111,814 research outputs found
Postilla. A proposito dell'Appendice di Dario Mantovani sul mio contributo
No full textThe Author replies to a critical intervention od Dario Mantovani concerning some points of his own essay about Ulpian's introductory to the edict on the pacta
Misure di resistività mediante OhmMapper finalizzate allo studio del sito di Torraccia di Chiusi
No full texthttp://www.fe.infn.it/u/mantovani/CV/Proceedings/Cavalieri_07.pd
Mechanisms of disease : mutations of G proteins and G-protein-coupled receptors in endocrine diseases
No full textG proteins and G-protein-coupled receptors (GPCRs) mediate the effects of a number of hormones. Genes that encode these molecules are subject to loss-of function or gain-of-function mutations that result in endocrine disorders. Loss-of-function mutations prevent signaling in response to the corresponding agonist and cause resistance to hormone actions, which mimics hormone deficiency. Gain-of-function mutations lead to constitutive, agonist-independent activation of signaling, which mimics hormone excess. Disease-causing mutations of GPCRs have been identified in patients with various disorders of the pituitary-thyroid, pituitary-gonadal and pituitary-adrenal axes, and in those with abnormalities in food intake, growth, water balance and mineral-ion turnover. The only mutational changes in G proteins unequivocally associated with endocrine disorders occur in GNAS (guanine nucleotide-binding protein G-stimulatory subunit α, or Gsα). Heterozygous loss-of-function mutations of GNAS in the active, maternal allele cause resistance to hormones that act through Gsα-coupled GPCRs, whereas somatic gain-of-function mutations cause proliferation of endocrine cells that recognize cyclic AMP as a mitogen. The study of mutations in G proteins and GPCRs has already had major implications for understanding the molecular basis of rare endocrine diseases, as well as susceptibility to multifactorial disorders that are associated with polymorphisms in these genes
G protein mutations in endocrine diseases
No full textThis review summarizes the pathogenetic role of naturally occurring mutations of G protein genes in endocrine diseases. Although in vitro mutagenesis and transfection assays indicate that several G proteins have mitogenic potential, to date only two G proteins have been identified which harbor naturally occurring mutations, Gsα, the activator of adenylyl cyclase and Gi2α, which is involved in several functions, including adenylyl cyclase inhibition and ion channel modulation. The gene encoding Gsα (GNAS1) may be altered by loss or gain of function mutations. Indeed, heterozygous inactivating germ line mutations in this gene cause pseudohypoparathyroidism type Ia, in which physical features of Albright hereditary osteodystrophy (AHO) are associated with resistance to several hormones, i.e. PTH, TSH and gonadotropins, that activate Gs-coupled receptors or pseudopseudohypoparathyroidism in which AHO is the only clinical manifestation. Evidence suggests that the variable and tissue-specific hormone resistance observed in PHP Ia may result from tissue-specific imprinting of the GNAS1 gene, although the Gsα knockout model only in part reproduces the human AHO phenotype. Activating somatic Gsα mutations leading to cell proliferation have been identified in endocrine tumors constituted by cells in which cAMP is a mitogenic signal, i.e. GH-secreting pituitary adenomas, hyperfunctioning thyroid adenomas and Leydig cell tumors. When the same mutations occur very early in embryogenesis they cause McCune-Albright syndrome. Although these mutations would in principle confer growth advantage, studies failed to detect differences in the clinical and hormonal phenotypes, suggesting the existence of mechanisms able to counteract the activation of the cAMP pathway. Activating mutations of Gi2α have been identified in a subset of ovarian, adrenal and pituitary tumors, but their prevalence and significance are still controversial. Finally, although Gα subunits are the only components of the heterotrimeric GTP binding proteins which harbor known mutations, β/γ subunits should be considered possible targets of genetic alterations as suggested by the frequent presence of β3 subunit variants in patients with essential hypertension
“Functional Anatomy of the Adipose Organ”
No full text“Functional Anatomy of the Adipose Organ” in: Cachexia and Wasting: A Modern Approach, Ed. by G. Mantovani, , 200
The Financial Value of Entrepreneurship. Using Applied Research to Quantify Entrepreneurial Competence
No full textThis Palgrave Pivot examines the essence of competence value in corporate and small business finance, offering empirical evidence to better understand financial practices within entrepreneurial settings. Mantovani suggests an innovative methodology to detect the financial value of entrepreneurial capabilities. He shows how the concept of competence value and T-ratio, its measurement tool, are necessary to arrange sound entrepreneurial finance deals. This book opens with an analysis of how entrepreneurial skills contribute to the economics of entrepreneurial business, and then provides a financial background to estimate the competence value even when the financial markets fail to do so. The book goes on to introduce the idea of an entrepreneurial life-cycle made of stages based on the transformation of human skills into competitive hallmarks. Applications across a large sample of companies and Mantovani's concluding suggestions about the financial practice make this book essential to both academics and executives
Employment of portable gamma-ray spectrometer in survey and mapping of intrusive complexes: a case study from the Buddusò pluton (Sardinia)
No full texthttp://www.fe.infn.it/u/mantovani/CV/Proceedings/Puccini_10a.pd
INTERNAL CROSSED MODULES AND PEIFFER CONDITION
No full textIn this paper we show that in a homological category in the sense of F.
Borceux and D. Bourn, the notion of an internal precrossed module
corresponding to a star-multiplicative graph, in the sense of G.
Janelidze, can be obtained by directly internalizing the usual axioms of
a crossed module, via equivariance. We then exhibit some sufficient
conditions on a homological category under which this notion coincides
with the notion of an internal crossed module due to G. Janelidze. We
show that this is the case for any category of distributive
Omega(2)-groups, in particular for the categories of groups with
operations in the sense of G. Orzech
Natural radioactivity in Sardinian granite dimension stones
No full texthttp://www.fe.infn.it/u/mantovani/CV/Proceedings/Puccini_10b.pd
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