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  1. Article ; Online: ¿Hay variantes genéticas que puedan modificar el curso de la pandemia por COVID-19?

    Azurmendi, Pablo J

    Medicina

    2020  Volume 80 Suppl 3, Page(s) 79–81

    Title translation Are there genetic variants that can modify the course of the COVID-19 pandemic?
    MeSH term(s) Angiotensin-Converting Enzyme 2 ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/genetics ; Humans ; Immunity, Cellular ; Pandemics ; Peptidyl-Dipeptidase A/genetics ; Pneumonia, Viral/genetics ; SARS-CoV-2
    Chemical Substances Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Keywords covid19
    Language Spanish
    Publishing date 2020-07-04
    Publishing country Argentina
    Document type Editorial
    ZDB-ID 411586-7
    ISSN 1669-9106 ; 0025-7680 ; 0325-951X
    ISSN (online) 1669-9106
    ISSN 0025-7680 ; 0325-951X
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  2. Article ; Online: Premio Nobel en Fisiología o Medicina 2022.

    Azurmendi, Pablo J / Lüthy, Isabel A

    Medicina

    2022  Volume 82, Issue 6, Page(s) 978–980

    Title translation Nobel Prize in Physiology or Medicine 2022.
    MeSH term(s) Humans ; Nobel Prize ; Medicine ; Physiology/history
    Language Spanish
    Publishing date 2022-12-26
    Publishing country Argentina
    Document type Editorial
    ZDB-ID 411586-7
    ISSN 1669-9106 ; 0025-7680 ; 0325-951X
    ISSN (online) 1669-9106
    ISSN 0025-7680 ; 0325-951X
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  4. Article ; Online: Are there genetic variants that can modify the course of the COVID-19 pandemic?

    Pablo J. Azurmendi

    Medicina (Buenos Aires), Vol 80, Iss Suppl 3, Pp 79-

    2020  Volume 81

    Keywords Medicine ; R ; Immunologic diseases. Allergy ; RC581-607 ; Infectious and parasitic diseases ; RC109-216 ; covid19
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Fundación Revista Medicina
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Premio Nobel en Química 2015. Mecanismos de reparación del ADN, desde las bacterias a los tumores.

    Azurmendi, Pablo J

    Medicina

    2016  Volume 76, Issue 3, Page(s) 183–186

    Title translation Nobel Prize in Chemistry 2015. DNA repair mechanisms, from bacteria to tumors.
    MeSH term(s) Bacteria ; Chemistry ; DNA Repair ; History, 20th Century ; Humans ; Neoplasms ; Nobel Prize
    Language Spanish
    Publishing date 2016-06-13
    Publishing country Argentina
    Document type Editorial ; Historical Article ; Comment
    ZDB-ID 411586-7
    ISSN 1669-9106 ; 0025-7680 ; 0325-951X
    ISSN (online) 1669-9106
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  6. Article ; Online: Role of Female Sex Hormones and Immune Response in Salt-Sensitive Hypertension Development: Evidence from Experimental Models.

    Vlachovsky, Sandra G / Di Ciano, Luis A / Oddo, Elisabet M / Azurmendi, Pablo J / Silberstein, Claudia / Ibarra, Fernando R

    Current hypertension reports

    2023  Volume 25, Issue 11, Page(s) 405–419

    Abstract: Purposeof review: Female sex hormones have systemic effects unrelated to their reproductive function. We describe experiences of different research groups and our own, on aspects related to the importance of female sex hormones on blood pressure (BP) ... ...

