The real SAP® Business one cost : a case study of ERP adoption in an SME

This paper reports on a UK based service management Small and Medium-sized Enterprise (SME) that invested into SAP® Business One. The action research case study highlights the real cost and difficulties faced in moving to the one single SAP system and the process that was followed in order to identify third-party vendors that can integrate or customise SAP® Business One. This paper highlights the additional costs required to ensure a ‘fit-for-purpose’ solution to close the gap between strategic needs and the existing SAP Business One solution. The gap itself is illustrated by highlighting 10 key functionalities expected by the given service management SME. The actual implementation cost of the Enterprise Resource Planning (ERP) was found to be approximately double the initial SAP costs. The real costs involve time for, among other things, process reengineering, strategic decision making, software add-ons, staff-training, project-management and software maintenance

The Upregulation of α2δ-1 Subunit Modulates Activity-Dependent Ca2+ Signals in Sensory Neurons.

As auxiliary subunits of voltage-gated Ca(2+) channels, the α2δ proteins modulate membrane trafficking of the channels and their localization to specific presynaptic sites. Following nerve injury, upregulation of the α2δ-1 subunit in sensory dorsal root ganglion neurons contributes to the generation of chronic pain states; however, very little is known about the underlying molecular mechanisms. Here we show that the increased expression of α2δ-1 in rat sensory neurons leads to prolonged Ca(2+) responses evoked by membrane depolarization. This mechanism is coupled to CaV2.2 channel-mediated responses, as it is blocked by a ω-conotoxin GVIA application. Once initiated, the prolonged Ca(2+) transients are not dependent on extracellular Ca(2+) and do not require Ca(2+) release from the endoplasmic reticulum. The selective inhibition of mitochondrial Ca(2+) uptake demonstrates that α2δ-1-mediated prolonged Ca(2+) signals are buffered by mitochondria, preferentially activated by Ca(2+) influx through CaV2.2 channels. Thus, by controlling channel abundance at the plasma membrane, the α2δ-1 subunit has a major impact on the organization of depolarization-induced intracellular Ca(2+) signaling in dorsal root ganglion neurons

Nitrification amplifies the decreasing trends of atmospheric oxygen and implies a larger land carbon uptake

[1] Atmospheric O-2 trend measurements are used to partition global oceanic and land biotic carbon sinks on a multiannual basis. The underlying principle is that a terrestrial uptake or release of CO₂ is accompanied by an opposite flux of O-2. The molar ratio of the CO₂ and O-2 terrestrial fluxes should be 1, if no other elements are considered. However, reactive nitrogen produced by human activities (e.g., fertilizers, N deposition) is also being incorporated into plant tissues. The various reaction pathways of the terrestrial nitrogen cycle cause fluxes of atmospheric O-2. Thus the cycles of nitrogen, carbon, and oxygen must be linked together. We report here on previously unconsidered anthropogenic nitrogen-related mechanisms which impact atmospheric O-2 trends and thus the derived global carbon sinks. In particular, we speculate that anthropogenic-driven changes are driving the global nitrogen cycle to a more oxidized state, primarily through nitrification, nitrate fertilizer industrial production, and combustion of fossil fuels and anthropogenic biomass burning. The sum of these nitrogen-related processes acts to additionally decrease atmospheric O-2 and slightly increase atmospheric CO₂. We have calculated that the effective land biotic O-2: CO₂ molar ratio ranges between 0.76 and 1.04 rather than 1.10 ( moles of O-2 produced per mole of CO₂ consumed) over the period 1993 - 2003, depending on which of four contrasting nitrogen oxidation and reduction pathway scenarios is used. Using the scenario in which we have most confidence, this implies a 0.23 PgC yr(-1) correction to the global land biotic and oceanic carbon sinks of most recently reported estimates over 1993 - 2003, with the land biotic sink becoming larger and the oceanic sink smaller. We have attributed large uncertainties of 100% to all nitrogen-related O-2 and CO₂ fluxes and this corresponds up to +/- 0.09 PgC yr(-1) increase in global carbon sink uncertainties. Thus accounting for anthropogenic nitrogen-related terrestrial fluxes of O-2 results in a 45% larger land biotic sink of 0.74 +/- 0.78 PgC yr(-1) and a slightly smaller oceanic sink of 2.01 +/- 0.66 PgC yr(-1) for the decade 1993 - 2003. [References: 38

The causes of full ocean depth interannual variability in Drake Passage

In recent years a number of large scale modes of Southern Hemisphere climate variability have been observed, most notably the Southern Annular Mode (SAM, e.g. Thompson and Solomon, 2002), the Pacific South American modes (PSA, e.g. Mo and Peagle, 2001), the Antarctic Dipole (e.g. Martinson and Ianuzzi, 2003), the Antarctic Circumpolar Wave (e.g. White and Peterson, 1996), and of course the El Niño Southern Oscillation (ENSO). All have pronounced effects over or in the Southern Ocean, and may be expected to account for a significant part of the interannual variability observed there. Most studies analyse these phenomena from a large-scale point of view, often by extracting modes from Southern Hemisphere atmospheric and oceanic fields using various mathematical techniques. In this study we have taken an alternative approach, and tried to understand the causes of the full ocean depth variability in Drake Passage observed in the WOCE SR1b repeat hydrographic sections (Cunningham et al. 2003)

