Gemma Calamandrei

Dr. Gemma Calamandrei

Centre for Behavioral sciences and Mental health Istituto Superiore di Sanità, Roma, Italy
orcid

Research Focus & Metrics

Academic Career Length

41Years (1986-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
27 September 2011 in Journal of Neuroendocrinology
Verified
Journal Article
Closed access
PDF file
Cheryl Anne FryeCheryl Anne Frye
Cheryl Anne Frye
EBE. Bo
E. Bo
Gemma CalamandreiGemma Calamandrei
Gemma Calamandrei
LCLaura Calzà
Laura Calzà
FDF. Dessì‐Fulgheri
F. Dessì‐Fulgheri
Giancarlo PanzicaGiancarlo Panzica
Giancarlo Panzica

20 June 2015 in Environmental Health
Verified
Journal Article
Open access
PDF file
JHJerrold J. Heindel
Jerrold J. Heindel
FSFrederick S. Vom Saal
Frederick S. Vom Saal
BBBruce Blumberg
Bruce Blumberg
PBPatrizia Bovolin
Patrizia Bovolin
Gemma CalamandreiGemma Calamandrei
Gemma Calamandrei
Paola PalanzaPaola Palanza
Paola Palanza
A multidisciplinary group of experts gathered in Parma Italy for a workshop hosted by the University of Parma, May 16–18, 2014 to address concerns about the potential relationship between environmental metabolic disrupting chemicals, obesity and related metabolic disorders. The objectives of the workshop were to: 1. Review findings related to the role of environmental chemicals, referred to as “metabolic disruptors”, in obesity and metabolic syndrome with special attention to recent discoveries from animal model and epidemiology studies; 2. Identify conclusions that could be drawn with confidence from existing animal and human data; 3. Develop predictions based on current data; and 4. Identify critical knowledge gaps and areas of uncertainty. The consensus statements are intended to aid in expanding understanding of the role of metabolic disruptors in the obesity and metabolic disease epidemics, to move the field forward by assessing the current state of the science and to identify research needs on the role of environmental chemical exposures in these diseases. We propose broadening the definition of obesogens to that of metabolic disruptors, to encompass chemicals that play a role in altered susceptibility to obesity, diabetes and related metabolic disorders including metabolic syndrome.

1 April 2008 in Molecular and Cellular Neuroscience
Verified
Journal Article
Closed access
Andrea FusoAndrea Fuso
Andrea Fuso
VNVincenzina Nicolia
Vincenzina Nicolia
RCRosaria A. Cavallaro
Rosaria A. Cavallaro
LRLaura Ricceri
Laura Ricceri
FDFabrizio D'ANselmi
Fabrizio D'ANselmi
SSSigfrido Scarpa
Sigfrido Scarpa

7 June 2006 in Toxicological Sciences
Verified
Journal Article
Open access
PDF file
LRLaura Ricceri
Laura Ricceri
AValdina Venerosi
aldina Venerosi
FCFrancesca Capone
Francesca Capone
MCMaria Francesca Cometa
Maria Francesca Cometa
PLPaola Lorenzini
Paola Lorenzini
Gemma CalamandreiGemma Calamandrei
Gemma Calamandrei
Developmental exposure to the organophosphorous insecticide chlorpyrifos (CPF) induces long-term effects on brain and behavior in laboratory rodents. We evaluated in adult mice the behavioral effects of either fetal and/or neonatal CPF exposure at doses not inhibiting fetal and neonatal brain cholinesterase. CPF (3 or 6 mg/kg) was given by oral treatment to pregnant females on gestational days 15–18 and offspring were treated sc (1 or 3 mg/kg) on postnatal days (PNDs) 11–14. Serum and brain acetylcholinesterase (AChE) activity was evaluated at birth and 24 h from termination of postnatal treatments. On PND 70, male mice were assessed for spontaneous motor activity in an open-field test and in a socioagonistic encounter with an unfamiliar conspecific. Virgin females underwent a maternal induction test following presentation of foster pups. Both sexes were subjected to a plus-maze test to evaluate exploration and anxiety levels. Gestational and postnatal CPF exposure (higher doses) affected motor activity in the open field and enhanced synergically agonistic behavior. Postnatal CPF exposure increased maternal responsiveness toward pups in females. Mice of both sexes exposed to postnatal CPF showed reduced anxiety response in the plus-maze, an effect greater in females. Altogether, developmental exposure to CPF at doses that do not cause brain AChE inhibition induces long-term alterations in sex-specific behavior patterns of the mouse species. Late neonatal exposure on PNDs 11–14 was the most effective in causing behavioral changes. These findings support the hypothesis that developmental CPF may represent a risk factor for increased vulnerability to neurodevelopmental disorders in humans.

1 January 2009 in Environmental Health Perspectives
Verified
Journal Article
Open access
SMSusan L. Makris
Susan L. Makris
KRKathleen Raffaele
Kathleen Raffaele
SASandra Allen
Sandra Allen
WBWayne J. Bowers
Wayne J. Bowers
UHUlla Hass
Ulla Hass
KCKevin M. Crofton
Kevin M. Crofton
A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

1 June 2007 in Environmental Health Perspectives
Verified
Journal Article
Open access
SCSandra Coecke
Sandra Coecke
AGAlan M Goldberg
Alan M Goldberg
SASandra Allen
Sandra Allen
Leonora BuzanskaLeonora Buzanska
Leonora Buzanska
Gemma CalamandreiGemma Calamandrei
Gemma Calamandrei
ABAnna Bal-Price
Anna Bal-Price
This is the report of the first workshop on Incorporating In Vitro Alternative Methods for Developmental Neurotoxicity (DNT) Testing into International Hazard and Risk Assessment Strategies, held in Ispra, Italy, on 19–21 April 2005. The workshop was hosted by the European Centre for the Validation of Alternative Methods (ECVAM) and jointly organized by ECVAM, the European Chemical Industry Council, and the Johns Hopkins University Center for Alternatives to Animal Testing. The primary aim of the workshop was to identify and catalog potential methods that could be used to assess how data from in vitro alternative methods could help to predict and identify DNT hazards. Working groups focused on two different aspects: a) details on the science available in the field of DNT, including discussions on the models available to capture the critical DNT mechanisms and processes, and b) policy and strategy aspects to assess the integration of alternative methods in a regulatory framework. This report summarizes these discussions and details the recommendations and priorities for future work.