Search Results - (Author, Cooperation:Y. Pinto)
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1Latest Papers from Table of Contents or Articles in PressStem cells. m6A mRNA methylation facilitates resolution of naive pluripotency toward differentiationS. Geula ; S. Moshitch-Moshkovitz ; D. Dominissini ; A. A. Mansour ; N. Kol ; M. Salmon-Divon ; V. Hershkovitz ; E. Peer ; N. Mor ; Y. S. Manor ; M. S. Ben-Haim ; E. Eyal ; S. Yunger ; Y. Pinto ; D. A. Jaitin ; S. Viukov ; Y. Rais ; V. Krupalnik ; E. Chomsky ; M. Zerbib ; I. Maza ; Y. Rechavi ; R. Massarwa ; S. Hanna ; I. Amit ; E. Y. Levanon ; N. Amariglio ; N. Stern-Ginossar ; N. Novershtern ; G. Rechavi ; J. H. Hanna
American Association for the Advancement of Science (AAAS)
Published 2015Staff ViewPublication Date: 2015-01-09Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Adenosine/*analogs & derivatives/metabolism ; Animals ; Blastocyst/enzymology ; Cell Differentiation/genetics/*physiology ; Cell Line ; Embryo Loss/genetics ; Epigenesis, Genetic ; Female ; Gene Knockout Techniques ; Male ; Methylation ; Methyltransferases/genetics/*physiology ; Mice ; Mice, Knockout ; Pluripotent Stem Cells/*cytology/enzymology ; RNA, Messenger/*metabolismPublished by: -
2Latest Papers from Table of Contents or Articles in PressStaff View
Publication Date: 2018-07-17Publisher: American Heart Association (AHA)Print ISSN: 1942-325XElectronic ISSN: 1942-3268Topics: MedicineKeywords: Genetics, Cardiomyopathy, Heart FailurePublished by: -
3Articles: DFG German National LicensesPinto, Y. M. ; van Veldhuisen, D. J. ; Tjon-Ka-Jie, R. T. ; Rooks, G. ; Netzer, T. ; Lie, K. I.
Springer
Published 1996Staff ViewISSN: 1432-1041Keywords: Key words Imidapril ; Angiotensin converting enzyme ; Heart failure; ACE inhibitor ; blood pressure ; circulating ACESource: Springer Online Journal Archives 1860-2000Topics: Chemistry and PharmacologyMedicineNotes: Abstract Objective: To study the haemodynamic profile and tolerability of imidapril, a new long-acting ACE inhibitor, and to investigate the effect of inhibition of circulating ACE on blood pressure in patients with stable chronic heart failure. Methods: Twenty-four patients with stable, chronic heart failure (New York Heart Association (NYHA) functional Class II–III) were randomised to receive either 2.5 mg or 5 mg imidapril. Other vasodilators were withheld for ≥ 5 half-lives. Blood pressure and ACE activity were carefully monitored for 24 h after dosing. Results: Both 2.5 mg and 5 mg imidapril decreased systolic blood pressure, while diastolic blood pressure fell only after 5 mg imidapril. The two doses produced a significant and similar inhibition of circulating (serum) ACE. No serious adverse effects were observed, although symptomatic hypotension occurred in 1 patient (5 mg). The decrease in blood pressure was not related to baseline ACE activity, serum sodium or serum creatinine concentration. Conclusions: Imidapril significantly lowered systolic blood pressure and was well tolerated. The difference in the first dose response to the two doses with respect to diastolic blood pressure suggests that this haemodynamic effect of ACE-inhibition is not related to inhibition of circulating ACE.Type of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesStaff View
ISSN: 1435-1803Keywords: Review-tissue renin-angiotensin systems ; heart failure ; experimental-clinicalSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract In this paper, we review the hypothesis that activated tissue renin-angiotensin systems play a detrimental role in heart failure. The main arguments for this idea are discussed: a) tissue renin-angiotensin systems behave functionally distinct from the circulating renin-angiotensin system; b) tissue renin-angiotensin systems are activated in heart failure; c) activated tissue renin-angiotensin systems induce cardiovascular dysfunction. Finally, this hypothesis predicts that optimal treatment in heart failure requires the inhibition of tissue renin-angiotensin systems. However, studies pertaining to this prediction are still lacking, particularly in human subjects.Type of Medium: Electronic ResourceURL: