[Is] ISSN:0917-5857
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Serum level of phosphate is regulated by the kidney, especially proximal tubule. The transcellular transport of phosphate in the proximal tubule is mediated via Na dependent transporters, i.e., NPT2a and NPT2b at the luminal membrane, and unknown channel at the basolateral side. The transport of phosphate via NPT2a and NPT2b is further regulated by factors, such as PTH, FGF23, and 1,25(OH)(2)D. Several hereditary diseases that cause hypophoshatemia specically are known. In addition, dysfunction of proximal tubule may develop Fanconi syndrome, which also causes hypherphosphaturia. In this section, I describe the renal mechanisms of phosphate handling and the causes of hypophosphatemia along with its treatment.
[Mh] Termos MeSH primário: Hipofosfatemia/etiologia
Hipofosfatemia/metabolismo
Túbulos Renais Proximais/metabolismo
Fosfatos/metabolismo
[Mh] Termos MeSH secundário: Administração Oral
Calcitriol/fisiologia
Canais de Cloreto
Doença de Dent/etiologia
Doença de Dent/genética
Doença de Dent/metabolismo
Síndrome de Fanconi/etiologia
Síndrome de Fanconi/metabolismo
Fatores de Crescimento de Fibroblastos/fisiologia
Seres Humanos
Hipofosfatemia/terapia
Doenças Mitocondriais
Síndrome Oculocerebrorrenal
Hormônio Paratireóideo/fisiologia
Monoéster Fosfórico Hidrolases
Compostos de Fósforo/administração & dosagem
Compostos de Fósforo/uso terapêutico
Proteínas Cotransportadoras de Sódio-Fosfato Tipo IIa/fisiologia
Proteínas Cotransportadoras de Sódio-Fosfato Tipo IIc/fisiologia
Vitamina D/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CLC-5 chloride channel); 0 (Chloride Channels); 0 (Parathyroid Hormone); 0 (Phosphates); 0 (Phosphorus Compounds); 0 (SLC34A1 protein, human); 0 (SLC34A3 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins, Type IIa); 0 (Sodium-Phosphate Cotransporter Proteins, Type IIc); 0 (fibroblast growth factor 23); 1406-16-2 (Vitamin D); 62031-54-3 (Fibroblast Growth Factors); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160128
[St] Status:MEDLINE
[do] DOI:CliCa1602284294



página 1 de 35 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde