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University of Modena and Reggio Emilia

EducationModena, Italy
About: University of Modena and Reggio Emilia is a education organization based out in Modena, Italy. It is known for research contribution in the topics: Population & Medicine. The organization has 8179 authors who have published 22418 publications receiving 671337 citations. The organization is also known as: Università degli Studi di Modena e Reggio Emilia & Universita degli Studi di Modena e Reggio Emilia.


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Journal ArticleDOI
Christopher D. Whelan1, Christopher D. Whelan2, Andre Altmann3, Juan A. Botía4, Neda Jahanshad1, Derrek P. Hibar1, Julie Absil5, Saud Alhusaini6, Saud Alhusaini2, Marina K. M. Alvim7, Pia Auvinen8, Emanuele Bartolini9, Felipe P. G. Bergo7, Tauana Bernardes7, Karen Blackmon10, Karen Blackmon11, Barbara Braga7, Maria Eugenia Caligiuri12, Anna Calvo, Sarah J. A. Carr13, Jian Chen14, Shuai Chen15, Andrea Cherubini12, Philippe David5, Martin Domin16, Sonya Foley17, Wendy Franca7, Gerrit Haaker18, Dmitry Isaev1, Simon S. Keller19, Raviteja Kotikalapudi20, Magdalena A. Kowalczyk21, Ruben Kuzniecky10, Soenke Langner16, Matteo Lenge9, Kelly M. Leyden22, Min Liu6, Richard Q. Loi22, Pascal Martin20, Mario Mascalchi9, Mario Mascalchi23, Marcia Elisabete Morita7, Jose C. Pariente, Raúl Rodríguez-Cruces24, Christian Rummel25, Taavi Saavalainen8, Mira Semmelroch21, Mariasavina Severino26, Rhys H. Thomas27, Rhys H. Thomas17, Manuela Tondelli28, Domenico Tortora26, Anna Elisabetta Vaudano28, Lucy Vivash29, Lucy Vivash30, Felix von Podewils16, Jan Wagner31, Jan Wagner32, Bernd Weber32, Yi Yao15, Clarissa L. Yasuda7, Guohao Zhang33, Núria Bargalló, Benjamin Bender20, Neda Bernasconi6, Andrea Bernasconi6, Boris C. Bernhardt6, Ingmar Blümcke18, Chad Carlson34, Chad Carlson10, Gianpiero L. Cavalleri2, Fernando Cendes7, Luis Concha24, Norman Delanty2, Norman Delanty35, Chantal Depondt5, Orrin Devinsky10, Colin P. Doherty2, Niels K. Focke20, Antonio Gambardella12, Renzo Guerrini9, Khalid Hamandi17, Khalid Hamandi27, Graeme D. Jackson30, Graeme D. Jackson21, Reetta Kälviäinen8, Peter Kochunov36, Patrick Kwan29, Angelo Labate12, Carrie R. McDonald22, Stefano Meletti28, Terence J. O'Brien29, Terence J. O'Brien30, Sebastien Ourselin3, Mark P. Richardson13, Mark P. Richardson37, Pasquale Striano38, Thomas Thesen11, Thomas Thesen10, Roland Wiest25, Junsong Zhang15, Annamaria Vezzani39, Mina Ryten4, Mina Ryten13, Paul M. Thompson1, Sanjay M. Sisodiya4 
01 Feb 2018-Brain
TL;DR: In the largest neuroimaging study to date, Whelan and colleagues report robust structural alterations across and within epilepsy syndromes, including shared volume loss in the thalamus, and widespread cortical thickness differences.
Abstract: Progressive functional decline in the epilepsies is largely unexplained. We formed the ENIGMA-Epilepsy consortium to understand factors that influence brain measures in epilepsy, pooling data from 24 research centres in 14 countries across Europe, North and South America, Asia, and Australia. Structural brain measures were extracted from MRI brain scans across 2149 individuals with epilepsy, divided into four epilepsy subgroups including idiopathic generalized epilepsies (n =367), mesial temporal lobe epilepsies with hippocampal sclerosis (MTLE; left, n = 415; right, n = 339), and all other epilepsies in aggregate (n = 1026), and compared to 1727 matched healthy controls. We ranked brain structures in order of greatest differences between patients and controls, by meta-analysing effect sizes across 16 subcortical and 68 cortical brain regions. We also tested effects of duration of disease, age at onset, and age-by-diagnosis interactions on structural measures. We observed widespread patterns of altered subcortical volume and reduced cortical grey matter thickness. Compared to controls, all epilepsy groups showed lower volume in the right thalamus (Cohen's d = -0.24 to -0.73; P < 1.49 × 10-4), and lower thickness in the precentral gyri bilaterally (d = -0.34 to -0.52; P < 4.31 × 10-6). Both MTLE subgroups showed profound volume reduction in the ipsilateral hippocampus (d = -1.73 to -1.91, P < 1.4 × 10-19), and lower thickness in extrahippocampal cortical regions, including the precentral and paracentral gyri, compared to controls (d = -0.36 to -0.52; P < 1.49 × 10-4). Thickness differences of the ipsilateral temporopolar, parahippocampal, entorhinal, and fusiform gyri, contralateral pars triangularis, and bilateral precuneus, superior frontal and caudal middle frontal gyri were observed in left, but not right, MTLE (d = -0.29 to -0.54; P < 1.49 × 10-4). Contrastingly, thickness differences of the ipsilateral pars opercularis, and contralateral transverse temporal gyrus, were observed in right, but not left, MTLE (d = -0.27 to -0.51; P < 1.49 × 10-4). Lower subcortical volume and cortical thickness associated with a longer duration of epilepsy in the all-epilepsies, all-other-epilepsies, and right MTLE groups (beta, b < -0.0018; P < 1.49 × 10-4). In the largest neuroimaging study of epilepsy to date, we provide information on the common epilepsies that could not be realistically acquired in any other way. Our study provides a robust ranking of brain measures that can be further targeted for study in genetic and neuropathological studies. This worldwide initiative identifies patterns of shared grey matter reduction across epilepsy syndromes, and distinctive abnormalities between epilepsy syndromes, which inform our understanding of epilepsy as a network disorder, and indicate that certain epilepsy syndromes involve more widespread structural compromise than previously assumed.

