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Institution

University of Florence

EducationFlorence, Toscana, Italy
About: University of Florence is a education organization based out in Florence, Toscana, Italy. It is known for research contribution in the topics: Population & Carbonic anhydrase. The organization has 27292 authors who have published 79599 publications receiving 2341684 citations. The organization is also known as: Università degli studi di Firenze & Universita degli studi di Firenze.


Papers
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Journal ArticleDOI
TL;DR: The diffusion approximation of the radiative transfer equation is a model used widely to describe photon migration in highly diffusing media and is an important matter in biological tissue optics as mentioned in this paper, however, it is not a suitable model for biological tissue imaging.
Abstract: The diffusion approximation of the radiative transfer equation is a model used widely to describe photon migration in highly diffusing media and is an important matter in biological tissue optics An analysis of the time-dependent diffusion equation together with its solutions for the slab geometry and for a semi-infinite diffusing medium are reported These solutions, presented for both the time-dependent and the continuous wave source, account for the refractive index mismatch between the turbid medium and the surrounding medium The results have been compared with those obtained when different boundary conditions were assumed The comparison has shown that the effect of the refractive index mismatch cannot be disregarded This effect is particularly important for the transmittance The discussion of results also provides an analysis of the role of the absorption coefficient in the expression of the diffusion coefficient

473 citations

Journal ArticleDOI
TL;DR: There was no clear correlation between percentage of mutant mitochondrial DNAs and severity of the biochemical defect, but there was a high concordance between clinical diagnosis of MELAS and transfer RNALeu(UUR) mutation.
Abstract: We studied 23 patients with clinically defined mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS), 25 oligosymptomatic or asymptomatic maternal relatives, and 50 mitochondrial disease control subjects for the presence of a previously reported heteroplasmic point mutation at nt 3,243 in the transfer RNA(Leu(UUR)) gene of mitochondrial DNA. We found a high concordance between clinical diagnosis of MELAS and transfer RNA(Leu(UUR)) mutation, which was present in 21 of the 23 patients with MELAS, all 11 oligosymptomatic and 12 of 14 asymptomatic relatives, but in only five of 50 patients without MELAS. The proportion of mutant genomes in muscle ranged from 56 to 95% and was significantly higher in the patients with MELAS than in their oligosymptomatic or asymptomatic relatives. In subjects in whom both muscle and blood were studied, the percentage of mutations was significantly lower in blood and was not detected in three of 12 asymptomatic relatives. The activities of complexes I + III, II + III, and IV were decreased in muscle biopsies harboring the mutation, but there was no clear correlation between percentage of mutant mitochondrial DNAs and severity of the biochemical defect.

473 citations

Journal ArticleDOI
TL;DR: Findings that implicate hypometabolism and oxidative stress as crucial players in the initiation and progression of synaptic pathology in AD are reviewed.
Abstract: One of the main features of Alzheimer’s disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc). In vivo imaging using positron emission tomography with 2-[18F]fluoro-2-deoxy-D-glucose (FDG–PET) demonstrates consistent and progressive CMRglc reductions in AD patients, the extent and topography of which correlate with symptom severity. Increasing evidence suggests that CMRglc reductions occur at the preclinical stages of AD. CMRglc reductions were observed on FDG–PET before the onset of disease in several groups of at-risk individuals, including patients with mild cognitive impairment (MCI), often a prodrome to AD; presymptomatic individuals carrying mutations responsible for early-onset familial AD; cognitively normal elderly individuals followed for several years until they declined to MCI and eventually to AD; normal, middle-aged individuals who expressed subjective memory complaints and were carriers of the apolipoprotein E epsilon-4 allele, a strong genetic risk factor for late-onset AD. However, the causes of the early metabolic dysfunction forerunning the onset of AD are not known. An increasing body of evidence indicates a deficient or altered energy metabolism that could change the overall oxidative microenvironment for neurons during the pathogenesis and progression of AD, leading to alterations in mitochondrial enzymes and in glucose metabolism in AD brain tissue. The present paper reviews findings that implicate hypometabolism and oxidative stress as crucial players in the initiation and progression of synaptic pathology in AD.

