Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria. - Wikidata - awgldk - TriplyDB

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

http://www.wikidata.org/entity/Q37494655

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Pregnancy as a critical window for blood pressure regulation in mother and child: programming and reprogramming.Nephron number and its determinants in early life: a primer.A best practice position statement on pregnancy in chronic kidney disease: the Italian Study Group on Kidney and Pregnancy.Developmental Origins and Nephron Endowment in Hypertension Type 1 diabetes, diabetic nephropathy, and pregnancy: a systematic review and meta-study.Intrinsic Age-Dependent Changes and Cell-Cell Contacts Regulate Nephron Progenitor Lifespan.Low Birth Weight due to Intrauterine Growth Restriction and/or Preterm Birth: Effects on Nephron Number and Long-Term Renal Health.Developmental programming of hypertension and kidney disease Extra-uterine renal growth in preterm infants: oligonephropathy and prematurity Renal consequences of preterm birth.Hypertensive pregnancy disorders and future renal disease.Birth weight, malnutrition and kidney-associated outcomes--a global concern.Fetal programming of chronic kidney disease: the role of maternal smoking, mitochondrial dysfunction, and epigenetic modfification.Programming of Essential Hypertension: What Pediatric Cardiologists Need to Know.Nephron number, hypertension, and CKD: physiological and genetic insight from humans and animal models.Is late-preterm birth a risk factor for hypertension in childhood?Fully Automated Evaluation of Total Glomerular Number and Capillary Tuft Size in Nephritic Kidneys Using Lightsheet Microscopy.Indomethacin administered early in the postnatal period results in reduced glomerular number in the adult rat.Cardiovascular dysfunction in adult mice following postnatal intermittent hypoxia.Exposure to famine in early life and chronic kidney diseases in adulthood.Prematurity and future kidney health: the growing risk of chronic kidney disease.Increased renal apoptosis and reduced renin-angiotensin system in fetal growth restriction.Developmental origins of health and adult disease: what should neonatologists/paediatricians be considering about the long-term health of their patients?Developmental Programming of Renal Function and Re-Programming Approaches.

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P2860

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

http://www.wikidata.org/entity/Q37494655

description

2011 nî lūn-bûn

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

@yue

2011年學術文章

@zh

2011年學術文章

@zh-hant

name

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@en

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@nl

type

label

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@en

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@nl

prefLabel

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@en

Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@nl

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J.TRSL.2011.10.004

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Translational Research

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Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.

@en

P2093

Alexandra Lerch-Gaggl

http://www.w3.org/2001/XMLSchema#string

Asraf El-Meanawy

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Cary Stelloh

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David L Mattson

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Kenneth P Allen

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Sreenivas Reddy

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P2860

Murine homolog of SALL1 is essential for ureteric bud invasion in kidney development

Very preterm birth is a risk factor for increased systolic blood pressure at a young adult age.

SALL1 mutations in Townes-Brocks syndrome and related disorders.

Mutation of PAX2 in two siblings with renal-coloboma syndrome.

Nephron number in patients with primary hypertension.

Screening for albuminuria identifies individuals at increased renal risk

The developmental origins of adult disease.

Very low birth weight is a risk factor for secondary focal segmental glomerulosclerosis.

Deficiency in Six2 during prenatal development is associated with reduced nephron number, chronic renal failure, and hypertension in Br/+ adult mice

Is low birth weight an antecedent of CKD in later life? A systematic review of observational studies.

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10.1016/J.TRSL.2011.10.004

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2

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2011-11-08T00:00:00Z

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arterial hypertension

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