José Pavı́a

Universidad de Málaga

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Elisa Martín‐Montañez

Universidad de Málaga

María García‐Fernández

Universidad de Málaga

Felipe Sánchez de la Cuesta

Universidad de Sevilla

Federica Boraldi

University of Modena and Reggio Emilia

Manuel Múñoz

Universidad de Málaga

Nadia Valverde

Universidad de Málaga

Francisco Martos Crespo

Universidad de Málaga

Estrella Lara

Universidad de Málaga

ÓF

Óscar Fernández

Universidad de Málaga

Susana Gómez‐Ramírez

Hospital Clínico Universitario Virgen de la Victoria

Cooperative Institutions

Universidad de Málaga

Instituto de Investigación Biomédica de Málaga

Instituto de Salud Carlos III

Hospital Regional Universitario de Málaga

Andalusian Centre for Nanomedicine and Biotechnology

Centro de Investigación Biomédica en Red

Hospital Clínico Universitario Virgen de la Victoria

Universidad Autónoma de Madrid

Consejo Superior de Investigaciones Científicas

Biomedical Research Networking Center on Neurodegenerative Diseases

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Insulin-like Growth Factor II Prevents MPP+ and Glucocorticoid Mitochondrial-Oxidative and Neuronal Damage in Dopaminergic Neurons

Antioxidants (2021)

Silvia Claros P. CABRERA Nadia Valverde Silvana Y. Romero-Zerbo Manuel Víctor López-González

Stress seems to contribute to Parkinson's disease (PD) neuropathology, probably by dysregulation of the hypothalamic-pituitary-adrenal axis. Key factors in this pathophysiology are oxidative stress and mitochondrial dysfunction and neuronal glucocorticoid-induced toxicity. The insulin-like growth factor II (IGF-II), a pleiotropic hormone, has shown antioxidant and neuroprotective effects in some neurodegenerative disorders. Our aim was to examine the protective effect of IGF-II on a dopaminergic cellular combined model of PD and mild to moderate stress measuring oxidative stress parameters, mitochondrial and neuronal markers, and signalling pathways. IGF-II counteracts the mitochondrial-oxidative damage produced by the toxic synergistic effect of corticosterone and 1-methyl-4-phenylpyridinium, protecting dopaminergic neurons from death and neurodegeneration. IGF-II promotes PKC activation and nuclear factor (erythroid-derived 2)-like 2 antioxidant response in a glucocorticoid receptor-dependent pathway, preventing oxidative cell damage and maintaining mitochondrial function. Thus, IGF-II is a potential therapeutic tool for treatment and prevention of disease progression in PD patients suffering mild to moderate emotional stress.

10.3390/antiox11010041

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Citations (7)

Molecular pharmacology of muscarinic receptor subtypes

N.J.M. Birdsall Edward C. Hulme Elisabetta Palazzi José Pavı́a Tracy A. Spalding

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Caracterización de receptores muscarínicos en células indiferenciadas tiroideas de ratas Fisher

Endocrinología y Nutrición (2009)

Francisco Botella Romero Elisa Martín‐Montañez Eugenio Gutierrez José Pavı́a

10.1016/s1575-0922(09)70839-3

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Platelet antiaggregatory effect of triflusal in human whole blood.

PubMed (1988)

J.P. De La Cruz José Pavı́a Inmaculada Bellido-Estévez María Carolina González F Sánchez de la Cuesta

An in vitro and ex vivo study has been made to determine the inhibition of platelet aggregation in human whole blood (WB) and platelet rich plasma by triflusal and its main metabolite HTB (2-hydroxy-4-trifluoromethylbenzoic acid). Triflusal was administered orally at 300 mg x 2/day, for 15 days, to 13 healthy volunteers (ex vivo tests). Triflusal and HTB, at concentrations lower than 1 mM, produced a significant inhibition of platelet aggregation induced by ADP (2.5 microM, final) and collagen (1 microgram/ml, final) in PRP, while about 50% inhibition was induced in WB samples at 0.12 mM. Ex vivo studies also revealed a stronger inhibitory effect of triflusal in WB samples against several inducers; differences were particularly pronounced against ADP (10.6 times more potent in WB). These results suggest an important role of red blood cells and/or leukocytes in the mechanism of action of triflusal. The antiplatelet effect of triflusal in WB was modified when incubated with HTB at therapeutic concentrations. The IC50 value against collagen increased from 82 to 140 microM with 37.5 microM HTB, but decreased in a dose-dependent manner when incubated with higher concentrations of HTB, suggesting that inhibition of platelet cyclooxygenase by HTB masks its negative interaction with triflusal.

