North-South technology transfer in unionised multinationals

We study how incentives for North-South technology transfers in multinational enterprises are affected by labour market institutions. If workers are collectively organised, incentives for technology transfers are partly governed by .rms. desire to curb trade union power. This will affect not only the extent but also the type of technology transfer. While skill upgrading of southern workers benefits these workers at the expense of northern worker welfare, quality upgrading of products produced in the South may harm not only northern but also southern workers. A minimum wage policy to raise the wage levels of southern workers may spur technology transfer, possibly to the extent that the utility of northern workers decline. These conclusions are reached in a setting where a unionised multinational multiproduct firm produces two vertically differentiated products in northern and southern subsidiaries, respectively.FEDERQRENCOMPETEFundação para a Ciência e a Tecnologia (FCT

Ready Both to Your and to My Hands: Mapping the Action Space of Others

To date, mutual interaction between action and perception has been investigated mainly by focusing on single individuals. However, we perceive affording objects and acts upon them in a surrounding world inhabited by other perceiving and acting bodies. Thus, the issue arises as to whether our action-oriented object perception might be modulated by the presence of another potential actor. To tackle this issue we used the spatial alignment effect paradigm and systematically examined this effect when a visually presented handled object was located close either to the perceiver or to another individual (a virtual avatar). We found that the spatial alignment effect occurred whenever the object was presented within the reaching space of a potential actor, regardless of whether it was the participant's own or the other's reaching space. These findings show that objects may afford a suitable motor act when they are ready not only to our own hand but also, and most importantly, to the other's hand. Our proposal is that this effect is likely to be due to a mapping of our own and the other's reaching space and we posit that such mapping could play a critical role in joining our own and the other's action

Knowledge of risk factors, beliefs and practices of female healthcare professionals towards breast cancer in a tertiary institution in Lagos, Nigeria

<p>Abstract</p> <p>Background</p> <p>Breast cancer is the leading female malignancy in Nigeria. Screening for early detection has led to reduction in mortality from the disease. It is known that attitudes of physicians and motivation by community nurses influence uptake of screening methods by women. This study aims to investigate knowledge of breast cancer risk factors, beliefs about treatment and practice of screening methods among a cohort of female healthcare professionals in Lagos, Nigeria.</p> <p>Methods</p> <p>A cross-sectional study was conducted using a self-administered questionnaire to assess the knowledge of breast cancer risk factors, beliefs about treatment and practice of screening methods among 207 female doctors, nurses and other healthcare professionals working in a university teaching hospital in Lagos, Nigeria. Stratified random sampling method was employed. Chi square test, analysis of variance and Mantel-Haenszel test were performed in data analysis using SPSS v10.0 and Epi Info version 6 statistical packages.</p> <p>Results</p> <p>Female doctors obtained a mean knowledge score of 74% and were the only professional group that had satisfactory knowledge of risk factors. Majority (86%) believed that early breast cancer is curable while half of participants believed that prayer can make breast cancer disappear from the affected breast. Eighty three percent practice breast self-examination (BSE) once a month and only 8% have ever had a mammogram. Age, knowledge of risk factors, profession and beliefs were not significantly associated with rate of BSE in this study.</p> <p>Conclusion</p> <p>Results from this study suggest the need for continuing medical education programmes aimed at improving knowledge of breast cancer among female healthcare providers other than doctors.</p

Peripersonal space representation develops independently from visual experience

Our daily-life actions are typically driven by vision. When acting upon an object, we need to represent its visual features (e.g. shape, orientation, etc.) and to map them into our own peripersonal space. But what happens with people who have never had any visual experience? How can they map object features into their own peripersonal space? Do they do it differently from sighted agents? To tackle these questions, we carried out a series of behavioral experiments in sighted and congenitally blind subjects. We took advantage of a spatial alignment effect paradigm, which typically refers to a decrease of reaction times when subjects perform an action (e.g., a reach-To-grasp pantomime) congruent with that afforded by a presented object. To systematically examine peripersonal space mapping, we presented visual or auditory affording objects both within and outside subjects' reach. The results showed that sighted and congenitally blind subjects did not differ in mapping objects into their own peripersonal space. Strikingly, this mapping occurred also when objects were presented outside subjects' reach, but within the peripersonal space of another agent. This suggests that (the lack of) visual experience does not significantly affect the development of both one's own and others' peripersonal space representation

Inhibition of the Progesterone Nuclear Receptor during the Bone Linear Growth Phase Increases Peak Bone Mass in Female Mice

Augmentation of the peak bone mass (PBM) may be one of the most effective interventions to reduce the risk of developing osteoporosis later in life; however treatments to augment PBM are currently limited. Our study evaluated whether a greater PBM could be achieved either in the progesterone nuclear receptor knockout mice (PRKO) or by using a nuclear progesterone receptor (nPR) antagonist, RU486 in mice. Compared to their wild type (WT) littermates the female PRKO mice developed significantly higher cancellous and cortical mass in the distal femurs, and this was associated with increased bone formation. The high bone mass phenotype was partially reproduced by administering RU486 in female WT mice from 1–3 months of age. Our results suggest that the inhibition of the nPR during the rapid bone growth period (1–3 months) increases osteogenesis, which results in acquisition of higher bone mass. Our findings suggest a crucial role for progesterone signaling in bone acquisition and inhibition of the nPR as a novel approach to augment bone mass, which may have the potential to reduce the burden of osteoporosis

A Pro-Cathepsin L Mutant Is a Luminal Substrate for Endoplasmic-Reticulum-Associated Degradation in C. elegans

