Professor Rosaria Alvaro of our Department is pleased to announce that the Research Assistant for Nursing Sciences, Dr. Gianluca Pucciarelli, has been awarded with the American Heart Association’s “2017 CVSN Stroke Article of the Year Award”.
Following is the statement by Prof. Alvaro:
I am pleased to inform you that Dr. Gianluca Pucciarelli, Research Assistant for Nursing Sciences, is the winner of the American Heart Association's “2017 CVSN Stroke Article of the Year Award”. This is probably the first time an Italian nurse is awarded this prestigious prize.
The article to which the award refers is the following:
Pucciarelli G, Vellone E, Savini S, Simeone S, Ausili D, Alvaro R, Lee CS, Lyons KS. Roles of Changing Physical Function and Caregiver Burden on Quality of Life in Stroke: A Longitudinal Dyadic Analysis. Stroke 2017; 48: 733-739.
The study, result of an international collaboration between the Department of Nursing Science and the School of Nursing at Oregon Health & Science University, Portland, USA, enrolled a group of 226 pairs of stroke patients with their respective caregivers and followed them for one year with follows-up every three months. The data analysis, very innovative by making use for the first time of multilevel methodologies on the reference population, has revealed that the physical fitness of the patient and the caregiver's burden not only affect the individual's quality of life, respectively of the patient and the caregiver , but also the quality of life of the other member of the pair. In addition, the study has shown that depression of the patient negatively affects the caregiver's depression and vice versa, and that better educated and better-prepared caregivers are less exposed to the adverse effects of the healthcare burden.
As you know, the study was funded by the Center for Excellence for Culture and Nursing Research at the IPASVI College in Rome.
Dr. Pucciarelli will receive the award during the upcoming American Heart Association Congress, which will be held in Anaheim, California (USA), November 11-15, 2017.
(From the left) Francesca Gioia Klinger e Luisa Campagnolo, researchers of Histology and Embryology at the Tor Vergata University of Rome (Department of Biomedicine and Prevention), and Rocco Rago, head of the Centre for Sterility and Assisted Procreation of the Pertini Hospital in Rome
GENEVA – She has the contagious enthusiasm and the incredulity of those who cannot believe of having won, together with her group. One of the three scholars awarded with the Gfi (Grant for Fertility Innovation) 2017, an award wanted and funded by Merck, is the Italian group of Luisa Campagnolo, researcher of Histology and Embryology of the Tor Vergata University of Rome, and her colleague Francesca Gioia Klinger. They work in collaboration with the Centre for Sterility and Assisted Procreation of the Pertini Hospital in Rome, headed by Rocco Rago. A public centre, which deals with basic research.
IN THE USA - Graduated at Sapienza University in Rome, Campagnolo worked for four years at the Scripps Research Institute in San Diego where - she tells - she happened to meet Laureates or talk with Dulbecco, and where it was easy to say "I'm a scientist", without anyone laughing, as it happens in Italy. Later she is tempted by nostalgia and takes part in a competition for researchers in Rome, winning it. In 2004 she goes back home. "Because Italy is my country, and maybe because I had some more expectation. Then, I realized that in Italy public research really is almost zero."
THE PROJECT – The project she is winning today was born at Tor Vergata when Luisa decided to proceed as in the United States and let her students do all the material work – she teaches Biotechnology – rather than just telling it. Thus, she prepares a teaching laboratory, with the collaboration of Rocco Rago of Pertini hospital, and shows how they manipulate oocytes (mice), how they crioconserve gametes (male ones are human but discarded) and how they are evaluated. A real success. From this didactic collaboration comes the research project, aimed at studying the EGFL7, which she had begun studying in the United States. Behind the abbreviation is an angiogenesis regulator (which is therefore also studied in oncology) but Luisa is convinced that it can play an important role in reproduction as it is also implicated in placental development.
