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  1. AU="Arribas, Silvia Magdalena"
  2. AU=Edry Efrat
  3. AU="James B. McCauley"
  4. AU="Offringa, Ite A"
  5. AU="Sakso, Salima Ahriz"
  6. AU="Huang, Zexiang"
  7. AU="Feleke, Sindew M"
  8. AU="van der Velden, Janielle"
  9. AU="Carmen Gonzalez"
  10. AU="Cheah, Jaime H"
  11. AU="Forte, Florence"
  12. AU="Anika Nier"
  13. AU="Bar, Adi"
  14. AU="Alvarado Pinedo, María F."
  15. AU="Scarlett, Garry"
  16. AU="Carlos G. Vanoye"
  17. AU=Lohrmann Jens
  18. AU="Petersen, Moritz"
  19. AU="Giovanni, L."
  20. AU="Liu, Xingzheng"
  21. AU="Głód, Mateusz"
  22. AU=Teo Kelvin Yi Chong
  23. AU="Khatmi, Aysan"
  24. AU="Erculiani, M"
  25. AU="Olivier Lortholary"
  26. AU="Lisnic, Vanda Juranic"
  27. AU="Seabloom, Eric W"
  28. AU="Odvina, Clarita V"
  29. AU="Singh, Inderbir"
  30. AU="Wonoh Lee"
  31. AU="Nelson, Warrick"
  32. AU="Douglas, David N"
  33. AU="King, Gary"
  34. AU="Barbera, Lauren"
  35. AU="Carlino, Antonio"
  36. AU="Shan, Qing-Hua"
  37. AU="Starko, S"
  38. AU="Lievre, Loïc"
  39. AU=Cammack N
  40. AU="Xia, Qin"
  41. AU="Ong, Ju Lynn"
  42. AU="Cullin, Christophe"
  43. AU="Georg K.S. Andersson"
  44. AU="Jeannel, Gaël-François"
  45. AU="Stuart Woods"
  46. AU="Shchegolev, A."
  47. AU="Nadeau, Pierre-Louis"
  48. AU="Gordon, David E A"
  49. AU="Shahid Mahmood"
  50. AU="Rosenblatt, Karin"
  51. AU="Dasgupta, Suvankar"
  52. AU=Nguyen Sylvain AU=Nguyen Sylvain

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  1. Artikel ; Online: Fetal programming and lactation: modulating gene expression in response to undernutrition during intrauterine life.

    Monedero Cobeta, Ignacio / Gomez Bris, Raquel / Rodríguez-Rodríguez, Pilar / Saez, Angela / Quintana-Villamandos, Begoña / González Granado, Jose Maria / Arribas, Silvia Magdalena

    Pediatric research

    2024  

    Abstract: Background: Adverse environmental conditions during intrauterine life, known as fetal programming, significantly contribute to the development of diseases in adulthood. Fetal programming induced by factors like maternal undernutrition leads to low birth ...

    Abstract Background: Adverse environmental conditions during intrauterine life, known as fetal programming, significantly contribute to the development of diseases in adulthood. Fetal programming induced by factors like maternal undernutrition leads to low birth weight and increases the risk of cardiometabolic diseases.
    Methods: We studied a rat model of maternal undernutrition during gestation (MUN) to investigate gene expression changes in cardiac tissue using RNA-sequencing of day 0-1 litters. Moreover, we analyzed the impact of lactation at day 21, in MUN model and cross-fostering experiments, on cardiac structure and function assessed by transthoracic echocardiography, and gene expression changes though qPCR.
    Results: Our analysis identified specific genes with altered expression in MUN rats at birth. Two of them, Agt and Pparg, stand out for being associated with cardiac hypertrophy and fibrosis. At the end of the lactation period, MUN males showed increased expression of Agt and decreased expression of Pparg, correlating with cardiac hypertrophy. Cross-fostering experiments revealed that lactation with control breastmilk mitigated these expression changes reducing cardiac hypertrophy in MUN males.
    Conclusions: Our findings highlight the interplay between fetal programming, gene expression, and cardiac hypertrophy suggesting that lactation period is a potential intervention window to mitigate the effects of fetal programming.
    Impact: Heart remodeling involves the alteration of several groups of genes and lactation period plays a key role in establishing gene expression modification caused by fetal programming. We could identify expression changes of relevant genes in cardiac tissue induced by undernutrition during fetal life. We expose the contribution of the lactation period in modulating the expression of Agt and Pparg, relevant genes associated with cardiac hypertrophy. This evidence reveal lactation as a crucial intervention window for preventing or countering fetal programming.
    Sprache Englisch
    Erscheinungsdatum 2024-02-07
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 4411-8
    ISSN 1530-0447 ; 0031-3998
    ISSN (online) 1530-0447
    ISSN 0031-3998
    DOI 10.1038/s41390-024-03042-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Maintenance over Time of the Effect Produced by Esmolol on the Structure and Function of Coronary Arteries in Hypertensive Heart Diseases.

