scholarly journals Developmental regulation of cardiovascular function is dependent on both genotype and environment

2009 ◽  
Vol 297 (6) ◽  
pp. H2234-H2241 ◽  
Author(s):  
Brian S. Knight ◽  
Nana Sunn ◽  
Craig E. Pennell ◽  
S. Lee Adamson ◽  
Stephen J. Lye
Keyword(s):  
Cardiovascular Disease ◽  
Arterial Pressure ◽  
Complex Traits ◽  
Developmental Regulation ◽  
Control Diet ◽  
Cardiovascular Function ◽  
Mouse Strains ◽  
Nutrient Restriction ◽  
Genetic Dissection ◽  
Age Range

Adverse developmental environments can increase the risk of adult cardiovascular disease, but not all individuals are affected, suggesting the importance of genotype. Genetically distinct mouse strains allow the genetic dissection of complex traits; however, they have not been used to evaluate the developmental origins of adult cardiovascular disease. Our objective was to determine the effect of prenatal nutrient restriction (R) on adult cardiovascular function in A/J (AJ) and C57BL/6J (B6) mice and whether a postnatal high-fat (HF) diet exacerbates these effects. Pregnant AJ and B6 mice underwent a 30% R or ad libitum diet, and their offspring underwent a HF or control diet. Hypertension (+17 mmHg; P < 0.001) was observed in B6R mice at 9 wk, and their arterial pressure tended to remain high at 25 wk (+13 mmHg; not significant). In AJR mice, the normal decrement in arterial pressure over this age range in this strain was abolished. Heart rate prematurely increased in B6R and decreased in AJR (all; P < 0.05) mice from 9 to 25 wk. There was no effect of postnatal HF diet on these relationships. The Tei index (from a 26-wk microultrasound) was increased in both AJR and B6R mice (all; P < 0.05), suggesting an improved global myocardial performance. Neither R nor HF alone changed diastolic (ratio of E wave to A wave) or systolic (%fractional shortening) function in either strain; however, R and HE combined improved diastolic function in B6 ( P < 0.05) but not in AJ mice. Therefore, there are strain-dependent alterations in adult cardiovascular function in response to prenatal nutrient restriction. Unexpectedly, a postnatal HF diet did not exacerbate the effects of prenatal nutrient restriction on postnatal cardiovascular outcomes.

Production of congenic mouse strains carrying NOD-derived diabetogenic genetic intervals: An approach for the genetic dissection of complex traits

1996 ◽  
Vol 7 (5) ◽  
pp. 331-334 ◽  
Author(s):  
M. A. Yui ◽  
K. Muralidharan ◽  
B. Moreno-Altamirano ◽  
G. Perrin ◽  
K. Chestnut ◽  
...  
Keyword(s):  
Complex Traits ◽  
Congenic Mouse ◽  
Mouse Strains ◽  
Genetic Dissection ◽  
Congenic Mouse Strains

scholarly journals Reciprocal F1 hybrids of two inbred mouse strains reveal parent-of-origin and perinatal diet effects on behavior and expression

2018 ◽  
Author(s):  
Daniel Oreperk ◽  
Sarah A Schoenrock ◽  
Rachel McMullan ◽  
Robin Ervin ◽  
Joseph Farrington ◽  
...  
Keyword(s):  
Complex Traits ◽  
Detection System ◽  
Inbred Mouse ◽  
F1 Hybrids ◽  
Hybrid Population ◽  
Psychiatric Disease ◽  
Mouse Strains ◽  
Imprinted Genes ◽  
F1 Hybrid ◽  
Parent Of Origin

ABSTRACTParent-of-origin effects (POEs) in mammals typically arise from maternal effects or from imprinting. Mutations in imprinted genes have been associated with psychiatric disorders, as well as with changes in a handful of animal behaviors. Nonetheless, POEs on complex traits such as behavior remain largely uncharacterized. Furthermore, although perinatal environmental exposures, such as nutrient deficiency, are known to modify both behavior and epigenetic effects generally, the architecture of environment-by-POE is almost completely unexplored. To study POE and environment-by-POE, we employ a relatively neglected but maximally powerful POE-detection system: a reciprocal F1 hybrid population. We exposed female NOD/ShiLtJxC57Bl/6J and C57Bl/6JxNOD/ShiLtJ mice, in utero, to one of four different diets, then after weaning recorded their whole-brain gene expression, as well as a set of behaviors that model psychiatric disease. Microarray expression data revealed an imprinting-enriched set of over a dozen genes subject to POE; the POE on the most significantly affected gene, Carmil1 (a.k.a. Lrrc16a), was validated using qPCR in the same and in a new set of mice. Several behaviors, especially locomotor behaviors, also showed POE. Interestingly, Bayesian mediation analysis suggests Carmil1 expression suppresses behavioral POE, and Airn suppresses POE on Carmil1 expression. A significant diet-by-POE was observed on one behavior, one imprinted gene, and over a dozen non-imprinted genes. Beyond our particular results, our study demonstrates a reciprocal F1 hybrid framework for studying POE and environment-by-POE on behavior.