    Abstract Purposeof review: Female sex hormones have systemic effects unrelated to their reproductive function. We describe experiences of different research groups and our own, on aspects related to the importance of female sex hormones on blood pressure (BP) regulation and salt-sensitivity-mediated BP response and salt sensitivity without alterations in BP, as well as renal sodium handling and interactions with the immune system.
    Recent findings: Changes in sodium intake in normotensive premenopausal women cause more BP variations than in men. After menopause, women often develop arterial hypertension (HT) with a profile of sodium sensitivity. Besides, experimental results have shown that in adult rat models resembling the postmenopausal hormonal state induced by ovariectomy, controlling BP is not enough to avoid renal and other tissue infiltration with immune cells, which does not occur when sodium intake is low or normal. Therefore, excess sodium promotes an inflammatory state with the involvement of immune cells. The evidence of activation of adaptive immunity, besides changes in T cell subpopulations, includes changes in sodium transporters and receptors. More studies are needed to evaluate the particular sodium sensitivity of women and its meaning. Changes in lifestyle and sodium intake reduction are the main therapeutic steps. However, to face the actual burden of salt-sensitive HT in postmenopausal women and its associated inflammatory/immune changes, it seems reasonable to work on immune cell activity by considering the peripheral blood mononuclear cell phenotypes of molecules and transport proteins related to sodium handle, both to screen for and treat cell activation.
    Language English
    Publishing date 2023-09-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2057367-4
    ISSN 1534-3111 ; 1522-6417
    ISSN (online) 1534-3111
    ISSN 1522-6417
    DOI 10.1007/s11906-023-01257-1
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  7. Article ; Online: NCoA3 upregulation in breast cancer‑associated adipocytes elicits an inflammatory profile.

    Lira, María Cecilia / Rosa, Francisco D / Aiello, Ignacio / Machado, Mileni Soares / Palma, Alejandra G / Paz, Leonardo / Güemes, María Cecilia Salazar / Burlando, Silvia / Azurmendi, Pablo J / Paladino, Natalia / Costas, Mónica A / Rubio, María Fernanda

    Oncology reports

    2023  Volume 49, Issue 5

    Abstract: Nuclear receptor coactivator 3 (NCoA3) is a transcriptional coactivator of NF‑κB and other factors, which is expressed at relatively low levels in normal cells and is amplified or overexpressed in several types of cancer, including breast tumors. NCoA3 ... ...

    Abstract Nuclear receptor coactivator 3 (NCoA3) is a transcriptional coactivator of NF‑κB and other factors, which is expressed at relatively low levels in normal cells and is amplified or overexpressed in several types of cancer, including breast tumors. NCoA3 levels have been shown to be decreased during adipogenesis; however, its role in tumor‑surrounding adipose tissue (AT) remains unknown. Therefore, the present study assessed the modulation of NCoA3 in breast cancer‑associated adipocytes and evaluated its association with the expression of inflammatory markers. 3T3‑L1 adipocytes were stimulated with conditioned medium from human breast cancer cell lines and the expression levels of NCoA3 were evaluated by reverse transcription‑quantitative (q)PCR. NF‑κB activation was measured by immunofluorescence, and tumor necrosis factor and monocyte chemoattractant protein 1 levels were analyzed by qPCR and dot blot assays. The results obtained from the
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Adipocytes/metabolism ; Breast Neoplasms/pathology ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Nuclear Receptor Coactivator 3/genetics ; Nuclear Receptor Coactivator 3/metabolism ; Up-Regulation ; 3T3-L1 Cells
    Chemical Substances NCOA3 protein, human (EC 2.3.1.48) ; NF-kappa B ; Nuclear Receptor Coactivator 3 (EC 2.3.1.48) ; Ncoa3 protein, mouse (EC 2.3.1.48)
    Language English
    Publishing date 2023-04-07
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 1222484-4
    ISSN 1791-2431 ; 1021-335X
    ISSN (online) 1791-2431
    ISSN 1021-335X
    DOI 10.3892/or.2023.8542
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  8. Article ; Online: Las hormonas femeninas en fisiología renal. Sensibilidad a la sal y regulación de la proliferación epitelial.