THE HYPOTESIS – And so – she supposes – why could EGFL7 not be important even for embryo implantation, the most problematic moment of assisted fertilization whose mechanisms are still ignored today? Rocco Rago defines it as a sort of "black hole", because the ways in which the embryo - once inserted into the uterus - converses with the endometrium are unknown. This is the most delicate instant, since up to 60% of the implants can fail. When embedded in the uterus, the embryo waits 48 to 72 hours before the implantation and perhaps it sends messages to the endometrium. Since in mice EGFL7 is released from the embryo shortly before implantation, could this not be how embryo and endometrium communicate?
THE FUTURE – This is a fascinating hypothesis that, if checked, could enable the detection of a factor responsible for the implant, and act on this in a specific way. Thus, unable to work in vivo for ethical problems, with the help of Pertini Hospital Tor Vergata's Obstetric Pathology (Carlo Ticconi) which will provide endometrial biopsies of women who suffer from recurrent abortions, Campagnolo and her team will study how the EGFL7 factor modulates the signal. "If, as we believe, this factor is important for uterine receptivity", said the researcher, "it may become a therapy target, perhaps even at a local level. We could speculate that a little quantity of EGLF7 brushed directly on the endometrium might promote implantation. By studying the moment when the embryo secretes this factor, it might be also possible to identify the right time for the transfer".
THE CELEBRATION – All this will happen in the next two years. Meanwhile - admits Campagnolo, who celebrated her birthday here in Geneva yesterday - this award was the most beautiful birthday present. "We have won and it has all happened in just a few months", she says, "and for me it is a great achievement." We had previously won another project of the Ministry of Health, but the funds came in after three years, and in the meantime, others published the results of what we had proposed. In this case, instead, we presented the project in December and already today we will have the required funds, all in the dark"
46 APPLICATIONS – The forty-six works submitted to the competition have been evaluated without any indication that could link the projects to the names of the proposers in order to ensure absolute impartiality. And today, Luisa - who is one of the winners - can go home and tell her children - without causing hilarity - that mom is really a scientist.
International study, coordinated for Italy by the haematologists of Tor Vergata, published in the New England Journal of Medicine
A molecular "target" drug, a new targeted therapy, will soon be available for about a third of the patients with acute myeloid leukaemia. In addition to conventional chemotherapy, this drug (midostaurin) has produced a significant benefit in the survival of patients with this disease, who exhibit specific mutations of a receptor, called FLT3.
The results of the international clinical study showing the benefits of this therapy have just been published on the New England Journal of Medicine, the most prestigious medical journal in the world. The randomized controlled trial assessed the effectiveness and tolerability of a FLT3 inhibitor against placebo in patients aged 18 to 60, in combination with chemotherapy.
The study saw the participation of 12 national co-operative groups and was supported by the National Cancer Institute in the USA and Novartis in Europe. The important Italian contribution is witnessed by the participation of 25 Centres that, through the cooperative group GIMEMA (Italian Group for the Study of Adult Haematological Diseases), enrolled 105 of the 717 patients studied. Co-authors of the newly published scientific work, as representatives of Italian haematologists, are Prof. Francesco Lo Coco, who has centralized at the Tor Vergata's laboratories the diagnostics and therefore the selection of the suitable patients, for all the Centres GIMEMA, and Prof. Sergio Amadori, Vice President of GIMEMA and Coordinator of the study Group of Acute Leukaemia.
It is worth noting that, thanks to this work, "midostaurin" has recently been approved in the USA by the Food and Drug Administration and will soon be approved as a new drug for the treatment of patients with acute myeloid leukaemia in Europe as well.
This has not happened for nearly 20 years!
Prof. William Arcese
Haematology and Stem Cell Transplantation
This is the title of a scientific publication on SCIENTIFIC REPORTS by an international team of experts that include also our Prof. Nicola Toschi.