Endoplasmic-reticulum associated degradation (ERAD) is a major cellular misfolded protein disposal pathway that is well conserved from yeast to mammals. In yeast, a mutant of carboxypeptidase Y (CPY*) was found to be a luminal ER substrate and has served as a useful marker to help identify modifiers of the ERAD pathway. Due to its ease of genetic manipulation and the ability to conduct a genome wide screen for modifiers of molecular pathways, C. elegans has become one of the preferred metazoans for studying cell biological processes, such as ERAD. However, a marker of ERAD activity comparable to CPY* has not been developed for this model system. We describe a mutant of pro-cathepsin L fused to YFP that no longer targets to the lysosome, but is efficiently eliminated by the ERAD pathway. Using this mutant pro-cathepsin L, we found that components of the mammalian ERAD system that participate in the degradation of ER luminal substrates were conserved in C. elegans. This transgenic line will facilitate high-throughput genetic or pharmacological screens for ERAD modifiers using widefield epifluorescence microscopy

HMGA1 drives stem cell, inflammatory pathway, and cell cycle progression genes during lymphoid tumorigenesis

<p>Abstract</p> <p>Background</p> <p>Although the <it>high mobility group A1 </it>(<it>HMGA1</it>) gene is widely overexpressed in diverse cancers and portends a poor prognosis in some tumors, the molecular mechanisms that mediate its role in transformation have remained elusive. <it>HMGA1 </it>functions as a potent oncogene in cultured cells and induces aggressive lymphoid tumors in transgenic mice. Because HMGA1 chromatin remodeling proteins regulate transcription, <it>HMGA1 </it>is thought to drive malignant transformation by modulating expression of specific genes. Genome-wide studies to define HMGA1 transcriptional networks during tumorigenesis, however, are lacking. To define the HMGA1 transcriptome, we analyzed gene expression profiles in lymphoid cells from <it>HMGA1a </it>transgenic mice at different stages in tumorigenesis.</p> <p>Results</p> <p>RNA from lymphoid samples at 2 months (before tumors develop) and 12 months (after tumors are well-established) was screened for differential expression of > 20,000 unique genes by microarray analysis (Affymetrix) using a parametric and nonparametric approach. Differential expression was confirmed by quantitative RT-PCR in a subset of genes. Differentially expressed genes were analyzed for cellular pathways and functions using Ingenuity Pathway Analysis. Early in tumorigenesis, HMGA1 induced inflammatory pathways with NFkappaB identified as a major node. In established tumors, HMGA1 induced pathways involved in cell cycle progression, cell-mediated immune response, and cancer. At both stages in tumorigenesis, HMGA1 induced pathways involved in cellular development, hematopoiesis, and hematologic development. Gene set enrichment analysis showed that stem cell and immature T cell genes are enriched in the established tumors. To determine if these results are relevant to human tumors, we knocked-down HMGA1 in human T-cell leukemia cells and identified a subset of genes dysregulated in both the transgenic and human lymphoid tumors.</p> <p>Conclusions</p> <p>We found that <it>HMGA1 </it>induces inflammatory pathways early in lymphoid tumorigenesis and pathways involved in stem cells, cell cycle progression, and cancer in established tumors. <it>HMGA1 </it>also dyregulates genes and pathways involved in stem cells, cellular development and hematopoiesis at both early and late stages of tumorigenesis. These results provide insight into <it>HMGA1 </it>function during tumor development and point to cellular pathways that could serve as therapeutic targets in lymphoid and other human cancers with aberrant <it>HMGA1 </it>expression.</p

Comparison of Expression Profiles in Ovarian Epithelium In Vivo and Ovarian Cancer Identifies Novel Candidate Genes Involved in Disease Pathogenesis

Molecular events leading to epithelial ovarian cancer are poorly understood but ovulatory hormones and a high number of life-time ovulations with concomitant proliferation, apoptosis, and inflammation, increases risk. We identified genes that are regulated during the estrous cycle in murine ovarian surface epithelium and analysed these profiles to identify genes dysregulated in human ovarian cancer, using publically available datasets. We identified 338 genes that are regulated in murine ovarian surface epithelium during the estrous cycle and dysregulated in ovarian cancer. Six of seven candidates selected for immunohistochemical validation were expressed in serous ovarian cancer, inclusion cysts, ovarian surface epithelium and in fallopian tube epithelium. Most were overexpressed in ovarian cancer compared with ovarian surface epithelium and/or inclusion cysts (EpCAM, EZH2, BIRC5) although BIRC5 and EZH2 were expressed as highly in fallopian tube epithelium as in ovarian cancer. We prioritised the 338 genes for those likely to be important for ovarian cancer development by in silico analyses of copy number aberration and mutation using publically available datasets and identified genes with established roles in ovarian cancer as well as novel genes for which we have evidence for involvement in ovarian cancer. Chromosome segregation emerged as an important process in which genes from our list of 338 were over-represented including two (BUB1, NCAPD2) for which there is evidence of amplification and mutation. NUAK2, upregulated in ovarian surface epithelium in proestrus and predicted to have a driver mutation in ovarian cancer, was examined in a larger cohort of serous ovarian cancer where patients with lower NUAK2 expression had shorter overall survival. In conclusion, defining genes that are activated in normal epithelium in the course of ovulation that are also dysregulated in cancer has identified a number of pathways and novel candidate genes that may contribute to the development of ovarian cancer

SS18 Together with Animal-Specific Factors Defines Human BAF-Type SWI/SNF Complexes

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