296 citations

Journal ArticleDOI
TL;DR: A strong correlation between serum AMH levels and ovarian response to gonadotrophin stimulation is demonstrated and for the first time, clinicians may have a reliable serum marker of ovarian response that can be measured independently of the day of the menstrual cycle.
Abstract: BACKGROUND: Recently, a new marker, the anti-Mullerian hormone (AMH), has been evaluated as a marker of ovarian response. Serum AMH levels have been measured at frequent time-points during the menstrual cycle, suggesting the complete absence of fluctuation. The aim of this study was to evaluate whether serum AMH measurement on any day of the menstrual cycle could predict ovarian response in women undergoing assisted reproductive technology (ART). METHODS: This study included 48 women attending the IVF/ICSI programme. Blood withdrawal for AMH measurement was performed in all the patients independently of the day of the menstrual cycle. RESULTS: Women in the lowest AMH quartile ( 7 ng/ml). All the cancelled cycles due to absent response were in the group of the lowest AMH quartile, whereas the cancelled cycles due to risk of ovarian hyperstimulation syndrome (OHSS) were in the group of the highest AMH quartile. This study demonstrated a strong correlation between serum AMH levels and ovarian response to gonadotrophin stimulation. CONCLUSION: For the first time, clinicians may have a reliable serum marker of ovarian response that can be measured independently of the day of the menstrual cycle.

295 citations

Journal ArticleDOI
TL;DR: There is insufficient and conflicting evidence to give any firm recommendations regarding green tea consumption for cancer prevention, and drinking green tea appears to be safe at moderate, regular and habitual use.
Abstract: Background Tea is one of the most commonly consumed beverages worldwide. Teas from the plant Camellia sinensis can be grouped into green, black and oolong tea. Cross-culturally tea drinking habits vary. Camellia sinensis contains the active ingredient polyphenol, which has a subgroup known as catechins. Catechins are powerful antioxidants. It has been suggested that green tea polyphenol may inhibit cell proliferation and observational studies have suggested that green tea may have cancer-preventative effects. Objectives To critically assess any associations between green tea consumption and the risk of cancer incidence and mortality. Search methods We searched eligible studies up to January 2009 in the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, Amed, CancerLit, Psych INFO and Phytobase and reference lists of previous reviews and included studies. Selection criteria We included all prospective, controlled interventional studies and observational studies, which either assessed the associations between green tea consumption and risk of cancer incidence or that reported on cancer mortality. Data collection and analysis At least two review authors independently applied the study criteria, extracted data and assessed methodological quality of studies. Due to the nature of included studies, which were mainly epidemiological, results were summarised descriptively according to cancer diagnosis. Main results Fifty-one studies with more than 1.6 million participants were included. Twenty-seven of them were case-control studies, 23 cohort studies and one randomised controlled trial (RCT). Twenty-seven studies tried to establish an association between green tea consumption and cancer of the digestive tract, mainly of the upper gastrointestinal tract, five with breast cancer, five with prostate cancer, three with lung cancer, two with ovarian cancer, two with urinary bladder cancer one with oral cancer, three further studies included patients with various cancer diagnoses. The methodological quality was measured with the Newcastle-Ottawa scale (NOS). The 9 nested case-control studies within prospective cohorts were of high methodological quality, 13 of medium, and 1 of low. One retrospective case-control study was of high methodological quality and 21 of medium and 5 of low. Results from studies assessing associations between green tea and risk of digestive tract cancer incidence were highly contradictory. There was limited evidence that green tea could reduce the incidence of liver cancer. The evidence for esophageal, gastric, colon, rectum, and pancreatic cancer was conflicting. In prostate cancer, observational studies with higher methodological quality and the only included RCT suggested a decreased risk in men consuming higher quantities green tea or green tea extracts. However, there was limited to moderate evidence that the consumption of green tea reduced the risk of lung cancer, especially in men, and urinary bladder cancer or that it could even increase the risk of the latter. There was moderate to strong evidence that green tea consumption does not decrease the risk of dying from gastric cancer. There was limited moderate to strong evidence for lung, pancreatic and colorectal cancer. Authors' conclusions There is insufficient and conflicting evidence to give any firm recommendations regarding green tea consumption for cancer prevention. The results of this review, including its trends of associations, need to be interpreted with caution and their generalisability is questionable, as the majority of included studies were carried out in Asia (n = 47) where the tea drinking culture is pronounced. Desirable green tea intake is 3 to 5 cups per day (up to 1200 ml/day), providing a minimum of 250 mg/day catechins. If not exceeding the daily recommended allowance, those who enjoy a cup of green tea should continue its consumption. Drinking green tea appears to be safe at moderate, regular and habitual use.

