Relevant bibliographies by topics / Diabetes insípida - Gene AVP (Arginine vasopressin)

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Academic literature on the topic 'Diabetes insípida - Gene AVP (Arginine vasopressin)'

Author: Grafiati
Published: 10 September 2021
Last updated: 29 July 2025

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Journal articles on the topic "Diabetes insípida - Gene AVP (Arginine vasopressin)"

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Nagasaki, H., H. Yokoi, H. Arima, et al. "Overexpression of vasopressin in the rat transgenic for the metallothionein-vasopressin fusion gene." Journal of Endocrinology 173, no. 1 (2002): 35–44. http://dx.doi.org/10.1677/joe.0.1730035.

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Arginine vasopressin (AVP) is a major antidiuretic hormone, the overproduction of which causes diluting hyponatremia in humans and is called the syndrome of inappropriate antidiuresis (SIAD). To study physiological changes resulting from AVP overproduction and to develop an animal model of hyponatremia, the human AVP gene was expressed under the control of the metallothionein promoter in transgenic (Tg) rats. Analyses of AVP immunoreactivity (irAVP) in the tissues revealed that the transgene is expressed mainly in the central nervous system. Gel filtration showed that irAVP in the brain and pl
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Kakiya, Satoshi, Hiroshi Arima, Hisashi Yokoi, Takashi Murase, Yuko Yambe, and Yutaka Oiso. "Effects of acute hypotensive stimuli on arginine vasopressin gene transcription in the rat hypothalamus." American Journal of Physiology-Endocrinology and Metabolism 279, no. 4 (2000): E886—E892. http://dx.doi.org/10.1152/ajpendo.2000.279.4.e886.

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We investigated the baroregulation of arginine vasopressin (AVP) gene transcription in the supraoptic (SON) and paraventricular nuclei (PVN) in conscious rats by use of intronic in situ hybridization. Hemorrhage of 16 ml/kg body wt decreased mean arterial pressure (MAP) by 57% and increased both plasma AVP (control, 1.2 ± 0.3 pg/ml; 16 ml/kg body wt, 38.9 ± 3.2 pg/ml) at 10 min and AVP heteronuclear (hn)RNA levels (SON, 150%; PVN, 140% of control values) at 20 min. On the other hand, hemorrhage of 7 ml/kg body wt had no significant effect on MAP, plasma AVP, or the AVP hnRNA levels. To better
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Feldkamp, Lara L. I., Elke Kaminsky, Tina Kienitz, and Marcus Quinkler. "Central Diabetes Insipidus Caused by Arginine Vasopressin Gene Mutation: Report of a Novel Mutation and Review of Literature." Hormone and Metabolic Research 52, no. 11 (2020): 796–802. http://dx.doi.org/10.1055/a-1175-1307.

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AbstractFamilial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant hereditary disorder characterized by severe polydipsia and polyuria that usually presents in early childhood. In this study, we describe a new arginine vasopressin (AVP) gene mutation in an ethnic German family with FNDI and provide an overview of disease-associated AVP-gene mutations that are already described in literature. Three members of a German family with neurohypophyseal diabetes insipidus were studied. Isolated DNA from peripheral blood samples was used for mutation analysis by sequencing the whole c
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Nicholson, H. D., A. J. Smith, S. D. Birkett, P. A. Denning-Kendall, and B. T. Pickering. "Two vasopressin-like peptides in the pig testis?" Journal of Endocrinology 117, no. 3 (1988): 441–46. http://dx.doi.org/10.1677/joe.0.1170441.

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ABSTRACT Vasopressin (VP)-like immunoreactivity (IR) has been located in the testes of several species of mammal. There is evidence that most of this IR in the rat does not represent authentic arginine vasopressin (AVP) and that a second AVP-like peptide may exist. We have studied testis samples from the pig, which produces lysine vasopressin (LVP) in its pituitary, and have found both LVP- and AVP-like IR. High-performance liquid chromatography (HPLC) of testis extracts showed two peaks of VP-IR. The first peak co-eluted with authentic LVP and was recognized only by antisera which cross-react
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Kim, J. K., S. N. Summer, W. M. Wood, J. L. Brown, and R. W. Schrier. "Arginine vasopressin secretion with mutants of wild-type and Brattleboro rats AVP gene." Journal of the American Society of Nephrology 8, no. 12 (1997): 1863–69. http://dx.doi.org/10.1681/asn.v8121863.

