17 research outputs found

    Import Substitution Industrialization [ISI]: An approach to Global Economic Sustainability

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    Globalisation has over the years brought about openness, thus creating an inextricable link among countries through various channels, including trade and investment. Consequently, there has been a substantial expansion in trade in goods and services and the flow of foreign direct investment between developed and developing countries. Even though, both have benefitted from this global openness, the balance of benefits is mainly tilted to developed countries, reinforced by the fact that developing countries have been importing more and exporting less to these countries – a reflection of the under-developed state of their industrial sector, which is evident in their export of mainly unrefined or primary products, with little or no value addition taking place. This gives attestation to the presence of an insignificant import substitution-oriented manufacturing activity in such countries, which have rendered them heavily reliant on imports for their survival – by extension making them highly susceptible to external risks and shocks. This brought about the inception of ISI, which originated from as early as in the 1930s through into the 1960s in Latin America and some parts of Asia and Africa – a notion that was meant to incorporate three stages, namely ‘domestic production of previously imported non-durable consumer goods, extension of production to a wide-range of consumer durables and complex manufactured items and finally, exporting of manufactured goods, with the vision of diversifying to multiple range of items’ (Bussell,, n/d)

    EMSY overexpression disrupts the BRCA2/RAD51 pathway in the DNA-damage response: implications for chromosomal instability/recombination syndromes as checkpoint diseases

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    EMSY links the BRCA2 pathway to sporadic breast/ovarian cancer. It encodes a nuclear protein that binds to the BRCA2 N-terminal domain implicated in chromatin/transcription regulation, but when sporadically amplified/overexpressed, increased EMSY level represses BRCA2 transactivation potential and induces chromosomal instability, mimicking the activity of BRCA2 mutations in the development of hereditary breast/ovarian cancer. In addition to chromatin/transcription regulation, EMSY may also play a role in the DNA-damage response, suggested by its ability to localize at chromatin sites of DNA damage/repair. This implies that EMSY overexpression may also repress BRCA2 in DNA-damage replication/checkpoint and recombination/repair, coordinated processes that also require its interacting proteins: PALB2, the partner and localizer of BRCA2; RPA, replication/checkpoint protein A; and RAD51, the inseparable recombination/repair enzyme. Here, using a well-characterized recombination/repair assay system, we demonstrate that a slight increase in EMSY level can indeed repress these two processes independently of transcriptional interference/repression. Since EMSY, RPA and PALB2 all bind to the same BRCA2 region, these findings further support a scenario wherein: (a) EMSY amplification may mimic BRCA2 deficiency, at least by overriding RPA and PALB2, crippling the BRCA2/RAD51 complex at DNA-damage and replication/transcription sites; and (b) BRCA2/RAD51 may coordinate these processes by employing at least EMSY, PALB2 and RPA. We extensively discuss the molecular details of how this can happen to ascertain its implications for a novel recombination mechanism apparently conceived as checkpoint rather than a DNA repair system for cell division, survival, death, and human diseases, including the tissue specificity of cancer predisposition, which may renew our thinking about targeted therapy and prevention

    Coronal plane segmental flexibility in thoracic adolescent idiopathic scoliosis assessed by fulcrum-bending radiographs

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    Knowledge about segmental flexibility in adolescent idiopathic scoliosis is crucial for a better biomechanical understanding, particularly for the development of fusionless, growth-guiding techniques. Currently, there is lack of data in this field. The objective of this study was, therefore, to compute segmental flexibility indices (standing angle minus corrected angle/standing angle). We compared segmental disc angles in 76 preoperative sets of standing and fulcrum-bending radiographs of thoracic curves (paired, two-tailed t tests, p > 0.05). The mean standing Cobb angle was 59.7 degrees (range 41.3 degrees -95 degrees ) and the flexibility index of the curve was 48.6% (range 16.6-78.8%). The disc angles showed symmetric periapical distribution with significant decrease (all p values >0.0001) for every cephalad (+) and caudad (-) level change. The periapical levels +1 and -1 wedged at 8.3 degrees and 8.7 degrees (range 3.5 degrees -14.8 degrees ), respectively. All angles were significantly smaller on the-bending views (p values >0.0001). We noted mean periapical flexibility indices of 46% (+1), 49% (-1), 57% (+2) and 81% (-2), which were significantly less (p > 0.001) than for the group of remote levels 105% (+3), 149% (-3), 231% (+4) and 300% (-4). The discal and bony wedging was 60 and 40%, respectively, and mean values 35 degrees and 24 degrees (p > 0.0001). Their relationship with the Cobb angle showed a moderate correlation (r = 0.56 and 0.45). Functional, radiographic analysis of idiopathic thoracic scoliosis revealed significant, homogenous segmental tethering confined to four periapical levels. Future research will aim at in vivo segmental measurements in three planes under defined load to provide in-depth data for novel therapeutic strategies
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