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Pesquisa : D12.776.157.530.400.175 [Categoria DeCS]
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Id: biblio-950023
Autor: Sancakli, Ozlem; Kulu, Bahar; Sakallioglu, Onur.
Título: Una nueva mutación de la enfermedad de Dent en un niño de 11 años con nefrolitiasis y nefrocalcinosis / A novel mutation of Dent's disease in an 11-year-old male with nephrolithiasis and nephrocalcinosis
Fonte: Arch. argent. pediatr;116(3):442-444, jun. 2018. ilus.
Idioma: en; es.
Resumo: La enfermedad de Dent es una tubulopatía recesiva ligada al cromosoma X caracterizada por proteinuria de bajo peso molecular (bpm), hipercalciuria, nefrocalcinosis o nefrolitiasis, disfunción tubular proximal e insuficiencia renal en la adultez. Las mujeres son portadoras y, en general, padecen una forma leve de la enfermedad. La progresión hacia la insuficiencia renal en estadio terminal se da entre los 30 y los 50 años de edad en el 30-80% de los varones afectados. A falta de un tratamiento dirigido al defecto molecular, en la actualidad, los pacientes con enfermedad de Dent reciben tratamientos complementarios orientados a prevenir la nefrolitiasis y la nefrocalcinosis. El caso que presentamos es el de un niño de 11 años con nefrocalcinosis y nefrolitiasis, en quien se detectó una nueva mutación en el gen CLCN5.

Dent's disease is a rare X-linked recessive tubulopathy characterized by low molecular weight (LMW) proteinuria, hypercalciuria, nephrolcalcinosis or nephrolithiasis, proximal tubular dysfunction and renal failure in adulthood. Females are carriers and usually mildly affected. Progression to endstage renal failure are at the 3rd-5th decades of life in 30-80% of affected males. In the absence of therapy targeting for the molecular defect, the current care of patients with Dent's disease is supportive, focusing on the prevention of nephrolithiasis and nephrocalcinosis. We present an 11-year-old child with nephrocalcinosis and nephrolithiasis caused by a new mutation at CLCN5 gene.
Descritores: Canais de Cloreto/genética
Nefrolitíase/etiologia
Doença de Dent/genética
Nefrocalcinose/etiologia
-Nefrolitíase/genética
Doença de Dent/fisiopatologia
Mutação
Nefrocalcinose/genética
Limites: Humanos
Masculino
Criança
Tipo de Publ: Relatos de Casos
Responsável: AR94.1 - Centro de Información Pediatrica


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Cunha, C. da
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Id: lil-623963
Autor: Izquierdo, I; Pereira, M. E; Cunha, C. da; Wolfman, C; Medina, J. H.
Título: Benzodiazepine receptor ligand influences on learning: an endogenous modulatory mechanism mediated by benzodiazepines possibly of alimentary origin
Fonte: Mem. Inst. Oswaldo Cruz;86(supl.2):169-171, 1991. tab.
Idioma: en.
Conferência: Apresentado em: Brazilian-Sino Symposium on Chemistry and Pharmacology of Natural Products, Rio de Janeiro, Dec. 10-14, 1989.
Resumo: In rats pre-but not post-training ip administration of either flumazenil, a central benzodiazepine (BSD) receptor antagonist, or of n-butyl-B-carboline-carboxylate (BCCB), an inverse agonist, enhanced retention of inhibitory avoidance learning. Flumazenil vlocked the enhancing effect of BCCB, and the inhibitory effect of the BZD agonists clonazepam and diazepam also given pre-training. Post-training administration of these drugs had no effects. The peripheral BZD receptor agonist/chloride channel blocker Ro5-4864 had no effect on the inhibitory avoidance task when given ip prior to training, buth it caused enhancement when given immediately post-training either ip or icv. This effect was blocked by PK11195, a competitive antagonist of Ro5-4864. These results suggest that ther is an endogenous mechanism mediated by BZD agonists, which is sensitive to inverse agonists and that normally down-regulates the formation of memories through a mechanism involving GABA-A receptors and the corresponding chloride channels. The most likely agonists for the endogenous mechanism suggested are the diazepam-like BZDs found in brain whose origin is possibly alimentary. Levels of these BZDs in the cortex were found to sharply decrease after inhibitory acoidance training or mere exposure to the training apparatus.
