International Differences in the Size and Roles of Corporate Headquarters: An Empirical Examination

This paper examines differences in the size and roles of corporate headquarters around the world. Based on a survey of over 600 multibusiness corporations in seven countries (France, Germany, Holland, UK, Japan, US, and Chile) the paper describes the differences among countries, and then applies a model of the factors determining the size of corporate headquarters (Young, Collis, and Goold, 2003) to systematically examine those differences. The data shows that there are significant differences among countries in the size and role of corporate headquarters, and strongly suggests the existence of a developing country model, a European model, a US model, and a Japanese model of corporate headquarters. Contrary to popular expectations, corporate headquarters in the US are about twice the size of European counterparts. Headquarters there exert a higher level of functional influence and have larger staffs in certain key areas, such as IT and R&D. US managers are generally more satisfied than their European counterparts with their larger more powerful headquarters which suggests that, at least in the US context, large corporate headquarters can create value. Japanese headquarters, as might have been expected, are substantially larger than elsewhere – a factor of four times larger than in Europe. However, those headquarters are becoming smaller because of dissatisfaction with their performance. It is clear that having headquarters the size of the Japanese firms in the survey is not conducive to value creation. More specifically, the evidence cannot refute a hypothesis that the slope of the relationship between firm size and the size of corporate headquarters is the same across all countries, but that there are significant differences in the intercept for Chile, the US, Japan, and the European countries. What the data indicates is that at a firm employing 20,000, a European corporate headquarters would on average employ 124 individuals, a US headquarters would have 255 employees, and Japan 467 employees. The paper also examines differences between countries in the extent to which they perform the two key corporate tasks of control and coordination. The US and Chile chose to be somewhat more interventionist in the traditional tools and processes used to monitor and control business units – setting strategy, budgets, and administering capital budgets. However, there was a significant difference in the degree of influence in operational affairs between countries. The US and Japan exerted far more influence than the other countries over every activity from IT and purchasing, to marketing, R&D and HR issues. The US was also found to have significantly larger legal, tax, and treasury functions than the common European model, perhaps reflecting a more legalistic institutional structure. Japan also has significantly larger tax, treasury, and corporate management functions, but overall was not that much larger than the common European model. While the causes of these observed differences cannot be directly determined from the research, suggestions are made that the institutional infrastructure, the size and homogeneity of the domestic market, and cultural factors within countries are important underlying drivers.

The Size and Composition of Corporate Headquarters in Multinational Companies: Empirical Evidence

Based on a six-country survey of nearly 250 multinationals (MNCs), this paper is the first empirical analysis to describe the size and composition of MNC headquarters and to account for differences among them. Findings are as follows: MNC corporate headquarters are more involved in "obligatory" and value creating and control functions than in operational activities; there are no systematic differences in the determinants of the size and composition of corporate headquarters between MNCs and purely domestic companies; and as the geographic scope of an MNC increases, two offsetting phenomena occur—headquarters decrease their influence over operational units that, ceteris paribus, reduces the size of headquarters, but the relative size of obligatory functions at headquarters increases with increased country heterogeneity. The net effect is that the size of corporate headquarters expands as MNC geographic scope increases. The notion of "administrative heritage" is validated as MNCs from different countries have substantially different corporate headquarters—U.S. headquarters are large (255 median staff for a 20,000 FTE MNC) and European headquarters smaller (124). Implications are drawn that countries will lose activities if domestic firms are acquired by foreign MNCs, and that MNCs need to allow more subsidiary autonomy as their geographic scope increases

Thermodynamics of a continuously monitored double quantum dot heat engine in the repeated interactions framework

Understanding the thermodynamic role of measurement in quantum mechanical systems is a burgeoning field of study. In this article, we study a double quantum dot (DQD) connected to two macroscopic fermionic thermal reservoirs. We assume that the DQD is continuously monitored by a quantum point contact (QPC), which serves as a charge detector. Starting from a minimalist microscopic model for the QPC and reservoirs, we show that the local master equation of the DQD can alternatively be derived in the framework of repeated interactions and that this framework guarantees a thermodynamically consistent description of the DQD and its environment (including the QPC). We analyze the effect of the measurement strength and identify a regime in which particle transport through the DQD is both assisted and stabilized by dephasing. We also find that in this regime the entropic cost of driving the particle current with fixed relative fluctuations through the DQD is reduced. We thus conclude that under continuous measurement a more constant particle current may be achieved at a fixed entropic cost.Comment: 11 pages, 7 figures; comments are welcom

