By K. Thapar, K. Kovacs, E. R. Laws (auth.), L. Symon, L. Calliauw, F. Cohadon, V. V. Dolenc, J. Lobo Antunes, H. Nornes, J. D. Pickard, H.-J. Reulen, A. J. Strong, N. de Tribolet (eds.)
As an addition to the eu postgraduate education process for younger neurosurgeons we started to post in 1974 this sequence of Advances and Technical criteria in Neurosurgery which was once later subsidized through the ecu organization of Neurosurgical Societies. This sequence used to be fust mentioned in 1972 at a mixed assembly of the Italian and German Neurosurgical Societies in Taormina, the founding fathers of the sequence being Jean Brihaye, Bernard Pertuiset, Fritz Loew and Hugo KrayenbUhl. therefore have been confirmed the rules of ecu co operation which were born from the ecu spirit, flourished within the ecu organization, and feature all through been linked to this sequence. the truth that the English language is definitely with the intention to changing into the foreign medium at eu medical meetings is a smart asset by way of mutual knowing. for this reason we've made up our minds to submit all contributions in English, whatever the local language of the authors. All contributions are submitted to the total editorial board sooner than publi cation of any quantity. Our sequence isn't really meant to compete with the guides of unique clinical papers in different neurosurgical journals. Our purpose is, particularly, to offer fields of neurosurgery and similar components within which very important contemporary advances were made. The contributions are written through experts within the given fields and represent the fust a part of every one volume.
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Moreover, the latter study demonstrated that constitutive activation of Gs could be accomplished by specific mutations involving the alpha chain gene. The alpha chain protein encoded by such mutations exhibited an intrinsic deficiency of GTPase activity, rendering it incapable of self-terminating its activated state. Therefore, such activating mutations stabilize Gs in its active conformation, thus mimicking the effect of persistent GHRH action. By-passing the normal regulatory control provided by GHRH, somatotrophs bearing the mutated alpha chain are conferred an autonomous and unrestrained capacity for GH secretion and cell proliferation, manifesting ultimately as neoplastic transformation.
Whereas such a somatic mutation perspective conforms well to contemporary paradigms of human tumorigenesis, it also tends to minimize the role of hypothalamic influences in pituitary tumor development. Such a tendency may not be fully justified, particularlY in view of the abundant clinical and experimental evidence implicating a hypothalamic component to pituitary tumorigenesis (see "endocrine factors", below). Thus, despite the compelling evidence favoring an intrinsic etiology to pituitary tumor development, the pathophysiologic component of hypothalamic dysfunction cannot be entirely ignored and must somehow be integrated in the current monoclonal model of pituitary tumorigenesis.
THAPAR et af. practical relevance, is the relationship between the behavior of corticotroph adenomas and thyrotroph adenomas treated with bilateral adrenalectomy and thyroidectomy, respectively. That such tumors tend to be notoriously more aggressive than those having intact pituitary-target gland axes emphasizes the pathophysiological importance of target gland feedback inhibition in modulating the progression of these tumors (Wilson et af. 1979). A final endocrine issue, one repeatedly implicated in the genesis of pituitary adenomas, particularly PRL producing adenomas, concerns the role of estrogens as mediators of transformation and/or neoplastic progression in the pituitary.