Descritores: Benzodiazepinas/metabolismo
Benzodiazepinas/farmacologia
Ativação do Canal Iônico/efeitos dos fármacos
Receptores de GABA-A/efeitos dos fármacos
Receptores de GABA-A/fisiologia
Diazepam/farmacologia
Proteínas de Membrana/efeitos dos fármacos
-Aprendizagem da Esquiva/efeitos dos fármacos
Ratos Wistar
Canais de Cloreto
Limites: Animais
Ratos
Responsável: BR1.1 - BIREME


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Id: lil-770496
Autor: Heilberg, Ita Pfeferman; Tótoli, Cláudia; Calado, Joaquim Tomaz.
Título: Adult presentation of Bartter syndrome type IV with erythrocytosis / Apresentação tardia de síndrome de Bartter tipo IV com eritrocitose
Fonte: Einstein (Säo Paulo);13(4):604-606, Oct.-Dec. 2015.
Idioma: pt.
Resumo: Abstract Bartter syndrome comprises a group of rare autosomal-recessive salt-losing disorders with distinct phenotypes, but one unifying pathophysiology consisting of severe reductions of sodium reabsorption caused by mutations in five genes expressed in the thick ascending limb of Henle, coupled with increased urinary excretion of potassium and hydrogen, which leads to hypokalemic alkalosis. Bartter syndrome type IV, caused by loss-of-function mutations in barttin, a subunit of chloride channel CLC-Kb expressed in the kidney and inner ear, usually occurs in the antenatal-neonatal period. We report an unusual case of late onset presentation of Bartter syndrome IV and mild phenotype in a 20 years-old man who had hypokalemia, deafness, secondary hyperparathyroidism and erythrocytosis.

Resumo A síndrome de Bartter compreende um grupo raro de doenças autossômicas recessivas perdedoras de sal, decorrentes de mutações em genes expressos na porção ascendente espessa da alça de Henle, com fenótipos distintos, porém fisiopatogenia única, que consiste em redução severa da reabsorção de sódio, e aumento da excreção urinária de hidrogênio e potássio, levando à alcalose hipocalêmica. A síndrome de Bartter tipo IV, causada por mutações com perda de função da bartina, uma subunidade do canal de cloro CLC-Kb expressa no rim e ouvido interno, geralmente se apresenta nos períodos ante e neonatal. No presente relato, descreve-se um caso não usual de síndrome de Bartter tipo IV com apresentação tardia e fenótipo atenuado, diagnosticado por análise molecular, em um homem adulto de 20 anos que se apresentava com hipocalemia, surdez, hiperparatireoidismo secundário e eritrocitose.
Descritores: Síndrome de Bartter/complicações
Policitemia/complicações
-Alcalose/metabolismo
Brasil
Síndrome de Bartter/genética
Canais de Cloreto/genética
Canais de Cloreto/metabolismo
Surdez/complicações
Hiperparatireoidismo Secundário/complicações
Hipopotassemia/complicações
Transtornos de Início Tardio/genética
Fenótipo
Potássio/urina
Limites: Humanos
Masculino
Adulto Jovem
Tipo de Publ: Relatos de Casos
Responsável: BR1.1 - BIREME


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Id: lil-759911
Autor: Scarparo, Henrique Clasen.
Título: Estudos farmacológicos dos bloqueadores dos canais de cloreto ativados pelo calcio e pelo volume celular na contratilidade do músculo liso longitudinal de fundo de estômago de rato / Studies of pharmacological blockers of chloride channels activated by calcium and the cell volume contractility in the longitudinal smooth muscle of rat stomach fundus.
Fonte: Fortaleza; s.n; 2001. 220 p.
Idioma: pt.
Tese: Apresentada a Universidade Federal do Ceará para obtenção do grau de Doutor.