Powering an autonomous clock with quantum electromechanics

We theoretically analyse an autonomous clock comprising a nanoelectromechanical system, which undergoes self-oscillations driven by electron tunnelling. The periodic mechanical motion behaves as the clockwork, similar to the swinging of a pendulum, while induced oscillations in the electrical current can be used to read out the ticks. We simulate the dynamics of the system in the quasi-adiabatic limit of slow mechanical motion, allowing us to infer statistical properties of the clock's ticks from the current auto-correlation function. The distribution of individual ticks exhibits a tradeoff between accuracy, resolution, and dissipation, as expected from previous literature. Going beyond the distribution of individual ticks, we investigate how clock accuracy varies over different integration times by computing the Allan variance. We observe non-monotonic features in the Allan variance as a function of time and applied voltage, which can be explained by the presence of temporal correlations between ticks. These correlations are shown to yield a precision advantage for timekeeping over the timescales that the correlations persist. Our results illustrate the non-trivial features of the tick series produced by nanoscale clocks, and pave the way for experimental investigation of clock thermodynamics using nanoelectromechanical systems.Comment: 10 pages, 8 figure

Entropy production in the mesoscopic-leads formulation of quantum thermodynamics

Understanding the entropy production of systems strongly coupled to thermal baths is a core problem of both quantum thermodynamics and mesoscopic physics. While there exist many techniques to accurately study entropy production in such systems, they typically require a microscopic description of the baths, which can become numerically intractable to study for large systems. Alternatively an open-systems approach can be employed with all the nuances associated with various levels of approximation. Recently, the mesoscopic leads approach has emerged as a powerful method for studying such quantum systems strongly coupled to multiple thermal baths. In this method, a set of discretised lead modes, each locally damped, provide a Markovian embedding. Here we show that this method proves extremely useful to describe entropy production of a strongly coupled open quantum system. We show numerically, for both non-interacting and interacting setups, that a system coupled to a single bath exhibits a thermal fixed point at the level of the embedding. This allows us to use various results from the thermodynamics of quantum dynamical semi-groups to infer the non-equilibrium thermodynamics of the strongly coupled, non-Markovian central systems. In particular, we show that the entropy production in the transient regime recovers the well established microscopic definitions of entropy production with a correction that can be computed explicitly for both the single- and multiple-lead cases.Comment: v1: 11 pages, 6 figures, comments welcome as always

FAN1 controls mismatch repair complex assembly via MLH1 retention to stabilize CAG repeat expansion in Huntington's disease.

CAG repeat expansion in the HTT gene drives Huntington's disease (HD) pathogenesis and is modulated by DNA damage repair pathways. In this context, the interaction between FAN1, a DNA-structure-specific nuclease, and MLH1, member of the DNA mismatch repair pathway (MMR), is not defined. Here, we identify a highly conserved SPYF motif at the N terminus of FAN1 that binds to MLH1. Our data support a model where FAN1 has two distinct functions to stabilize CAG repeats. On one hand, it binds MLH1 to restrict its recruitment by MSH3, thus inhibiting the assembly of a functional MMR complex that would otherwise promote CAG repeat expansion. On the other hand, it promotes accurate repair via its nuclease activity. These data highlight a potential avenue for HD therapeutics in attenuating somatic expansion

The Emergence and Evolution of the Multidimensional Organization

The article discusses multidimensional organizations and the evolution of complex organizations. The six characteristics of multidimensional organizations, disadvantages of the successful organizational structure that is categorized as a multidivisional, multi-unit or M-form, research by the Foundation for Management Studies which suggests that synergies across business divisions can be exploited by the M-form, a team approach to creating economic value, examples of multidimensional firms such as PricewaterhouseCoopers, and a comparison of various organization types including the matrix form are mentioned

FAN1 modifies Huntington's disease progression by stabilising the expanded HTT CAG repeat

