The Prospects For Coal Gasification

The prospects for coal gasification are considered in the light of ever increasing problems of high prices and uncertain supplies of fossil fuels throughout the world. A detailed analysis of the supply and demand for coal and gas in Britain now and in the next decade is an essential part of this work. This needs to be set in the overall context of world supply and demand. The consequences of social and political changes on energy supply are stressed as well as the consequences of technical changes. A review of the present position of coal gasification technology, both surface technology methods and underground coal gasification methods is given in some detail. The advantages of coal gasification compared with electricity production such as energy efficiency, capital cost and environmental impact are considered. The relatively poor position of the coal industry in relation to future markets for coal and the uncertainty surrounding ultimate natural gas reserves are two important factors which are relevant to the development of coal gasification. The domestic gas market is studied in some detail to determine the gas penetration within the various sectors and house types within this market. Future gas demand in the domestic market will be quite different from that in the 1970's. This will be due to several factors including price elasticity, insulation, low energy houses, housing policy, effect of high fuel prices on individual lifestyle etc., and each of these are considered in some detail. A close survey of the impact of various other heating vectors in the domestic sector is given to determine their future effect on gas demand. It is concluded that even allowing for some development of heat pump, CHP and other newer technologies, their effect on reducing future gas demand will be limited. There will remain a need for a substantial gas supply even when North Sea supplies decline. If this is linked to the need for the development of alternative coal markets and the need to promote the nuclear electricity plant programme, then a credible case for coal gasification emerges

Exploring Three-dimensional design worlds using Lindenmeyer systems and Genetic Programming

Since the end of the last century it has commonly been seen as decadent to simply apply aesthetics to the structure of a building to make it beautiful (with the exception of the deliberately ironic, although irony itself would have been thought decadent by the stern moralists of the modern movement ). Architects such as Louis Sullivan, Mies Van der Rohe, Le Corbusier and so on used the example of engineering to help to explain the relationship between form and function. Based on the simplistic assumption that engineers do not design form, but that it emerges from the correct solution to mechanical realities (cf. the Eiffel tower, Brunel's bridges and the "dom-ino" concrete frame) the modern movement declared such objects as pure and right . The functionalist tradition has suffered many blows in the last 50 years, partly because it was always an oversimplification, and partly because technology has now reached a point where the constraints of structure have almost vanished, with form becoming the precursor of function rather than it's determinant, ie. anything is possible (cf. Utzon's Sydney Opera House, The new Bilbao gallery etc.) The study of evolutionary algorithms allows us to get back to a more rigorous analysis of the basic determinants of form, where the global form of an object not only should not but actually cannot be predetermined on an aesthetic whim. Thus with genetic algorithms we have an opportunity to experiment with the true determinants of form in a way that the pioneers of the modern movement would have relished - an aesthetic of pure function whose outcome is totally embedded in the problem to be solved

Genetic determinants of hair and eye colours in the Scottish and Danish populations

<p>Abstract</p> <p>Background</p> <p>Eye and hair colour is highly variable in the European population, and is largely genetically determined. Both linkage and association studies have previously been used to identify candidate genes underlying this variation. Many of the genes found were previously known as underlying mutant mouse phenotypes or human genetic disease, but others, previously unsuspected as pigmentation genes, have also been discovered.</p> <p>Results</p> <p>We assayed the hair of a population of individuals of Scottish origin using tristimulus colorimetry, in order to produce a quantitative measure of hair colour. Cluster analysis of this data defined two groups, with overlapping borders, which corresponded to visually assessed dark versus red/light hair colour. The Danish population was assigned into categorical hair colour groups. Both cohorts were also assessed for eye colour. DNA from the Scottish group was genotyped at SNPs in 33 candidate genes, using 384 SNPs identified by HapMap as representatives of each gene. Associations found between SNPs and colorimetric hair data and eye colour categories were replicated in a cohort of the Danish population. The Danish population was also genotyped with SNPs in 4 previously described pigmentation genes. We found replicable associations of hair colour with the <it>KITLG </it>and <it>OCA2 </it>genes. <it>MC1R </it>variation correlated, as expected, with the red dimension of colorimetric hair colour in Scots. The Danish analysis excluded those with red hair, and no associations were found with <it>MC1R </it>in this group, emphasising that <it>MC1R </it>regulates the colour rather than the intensity of pigmentation. A previously unreported association with the <it>HPS3 </it>gene was seen in the Scottish population. However, although this replicated in the smaller cohort of the Danish population, no association was seen when the whole study population was analysed.</p> <p>Conclusions</p> <p>We have found novel associations with SNPs in known pigmentation genes and colorimetrically assessed hair colour in a Scottish and a Danish population.</p

