The aim of this paper is to explore a theoretical framework that can assist in under-standing the extent to which the increased integration of macro-regional economies (such as the European and North American) and the global economy is leading to divergence and/or convergence in the pattern of economic activity and the distribution of value-added and wealth. In particular, the paper focuses on the extent to which changing divisions of labour, the production, appropriation and allocation of value, and economic organization underpin these processes of convergence/divergence. We focus on developing an understanding of the changing divisions of labour across space in increasingly integrated macro-regional economies such as Europe and North America, and the (unequal) flows of value between places that underpin mosaics of territorial inequality. We argue that the production and flows of value associated with different forms of economic activities and commodity production and exchange in different localities provides a framework for understanding changing geographical divisions of labour. We also argue that a critical engagement with the range of work associated with analysing ‘commodity chains’ and ‘commodity networks’ provides a way into thinking about the (dis)organization of economic activity and value creation, appropriation and distribution. In particular, we argue that the focus on the commodity, while initially helpful, is misplaced because commodities embody and carry with them relations of value. Consequently, our attention should be focused on the organization of the production, appropriation and realization of value flows and the various forces that structure these processes, such as state governance, labour organization, corporate practices and so on, that are fundamental to understanding the (re)configuration of economic activity in macro-regional economies.
A number of cancers predominantly metastasize to bone, due to its complex microenvironment and multiple types of constitutive cells. Prostate cancer especially has been shown to localize preferentially to bones with higher marrow cellularity. Using an experimental prostate cancer metastasis model, we investigated the effects of cyclophosphamide, a bone marrow-suppressive chemotherapeutic drug, on the development and growth of metastatic tumors in bone. Priming the murine host with cyclophosphamide prior to intra-cardiac tumor cell inoculation was found to significantly promote tumor localization and subsequent growth in bone. Shortly after cyclophosphamide treatment, there was an abrupt expansion of myeloid lineage cells in the bone marrow and the peripheral blood, associated with increases in cytokines with myelogenic potential such as C-C chemokine ligand (CCL)-2, interleukin (IL)-6, and vascular endothelial growth factor (VEGF)-A. More importantly, neutralizing host-derived murine CCL2, but not IL-6, in the pre-metastatic murine host significantly reduced the pro-metastatic effects of cyclophosphamide. Together, our findings suggest that bone marrow perturbation by cytotoxic chemotherapy can contribute to bone metastasis via a transient increase in bone marrow myeloid cells and myelogenic cytokines. These changes can be reversed by inhibition of CCL2.
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