A design and implementation methodology for high variety electronics assembly systems

Small indigenous manufacturers of electronic equipment are coming under increasingly severe pressure to adopt a strong defensive position against large multinational and Far Eastern companies. A common response to this threat has been for these firms to adopt a 'market driven' business strategy based on quality and customer service, rather than a 'technology led' strategy which uses technical specification and price to compete. To successfully implement this type of strategy there is a need for production systems to be redesigned to suit the new demands of marketing. Increased range and fast response require economy of scope rather t ban economy or scale while the organisation's culture must promote quality and process consciousness. This paper describes the 'Modular Assembly Cascade' concept which addresses these needs by applying the principles of flexible manufacturing (FMS) and just in time (,JlT) to electronics assembly. A methodology for executing the concept is also outlined. This is called DRAMA (Design Houtirw !'or· Adopting Modular Assembly).

Design and implementation of production systems for high variety electronics assembly

Information technology companies are having to broaden their overall strategic view in deference to the premise that it is better to be market-driven than technology-led. Cost and technical performance are no longer the only considerations, as quality and service now demand equal recognition. The production of a high volume single item has given way to that of low volume multiple items, which in turn requires some modification of production systems and brings flexible manufacturing, Just-in-Time production and total quality control into sharper focus for the achievement of corporate objectives.

The 'law of requisite variety' may assist climate change negotiations:a review of the Kyoto and Durban meetings

Ashby wrote about cybernetics, during which discourse he described a Law that attempts to resolve difficulties arising in complex situations – he suggested using variety to combat complexity. In this paper, we note that the delegates to the UN Framework Convention on Climate Change (UNFCCC) meeting in Kyoto, 1997, were offered a ‘simplifying solution’ to cope with the complexity of discussing multiple pollutants allegedly contributing to ‘climate change’. We assert that the adoption of CO2eq has resulted in imprecise thinking regarding the ‘carbon footprint’ – that is, ‘CO2’ – to the exclusion of other pollutants. We propose, as Ashby might have done, that the CO2eq and other factors within the ‘climate change’ negotiations be disaggregated to allow careful and specific individual solutions to be agreed on each factor. We propose a new permanent and transparent ‘action group’ be in charge of agenda setting and to manage the messy annual meetings. This body would be responsible for achieving accords at these annual meetings, rather than forcing this task on national hosts. We acknowledge the task is daunting and we recommend moving on from Ashby's Law to Beer's Viable Systems approach.

Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer's disease

To determine whether genetic factors influence frontal lobe degeneration in Alzheimer's disease (AD), the laminar distributions of diffuse, primitive, and classic β-amyloid (Aβ) peptide deposits were compared in early-onset familial AD (EO-FAD) linked to mutations of the amyloid precursor protein (APP) or presenilin 1 (PSEN1) gene, late-onset familial AD (LO-FAD), and sporadic AD (SAD). The influence of apolipoprotein E (Apo E) genotype on laminar distribution was also studied. In the majority of FAD and SAD cases, maximum density of the diffuse and primitive Aβ deposits occurred in the upper cortical layers, whereas the distribution of the classic Aβ deposits was more variable, either occurring in the lower layers, or a double-peaked (bimodal) distribution was present, density peaks occurring in upper and lower layers. The cortical layer at which maximum density of Aβ deposits occurred and maximum density were similar in EO-FAD, LO-FAD and SAD. In addition, there were no significant differences in distributions in cases expressing Apo E ε4 alleles compared with cases expressing the ε2 or ε3 alleles. These results suggest that gene expression had relatively little effect on the laminar distribution of Aβ deposits in the frontal lobe of the AD cases studied. Hence, the pattern of frontal lobe degeneration in AD is similar regardless of whether it is associated with APP and PSEN1, mutation, allelic variation in Apo E, or with SAD.

A comparison of spatial patterns of TDP-43 cellular inclusions in familial and sporadic frontotemporal lobar degeneration with TDP-43 proteinopathy

Abnormal protein aggregates of transactive response (TAR) DNA-binding protein (TDP-43) in the form of neuronal cytoplasmic inclusions (NCI), oligodendroglial inclusions (GI), neuronal internuclear inclusions (NII), and dystrophic neurites (DN) are the pathological hallmark of frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP). To investigate the role of phosphorylated TDP-43 (pTDP-43) in neurodegeneration in FTLD-TDP, the spatial patterns of the pTDP-43-immunoreactive NCI, GI, NII, and DN were studied in frontal and temporal cortex in three groups of cases: (1) familial FTLD-TDP caused by progranulin (GRN) mutation, (2) a miscellaneous group of familial cases containing cases caused by valosin-containing protein (VCP) mutation, ubiquitin associated protein 1 (UBAP1) mutation, and cases not associated with currently known genes, and (3) sporadic FTLD-TDP. In a significant number of brain regions, the pTDP-43-immunoreactive inclusions developed in clusters and the clusters were distributed regularly parallel to the tissue boundary. The spatial patterns of the inclusions were similar to those revealed by a phosphorylation-independent anti-TDP-43 antibody. The spatial patterns and cluster sizes of the pTDP-43-immunoreactive inclusions were similar in GRN mutation cases, remaining familial cases, and in sporadic FTLD-TDP. Hence, pathological changes initiated by different genetic factors in familial cases and by unknown causes in sporadic FTLD-TDP appear to follow a parallel course resulting in very similar patterns of degeneration of frontal and temporal lobes.

