Globalization of biotechnology: The agglomeration of dispersed knowledge and information and its implications for the political economy of technology in developing countries

This study examines a contradictory development in the era of globalization wherein country-specific economic and socio-political institutional environment limits the global flow of technological knowledge and information, particularly in the biotechnology sector. International collaborations for developing new biotechnologies has increased significantly in recent years, but these have virtually bypassed firms in developing countries. The international flow of technologies tends to agglomerate in developed economies particularly in the US, where an appropriate mix of economic choices, social regulation and state action fostered institutional environments that facilitated the development and commercialization of biotechnologies. Moreover, with the heightening competition in the global economy, state and firms of developed economies have evolved into a relationship of close partnership. This shows that, far from being irrelevant, the state remains a political entity that structures the innovation system in order to promote the well-being of its firms. This calls for a re-thinking of the role of the state in technological and economic development, particularly among the developing economies.     

Pioneer settlement of the cold-water coral Desmophyllum dianthus (Esper, 1794) on plastic

Coral Reefs - Larval settlement is a critical step for sessile benthic species such as corals, whose ability to thrive on diverse natural and anthropogenic substrates may lead to a competitive...     

Virulence Factors and Antifungal Susceptibility in Candida Species Isolated from Dermatomycosis Patients

Mycopathologia - Dermatomycoses caused by Candida spp. are increasingly common, however there are few reports in the literature regarding their epidemiology, pathogenesis and antifungal...     

Prenatal and pubertal exposure to 17α-ethinylestradiol cause morphological changes in the prostate of old gerbils

This study evaluated such as exposure to ethinylestradiol during the prenatal (18th–22nd day) and pubertal (42nd–49th day) periods acts on the male ventral prostate and female prostate of 12-month old gerbils. We performed the analysis to serum hormone levels for estradiol and testosterone. The prostates were submitted to morphometric and immunohistochemical analyses. Exposure to ethinylestradiol during these developmental periods decreased the testosterone serum levels in males and increased the estradiol serum levels in females. Morphologically, prostate intraepithelial neoplasia and disorders in the arrangement of the fibrous components were observed in the prostate glands of both sexes of gerbil exposed to ethinylestradiol during development periods. In the male prostate, the ethinylestradiol promoted decreased in the frequency of positive epithelial cell for androgen receptor (AR) and increased the frequency of positive stromal cell for estrogen receptor α. However, in the female prostate, this synthetic estrogen caused AR upregulation and increased cell proliferation. This study shows that the exposure to ethinylestradiol during development phases alters the morphology and the hormonal signaling in the male and female prostates of old gerbils, confirming the action of ethinylestradiol as endocrine disruptor.     

Assessment of oxidative status and genotoxicity in photocopier operators: a pilot study

Occupational exposure to photocopiers has been indicated as being responsible for a number of health complaints, particularly effects on the respiratory, immunological, and nervous systems. In this study, we investigated oxidative and genotoxic damage in photocopier operators by assessing catalase activity (CAT), reduced vs. oxidized glutathione ratio (GSH/GSSG), level of lipid peroxidation (TBARS), damage index by Comet assay (DICA), and buccal cells with micronuclei (BCMN). Our results reveal that the TBARS levels in operators were increased (27%; p<0.05) but that no significant alterations to GSH/GSSG or CAT activity were observed. The DICA and the number of BCMN were significantly increased (134% and 100%, respectively; p<0.05) in the exposed group. There was a significant association between the time in months spent at work and DNA damage in lymphocytes (r(s)?=?0.720; p<0.001) and buccal cell with MN (r(s)?=?0.538; p<0.001). Because laser printers and photocopiers have become increasingly used, it is important to control human exposure using reliable biomarkers.     

Coordinated involvement of cathepsins S, D and cystatin C in the commitment of hematopoietic stem cells to dendritic cells

The identity of biochemical players which underpin the commitment of CD34(+) hematopoietic stem cells to immunogenic or tolerogenic dendritic cells is largely unknown. To explore this issue, we employed a previously established cell-based system amenable to shift dendritic cell differentiation from the immunogenic into the tolerogenic pathway upon supplementation with a conventional cytokine cocktail containing thrombopoietin (TPO) and IL-16. We show that stringent regulation of cathepsins S and D, two proteases involved in antigen presentation, is crucial to engage cell commitment to either route. In response to TPO+IL-16-dependent signaling, both cathepsins undergo earlier maturation and down-regulation. Additionally, cystatin C orchestrates cathepsin S expression through a tight but reversible interaction that, based on a screen of adult stem cells from disparate origins, CD14(+) cells, primary fibroblasts and the MCF7 cell line, appears unique to CD34(+) stem cells from peripheral and cord blood. As shown by CD4(+) T cell proliferation in mixed-lymphocyte reactions, cell commitment to either pathway is disrupted upon cathepsin knockdown by RNAi. Surprisingly, similar effects were also observed upon gene overexpression, which prompts atypically accelerated maturation of cathepsins S and D in cells of the immunogenic pathway, similar to the tolerogenic route. Furthermore, RNAi studies revealed that cystatin C is a proteolytic target of cathepsin D and has a direct, causal impact on cell differentiation. Together, these findings uncover a novel biochemical cluster that is subject to time-controlled and rigorously balanced expression to mediate specific stem cell commitment at the crossroads towards tolerance or immunity.     

Defect in mevalonate pathway induces pyroptosis in Raw 264.7 murine monocytes

The inhibition of mevalonate pathway by the aminobisphosphonate alendronate (ALD) has been previously associated with an augmented lipopolysaccharide-induced interleukin-1beta (IL-1β) secretion in monocytes, as demonstrated in an auto-inflammatory disease known as mevalonate kinase deficiency (MKD). In this study we investigated the effect of ALD + LPS on monocyte cell line (Raw 264.7) death. ALD strongly augmented LPS-induced programmed cell death (PCD) as well as IL-1β secretion in Raw murine monocytes, whereas necrosis was rather unaffected. ALD + LPS induced caspase-3 activation. Inhibition of IL-1β stimulation partially restored cell viability. These findings suggest that the inhibition of mevalonate pathway, together with a bacterial stimulus, induce a PCD partly sustained by the caspase-3-related apoptosis and partly by caspase-1-associated pyroptosis. The involvement of pyroptosis is a novel hit in our cell model and opens discussions about its role in inflammatory cells with chemical or genetic inhibition of mevalonate pathway.