    Martín-Oropesa, Raquel / Rodríguez-Rodríguez, Pilar / Pazó-Sayós, Laia / Arnalich-Montiel, Ana / Arribas, Silvia Magdalena / González, Maria Carmen / Quintana-Villamandos, Begoña

    Antioxidants (Basel, Switzerland)

    2022  Band 11, Heft 10

    Abstract: We previously observed that esmolol treatment for 48 h reduced vascular lesions in spontaneously hypertensive rats (SHRs). Therefore, we investigated whether this beneficial effect is persistent after withdrawal. Fourteen-month-old SHRs (SHR-Es) were ... ...

    Abstract We previously observed that esmolol treatment for 48 h reduced vascular lesions in spontaneously hypertensive rats (SHRs). Therefore, we investigated whether this beneficial effect is persistent after withdrawal. Fourteen-month-old SHRs (SHR-Es) were treated with esmolol (300 μg/kg/min) or a vehicle for 48 h. Two separate groups were also given identical treatment, but they were then monitored for a further 1 week and 1 month after drug withdrawal. We analyzed the geometry and composition of the coronary artery, vascular reactivity and plasma redox status. Esmolol significantly decreased wall thickness (medial layer thickness and cell count), external diameter and cross-sectional area of the artery, and this effect persisted 1 month after drug withdrawal. Esmolol significantly improved endothelium-dependent relaxation by ACh (10
    Sprache Englisch
    Erscheinungsdatum 2022-10-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11102042
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling.

    Vieira-Rocha, Maria Sofia / Rodriguez-Rodriguez, Pilar / Ferreira-Duarte, Mariana / Faria, Miguel / Sousa, Joana Beatriz / Morato, Manuela / Arribas, Silvia Magdalena / Diniz, Carmen

    International journal of molecular sciences

    2022  Band 23, Heft 3

    Abstract: Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal ... ...

    Abstract Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT
    Mesh-Begriff(e) Animals ; Blood Pressure ; Female ; Fetal Development ; Fetal Nutrition Disorders/physiopathology ; Male ; Maternal Nutritional Physiological Phenomena ; Mesenteric Arteries/metabolism ; Mesenteric Arteries/pathology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1/genetics ; Receptor, Angiotensin, Type 1/metabolism ; Receptor, Angiotensin, Type 2/genetics ; Receptor, Angiotensin, Type 2/metabolism ; Renin-Angiotensin System ; Vascular Remodeling
    Chemische Substanzen Receptor, Angiotensin, Type 1 ; Receptor, Angiotensin, Type 2
    Sprache Englisch
    Erscheinungsdatum 2022-01-22
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23031233
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Dronedarone induces regression of coronary artery remodeling related to better global antioxidant status.

    Quintana-Villamandos, Begoña / Pazó-Sayós, Laia / Arribas, Silvia Magdalena / Rodríguez-Rodríguez, Pilar / Böger, Rainer H / Lüneburg, Nicole / Delgado-Baeza, Emilio / González, Maria Carmen

    Hypertension research : official journal of the Japanese Society of Hypertension

    2019  Band 42, Heft 10, Seite(n) 1485–1494

    Abstract: Our group previously demonstrated that dronedarone induces regression of left ventricular hypertrophy in spontaneously hypertensive rats (SHRs). We assessed changes in vascular remodeling and oxidative stress following short-term use of this agent. The ... ...