Resumo: O presente estudo investigou o envolvimento dos canais de cloreto ativados pelo cálcio intracelular (Cl(Ca)) e pelo aumento do volume celular (ClSWELL) na contratilidade do músculo liso longitudinal de fundo de estômago de rato. Avaliamos os efeitos farmacológicos de vários bloqueadores de canais de cloreto: o ácido niflúmico (NFA), ácido 4,4'-diisotiocianatostilibeno-2,2'-dissulfônico (DIDS), ácido 3',5-diclorodifenilamina-2-carboxílico (DCDPC), ácido 5-nitro-2-(3-fenilpropilamino) benzóico (NPPB) e o tamoxifeno (TAM), assim como o envolvimento dos gradientes de cálcio e cloreto transmembrana sobre as respostas contráteis induzidas pelos agonistas 5-hidroxitriptamina (5-HT, serotonina), acetilcolina (ACh) e prostaglandina-F2α (PGF2α), pelo cloreto de potássio (KCl) e pela solução hipotônica (SH) em estômago de rato. Avaliamos também os efeitos eletrofisiológicos do NFA e da nifedipina (NIF) sobre as alterações elétricas induzidas pela SH sobre a membrana celular. O NFA inibiu, seletivamente, as contrações induzidas pela 5-HT, reduziu, em menor proporção, as respostas induzidas pela PGF2α e não alterou os efeitos da ACh. Além disso, não alterou a contração induzida por 60mM e 20mM de KCl, sugerindo não interagir com os canais de cálcio dependentes de voltagem (VDCC) e nem ativar canais de potássio, respectivamente. Em contraste, os efeitos do DCDPC não foram seletivos, inibindo as contrações induzidas pela 5-HT, ACh e pelo KCl. O DIDS foi menos potente do que o NFA e DCDPC, inibindo as respostas induzidas por 60mM de KCl apenas em alta concentração. As concentrações induzidas pela 5-HT foram mais sensíveis aos efeitos do NFA e a remoção do cálcio e cloreto extracelulares do que aquelas induzidas pela ACh e pela PGF2α...
Descritores: Canais de Cloreto
Canais Iônicos
Ratos
Serotonina
Limites: Animais
Ratos
Responsável: BR6.1 - BCS - Biblioteca de Ciências da Saúde


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Id: lil-529100
Autor: Flores, C. A; Cid, L. P; Sepúlveda, F. V; Niemeyer, M. I.
Título: TMEM16 proteins: the long awaited calcium-activated chloride channels?
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;42(11):993-1001, Nov. 2009. ilus.
Idioma: en.
Projeto: Fondecyt.
Resumo: Currents mediated by calcium-activated chloride channels (CaCCs), observed for the first time in Xenopus oocytes, have been recorded in many cells and tissues ranging from different types of neurons to epithelial and muscle cells. CaCCs play a role in the regulation of excitability in neurons including sensory receptors. In addition, they are crucial mediators of chloride movements in epithelial cells where their activity regulates electrolyte and fluid transport. The roles of CaCCs, particularly in epithelia, are briefly reviewed with emphasis on their function in secretory epithelia. The recent identification by three independent groups, using different strategies, of TMEM16A as the molecular counterpart of the CaCC is discussed. TMEM16A is part of a family that has 10 other members in mice. The discovery of the potential TMEM16 anion channel activity opens the way for the molecular investigation of the role of these anion channels in specific cells and in organ physiology and pathophysiology. The identification of TMEM16A protein as a CaCC chloride channel molecule represents a great triumph of scientific perseverance and ingenuity. The varied approaches used by the three independent research groups also augur well for the solidity of the discovery.
Descritores: Canais de Cloreto/metabolismo
Células Epiteliais
Proteínas de Membrana/metabolismo
Proteínas de Neoplasias/metabolismo
Proteínas de Xenopus/metabolismo
-Canais de Cloreto/genética
Células Epiteliais/metabolismo
Mucosa Intestinal
Proteínas de Membrana/genética
Proteínas de Neoplasias/genética
Xenopus
Proteínas de Xenopus/genética
Limites: Animais
Humanos
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME


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Malnic, G
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Id: lil-506881
Autor: Carraro-Lacroix, L. R; Lessa, L. M. A; Fernandez, R; Malnic, G.