McKinney, Mark. Redrawing French Empire Comics. Columbus, The Ohio State University Press, 2013. 304 pages. 9780814212202

The history of France and its empires is one that has been well trodden, particularly the French occupation, and subsequent war, in Algeria. In this companion to his earlier work, 2011’s The Colonial Heritage of French Comics,McKinney attempts to examine the reconstruction of French national identity in the wake of decolonisation through the medium of Francophonecomics. He endeavours to study the colonial affrontier (3), the space in which France and its colonies are connected and divided, where they seek to confront each other, or to seek peace and the removal of the division. McKinney argues this affrontier can be found most strongly in the Francophone comics produced dealing with the French colonial experience in Algeria, as well as that of Indochina,and does so from both sides of each conflict. McKinney examines in detail the French colonisation of Algeria (1830sonwards), the French war in Indochina (1946–54) and the Algerian war (1954–62), and his work is the first to approach these well-covered areas of research through the medium of comics. The resulting work takes the form of an investigation into the five forms of genealogical inquiry utilised in comics regarding these conflicts. His approach investigates the familial, ethnic, national, artistic and critical forms of genealogy relating to colonialism and imperialism from a variety of viewpoints, including the previously overlooked perspective of the pieds noirs. He aims to highlight both those cartoonists that critique the colonial ideology, as well as those cartoonists who to some extent attempt to gloss over or even romanticise the French empire, strengthening the affrontier. He positions himself alongside Foucault in seeing genealogy as a useful means of establishing ‘historical knowledge of struggles’ (Foucault1980, 85), but McKinney looks at the colonial representation in a popular medium,including the recent increase in comics produced which consider the French colonial experience. He argues that this consideration of the present, as well as European imperialism, is absent in the work of Foucault. The text is accompanied by a number of black and white facsimiles of pages from the comics he analyses to illustrate the different and often conflicting positions of cartoonists on these issues. Overall, McKinney’s work is a welcome addition to the study of the French colonial experience, which separates its elf from the rest by using Francophonecomics as lenses through which to look at these already well-trodden areas of study. He succeeds in determining if and how cartoonists critique colonial ideology and representations on both sides of the conflicts, a task in which he is unarguably successful. McKinney’s work, however, is unfortunately let down by typo graphicerrors, which occur throughout the text.Nevertheless, McKinney’s work is another important work in the field of Bande Dessine ́e scholarship, and useful for anyone interested in the representations of colonialism and imperialism in French comics, accompanied by anencyclopaedic bibliography of comics produced on this topic.

Uncovering the root cause of ethnic difference in ability testing:differential test functioning, test familiarity and trait optimism as explanations of ethnic group differences

The present research represents a coherent approach to understanding the root causes of ethnic group differences in ability test performance. Two studies were conducted, each of which was designed to address a key knowledge gap in the ethnic bias literature. In Study 1, both the LR Method of Differential Item Functioning (DIF) detection and Mixture Latent Variable Modelling were used to investigate the degree to which Differential Test Functioning (DTF) could explain ethnic group test performance differences in a large, previously unpublished dataset. Though mean test score differences were observed between a number of ethnic groups, neither technique was able to identify ethnic DTF. This calls into question the practical application of DTF to understanding these group differences. Study 2 investigated whether a number of non-cognitive factors might explain ethnic group test performance differences on a variety of ability tests. Two factors – test familiarity and trait optimism – were able to explain a large proportion of ethnic group test score differences. Furthermore, test familiarity was found to mediate the relationship between socio-economic factors – particularly participant educational level and familial social status – and test performance, suggesting that test familiarity develops over time through the mechanism of exposure to ability testing in other contexts. These findings represent a substantial contribution to the field’s understanding of two key issues surrounding ethnic test performance differences. The author calls for a new line of research into these performance facilitating and debilitating factors, before recommendations are offered for practitioners to ensure fairer deployment of ability testing in high-stakes selection processes.

Familial adrenal hypoplasia syndromes

The adrenal cortex secretes steroid hormones, including glucocorticoids and mineralocorticoids. Glucocorticoids control body homeostasis, stress, and immune responses, while mineralocorticoids regulate the water and electrolyte balance. A spectrum of genetic defects can disrupt the normal adrenal development, causing adrenal hypoplasia and various forms of adrenal insufficiency, which usually present in infancy or childhood with or without mineralocorticoid deficiency and with or without gonadal dysfunction. The genetic causes of adrenal hypoplasia can be broadly categorized into adrenal hypoplasia due to adrenocorticotropic hormone resistance syndromes (i.e., familial glucocorticoid deficiency and triple A syndrome) and adrenal hypoplasia due to primary defects in the development of the adrenal glands (i.e., X-linked adrenal hypoplasia congenita and primary adrenal hypoplasia caused by steroidogenic factor 1 mutations).