Huntington’s disease (HD) is an inherited neurodegenerative disease caused by an expanded CAG repeat in the HTT gene. CAG repeat length explains around half of the variation in age-at-onset, but genetic variation elsewhere in the genome accounts for a significant proportion of the remainder. Genome-wide association studies have identified a bidirectional signal on chromosome 15, likely underlain by FAN1 (FANCD2 and FANCI Associated Nuclease 1), a nuclease involved in DNA interstrand cross link repair. Here we show that increased FAN1 expression is significantly associated with delayed age-at-onset and slower progression of HD suggesting FAN1 is protective in the context of an expanded HTT CAG repeat. FAN1 overexpression in human cells reduces CAG repeat expansion in exogenously expressed mutant HTT exon 1, and in patient-derived stem cells and differentiated medium spiny neurons, FAN1 knockdown increases CAG repeat expansion. The stabilising effect is FAN1 concentration and CAG repeat length dependent. We show that FAN1 binds to the expanded HTT CAG repeat DNA and its nuclease activity is not required for protection against CAG repeat expansion. These data shed new mechanistic insights into how the genetic modifiers of HD act to alter disease progression, and show that FAN1 affects somatic expansion of the CAG repeat through a nuclease-independent mechanism. This provides new avenues for therapeutic interventions in HD and potentially other triplet repeat disorders

Partial loss of Tip60 slows mid-stage neurodegeneration in a spinocerebellar ataxia type 1 (SCA1) mouse model

Spinocerebellar ataxia type 1 (SCA1) is one of nine dominantly inherited neurodegenerative diseases caused by polyglutamine tract expansion. In SCA1, the expanded polyglutamine tract is in the ataxin-1 (ATXN1) protein. ATXN1 is part of an in vivo complex with retinoid acid receptor-related orphan receptor alpha (Rora) and the acetyltransferase tat-interactive protein 60 kDa (Tip60). ATXN1 and Tip60 interact directly via the ATXN1 and HMG-box protein 1 (AXH) domain of ATXN1. Moreover, the phospho-mimicking Asp amino acid at position 776, previously shown to enhance pathogenesis, increases the ability of ATXN1 to interact with Tip60. Using a genetic approach, the biological relevance of the ATXN1/Tip60 interaction was assessed by crossing ATXN1[82Q] mice with Tip60+/−animals. Partial Tip60 loss increased Rora and Rora-mediated gene expression and delayed ATXN1[82]-mediated cerebellar degeneration during mid-stage disease progression. These results suggested a specific, temporal role for Tip60 during disease progression. We also showed that genetic background modulated ATXN1[82Q]-induced phenotypes. Of interest, these latter studies showed that some phenotypes are enhanced on a mixed background while others are suppressed

Identification of novel risk loci and causal insights for sporadic Creutzfeldt-Jakob disease: a genome-wide association study

Background: Human prion diseases are rare and usually rapidly fatal neurodegenerative disorders, the most common being sporadic Creutzfeldt-Jakob disease (sCJD). Variants in the PRNP gene that encodes prion protein are strong risk factors for sCJD but, although the condition has similar heritability to other neurodegenerative disorders, no other genetic risk loci have been confirmed. We aimed to discover new genetic risk factors for sCJD, and their causal mechanisms. Methods: We did a genome-wide association study of sCJD in European ancestry populations (patients diagnosed with probable or definite sCJD identified at national CJD referral centres) with a two-stage study design using genotyping arrays and exome sequencing. Conditional, transcriptional, and histological analyses of implicated genes and proteins in brain tissues, and tests of the effects of risk variants on clinical phenotypes, were done using deep longitudinal clinical cohort data. Control data from healthy individuals were obtained from publicly available datasets matched for country. Findings: Samples from 5208 cases were obtained between 1990 and 2014. We found 41 genome-wide significant single nucleotide polymorphisms (SNPs) and independently replicated findings at three loci associated with sCJD risk; within PRNP (rs1799990; additive model odds ratio [OR] 1·23 [95% CI 1·17-1·30], p=2·68 × 10-15; heterozygous model p=1·01 × 10-135), STX6 (rs3747957; OR 1·16 [1·10-1·22], p=9·74 × 10-9), and GAL3ST1 (rs2267161; OR 1·18 [1·12-1·25], p=8·60 × 10-10). Follow-up analyses showed that associations at PRNP and GAL3ST1 are likely to be caused by common variants that alter the protein sequence, whereas risk variants in STX6 are associated with increased expression of the major transcripts in disease-relevant brain regions. Interpretation: We present, to our knowledge, the first evidence of statistically robust genetic associations in sporadic human prion disease that implicate intracellular trafficking and sphingolipid metabolism as molecular causal mechanisms. Risk SNPs in STX6 are shared with progressive supranuclear palsy, a neurodegenerative disease associated with misfolding of protein tau, indicating that sCJD might share the same causal mechanisms as prion-like disorders. Funding: Medical Research Council and the UK National Institute of Health Research in part through the Biomedical Research Centre at University College London Hospitals National Health Service Foundation Trust