Investigations over the last decade have established the essential role of growth factors and their receptors during angiogenesis. The biological significance of VEGF, EGF, and bFGF is mediated by their receptors, which belong to the family of tyrosine kinase receptors: Flt-1 (VEGFR-1), KDR (VEGFR-2), EGFR, FGFR-1, FGFR-2, FGFR-3, and FGFR-4. Deeper understanding of the mechanism of activation of these growth factor receptors has allowed the development of a new pharmacological strategy aimed at controlling cancer cell proliferation. The results of a large body of preclinical as well as early clinical studies conducted suggest that targeting the growth factor receptors could represent a significant contribution to cancer therapy.
Molecular biologic investigations in the past decades have begun to unravel the intracellular mechanisms involved in vasomotor regulation of cerebral blood vessels and their failure in delayed cerebral vasospasm produced by aneurysmal subarachnoid hemorrhage. Progress in deciphering macrovascular regulatory mechanisms and their failure in delayed cerebral vasospasm induced by aneurysmal subarachnoid hemorrhage have revealed that there are at least two important vasoactive substances-nitric oxide and endothelin-1-that play important roles in the clinical manifestations of subarachnoid-hemorrhage-induced cerebral vasospasm. Nitric oxide is a cell-membrane-permeable free radical gas that accounts for the phenomenon of vasodilatation by a variety of vasodilator agents. Endothelin-1, a 21 amino acid peptide, is one of the most potent constricting factors. Cerebral vasospasm is thought to represent a disturbance in the cerebral vasomotor equilibrium for which these two physiologically antagonistic compounds are at least partly responsible. Advances in our understanding of the molecular responses of the cerebral vasculature to subarachnoid hemorrhage should lead to more comprehensive management as knowledge becomes translated into development of effective pharmacologic agents to reverse or prevent cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
ABSTRACT:Objective:To describe simple modifications of the technique of opening and closure of the craniotomy to improve basal exposure and reconstruction.Methods:The modifications involve: a) additional soft-tissue dissection which is carried downward to the base of the ear and to the orbital rim, exposing the orbital rim and malar eminence without removing the bone; b) cutting the bone flap so that ‘bridges’ of bone remain that help to stabilize the flap when it is returned to the cranium at the end of the operation; c) the wedging of bone chips between the bone flap and native cranium at the time the bone is being reaffixed so as to provide firm stability by diminishing movement of the bone flap; d) the use of bone dust and bone chips mixed with the patient's blood to seal and bridge the gap between the bone flap and the native bone; e) reattachment of the temporalis muscle with the bone flap sutures. An ‘inlay’ technique of duraplasty is also described.Results and Conclusion:These simple modifications of craniotomy provide better basal exposure and reconstruction with little additional operating time at no additional cost.
The diversity inherent in every organ has its roots in gene-expression variation and is revealed through distinctions in the molecular profile and hence the identity of individual cell type. Study into the molecular mechanisms of the development of individual cell type within the pituitary, which is under the control of transcription factors, has provided a basis for a deeper insight into the molecular mechanisms underlying the pathogenesis of a variety of hormone-producing pituitary tumors. Identification of some of these transcription factors in pituitary adenomas further supports their role in the pathogenesis of pituitary adenomas. Understanding the molecular mechanisms of regulation of proliferation of pituitary cell types by transcription factors offers a basis for hope that rational genetic or pharmacologic therapies for pituitary tumors can be designed in the future.
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