On the massive gluon propagator, the PT-BFM scheme and the low-momentum behaviour of decoupling and scaling DSE solutions

We study the low-momentum behaviour of Yang-Mills propagators obtained from Landau-gauge Dyson-Schwinger equations (DSE) in the PT-BFM scheme. We compare the ghost propagator numerical results with the analytical ones obtained by analyzing the low-momentum behaviour of the ghost propagator DSE in Landau gauge, assuming for the truncation a constant ghost-gluon vertex and a simple model for a massive gluon propagator. The asymptotic expression obtained for the regular or decoupling ghost dressing function up to the order ${\cal O}(q^2)$ is proven to fit pretty well the numerical PT-BFM results. Furthermore, when the size of the coupling renormalized at some scale approaches some critical value, the numerical PT-BFM propagators tend to behave as the scaling ones. We also show that the scaling solution, implying a diverging ghost dressing function, cannot be a DSE solution in the PT-BFM scheme but an unattainable limiting case.Comment: 16 pages, 2 figs., 2 tabs (updated version to be published in JHEP

Gray-matter volume, midbrain dopamine D2/D3 receptors and drug craving in methamphetamine users.

Dysfunction of the mesocorticolimbic system has a critical role in clinical features of addiction. Despite evidence suggesting that midbrain dopamine receptors influence amphetamine-induced dopamine release and that dopamine is involved in methamphetamine-induced neurotoxicity, associations between dopamine receptors and gray-matter volume have been unexplored in methamphetamine users. Here we used magnetic resonance imaging and [(18)F]fallypride positron emission tomography, respectively, to measure gray-matter volume (in 58 methamphetamine users) and dopamine D2/D3 receptor availability (binding potential relative to nondisplaceable uptake of the radiotracer, BPnd) (in 31 methamphetamine users and 37 control participants). Relationships between these measures and self-reported drug craving were examined. Although no difference in midbrain D2/D3 BPnd was detected between methamphetamine and control groups, midbrain D2/D3 BPnd was positively correlated with gray-matter volume in the striatum, prefrontal cortex, insula, hippocampus and temporal cortex in methamphetamine users, but not in control participants (group-by-midbrain D2/D3 BPnd interaction, P<0.05 corrected for multiple comparisons). Craving for methamphetamine was negatively associated with gray-matter volume in the insula, prefrontal cortex, amygdala, temporal cortex, occipital cortex, cerebellum and thalamus (P<0.05 corrected for multiple comparisons). A relationship between midbrain D2/D3 BPnd and methamphetamine craving was not detected. Lower midbrain D2/D3 BPnd may increase vulnerability to deficits in gray-matter volume in mesocorticolimbic circuitry in methamphetamine users, possibly reflecting greater dopamine-induced toxicity. Identifying factors that influence prefrontal and limbic volume, such as midbrain BPnd, may be important for understanding the basis of drug craving, a key factor in the maintenance of substance-use disorders

The Gut Microbiome in Neuromyelitis Optica.

Neuromyelitis optica (NMO) is a rare, disabling, sometimes fatal central nervous system inflammatory demyelinating disease that is associated with antibodies ("NMO IgG") that target the water channel protein aquaporin-4 (AQP4) expressed on astrocytes. There is considerable interest in identifying environmental triggers that may elicit production of NMO IgG by AQP4-reactive B cells. Although NMO is considered principally a humoral autoimmune disease, antibodies of NMO IgG are IgG1, a T-cell-dependent immunoglobulin subclass, indicating that AQP4-reactive T cells have a pivotal role in NMO pathogenesis. When AQP4-specific proliferative T cells were first identified in patients with NMO it was discovered that T cells recognizing the dominant AQP4 T-cell epitope exhibited a T helper 17 (Th17) phenotype and displayed cross-reactivity to a homologous peptide sequence within a protein of Clostridium perfringens, a commensal bacterium found in human gut flora. The initial analysis of gut microbiota in NMO demonstrated that, in comparison to healthy controls (HC) and patients with multiple sclerosis, the microbiome of NMO is distinct. Remarkably, C. perfringens was the second most significantly enriched taxon in NMO, and among bacteria identified at the species level, C. perfringens was the one most highly associated with NMO. Those discoveries, along with evidence that certain Clostridia in the gut can regulate the balance between regulatory T cells and Th17 cells, indicate that gut microbiota, and possibly C. perfringens itself, could participate in NMO pathogenesis. Collectively, the evidence linking microbiota to humoral and cellular immunity in NMO underscores the importance for further investigating this relationship