    Abstract Our group previously demonstrated that dronedarone induces regression of left ventricular hypertrophy in spontaneously hypertensive rats (SHRs). We assessed changes in vascular remodeling and oxidative stress following short-term use of this agent. The coronary artery was isolated from 10-month-old male SHRs treated with 100 mg kg
    Mesh-Begriff(e) Animals ; Antioxidants/metabolism ; Arginine/analogs & derivatives ; Arginine/blood ; Coronary Vessels/drug effects ; Coronary Vessels/pathology ; Coronary Vessels/physiology ; Dronedarone/pharmacology ; Male ; Nitric Oxide/physiology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Vascular Remodeling/drug effects ; Vasoconstriction/drug effects
    Chemische Substanzen Antioxidants ; Nitric Oxide (31C4KY9ESH) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Dronedarone (JQZ1L091Y2)
    Sprache Englisch
    Erscheinungsdatum 2019-04-16
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1175297-x
    ISSN 1348-4214 ; 0916-9636
    ISSN (online) 1348-4214
    ISSN 0916-9636
    DOI 10.1038/s41440-019-0257-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 3898: Hefte anzeigen Standort:
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  5. Artikel ; Online: Impaired inhibitory function of presynaptic A1-adenosine receptors in SHR mesenteric arteries.

    Rocha-Pereira, Carolina / Arribas, Silvia Magdalena / Fresco, Paula / González, Maria Carmen / Gonçalves, Jorge / Diniz, Carmen

    Journal of pharmacological sciences

    2013  Band 122, Heft 2, Seite(n) 59–70

    Abstract: In hypertension, vascular reactivity alterations have been attributed to numerous factors, including higher sympathetic innervation/adenosine. This study examined the modulation of adenosine receptors on vascular sympathetic nerves and their putative ... ...

    Abstract In hypertension, vascular reactivity alterations have been attributed to numerous factors, including higher sympathetic innervation/adenosine. This study examined the modulation of adenosine receptors on vascular sympathetic nerves and their putative contribution to higher noradrenaline spillover in hypertension. We assessed adenosine receptors distribution in the adventitia through confocal microscopy, histomorphometry, and their regulatory function on electrically-evoked [(3)H]-noradrenaline overflow, using selective agonists/antagonists. We found that: i) A1-adenosine receptor agonist (CPA: 100 nM) inhibited tritium overflow to a lower extent in SHR (25% ± 3%, n = 14) compared to WKY (38% ± 3%, n = 14) mesenteric arteries; ii) A2A-adenosine receptor agonist (CGS 21680: 100 nM) induced a slight increase of tritium overflow that was similar in SHR (22% ± 8%, n = 8) and WKY (24% ± 5%, n = 8) mesenteric arteries; iii) A2B- and A3-adenosine receptors did not alter tritium overflow in either strain; iv) all adenosine receptors were present on mesenteric artery sympathetic nerves and/or some adventitial cells of both strains; and v) A1-adenosine receptor staining fractional area was lower in SHR than in WKY mesenteric arteries. We conclude that there is an impaired inhibitory function of vascular presynaptic A1-adenosine receptors in SHR, likely related to a reduced presence of these receptors on sympathetic innervation, which might lead to higher levels of noradrenaline in the synaptic cleft and contribute to hypertension in this strain.
    Mesh-Begriff(e) Animals ; Hypertension/etiology ; Hypertension/metabolism ; Male ; Mesenteric Arteries/innervation ; Mesenteric Arteries/metabolism ; Microscopy, Confocal ; Molecular Imaging ; Norepinephrine/metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptor, Adenosine A1/metabolism ; Receptor, Adenosine A1/physiology ; Sympathetic Nervous System/metabolism ; Synapses/metabolism ; Tritium/metabolism
    Chemische Substanzen Receptor, Adenosine A1 ; Tritium (10028-17-8) ; Norepinephrine (X4W3ENH1CV)
    Sprache Englisch
    Erscheinungsdatum 2013-06-05
    Erscheinungsland Japan
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2104264-0
    ISSN 1347-8648 ; 1347-8613
    ISSN (online) 1347-8648
    ISSN 1347-8613
    DOI 10.1254/jphs.12266fp
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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