    Vlachovsky, Sandra G / Sánchez, Daiana S / Di Ciano, Luis A / Oddo, Elisabet M / Azurmendi, Pablo J / Silberstein, Claudia / Ibarra, Fernando R

    Medicina

    2020  Volume 80, Issue 2, Page(s) 157–161

    Abstract: Female sex hormones participate in the regulation of blood pressure and renal epithelial proliferation, effects not related to their reproductive function. About one-third of the world's population has abnormally high levels of blood pressure, ... ...

    Title translation Female hormones in renal physiology. Salt sensitivity and regulation of epithelial proliferation.
    Abstract Female sex hormones participate in the regulation of blood pressure and renal epithelial proliferation, effects not related to their reproductive function. About one-third of the world's population has abnormally high levels of blood pressure, hypertension, which is responsible for almost 50% of deaths from stroke and coronary heart disease. Salt sensitivity is a risk factor for cardiovascular morbidity and mortality and other diseases as well. We reported a model of salt sensitive hypertension in adult ovariectomized (oVx) Wistar rats. oVx rats are normotensive under normal salt intake (NS, 0.24% NaCl), but upon a high salt intake (HS, 1% NaCl) oVx rats developed a blood pressure profile of salt-sensitive hypertension. Our studies on kidney molecules related to sodium balance found that the circuit dopamine D1-like receptor, cytochrome P450 4A and Na+, K+-ATPase is altered by the absence of ovary hormones which is accompanied by a reduced ability to excrete sodium. In oVx rats HS intake also promotes changes in the expression of proteins related to sodium transport in peripheral blood mononuclear cells, mainly peripheral lymphocytes. Therefore, sodium transport is modified at several levels of normal physiology. Lately, we described that estradiol increases the rate of renal epithelial cell proliferation in primary cultures developed from human renal cortex. Thus, salt sensitivity, adaptive immunity, blood pressure and renal cell proliferation are complex biological responses regulated by female sex hormones.
    MeSH term(s) Animals ; Blood Pressure ; Cell Proliferation ; Estradiol/metabolism ; Female ; Humans ; Hypertension/metabolism ; Hypertension/physiopathology ; Kidney/metabolism ; Rats ; Rats, Wistar ; Sodium Chloride/adverse effects ; Sodium Chloride/metabolism ; Sodium-Potassium-Exchanging ATPase
    Chemical Substances Sodium Chloride (451W47IQ8X) ; Estradiol (4TI98Z838E) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
    Language Spanish
    Publishing date 2020-04-13
    Publishing country Argentina
    Document type Journal Article
    ZDB-ID 411586-7
    ISSN 1669-9106 ; 0025-7680 ; 0325-951X
    ISSN (online) 1669-9106
    ISSN 0025-7680 ; 0325-951X
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  9. Article ; Online: Ovariectomy and high salt increase blood pressure and alter sodium transport proteins in peripheral blood mononuclear cells of adult Wistar rats.

    Vlachovsky, Sandra G / Di Ciano, Luis A / Oddo, Elisabet M / Azurmendi, Pablo J / Goette, Nora P / Arrizurieta, Elvira E / Silberstein, Claudia / Ibarra, Fernando R

    Experimental physiology

    2021  Volume 106, Issue 10, Page(s) 2107–2123

    Abstract: New findings: What is the central question of this study? In a model of salt-sensitive hypertension in ovariectomized (oVx) adult Wistar rats, what is the expression of proteins related to sodium transport in peripheral blood mononuclear cells (PBMCs), ... ...