On Shanks' algorithm for computing the continued fraction of log b a

Abstract. We give a more practical variant of Shanks ’ 1954 algorithm for computing the continued fraction of log b a, for integers a&gt; b&gt; 1, using the floor and ceiling functions and an integer parameter c&gt; 1. The variant, when repeated for a few values of c = 10 r, enables one to guess if log b a is rational and to find approximately r partial quotients. 1. Shanks ’ algorithm In his article [1], Shanks gave an algorithm for computing the partial quotients of log b a, where a&gt; b are positive integers greater than 1. Construct two sequences a0 = a, a1 = b, a2,... and n0, n1, n2,..., where the ai are positive rationals and the ni are positive integers, by the following rule: If i ≥ 1 and ai−1&gt; ai&gt; 1, then a ni−1 i ≤ ai−1 &lt; a ni−1+1 i (1.1) ai+1 = ai−1/a ni−1 i. (1.2) Clearly (1.1) and (1.2) imply ai&gt; ai+1 ≥ 1. Also (1.1) implies ai ≤ a 1/ni−1 i−1 hence by induction on i ≥ 0, Also by induction on j ≥ 0, we get for i ≥ 1 and ai+1 ≤ a 1/n0···ni 0. (1.3) a2j = a r 0/a s 1, a2j+1 = a u 1/a v 0, (1.4) where r and u are positive integers and s and v are non–negative integers. Two possibilities arise: 1 2 TERENCE JACKSON 1 AND KEITH MATTHEWS 2 (i) ar+1 = 1 for some r ≥ 1. Then equations (1.4) imply a relation a q 0 = a p 1 for positive integers p and q and so log a1 a0 = p/q. (ii) ai+1&gt; 1 for all i. In this case the decreasing sequence {ai} tends to a ≥ 1. Also (1.3) implies a = 1, unless perhaps ni = 1 for all sufficiently large i; but then (1.2) becomes ai+1 = ai−1/ai and hence a = a/a = 1. If ai−1&gt; ai&gt; 1, then from (1.1) we have log ai−1 ni−1 =. (1.5) log ai Let xi = log ai+1 ai if ai+1&gt; 1. Then we have Lemma 1. If ai+2&gt; 1, then xi = ni + 1/xi+1. (1.6) Proof. From (1.2), we have log ai+2 = log ai − ni log ai+1 (1.7) from which (1.6) follows. 1 = log ai log ai+1 log ai+1 · − ni · log ai+1 log ai+2 log ai+2 (1.8) = xixi+1 − nixi+1, (1.9) From Lemma 1.1 and (1.5), we deduc

Review essay: Anthony Howe. Byron and the Forms of Thought (Liverpool: Liverpool UP, 2013) and Carla Pomare. Byron and the Discourse of History (Farnham and Burlington: Ashgate, 2013).

This essay is a comparative review of two recently published books in Byron studies: Anthony Howe's Byron and the Forms of Thought (Liverpool: Liverpool UP, 2013) and Carla Pomare's Byron and the Discourse of History (Farnham and Burlington: Ashgate, 2013)

Rosiglitazone Induces Mitochondrial Biogenesis in Differentiated Murine 3T3-L1 and C3H/10T1/2 Adipocytes

Growing evidence indicates that PPARγ agonists, including rosiglitazone (RSG), induce adipose mitochondrial biogenesis. By systematically analyzing mitochondrial gene expression in two common murine adipocyte models, the current study aimed to further establish the direct role of RSG and capture temporal changes in gene transcription. Microarray profiling revealed that in fully differentiated 3T3-L1 and C3H/10T1/2 adipocytes treated with RSG or DMSO vehicle for 1, 2, 4, 7, 24, and 48 hrs, RSG overwhelmingly increased mitochondrial gene transcripts time dependently. The timing of the increases was consistent with the cascade of organelle biogenesis, that is, initiated by induction of transcription factor(s), followed by increases in the biosynthesis machinery, and then by increases in functional components. The transcriptional increases were further validated by increased mitochondrial staining, citrate synthase activity, and O2 consumption, and were found to be associated with increased adiponectin secretion. The work provided further insight on the mechanism of PPARγ-induced mitochondrial biogenesis in differentiated adipocytes

Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice

Atypical hemolytic uremic syndrome (aHUS) is frequently associated in humans with loss-of-function mutations in complement-regulating proteins or gain-of-function mutations in complement-activating proteins. Thus, aHUS provides an archetypal complement-mediated disease with which to model new therapeutic strategies and treatments. Herein, we show that, when transferred to mice, an aHUS-associated gain-of-function change (D1115N) to the complement-activation protein C3 results in aHUS. Homozygous C3 p.D1115N (C3KI) mice developed spontaneous chronic thrombotic microangiopathy together with hematuria, thrombocytopenia, elevated creatinine, and evidence of hemolysis. Mice with active disease had reduced plasma C3 with C3 fragment and C9 deposition within the kidney. Therapeutic blockade or genetic deletion of C5, a protein downstream of C3 in the complement cascade, protected homozygous C3KI mice from thrombotic microangiopathy and aHUS. Thus, our data provide in vivo modeling evidence that gain-of-function changes in complement C3 drive aHUS. They also show that long-term C5 deficiency is not accompanied by development of other renal complications (such as C3 glomerulopathy) despite sustained dysregulation of C3. Our results suggest that this preclinical model will allow testing of novel complement inhibitors with the aim of developing precisely targeted therapeutics that could have application in many complement-mediated diseases