Título: Physiological implications of the regulation of vacuolar H+-ATPase by chloride ions
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;42(2):155-163, Feb. 2009. ilus.
Idioma: en.
Projeto: FAPESP; . CNPq.
Resumo: Vacuolar H+-ATPase is a large multi-subunit protein that mediates ATP-driven vectorial H+ transport across the membranes. It is widely distributed and present in virtually all eukaryotic cells in intracellular membranes or in the plasma membrane of specialized cells. In subcellular organelles, ATPase is responsible for the acidification of the vesicular interior, which requires an intraorganellar acidic pH to maintain optimal enzyme activity. Control of vacuolar H+-ATPase depends on the potential difference across the membrane in which the proton ATPase is inserted. Since the transport performed by H+-ATPase is electrogenic, translocation of H+-ions across the membranes by the pump creates a lumen-positive voltage in the absence of a neutralizing current, generating an electrochemical potential gradient that limits the activity of H+-ATPase. In many intracellular organelles and cell plasma membranes, this potential difference established by the ATPase gradient is normally dissipated by a parallel and passive Cl- movement, which provides an electric shunt compensating for the positive charge transferred by the pump. The underlying mechanisms for the differences in the requirement for chloride by different tissues have not yet been adequately identified, and there is still some controversy as to the molecular identity of the associated Cl--conducting proteins. Several candidates have been identified: the ClC family members, which may or may not mediate nCl-/H+ exchange, and the cystic fibrosis transmembrane conductance regulator. In this review, we discuss some tissues where the association between H+-ATPase and chloride channels has been demonstrated and plays a relevant physiologic role.
Descritores: Membrana Celular/metabolismo
Canais de Cloreto/metabolismo
ATPases Vacuolares Próton-Translocadoras/metabolismo
-Osso e Ossos/enzimologia
Sistema Nervoso Central/enzimologia
Canais de Cloreto/fisiologia
Rim/enzimologia
Fígado/enzimologia
ATPases Vacuolares Próton-Translocadoras/fisiologia
Limites: Animais
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME


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Id: lil-496393
Autor: Morales, Fernando; Cuenca, Patricia; Valle, Gerardo del; Vásquez, Melissa; Brian, Roberto; Sittenfeld, Mauricio; Johnson, Keith; Lin, Xi; Ashizawa, Tetsuo.
Título: Clinical and molecular diagnosis of a Costa Rican family with autosomal recessive myotonia congenita (Becker disease) carrying a new mutation in the CLCN1 gene
Fonte: Rev. biol. trop;56(1):1-11, mar. 2008. ilus, graf, tab.
Idioma: en.
Resumo: Myotonia congenita is a muscular disease characterized by myotonia, hypertrophy, and stiffness. It is inherited as either autosomal dominant or recessive known as Thomsen and Becker diseases, respectively. Here we confirm the clinical diagnosis of a family diagnosed with a myotonic condition many years ago and report a new mutation in the CLCN1 gene. The clinical diagnosis was established using ocular, cardiac, neurological and electrophysiological tests and the molecular diagnosis was done by PCR, SSCP and sequencing of the CLCN1 gene. The proband and the other affected individuals exhibited proximal and distal muscle weakness but no hypertrophy or muscular pain was found. The myotatic reflexes were lessened and sensibility was normal. Electrical and clinical myotonia was found only in the sufferers. Slit lamp and electrocardiogram tests were normal. Two affected probands presented diminution of the sensitive conduction velocities and prolonged sensory distal latencies. The clinical spectrum for this family is in agreement with a clinical diagnosis of Becker myotonia. This was confirmed by molecular diagnosis where a new disease-causing mutation (Q412P) was found in the family and absent in 200 unaffected chromosomes. No latent myotonia was found in this family; therefore the ability to cause this subclinical sign might be intrinsic to each mutation. Implications of the structure-function-genotype relationship for this and other mutations are discussed. Adequate clinical diagnosis of a neuromuscular disorder would allow focusing the molecular studies toward the confirmation of the initial diagnosis, leading to a proper clinical management, genetic counseling and improving in the quality of life of the patients and relatives.