    Abstract New findings: What is the central question of this study? In a model of salt-sensitive hypertension in ovariectomized (oVx) adult Wistar rats, what is the expression of proteins related to sodium transport in peripheral blood mononuclear cells (PBMCs), and how does the response of proteins to high sodium intake compare with changes in blood pressure in intact female rats? What is the main finding and its importance? Sodium transport proteins in PBMCs react to high sodium and blood pressure markedly differently in oVx versus intact female rats. Protein expression shows sodium and pressure sensitivity. Renal immune cells increase in oVx under high salt.
    Abstract: Hypertension is a worldwide public health problem. High sodium consumption is associated with hypertension, and hypertensive mechanisms involve immunity cells. Peripheral blood mononuclear cells (PBMCs) are endowed with proteins related to sodium transport. We studied their abundance in PBMCs from intact (IF) or ovariectomized (oVx) adult Wistar rats under normal (NS) or high (HS) salt intake. Ovariectomy was performed at 60 days of life. At 145 days, one group of IF and oVx rats received NS or HS intake for 5 days. Another group of IF HS and oVx HS rats received hydralazine (HDZ) to reduce blood pressure (BP). Sodium balance and BP were recorded. Expression of Na
    MeSH term(s) Animals ; Blood Pressure/physiology ; Carrier Proteins ; Female ; Humans ; Hypertension ; Leukocytes, Mononuclear/metabolism ; Ovariectomy ; Rats ; Rats, Wistar ; Sodium/metabolism ; Sodium Chloride, Dietary/metabolism ; Sodium-Potassium-Exchanging ATPase
    Chemical Substances Carrier Proteins ; Sodium Chloride, Dietary ; Sodium (9NEZ333N27) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
    Language English
    Publishing date 2021-08-17
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1016295-1
    ISSN 1469-445X ; 0958-0670
    ISSN (online) 1469-445X
    ISSN 0958-0670
    DOI 10.1113/EP089553
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  10. Article ; Online: Estradiol stimulates cell proliferation via classic estrogen receptor-alpha and G protein-coupled estrogen receptor-1 in human renal tubular epithelial cell primary cultures.

    Sánchez, Daiana S / Fischer Sigel, Lilian K / Azurmendi, Pablo J / Vlachovsky, Sandra G / Oddo, Elisabet M / Armando, Inés / Ibarra, Fernando R / Silberstein, Claudia

    Biochemical and biophysical research communications

    2019  Volume 512, Issue 2, Page(s) 170–175

    Abstract: This work was aimed to determine the effect of 17β-estradiol (17βE) on cell proliferation in human renal tubular epithelial cells (HRTEC) isolated from kidneys from pediatric subjects, as well as the role of estrogen receptors involved in the 17βE ... ...

    Abstract This work was aimed to determine the effect of 17β-estradiol (17βE) on cell proliferation in human renal tubular epithelial cells (HRTEC) isolated from kidneys from pediatric subjects, as well as the role of estrogen receptors involved in the 17βE proliferative response. Treatment with 17βE (10 nmol/L, 24 h) significantly stimulated cell proliferation, measured by 5-bromo-2-deoxyuridine (BrdU) uptake, in HRTEC primary cultures and in tubular structures obtained by 3D cultured-HRTEC. Incubation of HRTEC with the G protein-coupled estrogen receptor 1 (GPER-1) agonist G-1 increased BrdU uptake. Incubation of HRTEC with 17βE activated the classic estrogen receptor alpha (ERα) but not ERβ. Treatment of HRTEC with the GPER-1 antagonist G-15, the ER inhibitor ICI182,780, or the β-catenin inhibitor iCRT14, completely abrogated the increase in BrdU uptake induced by 17βE. We also show that 17βE stimulated β-catenin protein expression and translocation to the nucleus of HRTEC, effects that were abrogated by G-15 and ICI 182,780. In conclusion, estradiol stimulates cell proliferation in HRTEC primary cultures through both ERα and GPER-1 estrogen receptors and involves β-catenin activation.
    MeSH term(s) Cell Proliferation ; Cells, Cultured ; Child ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Humans ; Kidney Tubules/cytology ; Kidney Tubules/metabolism ; Receptors, Estrogen/metabolism ; Receptors, G-Protein-Coupled/metabolism
    Chemical Substances ESR1 protein, human ; Estrogen Receptor alpha ; GPER1 protein, human ; Receptors, Estrogen ; Receptors, G-Protein-Coupled ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2019-03-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2019.03.056
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