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Milton Wainwright and Sulamein Al Harbi. Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, S10 2TN, UK, m.wainwright sheffield.ac The role of microorganisms in the transformations of silicon has been little studied and, as a result, is little understood; most of the studies having been directed towards the use of silicon by diatoms. The lack of interest in silicon microbiology obviously relates to the fact that there is no evidence that silicon can be oxidised and reduced; as a result, there is no silicon cycle that is comparable to, for example, the sulphur or nitrogen cycles. Similarly, there is little evidence that silicon can be used as an energy source by microorganisms However, as I hope to show in this lecture, microorganisms can influence the availability of silicon in soils, and stimulate the growth of both bacteria and fungi in vitro. My aim is to review the available literature on the microbiology of silicon and to show how silicon affects microorganisms in relation to microbial growth in the environment and microbial pathogenesis. s Compounds of silicon are very common, comprising around 28 % of the earth' crust. The element occurs in two forms: silica or the oxides of silicon, which exist in crystalline or amorphous forms as in quartz, flint, sandstone, opal and diatomaceous earths and silicates, of which clay is an example. Silicon, as silicic acid 0.1-0.6 mM ; occurs as one of the main constituents of soil solution and it can be regarded as a plant nutrient Epstein, 1994 ; . Although silicon is close to carbon in the Periodic Table, its chemistry is dominated by stable Si-O bonds, so direct replacement of silicon for carbon in normal biochemistry appears impossible A wide range of bacteria and fungi can solubilize insoluble silicates by producing mineral and organic acids, and chelating agents Henderson and Duff, 1965 ; . Most of these silicate solubilizers are common soil microorganisms, although a specialized silicon solubilizing bacterium, Bacillus mucilaginosus, has been described by Russian workers. Silicate-dissolving micro-organisms have been used to remove silicon from low-grade mineral raw materials, like bauxite, and to extract valuable metals from silicate and aluminosilicate ores and minerals Karavaiko et al., 1988 ; . It has long been known that silicon compounds can stimulate microbial growth; for example, Borrell et al. 1922 ; found that the addition of a small amount of K2Si03 augments the yield of cultures of Bacille tuberculeux. Price 1932 ; also showed that the growth rate of Amoeba proteus was greatly increased by the addition of sodium silicate. Similarly, Mast and Pace 1937 ; found that Chilomonas paramecium will not grow in inorganic solutions lacking silicon and also that silicon stimulated starch production, growth and respiration in this organism. Bacteria, such as Bacillus licheniformis, can also accumulate silicon from growth media Mohanty et al., 1990 ; . Much of the early work on the interaction between silicon and bacteria relates to studies on the lung diseases silicosis a form of pneumoconiosis ; and tuberculosis. In the past, silicosis was very common amongst industrial workers especially coal miners ; exposed to dust rich in crystalline silica, but not amorphous silica and silicates. Many silicosis sufferers died from tuberculosis which spread rapidly through the lungs and caused death in a relatively short time. Price 1932 ; showed that sodium silicate and silicic acid stimulates the growth of Mycobacterium tuberculosis, and that even small amounts of silicon compounds, notably the easily soluble forms, produced the stimulatory effect. More recently, Yoshino 1990 ; found that 100 g g silicon ml-1 has a remarkable stimulatory effect on the growth of Staphylococcus aureus. He also showed that a high concentration of silicon present in the mucous membrane acts to enhance the growth of Pseudomonas aeruginosa. Sufferers from chronic sinusitis apparently have a high concentration of silicon in their mucous membranes, a fact which led Yoshino to suggest that this stimulatory effect of silicon on bacteria exacerbates the condition.