Here the abstract:
"The application of complex systems theory to physiology and medicine has provided meaningful information about the nonlinear aspects underlying the dynamics of a wide range of biological processes and their disease-related aberrations. However, no studies have investigated whether meaningful information can be extracted by quantifying second-order moments of time-varying cardiovascular complexity. To this extent, we introduce a novel mathematical framework termed complexity variability, in which the variance of instantaneous Lyapunov spectra estimated over time serves as a reference quantifier. We apply the proposed methodology to four exemplary studies involving disorders which stem from cardiology, neurology and psychiatry: Congestive Heart Failure (CHF), Major Depression Disorder (MDD), Parkinson’s Disease (PD), and Post-Traumatic Stress Disorder (PTSD) patients with insomnia under a yoga training regime. We show that complexity assessments derived from simple time-averaging are not able to discern pathology-related changes in autonomic control, and we demonstrate that between-group differences in measures of complexity variability are consistent across pathologies. Pathological states such as CHF, MDD, and PD are associated with an increased complexity variability when compared to healthy controls, whereas wellbeing derived from yoga in PTSD is associated with lower time-variance of complexity."
to read more click HERE
In women, fertility preservation and health related to ovarian function are among the emerging health problems. More often, pathologies with progressive or immediate ovarian exhaustion afflict women between 18 and 40 years, and, in the case of oncological diseases, women with a greater probability of survival of 50%.
The development of new molecules, together with the testing of new cell and drug therapies, can help ease the pathologies linked to the loss of ovarian function. In the contest of these issues, the research team led by Dr. Francesca Gioia Klinger and coordinated by Prof. Massimo De Felici has discovered a new function of the luteinizing hormone LH in women. Until now it was thought that the functions of LH, secreted from the pituitary gland, were in women of childbearing age, ovulation, induction and maintenance of the corpus luteum, which is necessary for the early stages of embryo development. New researches has shown that LH is able to defend the primordial follicles (containing the eggs destined to be ovulated and fertilized after a long process of maturation), from the deleterious effects of a known chemotherapeutic, cisplatin, used in treatment of different types of tumors, including those that most frequently affect women, such as breast cancer. In fact, the researchers have found that treatment with cisplatin destroys the primordial follicles and render sterile prepubertal mice; in contrast, when chemotherapy is administered with LH, most primordial follicles don’ t degenerate and adult female mice are fertile. The group has also shown that the cause of the degeneration of the follicles is probably due to the damage that cisplatin causes to the oocytes’ DNA; LH stimulate the DNA repair mechanisms and at the same time block the apoptotic pathways activated by cisplatin in oocytes. Through which mechanisms LH plays this important new function, and if it occurs in human ovaries, is what the researchers are currently investigating. These findings could lead to the development of a physiological strategy to protect the ovarian function of young cancer patients.
This research is funded by Merck and the European Society for Human Reproduction (ESHRE).
The work was published in the journal Cell Death and Differentiation1, at the beginning of this year. The group works in the Section of Histology and Embryology of our Department and that has been studying the molecular mechanisms that control the formation and maturation of female germ cells since many years.
1. Rossi V, Lispi M, Longobardi S, Mattei M, Rella FD, Salustri A, De Felici M, Klinger FG. LH prevents cisplatin-induced apoptosis in oocytes and preserves female fertility in mouse. Cell Death Differ. 2017 Jan;24(1):72-82. doi: 10.1038/cdd.2016.97.
RARE DISEASE DAY 2017 – FRIEDREICH ATAXIA:RESEARCHERS AT FRATAGENE THERAPEUTICS AND UNVERSITY OF ROME “TOR VERGATA” HAVE IDENTIFIED A NEW THERAPEUTIC TARGET
Researchers at Fratagene Therapeutics, led by Dr. Alessandra Rufini, in collaboration with researchers at the Department of Biomedicine and Prevention of the University of Rome “Tor Vergata”, coordinated by Prof. Roberto Testi, have identified a new therapeutic target relevant for Friedreich ataxia (FA).
FA is a rare disease, a genetic neurodegenerative affection of children and young adults that progressively leads to disability and that still lacks an approved therapy. The discovery of a new therapeutic target, the enzyme RNF126, paves the way to the development of a new class of drugs able to restore the levels of frataxin, the protein defective in FA, therefore providing hope of cure. The results of this work have just been published in the prestigious journal Cell Reports.