295 citations

Journal ArticleDOI
TL;DR: Findings suggest that aerobic glycolysis endows cancer cells with particular metabolic properties and at the same time sustains transcription factors with potent pro‐tumorigenic activities such as YAP/TAZ.
Abstract: Increased glucose metabolism and reprogramming toward aerobic glycolysis are a hallmark of cancer cells, meeting their metabolic needs for sustained cell proliferation. Metabolic reprogramming is usually considered as a downstream consequence of tumor development and oncogene activation; growing evidence indicates, however, that metabolism on its turn can support oncogenic signaling to foster tumor malignancy. Here, we explored how glucose metabolism regulates gene transcription and found an unexpected link with YAP/TAZ, key transcription factors regulating organ growth, tumor cell proliferation and aggressiveness. When cells actively incorporate glucose and route it through glycolysis, YAP/TAZ are fully active; when glucose metabolism is blocked, or glycolysis is reduced, YAP/TAZ transcriptional activity is decreased. Accordingly, glycolysis is required to sustain YAP/TAZ pro-tumorigenic functions, and YAP/TAZ are required for the full deployment of glucose growth-promoting activity. Mechanistically we found that phosphofructokinase (PFK1), the enzyme regulating the first committed step of glycolysis, binds the YAP/TAZ transcriptional cofactors TEADs and promotes their functional and biochemical cooperation with YAP/TAZ. Strikingly, this regulation is conserved in Drosophila, where phosphofructokinase is required for tissue overgrowth promoted by Yki, the fly homologue of YAP. Moreover, gene expression regulated by glucose metabolism in breast cancer cells is strongly associated in a large dataset of primary human mammary tumors with YAP/TAZ activation and with the progression toward more advanced and malignant stages. These findings suggest that aerobic glycolysis endows cancer cells with particular metabolic properties and at the same time sustains transcription factors with potent pro-tumorigenic activities such as YAP/TAZ.

295 citations

Journal ArticleDOI
TL;DR: In response to fluctuations in the level of the 'labile iron pool', IRPs act as key regulators of cellular iron homoeostasis as a result of the translational control of the expression of a number of iron metabolism-related genes.
Abstract: The capacity of readily exchanging electrons makes iron not only essential for fundamental cell functions, but also a potential catalyst for chemical reactions involving free-radical formation and subsequent oxidative stress and cell damage. Cellular iron levels are therefore carefully regulated in order to maintain an adequate substrate while also minimizing the pool of potentially toxic ‘free iron’. Iron homoeostasis is controlled through several genes, an increasing number of which have been found to contain non-coding sequences [i.e. the iron-responsive elements (IREs)] which are recognized at the mRNA level by two cytoplasmic iron-regulatory proteins (IRP-1 and IRP-2). The IRPs belong to the aconitase superfamily. By means of an Fe-S-cluster-dependent switch, IRP-1 can function as an mRNA-binding protein or as an enzyme that converts citrate into isocitrate. Although structurally and functionally similar to IRP-1, IRP-2 does not seem to assemble a cluster nor to possess aconitase activity; moreover, it has a distinct pattern of tissue expression and is modulated by means of proteasome-mediated degradation. In response to fluctuations in the level of the ‘labile iron pool’, IRPs act as key regulators of cellular iron homoeostasis as a result of the translational control of the expression of a number of iron metabolism-related genes. Conversely, various agents and conditions may affect IRP activity, thereby modulating iron and oxygen radical levels in different pathobiological settings. As the number of mRNAs regulated through IRE–IRP interactions keeps growing, the definition of IRPs as iron-regulatory proteins may in the near future become limiting as their role expands to other essential metabolic pathways.

294 citations


Authors

Showing all 8322 results

NameH-indexPapersCitations
Carlo M. Croce1981135189007
Gregory Y.H. Lip1693159171742
Geoffrey Burnstock141148899525
Peter M. Rothwell13477967382
Claudio Franceschi12085659868
Lorenzo Galluzzi11847771436
Leonardo M. Fabbri10956660838
David N. Reinhoudt107108248814
Stefano Pileri10063543369
Andrea Bizzeti99116846880
Brian K. Shoichet9828140313
Dante Gatteschi9772748729
Roberta Sessoli9542441458
Thomas A. Buchholz9349433409
Pier Luigi Zinzani9285735476
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202376
2022230
20212,354
20202,083
20191,633
20181,450