Literature DB >> 7814859

Short report: HYPERGENE: a clinical and genetic database for genetic analysis of human hypertension.

A Charru1, X Jeunemaitre, F Soubrier, P Corvol, G Chatellier.   

Abstract

OBJECTIVE: Genetic studies of essential human hypertension require the recording and management of numerous data concerning multiple hypertensive families. The present report describes a new family database, HYPERGENE, and demonstrates its potential usefulness in such a complex disease.
METHODS: The database was implemented on an Apple Macintosh computer using the 4TH DIMENSION software program. Through a user-friendly interface, it offers a high-quality data record, easy data retrieval and compatibility with other software. PATIENTS: HYPERGENE contains a prospective collection of 187 families with at least two hypertensive sibs (826 subjects). Each subject was analysed according to the same protocol. To allow definition of clinical and biological phenotypes and genetic analysis, clinical and biological data were recorded and, at the same time, plasma, urine and DNA libraries were stored.
RESULTS: Probands were 50.6 years old with an early onset (39.1 years of age) of hypertension (157.7/97.8 mmHg); 125 had moderate-to-severe hypertension. According to our selection criteria, only one out of 187 sibships had familial dislipidaemic hypertension. Of the living fathers, 45% were examined, and 54% of the living mothers: 48.6% had an onset of hypertension before age 50 years. Children (mean age 28.7 years) of hypertensive sibs presented a high percentage of hypertension (8.3%).
CONCLUSION: The HYPERGENE database facilitates data storage and analysis on familial hypertension, and should prove a useful tool for assessing molecular biology results in the field of hypertension and for allowing collaborative research.

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Year:  1994        PMID: 7814859

Source DB:  PubMed          Journal:  J Hypertens        ISSN: 0263-6352            Impact factor:   4.844


  3 in total

1.  Haplotypes of angiotensinogen in essential hypertension.

Authors:  X Jeunemaitre; I Inoue; C Williams; A Charru; J Tichet; M Powers; A M Sharma; A P Gimenez-Roqueplo; A Hata; P Corvol; J M Lalouel
Journal:  Am J Hum Genet       Date:  1997-06       Impact factor: 11.025

Review 2.  Pathologic consequences of increased angiotensin II activity.

Authors:  C M Ferrario; J M Flack
Journal:  Cardiovasc Drugs Ther       Date:  1996-11       Impact factor: 3.727

3.  KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron.

Authors:  Hélène Louis-Dit-Picard; Julien Barc; Daniel Trujillano; Stéphanie Miserey-Lenkei; Nabila Bouatia-Naji; Olena Pylypenko; Geneviève Beaurain; Amélie Bonnefond; Olivier Sand; Christophe Simian; Emmanuelle Vidal-Petiot; Christelle Soukaseum; Chantal Mandet; Françoise Broux; Olivier Chabre; Michel Delahousse; Vincent Esnault; Béatrice Fiquet; Pascal Houillier; Corinne Isnard Bagnis; Jens Koenig; Martin Konrad; Paul Landais; Chebel Mourani; Patrick Niaudet; Vincent Probst; Christel Thauvin; Robert J Unwin; Steven D Soroka; Georg Ehret; Stephan Ossowski; Mark Caulfield; Patrick Bruneval; Xavier Estivill; Philippe Froguel; Juliette Hadchouel; Jean-Jacques Schott; Xavier Jeunemaitre
Journal:  Nat Genet       Date:  2012-03-11       Impact factor: 38.330

  3 in total

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