473 citations

Journal ArticleDOI
TL;DR: 20 international experts including 19 members of the European Society for Radiotherapy and Oncology and European Organisation for Research and Treatment of Cancer OligoCare project developed a comprehensive system for characterisation and classification of oligometastatic disease.
Abstract: Oligometastatic disease has been proposed as an intermediate state between localised and systemically metastasised disease. In the absence of randomised phase 3 trials, early clinical studies show improved survival when radical local therapy is added to standard systemic therapy for oligometastatic disease. However, since no biomarker for the identification of patients with true oligometastatic disease is clinically available, the diagnosis of oligometastatic disease is based solely on imaging findings. A small number of metastases on imaging could represent different clinical scenarios, which are associated with different prognoses and might require different treatment strategies. 20 international experts including 19 members of the European Society for Radiotherapy and Oncology and European Organisation for Research and Treatment of Cancer OligoCare project developed a comprehensive system for characterisation and classification of oligometastatic disease. We first did a systematic review of the literature to identify inclusion and exclusion criteria of prospective interventional oligometastatic disease clinical trials. Next, we used a Delphi consensus process to select a total of 17 oligometastatic disease characterisation factors that should be assessed in all patients treated with radical local therapy for oligometastatic disease, both within and outside of clinical trials. Using a second round of the Delphi method, we established a decision tree for oligometastatic disease classification together with a nomenclature. We agreed oligometastatic disease as the overall umbrella term. A history of polymetastatic disease before diagnosis of oligometastatic disease was used as the criterion to differentiate between induced oligometastatic disease (previous history of polymetastatic disease) and genuine oligometastatic disease (no history of polymetastatic disease). We further subclassified genuine oligometastatic disease into repeat oligometastatic disease (previous history of oligometastatic disease) and de-novo oligometastatic disease (first time diagnosis of oligometastatic disease). In de-novo oligometastatic disease, we differentiated between synchronous and metachronous oligometastatic disease. We did a final subclassification into oligorecurrence, oligoprogression, and oligopersistence, considering whether oligometastatic disease is diagnosed during a treatment-free interval or during active systemic therapy and whether or not an oligometastatic lesion is progressing on current imaging. This oligometastatic disease classification and nomenclature needs to be prospectively evaluated by the OligoCare study.

472 citations

Journal ArticleDOI
TL;DR: Classifying LOH into different categories by combining LH with T may improve the diagnosis and management of LOH, and Symptomatic elderly men considered to have LOH can be differentiated on the basis of endocrine and clinical features and predisposing risk factors.
Abstract: Context: The diagnosis of late-onset hypogonadism (LOH) in older men with age-related declines in testosterone (T) is currently not well characterized. Objective: Our objective was to investigate whether different forms of hypogonadism can be distinguished among aging men. Design: The study was a cross-sectional survey on 3369 community-dwelling men aged 40-79 yr in eight European centers. Methods: Four groups of subjects were defined: eugonadal (normal T and normal LH), secondary (low T and low/normal LH), primary (low T and elevated LH), and compensated (normal T and elevated LH) hypogonadism. Relationships between the defined gonadal status with potential risk factors and clinical symptoms were investigated by multilevel regression models. Results: Among the men, 11.8, 2.0, and 9.5% were classified into the secondary, primary, and compensated hypogonadism categories, respectively. Older men were more likely to have primary [relative risk ratio (RRR) = 3.04; P < 0.001] and compensated (RRR = 2.41; P < 0.001) hypogonadism. Body mass index of 30 kg/m(2) or higher was associated with secondary hypogonadism (RRR = 8.74; P < 0.001). Comorbidity was associated with both secondary and primary hypogonadism. Sexual symptoms were more prevalent in secondary and primary hypogonadism, whereas physical symptoms were more likely in compensated hypogonadism. Conclusions: Symptomatic elderly men considered to have LOH can be differentiated on the basis of endocrine and clinical features and predisposing risk factors. Secondary hypogonadism is associated with obesity and primary hypogonadism predominately with age. Compensated hypogonadism can be considered a distinct clinical state associated with aging. Classification of LOH into different categories by combining LH with T may improve the diagnosis and management of LOH.

472 citations


Authors

Showing all 27699 results

NameH-indexPapersCitations
Charles A. Dinarello1901058139668
D. M. Strom1763167194314
Gregory Y.H. Lip1693159171742
Christopher M. Dobson1501008105475
Dirk Inzé14964774468
Thomas Hebbeker1481984114004
Marco Zanetti1451439104610
Richard B. Devereux144962116403
Gunther Roland1411471100681
Markus Klute1391447104196
Tariq Aziz138164696586
Guido Tonelli138145897248
Giorgio Trinchieri13843378028
Christof Roland137130896632
Christoph Paus1371585100801
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023244
2022631
20215,298
20205,251
20194,652
20184,147