Fratagene Therapeutics is a biotech company created by Prof. Roberto Testi, at the Department of Biomedicine and Prevention of the University of Rome “Tor Vergata”, with the aim of attracting the necessary resources to the development of a cure for FA. Fratagene Therapeutics is part of a long-term research endehavour in innovative drug discovery carried out by Prof. Testi group, funded by Telethon, by the Friedreich Ataxia Research Alliance USA and by two European Research Council grants (an Advanced Grant and a Proof-of-Concept grant).
Benini et a., http://www.cell.com/cell-reports/fulltext/S2211-1247(17)30149-3
“Human Connectome Project”: Personality traits linked to differences in brain structure. PROF. NICOLA TOSCHI
Our personality may be shaped by how our brain works, but in fact the shape of our brain can itself provide surprising clues about how we behave - and our risk of developing mental health disorders - suggests a study published today. According to psychologists, the extraordinary variety of human personality can be broken down into the so-called 'Big Five' personality traits, namely neuroticism (how moody a person is), extraversion (how enthusiastic a person is), openness (how open-minded a person is), agreeableness (a measure of altruism), and conscientiousness (a measure of self-control).
In a study published today in the journal Social Cognitive and Affective Neuroscience, an international team of researchers from the UK, US, and Italy have analysed a brain imaging dataset from over 500 individuals that has been made publicly available by the Human Connectome Project, a major US initiative funded by the National Institutes of Health. In particular, the researchers looked at differences in the brain cortical anatomy (the structure of the outer layer of the brain) as indexed by three measures - the thickness, area, and amount of folding in the cortex - and how these measures related to the Big Five personality traits.
"Evolution has shaped our brain anatomy in a way that maximizes its area and folding at the expense of reduced thickness of the cortex," explains Dr Luca Passamonti from the Department of Clinical Neurosciences at the University of Cambridge. "It's like stretching and folding a rubber sheet - this increases the surface area, but at the same time the sheet itself becomes thinner. We refer to this as the 'cortical stretching hypothesis'."
"Cortical stretching is a key evolutionary mechanism that enabled human brains to expand rapidly while still fitting into our skulls, which grew at a slower rate than the brain," adds Professor Antonio Terracciano from the Department of Geriatrics at the Florida State University. "Interestingly, this same process occurs as we develop and grow in the womb and throughout childhood, adolescence, and into adulthood: the thickness of the cortex tends to decrease while the area and folding increase."
In addition, as we get older, neuroticism goes down - we become better at handling emotions. At the same time, conscientiousness and agreeableness go up - we become progressively more responsible and less antagonistic.
The researchers found that high levels of neuroticism, which may predispose people to develop neuropsychiatric disorders, were associated with increased thickness as well as reduced area and folding in some regions of the cortex such as the prefrontal-temporal cortices at the front of the brain.
In contrast, openness, which is a personality trait linked with curiosity, creativity and a preference for variety and novelty, was associated with the opposite pattern, reduced thickness and an increase in area and folding in some prefrontal cortices.
"Our work supports the notion that personality is, to some degree, associated with brain maturation, a developmental process that is strongly influenced by genetic factors," says Dr Roberta Riccelli from Italy.
"Of course, we are continually shaped by our experiences and environment, but the fact that we see clear differences in brain structure which are linked with differences in personality traits suggests that there will almost certainly be an element of genetics involved," says Professor Nicola Toschi from the University 'Tor Vergata' in Rome. "This is also in keeping with the notion that differences in personality traits can be detected early on during development, for example in toddlers or infants."
The volunteers whose brains were imaged as part of the Human Connectome Project were all healthy individuals aged between 22 and 36 years with no history of neuro-psychiatric or other major medical problems. However, the relationship between differences in brain structure and personality traits in these people suggests that the differences may be even more pronounced in people who are more likely to experience neuro-psychiatric illnesses.
