Wide-ranging Implications (wide-ranging + implication)

Distribution by Scientific Domains


Selected Abstracts


Slave prices, the African slave trade, and productivity in the Caribbean, 1674,18071

ECONOMIC HISTORY REVIEW, Issue 4 2005
DAVID ELTIS
We draw wide-ranging implications about slave productivity change by making use of newly collected data on the prices paid for nearly 230,000 slaves as they arrived in the Americas from Africa between 1674 and 1807. Prices for the product that most slaves were destined to produce-sugar-are also available. Together the comprehensive series allow us to derive annual measures of average slave productivity and to compare productivity trends across different sectors of the Caribbean. Average productivity rose throughout the Caribbean, and the pattern of average productivity change across regions was similar, indicating an open slave market. These averages mask sharp differences in the growth of demand for slaves among regions, as reflected by their slave populations. Between 1700 and 1790 the increase in demand ranged from 90 per cent in Barbados to 600 per cent in Jamaica and Cuba; while total factor productivity overall may have doubled. The slave trade accommodated the rising demand. It also served to offset population attrition among the slaves. [source]


Challenging the omnipotence of the suprachiasmatic timekeeper: are circadian oscillators present throughout the mammalian brain?

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2007
Clare Guilding
Abstract The suprachiasmatic nucleus of the hypothalamus (SCN) is the master circadian pacemaker or clock in the mammalian brain. Canonical theory holds that the output from this single, dominant clock is responsible for driving most daily rhythms in physiology and behaviour. However, important recent findings challenge this uniclock model and reveal clock-like activities in many neural and non-neural tissues. Thus, in addition to the SCN, a number of areas of the mammalian brain including the olfactory bulb, amygdala, lateral habenula and a variety of nuclei in the hypothalamus, express circadian rhythms in core clock gene expression, hormone output and electrical activity. This review examines the evidence for extra-SCN circadian oscillators in the mammalian brain and highlights some of the essential properties and key differences between brain oscillators. The demonstration of neural pacemakers outside the SCN has wide-ranging implications for models of the circadian system at a whole-organism level. [source]


The pathology of hypertrophic cardiomyopathy

HISTOPATHOLOGY, Issue 5 2004
S E Hughes
Sudden cardiac death (SCD) is devastating at any age, but even more so when the individual affected is young and asymptomatic, and the death is entirely unexpected. SCD is a catastrophic complication of hypertrophic cardiomyopathy (HCM) and may be the first manifestation of this disease. HCM is an inherited intrinsic disease of the myocardium characterized by left ventricular hypertophy without chamber dilatation, in the absence of either a systemic or other cardiac disease, which may cause a similar magnitude of hypertrophy. HCM may be a clinically silent disease. Indeed, the pathologist may be the first to encounter a case of HCM at autopsy. HCM has wide-ranging implications for affected families, who will require cardiac screening and genetic counselling even if mutations are not known. Therefore, prompt and accurate diagnosis of HCM is vital. This review article will focus on the pathological diagnosis of HCM, recent advances in the genetics of this disease, and common pitfalls which may arise, leading to diagnostic uncertainty. [source]


Apoptosis: a basic biological phenomenon with wide-ranging implications in human disease

JOURNAL OF INTERNAL MEDICINE, Issue 6 2005
B. FADEEL
Abstract. Apoptosis is a highly regulated process of cell deletion and plays a fundamental role in the maintenance of tissue homeostasis in the adult organism. Numerous studies in recent years have revealed that apoptosis is a constitutive suicide programme expressed in most, if not all cells, and can be triggered by a variety of extrinsic and intrinsic signals. Many human diseases can be attributed directly or indirectly to a derangement of apoptosis, resulting in either cell accumulation, in which cell eradication or cell turnover is impaired, or cell loss, in which the apoptotic programme is inadvertently triggered. In addition, defective macrophage engulfment and degradation of cell corpses may also contribute to a dysregulation of tissue homeostasis. An increased understanding of the signalling pathways that govern the execution of apoptosis and the subsequent clearance of dying cells may thus yield novel targets for therapeutic intervention in a wide range of human maladies. [source]


Current and emerging concepts in tumour metastasis,

THE JOURNAL OF PATHOLOGY, Issue 1 2010
Caroline Coghlin
Abstract Disseminated cancer accounts for most deaths due to malignancy. Despite this, research has focused predominantly on tumour development and progression at the primary site. Recently, attention has shifted towards the field of tumour metastasis. Several new and exciting concepts that have emerged in the past few years may shed light on this complex area. The established canonical theory of tumour metastasis, as a process emerging from a stepwise accumulation of genetic events fuelled by clonal evolution, has been challenged. New evidence suggests that malignant cells can disseminate at a much earlier stage than previously recognized in tumourigenesis. These findings have direct relevance to clinical practice and shed new light on tumour biology. Gene-profiling studies support this theory, suggesting that metastatic ability may be an innate property shared by the bulk of cells present early in a developing tumour mass. There is a growing recognition of the importance of host factors outside the primary site in the development of metastatic disease. The role of the ,pre-metastatic niche' is being defined and with this comes a new understanding of the function of bone marrow-derived progenitor cells in directing the dissemination of malignant cells to distant sites. Current research has highlighted the crucial roles played by non-neoplastic host cells within the tumour microenvironment in regulating metastasis. These new concepts have wide-ranging implications for our overall understanding of tumour metastasis and for the development of cancer therapeutics. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]


Molecular complementarity between tetracycline and the GTPase active site of elongation factor Tu

ACTA CRYSTALLOGRAPHICA SECTION D, Issue 11 2006
Susan E. Heffron
Two crystal forms of a complex between trypsin-modified elongation factor Tu,MgGDP from Escherichia coli and the antibiotic tetracycline have been solved by X-ray diffraction analysis to resolutions of 2.8 and 2.1,Å, respectively. In the P21 form, cocrystals were grown from a solution mixture of the protein and tetracycline. Six copies of the trypsin-modified EF-Tu,MgGDP,tetracycline complex are arranged as three sets of dimers in the asymmetric unit. In the second crystal form, tetracycline was diffused into P43212 crystals, resulting in a monomeric complex in the asymmetric unit. Atomic coordinates have been refined to crystallographic R factors of 18.0% for the P21 form and 20.0% for the P43212 form. In both complexes, tetracycline makes significant interactions with the GTPase active site of EF-Tu. The phenoldiketone moiety of tetracycline interacts directly with the Mg2+, the ,-­phosphate group of GDP and two amino acids, Thr25 and Asp80, which are conserved in the GX4GKS/T and DX2G sequence motifs found in all GTPases and many ATPases. The molecular complementarity, previously unrecognized between invariant groups present in all GTPase/ATPases and the active moiety of tetracycline, may have wide-ranging implications for all drugs containing the phenoldiketone moiety as well as for the design of new compounds targeted against a broad range of GTPases or ATPases. [source]