Autologous endometrial cell co-culture improves human embryo development to high-quality blastocysts: a randomized controlled trial.

Research Question: Does autologous endometrial cell co-culture (AECC) improve the number of good-quality blastocysts obtained by IVF/intracytoplasmic sperm injection (ICSI), compared with conventional embryo culture medium in a broad group of patients referred to assisted reproductive technology (ART)?

Design: This interventional, randomized, double-blind study took place at Clinique Ovo from March 2013 to October 2015 and included 207 healthy patients undergoing an IVF or ICSI protocol, of which 71 were excluded before randomization. On the previous cycle, all participants underwent an endometrial biopsy at D5 to D7 post-ovulation, following which the endometrial cells were prepared for AECC.

Results: The data demonstrated that AECC significantly increased the incidence of good-quality blastocysts compared with culture in conventional media (42.

Retinoblastoma-associated protein 140 as a candidate for a novel etiological gene to hypertension.

Gene discovery in animal models may lead to the revelation of therapeutic targets for essential hypertension as well as mechanistic insights into blood pressure (BP) regulation. Our aim was to identify a disease-causing gene for a component of polygenic hypertension contrasting inbred hypertensive Dahl salt-sensitive (DSS) and normotensive Lewis rats. The chromosome segment harboring a quantitative trait locus (QTL), C16QTL, was first isolated from the rat genome via congenic strains.

Hypertension Suppression, Not a Cumulative Thrust of Quantitative Trait Loci, Predisposes Blood Pressure Homeostasis to Normotension.

Background: Genetics of high blood pressure (BP) has revealed causes of hypertension. The cause of normotension, however, is poorly understood. Inbred Lewis rats sustain normotension despite a genetic push in altering BP.

Modularization and epistatic hierarchy determine homeostatic actions of multiple blood pressure quantitative trait loci.

Hypertension, the most frequently diagnosed clinical condition world-wide, predisposes individuals to morbidity and mortality, yet its underlying pathological etiologies are poorly understood. So far, a large number of quantitative trait loci (QTLs) have been identified in both humans and animal models, but how they function together in determining overall blood pressure (BP) in physiological settings is unknown. Here, we systematically and comprehensively performed pair-wise comparisons of individual QTLs to create a global picture of their functionality in an inbred rat model.

Unique quantitative trait loci in synergy permanently improve diastolic dysfunction.

Background: Diastolic dysfunction often precedes the onset of diastolic heart failure. We previously demonstrated that diastolic dysfunction and left ventricular hypertrophy (LVH) in Dahl salt-sensitive rats can be ameliorated by quantitative trait loci (QTLs).

Methods: We analyzed cardiac phenotypes of 2 "single" congenic strains, C10S.

Combining distinctive and novel loci doubles BP reduction, reverses diastolic dysfunction and mitigates LV hypertrophy.

Objectives: Diastolic dysfunction often represents the onset of diastolic heart failure (DHF). We previously showed in principle that diastolic function in Dahl salt-sensitive rats (DSS) can be genetically determined by quantitative trait loci (QTLs) that also modulate blood pressure (BP).

Methods: We analyzed cardiac phenotypes of four 'single' congenic strains by echocardiography, in which a specific DSS chromosome segment was replaced by its normotensive Lewis homologue.

α-Kinase 2 is a novel candidate gene for inherited hypertension in Dahl rats.

Objectives: The interval harboring a quantitative trait locus for blood pressure (BP), C18QTL3, contains β-2 adrenergic receptor (Adrb2) and neural precursor cell expressed, developmentally downregulated 4-like (Nedd4l) genes. None of the other genes in the C18QTL3-residing interval is known to affect BP. The identification of C18QTL3 might uncover a brand new gene that could prosper into a novel diagnostic and/or therapeutic target for essential hypertension, if neither Adrb2 nor Nedd4l could be upheld as candidate genes.

Normotension in Lewis and Dahl salt-resistant rats is governed by different genes.

Objectives: Inbred rodent models simulating essential hypertension and normotension are useful tools in discovering genes controlling blood pressure (BP) homeostasis. An analysis of a F2 population made from crosses of hypertensive Dahl salt-sensitive (DSS) and normotensive Lewis rats did not detect a BP quantitative trait locus (QTL) on chromosome 7 (Chr 7). However, false negativity could not be excluded.