La miotonía congénita es una enfermedad muscular caracterizada por miotonía, hipertrofia y rigidez. Se presenta con dos patrones de herencia, autosómica dominante en cuyo caso recibe el nombre de miotonía de Thomsen, o autosómica recesiva conocida como miotonía de Becker. En este trabajo se confirmó el diagnóstico clínico presuntivo hecho hace algunos años en una familia con una condición miotónica y se reporta una nueva mutación en el gen CLCN1. El diagnóstico clínico se estableció después de estudios oculares, cardíacos, neurológicos y electrofisiológicos. El diagnóstico molecular fue hecho mediante la PCR, SSCP y secuenciación del gen CLCN1. El caso índice y los otros individuos afectados exhibieron debilidad muscular proximal y distal, pero no se encontró hipertrofia ni dolor muscular. Los reflejos miotáticos estuvieron disminuidos y la sensibilidad fue normal. Se encontró miotonía clínica y eléctrica solo en los individuos afectados. Las pruebas de lámpara de hendidura y electrocardiograma resultaron normales. Dos individuos afectados presentaron disminución de las velocidades de conducción sensitiva y latencias distales sensoriales prolongadas. El cuadro clínico concuerda con la miotonía de Becker, lo cual se confirmó con el hallazgo de una mutación responsable de la enfermedad en el gen CLCN1 (Q412P), la cual se encontró en la familia y estuvo ausente en 200 cromosomas provenientes de la población general. No se encontró miotonía latente, por lo que probablemente la habilidad de causar este signo subclínico es intrínsica de cada mutación. Afinar el diagnóstico clínico diferencial de las enfermedades neuromusculares permitiría enfocar los estudios moleculares hacia la confirmación del diagnóstico inicial en forma eficiente, lo cual permitiría un manejo clínico y asesoramiento genético más adecuados y una mejora en la calidad de vida de los pacientes y sus familias.
Descritores: Canais de Cloreto/genética
Miotonia Congênita/diagnóstico
Mutação/genética
-Costa Rica
Enzimas de Restrição do DNA
Marcadores Genéticos
Miotonia Congênita/genética
Linhagem
Fenótipo
Reação em Cadeia da Polimerase
Polimorfismo Conformacional de Fita Simples
Limites: Humanos
Masculino
Feminino
Criança
Adolescente
Adulto
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  8 / 15 LILACS  
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Malnic, G
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Id: lil-449084
Autor: Tararthuch, A. L; Fernandez, R; Malnic, G.
Título: Cl- and regulation of pH by MDCK-C11 cells
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;40(5):687-696, May 2007. graf, tab.
Idioma: en.
Projeto: FAPESP; . CNPq.
Resumo: The interaction between H+ extrusion via H+-ATPase and Cl- conductance was studied in the C11 clone of MDCK cells, akin to the intercalated cells of the collecting duct. Cell pH (pHi) was measured by fluorescence microscopy using the fluorescein-derived probe BCECF-AM. Control recovery rate measured after a 20 mM NH4Cl acid pulse was 0.136 ± 0.008 pH units/min (dpHi/dt) in Na+ Ringer and 0.032 ± 0.003 in the absence of Na+ (0 Na+). With 0 Na+ plus the Cl- channel inhibitor NPPB (10 æM), recovery was reduced to 0.014 ± 0.001 dpHi/dt. 8-Br-cAMP, known to activate CFTR Cl- channels, increased dpHi/dt in 0 Na+ to 0.061 ± 0.009 and also in the presence of 46 nM concanamycin and 50 æM Schering 28080. Since it is thought that the Cl- dependence of H+-ATPase might be due to its electrogenic nature and the establishment of a +PD (potential difference) across the cell membrane, the effect of 10 æM valinomycin at high (100 mM) K+ was tested in our cells. In Na+ Ringer, dpHi/dt was increased, but no effect was detected in 0 Na+ Ringer in the presence of NPPB, indicating that in intact C11 cells the effect of blocking Cl- channels on dpHi/dt was not due to an adverse electrical gradient. The effect of 100 æM ATP was studied in 0 Na+ Ringer solution; this treatment caused a significant inhibition of dpHi/dt, reversed by 50 æM Bapta. We have shown that H+-ATPase present in MDCK C11 cells depends on Cl- ions and their channels, being regulated by cAMP and ATP, but not by the electrical gradient established by electrogenic H+ transport.