"Linking how brain structure is related to basic personality traits is a crucial step to improving our understanding of the link between the brain morphology and particular mood, cognitive, or behavioural disorders," adds Dr Passamonti. "We also need to have a better understanding of the relation between brain structure and function in healthy people to figure out what is different in people with neuropsychiatric disorders."
This is not the first time the researchers have found links between our brain structure and behaviour. A study published by the group last year found that the brains of teenagers with serious antisocial behaviour problems differ significantly in structure to those of their peers.
Riccelli, R et al. Surface-based morphometry reveals the neuroanatomical basis of the five-factor Model. Social Cognitive and Affective Neuroscience; 25 Jan 2016; DOI: 10.1093/scan/nsw175
The launch event for the journal Biomedicine & Prevention, which met with success, was held on December 14, 2016 at the Rome headquarters of the Italian National Research Council (Centro Nazionale delle Ricerche).
The occasion was attended by over a hundred guests hailing not only from the medical sphere but also from the fields of biology, chemistry, physics, and engineering. Many colleagues from the Department were also present.
Prof. Leonardo Palombi, Editor-in-chief of the journal and Head of the eponymous Biomedicine and Prevention Department at the University of Rome “Tor Vergata”, together with Prof. Sandro Mancinelli, who served as moderator for the event, presided over interesting addresses delivered by the Honorable Rector of the University, Prof. Giuseppe Novelli, and by the President of the Italian National Institute of Health (Istituto Superiore di Sanità), Prof. Walter Ricciardi.
These opening addresses were followed by technical presentations from the event’s overseas guest speakers:
- Prof. Felicity Astin
- Prof. Lang Tran
- Dr. Cornelius Bartels
- Dr. Graham Fraser
In closing, well-wishes and expressions of interest in participating were conveyed by:
- Società Italiana di Igiene e Medicina Preventiva
- Fondazione SIMG
- Federazione Nazionale Collegi IPASVI
- Società Italiana di Scienze Infermieristiche
- Società Italiana di Medicina del Lavoro e Igiene Industriale
- Società Italiana di Ematologia
- Società Italiana di Psichiatria
- Società Italiana di Ginecologia e Ostetricia
- Società Italiana di Mutagenesi Ambientale
- Società Italiana di Fisica Medica
- Collegio Italiano dei Professori di Anatomia Patologica
Compared with their peers, male youths with severe antisocial behavior problems appear to have significant differences in brain structure, suggesting their problem behavior stems from early life changes in brain development.
So concludes a study by an international team published in the Journal of Child Psychology and Psychiatry.
First author Graeme Fairchild, associate professor in abnormal psychology at the University of Southampton in the United Kingdom, and colleagues used magnetic resonance imaging (MRI) to examine the brain structure of teenage and young adult men diagnosed with conduct disorder.
First author Graeme Fairchild, associate professor in abnormal psychology at the University of Southampton in the United Kingdom, and colleagues used magnetic resonance imaging (MRI) to examine the brain structure of teenage and young adult men diagnosed with conduct disorder.
Conduct disorder is a cluster of persistent behavioral problems displayed in childhood and adolescence, such as aggressive and destructive behavior, stealing, and lying. In older children, it can also include staying out all night and use of weapons.
The researchers note that evidence already exists that the brains of people with serious behavior problems are different, but this tends to be simplistic and focused in limited regions, such as the amygdala - the brain's emotion center.
However, conduct disorder is a complex behavioral disorder, and one might expect the brain differences to be more complex and affect more than one brain region, they suggest.
Therefore, in their investigation, the team looked for brain regions with similar or different thicknesses as this might indicate coordinated or non-coordinated development between regions.
For the study, the researchers carried out MRI brain scans on 58 male teenagers and young adults diagnosed with conduct disorder. They also included 25 peers without such a diagnosis, as typically developing, "healthy" controls. The participants were all aged 16-21.
'Most of the brain is involved'
The researchers found that participants with childhood onset conduct disorder - sometimes referred to as "early starters" - had a strikingly higher number of cases where brain regions had the same thickness as controls.
