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Principal Role (principal + role)
Selected AbstractsVillein rents in thirteenth,century England: an analysis of the Hundred Rolls of 1279,1280ECONOMIC HISTORY REVIEW, Issue 4 2002Junichi Kanzaka What factors played the principal role in determining the level of villein rents in thirteenth,century England? Historians have assumed three factors: economic and demographic forces, seigneurial power, and custom. This analysis of the Hundred Rolls of 1279,80 for Cambridgeshire, Huntingdonshire, Oxfordshire, and Warwickshire indicates that community custom was the most important factor. It is only on ecclesiastical estates in Huntingdonshire that seigneurial power had a decisive influence in imposing heavy labour services on villeins. Furthermore, since villeins were protected by custom, the level of their rents was usually lower than that of competitive freehold rents, which reflected market forces. [source] Differential expression of E-cadherin in metastatic lesionscomparing to primary oral squamous cell carcinomaJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 10 2006K.-F. Hung Background:, The main cause of treatment failure in resectable oral squamous cell carcinoma (OSCC) is metastasis. E-cadherin (E-cad) plays a principal role in cell adhesion and motility, and is associated with OSCC progression. The aim of this study was to investigate the clinical significance of E-cad expression in OSCC with lymph node metastasis which had radical neck dissection done. Method:, Immunohistochemistry was used to detect E-cad expression in normal oral mucosa (NOM) (n = 10), oral precancerous lesions (OPLs) (n = 20), primary OSCC (n = 45), and their paired metastatic lesions (n = 45). E-cad immunoreactivity correlated with the clinicopathologic features. Results:, E-cadherin immunoreactivity was progressively reduced in the NOM followed by OPLs and primary OSCC (58%). It decreased significantly in the advanced stages of OSCC. However, the increase in E-cad immunoreactivity was observed in the majority (60%) of metastatic lesions in relation to primary OSCC. Patients with such increased or positive immunoreactivity of E-cad in metastatic lesions exhibited worse prognosis. Conclusion:, The findings suggested a dynamic change in E-cad immunoreactivity during tumorigenesis and metastasis of OSCC. In a multivariate analysis, E-cad immunoreactivity in metastasis lesions (odds ratio 3.74, 95% CI 1.15,14.67; P = 0.040) implied the potential role of mortality predictors for OSCC cases with nodal involvement. [source] Molecular determinants of inactivation in voltage-gated Ca2+ channelsTHE JOURNAL OF PHYSIOLOGY, Issue 2 2000Steffen Hering Evolution has created a large family of different classes of voltage-gated Ca2+ channels and a variety of additional splice variants with different inactivation properties. Inactivation controls the amount of Ca2+ entry during an action potential and is, therefore, believed to play an important role in tissue-specific Ca2+ signalling. Furthermore, mutations in a neuronal Ca2+ channel (Cav2.1) that are associated with the aetiology of neurological disorders such as familial hemiplegic migraine and ataxia cause significant changes in the process of channel inactivation. Ca2+ channels of a given subtype may inactivate by three different conformational changes: a fast and a slow voltage-dependent inactivation process and in some channel types by an additional Ca2+ -dependent inactivation mechanism. Inactivation kinetics of Ca2+ channels are determined by the intrinsic properties of their pore-forming ,1 -subunits and by interactions with other channel subunits. This review focuses on structural determinants of Ca2+ channel inactivation in different parts of Ca2+ channel ,1 -subunits, including pore-forming transmembrane segments and loops, intracellular domain linkers and the carboxyl terminus. Inactivation is also affected by the interaction of the ,1 -subunits with auxiliary ,-subunits and intracellular regulator proteins. The evidence shows that pore-forming S6 segments and conformational changes in extra- (pore loop) and intracellular linkers connected to pore-forming segments may play a principal role in the modulation of Ca2+ channel inactivation. Structural concepts of Ca2+ channel inactivation are discussed. [source] Local helioseismology in the SDO HMI/AIA data analysis pipelineASTRONOMISCHE NACHRICHTEN, Issue 3-4 2007R. S. Bogart Abstract Local helioseismology techniques will play a principal role in the pipeline processing of data from HMI to produce standard data products suitable for scientific analysis. Many of these techniques are undergoing rapid development, and it is expected that new or enhanced algorithms and models will be contributed by members of the community. We describe the design and implementation of the data analysis environment of the SDO Joint Science Operations Center for the benefit of potential contributors and users. (© 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] DNA repair dysfunction in gastrointestinal tract cancersCANCER SCIENCE, Issue 3 2008Yoshihiko Maehara The DNA repair system surveys the genome, which is always suffering from exposure to both exogenous as well as endogenous mutagens, to maintain the genetic information. The fact that the basis of this DNA repair system is highly conserved, from prokaryote to mammalian cells, suggests the importance of precise genome maintenance mechanisms for organisms. In the past 15 years, considerable progress has been made in understanding how repair processes interact and how disruptions of these mechanisms lead to the accumulation of mutations and carcinogenesis. In 1993, two groups reported that DNA mismatch repair could be associated with hereditary non-polyposis colorectal cancer, indicating a connection between faulty DNA repair function and cancer. More recently, an inherited disorder of DNA glycosylase, which removes mutagenic oxidized base from DNA, has been reported in individuals with a predisposition to multiple colorectal adenomas and carcinomas. This is the first report that directly indicates the role of the repair of oxidative DNA in human inherited cancer. Studies from gene knockout mice have elucidated the principal role of these repair systems in the process of carcinogenesis. Moreover, clinical samples derived from cancer patients have shown the direct involvement. This review focuses on the function of DNA mismatch repair and oxidative DNA/nucleotide repair among various DNA repair systems in cells, both of which are essentially involved in the carcinogenesis of gastrointestinal tract cancer. (Cancer Sci 2008; 99: 451,458) [source] Functions and effectors of the Salmonella pathogenicity island 2 type III secretion systemCELLULAR MICROBIOLOGY, Issue 8 2003Scott R. Waterman Summary Salmonella enterica uses two functionally distinct type III secretion systems encoded on the pathogenicity islands SPI-1 and SPI-2 to transfer effector proteins into host cells. A major function of the SPI-1 secretion system is to enable bacterial invasion of epithelial cells and the principal role of SPI-2 is to facilitate the replication of intracellular bacteria within membrane-bound Salmonella -containing vacuoles (SCVs). Studies of mutant bacteria defective for SPI-2-dependent secretion have revealed a variety of functions that can be attributed to this secretion system. These include an inhibition of various aspects of endocytic trafficking, an avoidance of NADPH oxidase-dependent killing, the induction of a delayed apoptosis-like host cell death, the control of SCV membrane dynamics, the assembly of a meshwork of F-actin around the SCV, an accumulation of cholesterol around the SCV and interference with the localization of inducible nitric oxide synthase to the SCV. Several effector proteins that are translocated across the vacuolar membrane in a SPI-2-dependent manner have now been identified. These are encoded both within and outside SPI-2. The characteristics of these effectors, and their relationship to the physiological functions listed above, are the subject of this review. The emerging picture is of a multifunctional system, whose activities are explained in part by effectors that control interactions between the SCV and intracellular membrane compartments. [source] |