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December 2-4, 2019

Instituto Ferreyra, Friuli 2434, CP 5016, Córdoba Capital, Argentina

WORKSHOP

“The neurohumoral control of body fluid and cardiovascular homeostasis in males and females - vive la difference!

 

Córdoba, Argentina,  2-4 December 2019

REGISTRATION 

To register for the meeting please send the following information to this e-mail (workshopcba2019@gmail.com).

*Please note that it is requested that you send the registration information by November 25th, 2019. This is very important for the organization of the event.

 

Register information:

Name

Affiliation

Country

E-mail

Occupation (PI/ senior researcher/postdoctoral/young researcher/graduate student/

undergraduate student)

 

There will be an abstract submission fee of 20 US$ or Argentinean equivalent pesos in the case you are participating in the poster sessions.

This payment will be charged AT THE REGISTRATION DESK AFTER ARRIVAL TO THE Meeting. If you want to be selected for  "The Young Investigators Talks" please indicate this in the final of your abstract.

 

Local Organizer: Dr. Laura Vivas, Dr. Ximena Caeiro and Dr. Andrea Godino (Instituto de Investigación Médica Mercedes y Martin  Ferreyra, Fac. cs Ex. Fis. y Nat. UNC, Córdoba, Argentina.)

Foreign Organizer: Dr. Professor David Murphy (University of Bristol, Faculty of Medicine, Bristol, United Kingdom.

 

Location: Auditory of the Instituto de Investigación Médica M. y M. Ferreyra, Friuli 2434 (o Friuli esquina Finochietto), Barrio Parque Vélez Sarsfield,  

5016 - Córdoba, Córdoba, Argentina

Support: BBSRC, Mincyt-Cba, SECyT.

Description of Event:

The Workshop, which will take place over 3 days in early December in Cordoba, Argentina, will be organised by The Instituto de Investigación Médica Mercedes y Martin Ferreyra, a non-profit organization dedicated to scientific research and the development of scientific and technical human resources in medical science http://www.institutoferreyra.org/

Prof David Murphy (UK main Lead) and Prof Laura Vivas (local main Lead), proposed a Workshop that will cement the formation of a collaborative network that will apply state-of-the art molecular genetic and genomic technologies to study sex differences in cardiovascular diseases.

The Workshop will include a combination of lectures given by experts, followed by posters sessions, and round tables, giving the opportunity to the participants to design a new approach addressing their individual/collaborative research projects.  The estimated number of attendees is approximately 80 among researchers, posdoctoral students and young researchers. The goal of these discussions is not only to provide understanding of how to design and use modern molecular tools, but also provide novel insight into integrative physiology of the cardiovascular sexual differences during health and disease. Our collaborative network will advance understanding of the mechanisms underlying normal physiology and their homeostatic control or the genesis of pathophysiology with a view to improving human health and wellbeing across the life-course.

Men and women are different, not only in rates of cardiovascular disease, but also in terms of symptoms and risk factors, but studies on females have lagged behind those on males. We will address the sources of physiological disparity between sexes, in particular the contribution of the genetic and sex chromosome factors, with a view to designing sex-tailored therapeutic strategies.

Cardiovascular diseases are the leading cause of death in both men and women, but there are significant differences in the incidence, etiology, and outcomes of the disease between the genders. Whilst awareness of the importance of sex differences in cardiovascular disease has increased of late, much of what we know about cardiovascular regulation has been derived from studies in males, and lessons learnt in males do not necessarily apply to females. In addition, the impact of uniquely female characteristics and physiological activities (oestrous cycle, pregnancy, lactation, menopause) on cardiovascular health are not well understood. For example, hypertension is less prevalent in young women compared with young men, but menopausal women are at greater risk for hypertension compared with men of similar age. Despite these risks, women do not consistently receive first line treatment for the early stages of hypertension, and the greater morbidity in menopause reflects this neglect.

But why are male and female different? For a long time, it was assumed that male female differences were completely determined by gonadal hormonal actions. In most of the cases, XX females developed a masculine phenotype when they were treated with testosterone whilst XY males showed a feminine phenotype when the effects of testosterone were blocked. However in the late 80's, it was shown that some dimorphic phenotypes appeared before gonadal differentiation and thus could not be explained as the solely result of sex hormones actions. Rather, it was recognised that sex chromosome complement itself is important. Some X and Y genes act in a sex-specific manner on the gonads and other tissues to cause sex differences in XX and XY cells. Thus, the genetic and/or hormone pathways could, thus, act independently or interact (synergistically/ antagonistically) in modulating sexual dimorphic development.

The renin angiotensin system (RAS) and the vasopressinergic systems are involved in blood pressure and hydroelectrolyte balance control with clear sex differences in cardiovascular parameters in males and females. Clinical and basic findings demonstrate major sex differences in the way males and females respond to stimulation and inhibition of the RAS under physiological and pathophysiological circumstances. Although sex hormones (activational effects) are known to directly interact with RAS, the potential contribution of organizational hormonal and SCC effects on physiological sex-based differences in the regulation of the RAS and vasopressin remains undefined. It is, however, tempting to speculate that genes residing in the sex chromosomes may serve as regulators of sexually dimorphic cardiovascular phenotypes. We will thus assess whether sex-related genetic and transcriptomic differences may differentially modulate sexually dimorphic  cardiovascular outcomes.

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