A Comparative Analysis of Case Studies from the Old World

The present contribution deals with the concepts of marginal habitats in selected regions of the ancient world, ranging from modern Spain to the Jordanian desert and from Turkey to the Ethiopian highlands. Central to this research is the hypothesis that the occupation of areas beyond the ‘normal’ settlement patterns corresponds to colonization processes which reflect specific social strategies and may have stimulated the development of new technological skills. A review of ‘marginality’ research in various disciplines indicates that there is no comprehensive definition of the concept, which can be approached from a multitude of perspectives and with manifold objectives. A survey of the eight case studies and two more in-depth discussions of the sites of Musawwarat (Sudan) and Ayamonte (Spain) highlight the potentials as well as the limits of the archaeological investigation into past marginalities. Patterns of spatial marginalization are the easiest to detect. The studies also show that we must not limit our analysis to the adverse factors connected to different kinds of marginalities. Instead, our analyses suggest that spatially marginal areas were deliberately chosen for settlement – an integration with core-periphery approaches may help us to understand these scenarios, which have received little attention in ‘marginality’ research in archaeology or elsewhere so far

Observation of enhanced subthreshold K+ production in central collisions between heavy nuclei

In the very heavy collision system 197Au+197Au the K+ production process was studied as a function of impact parameter at 1 GeV/nucleon, a beam energy well below the free N-N threshold. The K+ multiplicity increases more than linearly with the number of participant nucleons and the K+/ pi + ratio rises significantly when going from peripheral to central collisions. The measured K+ double differential cross section is enhanced by a factor of 6 compared to microscopic transport calculations if secondary processes (Delta N-->K Lambda N and Delta Delta -->K Lambda N) are ignored

Ultraviolet-radiation-induced inflammation promotes angiotropism and metastasis in melanoma

Intermittent intense ultraviolet (UV) exposure represents an important aetiological factor in the development of malignant melanoma(1). The ability of UV radiation to cause tumour-initiating DNA mutations in melanocytes is now firmly established(2), but how the microenvironmental effects of UV radiation(3,4) influence melanoma pathogenesis is not fully understood. Here we report that repetitive UV exposure of primary cutaneous melanomas in a genetically engineered mouse model(5) promotes metastatic progression, independent of its tumour-initiating effects. UV irradiation enhanced the expansion of tumour cells along abluminal blood vessel surfaces and increased the number of lung metastases. This effect depended on the recruitment and activation of neutrophils, initiated by the release of high mobility group box 1 (HMGB1) from UV-damaged epidermal keratinocytes and driven by Toll-like receptor 4 (TLR4). The UV-induced neutrophilic inflammatory response stimulated angiogenesis and promoted the ability of melanoma cells to migrate towards endothelial cells and use selective motility cues on their surfaces. Our results not only reveal how UV irradiation of epidermal keratinocytes is sensed by the innate immune system, but also show that the resulting inflammatory response catalyses reciprocal melanoma-endothelial cell interactions leading to perivascular invasion, a phenomenon originally described as angiotropism in human melanomas by histopathologists(6). Angiotropism represents a hitherto underappreciated mechanism of metastasis(7) that also increases the likelihood of intravasation and haematogenous dissemination. Consistent with our findings, ulcerated primary human melanomas with abundant neutrophils and reactive angiogenesis frequently show angiotropism and a high risk for metastases. Our work indicates that targeting the inflammation-induced phenotypic plasticity of melanoma cells and their association with endothelial cells represent rational strategies to specifically interfere with metastatic progression