In contrast, the participants with adolescent-onset conduct disorder - sometimes termed "late starters" - had a lower number of cases where brain regions had the same thickness compared with controls.
The researchers confirmed the findings with a separate, independent sample of 37 participants with conduct disorder and 32 healthy controls. All participants in this second sample were male, aged 13-18.
Prof. Fairchild says the differences between the youths with both forms of conduct disorder and their healthy peers "show that most of the brain is involved, but particularly the frontal and temporal regions of the brain."
He argues that the findings are "compelling evidence" that conduct disorder is a "real psychiatric disorder," and not just an exaggerated form of teenage rebellion as some experts have suggested.
The study also indicates there are important differences in the brains of people who develop conduct disorder early in childhood and those who develop it later during their teens.
However, while the findings highlight the key role the brain plays in the development of conduct disorder, they do not explain how the changes come about. For example, to what extent are they influenced by people's genes, and to what extent are they affected by the environment they are raised in?
While the study does not answer these questions, the researchers believe the findings could help to measure the effect of interventions. Using a brain map of conduct disorder it might be possible, for example, to see if interventions such as psychological therapy can reverse some of the changes noted in the study.
ROME – A group of researchers from the University of Rome “Tor Vergata” and the Fondazione Santa Lucia has identified a potential new approach to treating spinal muscular atrophy (SMA) which directly tackles the gene mutation responsible for the disease.
The study, funded by the Fondazione Telethon, was coordinated by Claudio Sette, Associate Professor at the Department of Biomedicine and Prevention, University of Rome “Tor Vergata”. The study’s findings have appeared in the scientific publication The Journal of Cell Biology.
Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by the progressive death of motor neurons, the nerve cells in the spinal cord that relay motor commands to the muscles. The disease is caused by mutations in the genes called SMN1 and SMN2, which lead to the production of insufficient levels of the SMN protein that is associated with the survival of motor neurons. To date, all attempts to correct the genetic defect responsible have failed to yield the desired results.
The research group led by Claudio Sette had already in recent years identified a protein, called Sam68, involved in certain processes key to the progression of the disease. In this new study, the researchers developed animal (mouse) models of SMA in which Sam68 was eliminated. They were thus able to observe that mice lacking the Sam68 protein showed a significant improvement in the survival of motor neurons and, more generally, in the health and functionality of affected muscles. This thus paves the way for a new therapeutic approach to this as-yet incurable disease, in respect of which however very interesting prospects have emerged in recent years thanks to research. In particular, at the start of 2015 two international clinical trials got underway, in which Italian patients will also be able to participate, testing the efficacy of two different drugs in combating the disease. According to a statement issued by the University of Rome “Tor Vergata”, this undertaking has in part been made possible with the support of the Fondazione Telethon.
Spinal muscular atrophy (SMA) – Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by the progressive death of motor neurons, the nerve cells in the spinal cord that control muscle movement.
It affects around 1 in every 10,000 newborn babies and is the most common genetic cause of infant death. There are three forms of the disease, of which type I is the most serious and affects about half of SMA patients. In this type, affected infants exhibit signs of the disease already from birth or within their first few months of life, manifesting as severe and progressive signs of respiratory insufficiency.
Children suffering from type II, also termed the “intermediate form”, acquire the ability to sit but not to walk unaided, and often present respiratory complications as well as other signs, such as scoliosis.
Type III is the least severe, often begins to manifest after the first few years of life, and is always accompanied by successful development of the ability to walk, although in some cases this capability may subsequently be lost.
The disease is caused by a defect in the SMN1 gene that encodes for a protein called SMN. The counterpart SMN2 gene remains functional in SMA patients, but leads to the production of insufficient levels of the SMN protein.
The mode of transmission is autosomal recessive: parents are healthy carriers of the genetic defect and have a 25% probability of transmitting the disease to each of their children. The disease is diagnosed through genetic testing. At present, there is no definitive cure, though numerous studies are underway to evaluate potential treatments. A few drugs are currently being trialed.