Ex vivo

IC50

Bleeding time

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Citations (16)

Activation of muscarinic acetylcholine receptors induces Ca2+ mobilization in FRT cells

Cellular Signalling (2001)

Mercedes Montiel José Pavı́a Santo Marsigliante Eugenio Jiménez

Thapsigargin

Muscarinic agonist

10.1016/s0898-6568(01)00133-4

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Cost of post-operative intravenous iron therapy in total lower limb arthroplasty: a retrospective, matched cohort study.

PubMed (2014)

Manuel Múñoz Susana Gómez‐Ramírez Elisa Martín‐Montañez E. Naveira Javier García Seara

Requirements for allogeneic red cell transfusion after total lower limb arthroplasty are still high (20-50%), and post-operative intravenous iron has been shown to reduce transfusion requirements for this surgery. We performed a cost analysis to ascertain whether this alternative is also likely to be cost-effective.

10.2450/2013.0088-13

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Citations (40)

The cost of post-operative shed blood salvage after total knee arthroplasty: an analysis of 1,093 consecutive procedures.

PubMed (2013)

Manuel Múñoz Daniel Ariza Arturo Campos Elisa Martín‐Montañez José Pavı́a

Requirements for allogeneic red cell transfusion after total knee arthroplasty are still high (20-50%), and salvage and reinfusion of unwashed, filtered post-operative shed blood is an established method for reducing transfusion requirements following this operation. We performed a cost analysis to ascertain whether this alternative is likely to be cost-effective.

Autologous blood

Blood management

10.2450/2012.0139-12

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Citations (37)

Perioperative intravenous iron: an upfront therapy for treating anaemia and reducing transfusion requirements.

PubMed (2013)

Manuel Múñoz Susana Gómez‐Ramírez Elisa Martín‐Montañez José Pavı́a Jorge Cuenca

Perioperative anaemia, with iron deficiency being its leading cause, is a frequent condition among surgical patients, and has been linked to increased postoperative morbidity and mortality, and decreased quality of life. Postoperative anaemia is even more frequent and is mainly caused by perioperative blood loss, aggravated by inflammation-induced blunting of erythropoiesis. Allogenic transfusion is commonly used for treating acute perioperative anaemia, but it also increases the rate of morbidity and mortality in surgical and critically ill patients. Thus, overall concerns about adverse effects of both preoperative anaemia and allogeneic transfusion have prompted the review of transfusion practice and the search for safer and more biologically rational treatment options. In this paper, the role of intravenous iron therapy (mostly with iron sucrose and ferric carboxymaltose), as a safe and efficacious tool for treating anaemia and reducing transfusion requirements in surgical patients, as well as in other medical areas, has been reviewed. From the analysis of published data and despite the lack of high quality evidence in some areas, it seems fair to conclude that perioperative intravenous iron administration, with or without erythropoiesis stimulating agents, is safe, results in lower transfusion requirements and hastens recovery from postoperative anaemia. In addition, some studies have reported decreased rates of postoperative infection and mortality, and shorter length of hospital stay in surgical patients receiving intravenous iron.

Iron sucrose

10.3305/nh.2012.27.6.6087

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Citations (19)

“Patient blood management” en cirugía ortopédica

Revista Española de Cirugía Ortopédica y Traumatología (2015)

Fernando Alamillo Canillas Susana Gómez‐Ramírez José Antonio García‐Erce José Pavı́a A. Gómez‐Luque

Blood management

10.1016/j.recot.2014.11.005

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Citations (30)

Effects of chronic administration of S-adenosyl-l-methionine on brain oxidative stress in rats