Subsidiaries within a High-Tech MNC. A reappraisal of the Role of Functions

The recent management literature on multinational corporations (MNCs) has mainly focused on the new role played by subsidiaries within the international firms. Many scholars have underlined that MNCs tend to organise themselves along a differentiated network approach, where subsidiaries play a very different role according to their internal resources and the significance of the local environment. This strategic and organisational model dates back to the pioneering work of Bartlett and Goshal, who called this new international strategy “Transnational” so as to differentiate it from the classical Multidomestic and Global strategies. Along with the different roles played by the subsidiaries, this model is characterised by the simultaneous existence of cooperation and competition within the multinational corporations. The present work focuses on the role of the Italian subsidiary of AgilentTechnologies, a multinational firm with around 36,000 employees that is active in more than 40 countries in high-tech sectors such as electronics, telecommunications and life science. The case study brought new light to the usual distinction that is commonly made with regard to the role of a subsidiary. When we try to apply the Transnational model to Agilent we realise that neither this model nor the traditional typologies (Multidomestic, Global) apply to the case we have studied. The role of the subsidiary changes significantly according to the function being considered. Therefore, we conclude that the role of function should be re-evaluated when the strategy and the structure of an MNC is defined. Not only does the classification of subsidiaries change according to the function in question, but the strategic posture and the organisational structure of MNCs should also be re-evaluated in light of the function under consideration. Our study shows how activities such as R&D, where coopetition represents a strategic source of advantage, seem to follow the Transnational scheme, while others such as sales are mainly globally managed

Where is the Role of Philanthropy in the RESTORE Act?

The RESTORE Act presents an historic opportunity to invest in the revitalization of the Gulf of Mexico ecosystem on an unprecedented scale. The Act also can provide support for spurring economic recovery for a region hit hard by the BP Deepwater Horizon spill of 2010. Though much remains uncertain about how the Act will be funded and put to use, enough is clear to take stock of what the Act can do, what it will not do, and how affected communities and stakeholders might best engage the RESTORE Act process to ensure it fulfills its promise of a revitalized Gulf of Mexico.Given the unprecedented nature of the RESTORE Act and the hopes and expectations that many have for the Act, it is important to keep in mind what the Act will not and cannot be expected to do. Simply put, the Act does not address, much less solve, the deep ecologic challenges facing the Gulf of Mexico and its associated coastal ecosystems. Nor does it address the longstanding challenges to the sustainability and resilience of the communities of the region, many of which are tied to past and projected environmental trends in the coast and the Gulf. The Act can certainly improve conditions and create greater possibilities for the future, but it will take much more than RESTORE Act dollars to create the intellectual, civic, and financial capacity to achieve the goal of a Gulf and coast that are ecologically, culturally, and economically vibrant and sustainable. Indeed, it is far more certain that the challenges of participating in the RESTORE Act process -- which will stretch on for some years -- and ensuring that the Act in fact lives up to its promise will put new demands on communities and stakeholders that the Act does not meet in any way. Those demands and the broader demands of creating sustainable communities and environments will likely have to be met by the sort of civic, academic, and philanthropic investment that helped make the RESTORE Act a plausible public investment

Analysis of shared common genetic risk between amyotrophic lateral sclerosis and epilepsy

Because hyper-excitability has been shown to be a shared pathophysiological mechanism, we used the latest and largest genome-wide studies in amyotrophic lateral sclerosis (n = 36,052) and epilepsy (n = 38,349) to determine genetic overlap between these conditions. First, we showed no significant genetic correlation, also when binned on minor allele frequency. Second, we confirmed the absence of polygenic overlap using genomic risk score analysis. Finally, we did not identify pleiotropic variants in meta-analyses of the 2 diseases. Our findings indicate that amyotrophic lateral sclerosis and epilepsy do not share common genetic risk, showing that hyper-excitability in both disorders has distinct origins

Senataxin associates with replication forks to protect fork integrity across RNA-polymerase-II-transcribed genes

Transcription hinders replication fork progression and stability. The ATR checkpoint and specialized DNA helicases assist DNA synthesis across transcription units to protect genome integrity. Combining genomic and genetic approaches together with the analysis of replication intermediates, we searched for factors coordinating replication with transcription. We show that the Sen1/Senataxin DNA/RNA helicase associates with forks, promoting their progression across RNA polymerase II (RNAPII)-transcribed genes. sen1 mutants accumulate aberrant DNA structures and DNA-RNA hybrids while forks clash head-on with RNAPII transcription units. These replication defects correlate with hyperrecombination and checkpoint activation in sen1 mutants. The Sen1 function at the forks is separable from its role in RNA processing. Our data, besides unmasking a key role for Senataxin in coordinating replication with transcription, provide a framework for understanding the pathological mechanisms caused by Senataxin deficiencies and leading to the severe neurodegenerative diseases ataxia with oculomotor apraxia type 2 and amyotrophic lateral sclerosis 4

MYCOBACTERIAL ANTIGEN COMPLEX A60-SPECIFIC T-CELL REPERTOIRE DURING THE COURSE OF PULMONARY TUBERCULOSIS

The Mycobacterium bovis antigen complex A60 is known to be immunodominant in tuberculosis and to have a protective effect against experimental infection in vitro and in vivo. To identify immunodominant and possibly protective antigens in pulmonary tuberculosis, the T-cell repertoire directed to nitrocellulose-bound fractions of A60 antigen was analyzed in active tuberculosis patients during the course of the infection and after recovery. The results show that patients infected with Mycobacterium tuberculosis acquired reactivity only in the late phases of infection. At disease onset, patients with active tuberculosis were characterized by (i) T-cell unresponsiveness to most A60 fractions, (ii) high tumor necrosis factor alpha production, and (iii) low gamma interferon (IFN-gamma) release. Several weeks after chemotherapy, the unresponsive state disappeared and the following reverse situation was observed: (i) high blastogenic response to almost all A60 fractions, (ii) low tumor necrosis factor alpha release, and (iii) high IFN-gamma production. In addition, 60% of these patients significantly responded against seven A60 fractions (61 to 58, 56 to 53, 49 to 46, 46 to 44, 35 to 33, 33 to 30, and 30 to 28 kDa), indicating that they included immunodominant antigens. Furthermore, only the fractions within the molecular mass ranges of 56 to 44 and 35 to 28 kDa induced IFN-gamma synthesis. One year after complete recovery from infection, more than 60% of past-active tuberculosis subjects had memory T cells specific for the immunodominant fractions of 61 to 58, 56 to 53, 49 to 46, and 33 to 30 kDa. Since the same fractions induced the strongest IFN-gamma production, known to exhibit antimycobacterial effects, it is suggested that these may represent the inducers of a protective immune response