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Defects in peptide processing are associated with several disorders, including central diabetes insipidus (CDI). In the Brattleboro (BB) rat with CDI, the mRNA and protein of arginine vasopressin (AVP) are present in the hypothalamus, but no circulating AVP is detectable, thus suggesting a processing defect. The present study examined AVP secretion in cultured COS cells transfected with various constructs from wild-type and mutated Brattleboro AVP gene precursors. The precursor contains three exons encoding for vasopressin (VP), neurophysin (NP), and glycopeptide (GP). The Brattleboro rat has
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Marzocchi, Carlotta, Silvia Cantara, Alfonso Sagnella, Maria Grazia Castagna, and Marco Capezzone. "Autosomal dominant familial neurohypophyseal diabetes insipidus caused by a novel missense mutation in AVP gene in a large Italian kindred." Endocrine 74, no. 1 (2021): 188–92. http://dx.doi.org/10.1007/s12020-021-02830-x.

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Abstract Purpose Familial neurohypophysial diabetes insipidus (FNDI), commonly caused by autosomal dominant arginine vasopressin (AVP) mutations, is a rare condition in which vasopressin fails in regulating body’s level of water with final polyuria and polydipsia. Genetic testing in familial cases of FNDI should be carry out to ensure adequate treatments and avoid disease manifestations especially in infants. Methods In this study, we investigated three-generations of a large Italian family with clinical diagnosis of familial central diabetes insipidus for the presence of potential pathogenic
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Melo, Maria Edna de, Suemi Marui, Vinícius Nahime de Brito, Marcio Corrêa Mancini, Berenice B. Mendonca, and Mirta Knoepfelmacher. "Autosomal dominant familial neurohypophyseal diabetes insipidus caused by a novel mutation in arginine-vasopressin gene in a Brazilian family." Arquivos Brasileiros de Endocrinologia & Metabologia 52, no. 8 (2008): 1272–76. http://dx.doi.org/10.1590/s0004-27302008000800011.

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Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare autosomal dominant disorder characterized by polyuria and polydipsia due to deficiency of arginine vasopressin (AVP). More than 50 mutations causing adFNDI have been already reported in the AVP gene. The aim of the present study is to analyze the AVP gene in four generations of one Brazilian kindred with adFNDI. The proband was a 31-year old female with huge hypotonic polyuria (10 L/day) dated from childhood. Molecular analysis included amplification of all exons and exon-intron regions of the AVP gene by PCR an
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Ma, X.-M., A. Levy, and S. L. Lightman. "Rapid changes in heteronuclear RNA for corticotrophin-releasing hormone and arginine vasopressin in response to acute stress." Journal of Endocrinology 152, no. 1 (1997): 81–89. http://dx.doi.org/10.1677/joe.0.1520081.

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Abstract The rapid detection of gene activation is important for our understanding of gene regulation. We have therefore studied heteronuclear (i.e. nascent) RNA (hnRNA) by using 35S-labelled corticotrophin-releasing hormone (CRH) riboprobes and arginine vasopressin (AVP) oligonucleotide probes directed against intronic and exonic sequences of both CRH and AVP transcripts for in situ hybridization studies of transcriptional changes during acute stress. CRH and AVP intronic signals (found in newly synthesized transcripts) were confined to the nuclei of the parvocellular cells in the paraventric
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Vargas-Poussou, R., L. Forestier, M. D. Dautzenberg, P. Niaudet, M. Déchaux, and C. Antignac. "Mutations in the vasopressin V2 receptor and aquaporin-2 genes in 12 families with congenital nephrogenic diabetes insipidus." Journal of the American Society of Nephrology 8, no. 12 (1997): 1855–62. http://dx.doi.org/10.1681/asn.v8121855.