scholarly journals High-level Exposure of Uric Acid in Asymptomatic Hyperuricemia Could Be An Isolated Risk Factors of Cardio-Cerebrovascular Diseases: A Prospective Cohort Study

2021 ◽  
Author(s):  
Zhiyuan Cheng ◽  
Tongzhang Zheng ◽  
Desheng Zhang ◽  
Jingli Yang ◽  
Xiaobin Hu ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Uric Acid ◽  
Cox Regression ◽  
Cerebrovascular Diseases ◽  
Healthy Population ◽  
Incidence Risk ◽  
High Level ◽  
Age Range ◽  
Fourth Quartile

Abstract Background: Whether the asymptomatic hyperuricemia (AH) raises the risk of cardiovascular disease with or without hyperuricemia-related comorbidities still remains contentious. Our study was aimed to quantitatively access the incidence risk of coronary heart disease (CHD) and stroke associated with AH.Methods: Multivariate-adjusted Cox regression models were applied to evaluate the risk of cardiovascular disease (CVD). Serum uric acid beyond normouricemia was quarterly stratified based on the distribution of healthy population without CVD onset.Results: 1,062 CVD first attack cases were collected among the 48,001 cohort participants (age range: 18-92, mean age: 47.2±13.9 years-old) with a mean follow-up duration of 5.78±0.83 years. 14,464 baseline population with comorbidities were excluded to further study the association between AH and CVD incidence. The AH showed overall non-association with CVD incident. However, significantly increased adjusted hazard ratio (HR) of CVD with 95% confidence interval (CI) were observed when the fourth quartile compared with normouricemia stratum in the total cohort population (CHD: 1.70, 1.34-2.16; stroke: 1.55, 1.13-2.13), male (CHD: 1.94, 1.47-2.56), female (CHD: 1.71, 1.03-2.35; stroke: 2.02, 1.14-3.58) and aged over 50 years-old population. Meanwhile, the age-standardized incidence rate of CVD in the fourth quartile was 2 to 3 time higher than the normouricemia population. Consistent results were also observed in the AH population in absence of comorbidities (CHD: 2.40, 1.39-4.14; stroke: 1.85, 1.12-3.59).Conclusion: Asymptomatic hyperuricemia patients exposed to higher level of uric acid (male>487 mmol/L, female>422 mmol/L) could significantly increase the incidence risk of CHD and stroke, with or without hyperuricemia-related comorbidities.

T WAVE CONTOUR IN THE PRECORDIAL LEADS DURING CHILDHOOD

PEDIATRICS ◽  
1951 ◽  
Vol 7 (3) ◽  
pp. 400-407
Author(s):  
R. W. REYNOLDS
Keyword(s):  
Cardiovascular Disease ◽  
Young Adults ◽  
Cardiovascular System ◽  
Normal Children ◽  
Positive Wave ◽  
T Wave ◽  
Children And Young Adults ◽  
Transitional Forms ◽  
The Right ◽  
Age Range

The T wave in the precordial V leads was studied in 187 normal children and young adults in the age range of 2 weeks to 20 years and in 164 individuals of like age with cardiovascular disease or with disease or medication capable of affecting the cardiovascular system. On the basis of this analysis correlated with a survey of the literature, it is concluded that: a. An upright T wave in lead V2 or leads further to the right should be considered abnormal in children between 2 weeks and 9 years of age until proved otherwise. b. The normal sequence in the direction of the T wave from V4R to V6 is from a negative to a positive wave with transitional forms which may be notched or diphasic. The reversal of this pattern is to be considered abnormal. c. The presence of unexpected T wave contours in specific leads at the different ages should be considered as evidence demanding re-examination of the ECG and of the child for abnormalities.

Ovine fetal adrenal gland and cardiovascular function

1988 ◽  
Vol 254 (4) ◽  
pp. R706-R710 ◽  
Author(s):  
N. D. Ray ◽  
C. S. Turner ◽  
N. M. Rawashdeh ◽  
J. C. Rose
Keyword(s):  
Heart Rate ◽  
Adrenal Gland ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Cardiovascular Function ◽  
Late Gestation ◽  
Arterial Blood ◽  
Significant Difference ◽  
Ovine Fetus ◽  
Ovine Fetal