Descritores: Canais de Cloreto/metabolismo
ATPases Translocadoras de Prótons/metabolismo
-Linhagem Celular
Células Clonais
Fluoresceínas
Corantes Fluorescentes
Concentração de Íons de Hidrogênio
Microscopia de Fluorescência
Limites: Animais
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Texto completo SciELO Chile
Texto completo
Id: lil-437377
Autor: Riquelme, Gloria.
Título: Apical Maxi-chloride channel from human placenta: 12 years after the first electrophysiological recordings
Fonte: Biol. Res;39(3):437-445, 2006.
Idioma: en.
Projeto: Fondo Nacional de Desarrollo Científico y Tecnológico.
Resumo: The Maxi-chloride channel was the first ion channel described by electrophysiological methods in placenta. Because it is difficult to access a complex epithelium such as the placenta for electrophysiological procedures, the studies of ion channels from placental membranes have been performed only very recently. It was only in 1993 that a direct demonstration of a high-conductance chloride channel in apical membranes of intact trophoblastic epithelium was mentioned, and two years later, the description of this channel was reported from purified placental apical membranes reconstituted into artificial lipid membranes suitable for patch-clamp recordings. This brief review comments on the work done with regard to the electrophysiological characterization and regulation of the large-conductance or "Maxi" chloride channel and its contribution to the development of a cellular model for syncytiotrophoblast ion transport.
Descritores: Canais de Cloreto/metabolismo
Potenciais da Membrana/fisiologia
Placenta/metabolismo
Trofoblastos/metabolismo
-Eletrofisiologia
Transporte de Íons
Técnicas de Patch-Clamp
Placenta/fisiologia
Limites: Feminino
Humanos
Gravidez
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: lil-305196
Autor: Battaglini, Yamila; Fernández, Roxana; Marcano, Durvin; Hutton, Brenda.
Título: Líquidos y electrolitos en la nutrición parenteral en pediatría / Liquids and electrolyte in the parenteral nutrition in pediatric
Fonte: Bol. Hosp. Niños J. M. de los Ríos;36(1):21-23, ene.-abr. 2000. tab.
Idioma: es.
Resumo: El mayor componente de la nutrición parenteral total(NPT) se encuentra representado por el agua y los electrolitos dos elementos esenciales para la vida. El agua se encuentra distribuida en el cuerpo humano en dos grandes compartamientos: intracelular y extracelular, este último se divide en tres espacios: plasmático, intersticial-linfático y transcelular (líquido cefalorraquídeo, intestinal y renal). Contribuye al 80 por ciento del peso corporal total del prematuro, al 70 por ciento del recién nacido a término y aproximadamente al 60 por ciento en el adulto. La disminución se debe a la sustitución del agua por grasa a medida que crece el individuo. Así tenemos que la concentración del agua corporal total en el recién nacido sufre un descenso de 3 a 5 por ciento en los primeros tres a cinco días de vida, alcanzando los valores del adulto al año de edad
Descritores: Canais de Cloreto
Eletrólitos
Líquido Intracelular/fisiologia
Nutrição Parenteral
Potássio
Sódio
Água
-Medicina
Pediatria
Venezuela
Limites: Humanos
Masculino
Feminino
Recém-Nascido
Tipo de Publ: Relatos de Casos
Responsável: VE1.1 - Biblioteca Humberto Garcia Arocha



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