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Congenital nephrogenic diabetes insipidus (CNDI) is a rare inherited disorder characterized by renal tubular insensitivity to the antidiuretic effect of arginine vasopressin (AVP). In a large majority of the cases, nephrogenic diabetes insipidus is an X-linked recessive disorder caused by mutations in the AVP V2 receptor gene (AVPR2). In the remaining cases, the disease is autosomal recessive or dominant and, for these patients, mutations in the aquaporin 2 gene (AQP2) have been reported. Fourteen probands belonging to 12 families were analyzed by single-strand conformational polymorphism and
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10

Pak, Toni R., Wilson C. J. Chung, Laura R. Hinds та Robert J. Handa. "Arginine vasopressin regulation in pre- and postpubertal male rats by the androgen metabolite 3β-diol". American Journal of Physiology-Endocrinology and Metabolism 296, № 6 (2009): E1409—E1413. http://dx.doi.org/10.1152/ajpendo.00037.2009.

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Arginine vasopressin (AVP) is a nonapeptide expressed in several brain regions. In addition to its well-characterized role in osmoregulation, AVP regulates paternal behavior, aggression, circadian rhythms, and the stress response. In the bed nucleus of the stria terminalis (BST), AVP gene expression is tightly regulated by gonadal steroid hormones. However, the degree by which AVP is regulated by gonadal steroid hormones in the suprachiasmatic nucleus (SCN) and medial amygdala (MeA) is unclear. Previous studies have shown that AVP expression in the brain of gonadectomized rats is restored with
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Dissertations / Theses on the topic "Diabetes insípida - Gene AVP (Arginine vasopressin)"

1

Hedrich, Christian Michael, Agnieszka Zachurzok-Buczynska, Aneta Gawlik, et al. "Autosomal Dominant Neurohypophyseal Diabetes Insipidus in Two Families." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-134493.

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Background: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare disease with symptoms of polydipsia, polyuria and dehydration caused by arginine vasopressin deficiency. Disease onset is within infancy or adolescence. A variety of disease-causing mutations of the arginine vasopressin neurophysin II gene (AVP) on chromosome 20p13 have been described. Methods: Two Polish families with adFNDI were screened for mutations. Processing of wild-type (WT) and mutant AVP was monitored using immunocytochemical methods in stably transfected Neuro2A cells. AVP secretion into t
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2

Hedrich, Christian Michael, Agnieszka Zachurzok-Buczynska, Aneta Gawlik, et al. "Autosomal Dominant Neurohypophyseal Diabetes Insipidus in Two Families: Molecular Analysis of the Vasopressin-Neurophysin II Gene and Functional Studies of Three Missense Mutations." Karger, 2009. https://tud.qucosa.de/id/qucosa%3A27572.

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Background: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare disease with symptoms of polydipsia, polyuria and dehydration caused by arginine vasopressin deficiency. Disease onset is within infancy or adolescence. A variety of disease-causing mutations of the arginine vasopressin neurophysin II gene (AVP) on chromosome 20p13 have been described. Methods: Two Polish families with adFNDI were screened for mutations. Processing of wild-type (WT) and mutant AVP was monitored using immunocytochemical methods in stably transfected Neuro2A cells. AVP secretion into t
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3

Francisco, Ângela Sofia Fernandes Alves. "Identification of genetic mutations in patients with familial central diabetes insipidus." Master's thesis, 2012. http://hdl.handle.net/10400.6/3266.

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Diabetes insipidus (DI) is associated with defects that involve the secretion and the action of hormone arginine vasopressin (AVP) resulting in the excretion of abnormally large volumes of diluted urine. The most common defect that results in disease development is the deficient secretion of the hormone AVP and the disease is referred to as central or neurohypophyseal DI. The AVP hormone is synthesized in magnocellular neurons, that originate in the supraoptic and paraventricular nuclei of the hypothalamus and are projected to neurohypophysis, and the destruction of these neurons leads to a de
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