Given the necessity of the adrenal gland in maintaining cardiovascular function in adults of various species, these experiments were conducted to determine if fetal bilateral adrenalectomy results in altered resting heart rate, hypotension, and decreased basal blood volume as well as a diminished ability of the fetus to maintain arterial pressure and restore blood volume in response to hemorrhage. We studied heart rate, arterial blood pressure, and blood volume changes in response to hemorrhage of 20% of blood volume at 2%/min in seven adrenalectomized and six intact chronically cannulated unanesthetized lambs between 119 and 133 days of gestation. Blood volumes and percent restitution of shed volume were determined using 51Cr-tagged red blood cells and changes in hematocrit. There was no significant difference between groups in basal heart rate, mean arterial pressure, hematocrit, and blood volume. The two groups were similar to hemorrhage-induced changes in these and restitution of volume. Therefore, fetal adrenal glands are not necessary for basal cardiovascular function or regulation subsequent to moderate hemorrhage in the late gestation ovine fetus.

scholarly journals Mouse Age Matters: How Age Affects the Murine Plasma Metabolome

Metabolites ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 472
Author(s):  
Patrick Pann ◽  
Martin Hrabě de Angelis ◽  
Cornelia Prehn ◽  
Jerzy Adamski
Keyword(s):  
Age Differences ◽  
Early Adulthood ◽  
High Variability ◽  
Developmental Changes ◽  
Mouse Strains ◽  
Targeted Metabolomics ◽  
Age Related ◽  
Plasma Metabolome ◽  
Metabolite Profiles ◽  
Age Range

A large part of metabolomics research relies on experiments involving mouse models, which are usually 6 to 20 weeks of age. However, in this age range mice undergo dramatic developmental changes. Even small age differences may lead to different metabolomes, which in turn could increase inter-sample variability and impair the reproducibility and comparability of metabolomics results. In order to learn more about the variability of the murine plasma metabolome, we analyzed male and female C57BL/6J, C57BL/6NTac, 129S1/SvImJ, and C3HeB/FeJ mice at 6, 10, 14, and 20 weeks of age, using targeted metabolomics (BIOCRATES AbsoluteIDQ™ p150 Kit). Our analysis revealed high variability of the murine plasma metabolome during adolescence and early adulthood. A general age range with minimal variability, and thus a stable metabolome, could not be identified. Age-related metabolomic changes as well as the metabolite profiles at specific ages differed markedly between mouse strains. This observation illustrates the fact that the developmental timing in mice is strain specific. We therefore stress the importance of deliberate strain choice, as well as consistency and precise documentation of animal age, in metabolomics studies.

scholarly journals Postnatal Enalapril to Improve Cardiovascular Function Following Preterm Preeclampsia (PICk-UP):

Hypertension ◽  
2020 ◽  
Vol 76 (6) ◽  
pp. 1828-1837 ◽  
Author(s):  
Laura Ormesher ◽  
Suzanne Higson ◽  
Matthew Luckie ◽  
Stephen A Roberts ◽  
Heather Glossop ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Randomized Controlled Trial ◽  
Controlled Trial ◽  
Global Longitudinal Strain ◽  
Cardiovascular Function ◽  
Left Ventricular ◽  
Targeted Interventions ◽  
Risk Of Death ◽  
Randomized Controlled ◽  
Multicenter Randomized Controlled Trial

Hypertensive disease in pregnancy is associated with future cardiovascular disease and, therefore, provides an opportunity to identify women who could benefit from targeted interventions aimed at reducing cardiovascular morbidity. This study focused on the highest-risk group, women with preterm preeclampsia, who have an 8-fold risk of death from future cardiovascular disease. We performed a single-center feasibility randomized controlled trial of 6 months’ treatment with enalapril to improve postnatal cardiovascular function. Echocardiography and hemodynamic measurements were performed at baseline (<3 days), 6 weeks, and 6 months postdelivery on 60 women. At randomization, 88% of women had diastolic dysfunction, and 68% had concentric remodeling/hypertrophy. No difference was seen in total vascular resistance ( P =0.59) or systolic function (global longitudinal strain: P =0.14) between groups at 6 months. However, women treated with enalapril had echocardiographic measurements consistent with improved diastolic function (E/E′[the ratio of early mitral inflow velocity and early mitral annular diastolic velocity]: P =0.04) and left ventricular remodeling (relative wall thickness: P =0.01; left ventricular mass index: P =0.03) at 6 months, compared with placebo. Urinary enalapril was detectable in 85% and 63% of women in the enalapril arm at 6 weeks and 6 months, respectively. All women responded positively to taking enalapril in the future. Our study confirmed acceptability and feasibility of the study protocol with a recruitment to completion rate of 2.2 women per month. Importantly, postnatal enalapril treatment was associated with improved echocardiographic measurements; these early improvements have the potential to reduce long-term cardiovascular disease risk. A definitive, multicenter randomized controlled trial is now required to confirm these findings. Registration— URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03466333.

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