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The first shift of 0.05 pixels causes a tiny pimple to appear at the right edge; after another small shift the pimple has grown into a mole, and the left edge has become too flat. A designer who is asked to make a digital `O' that is 22 pixels wide will certainly have pixels in mind when making the design. Therefore it's not surprising that our program to generate a digital `O' should pay attention to actual pixel positions by rounding curve sidebar as in this example. We have distorted the infinite-resolution curve slightly so that it will digitize well, before digitizing it. A path z t ; will digitize well if the digitization process doesn't change it too much; thus, we want z t ; to essentially the same as round z t ; , at all the important places. But what places are "important"? Experience shows that the most critical points are those where the path travels horizontally or vertically, i.e., where it runs parallel to the raster lines. It's best to arrange things so that a curve becomes parallel to the raster lines just when it touches or nearly touches those lines; then it will appear to have the right curvature after digitization. The worst case occurs when a curve becomes parallel to the raster just when it's halfway between raster lines; then it gets a pimple or a flat spot. Diagonal slopes, where a curve has a 45 tangent angle, are also potential sources of unwanted pimples and flats. Similarly, at higher resolutions it is sometimes possible to detect small glitches when a curve travels with slopes of 1 2 Rational slopes m n where m and n are small integers turn out to be somewhat dangerous. But diagonals are of secondary importance; horizontal and vertical slopes lead to more severe problems. These considerations suggest a simple general principle for adapting the outlines of shapes to be digitized: If you know that the outline will have a vertical tangent at some point, round the x coordinate to an integer and leave the y coordinate unchanged. If you know that the outline will have a horizontal tangent at some point, round the y coordinate to an integer and leave the x coordinate unchanged. Incidentally, the horizontal tangent points in our ` ' examples were taken care of by the fact that `define corrected pixels' makes the overshoot parameter o nearly an integer, together with the fact that beginchar makes h an integer. If the y coordinates had not been rounded at the horizontal tangent points, our bad examples would have looked even worse. Before we go further into the study of rounding, we had better face up to a technicality that's sometimes important: We said that the pixels of a digitized region are those whose centers lie inside the undigitized region; but this rule is vague about what happens when the centers happen to fall precisely on the undigitized boundary. Similarly, when we said that round z t ; jumps from one point to an adjacent point, we ignored the fact that a curve such as z t ; t, actually jumps from 0, 0 ; to 1, ; when it is rounded as t passes 1 2; those points are not adjacent. skirts both of these problems in an interesting way: It shifts all of its paths to the right by an infinitesimal amount , and it also shifts them upward by an even smaller infinitesimal amount , so that no path actually touches a pixel center. Here and are positive numbers that are chosen to be so small that their actual values don't matter. For example, the path z t ; t, t ; becomes t + , t which jumps from 0, 0 ; to 1, 0 ; because it momentarily rounds to 1, 0 ; when t 1 2.
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If any Maori customary activity is and has been - general and widespread among the different and distinct iwi, it is fishing with no distinction made between freshwater and seawater fishing. Their association to water and the coastal marine area is particularly strong. The fishing provisions also apply more generally, with separate regulations for the North and South Islands, than, for instance, various gathering rights. The New Zealand fishing regime is quite complex, and a number of statutes and regulations apply to Maori fishing rights, both customary rights and commercial fishing rights. An initial distinction is made between commercial and non-commercial fishing and sometimes also between freshwater426 and marine fishing. Importantly, the Maori customary fishing rights do not merely include "fishing", but also include gathering rights of other aquatic life, including seaweed, as well as managing rights of such fisheries resources. Even if Maori commercial fishing rights, with rights to a fixed percentage of the annual catch quota, are a part of a separate legal system, the basis of this system has been aroused, at least partly, by acknowledged Maori customary rights to commercial fishing. This regime will, however, be presented in subsection 5.2.2.3 since the legal regime draws from the two fisheries settlements.
Inhibition could be described by a first order reaction between the drug and the channel that was apparently independent of HERG channel gating. Although the unbinding rate constant of the drug was constant, the apparent binding rate constant increased as the membrane was more depolarized and the drug concentration was raised. This model also could explain the fast recovery from the drug's effect at hyperpolarized potentials and its rate-dependent inhibition of HERG. Therefore, the effect of vesnarinone on the HERG-K current could be adequately described by a simple kinetic model of drug-channel interaction.
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Nilsen DW, Naess-Andresen KF, Kierulf P, et al. Graded pressure stockings in prevention of deep vein thrombosis following total hip replacement. Acta Chir Scand 1984; 150: 531-4. Nilsen DW, Jeremic M, Weisert OK. An attempt at predicting postoperative deep vein thrombosis by preoperative coagulation studies in patients undergoing total hip replacement. Thromb Haemost 1980; 43: 194-7. Owen TD, Moran CG, Smith SR, Pinder IM. Results of uncemented porous-coated anatomic total hip replacment. J Bone Joint Surg [Br] 1994; 76-B: 258-62. Paiement G, Wessinger SJ, Waltman AC, Harris WH. Low-dose warfarin versus external pneumatic compression for prophylaxis against venous thromboembolism following total hip replacement. J Arthroplasty 1987; 2: 23-6. Paiement G, Wessinger SJ, Waltman AC, Harris WH. Surveillance of deep vein thrombosis in asymptomatic total hip replacement patients. J Surg 1988; 155: 400-4. Paiement GD, Wessinger SJ, Hughes R, Harris WH. Routine use of adjusted low-dose warfarin to prevent venous thromboembolism after total hip replacement. J Bone Joint Surg [Am] 1993; 75-A: 893-8. Paramo JA, Alfaro MJ, Rocha E. Postoperative changes in the plasmatic levels of tissue type plasminogen activator and its fast acting inhibitor: relationship to deep vein thrombosis and influence of prophylaxis. Thromb Haemostas 1985; 54: 713-6. Paramo JA, Rocha E. Deep vein thrombosis and related platelet changes after total hip replacement. Haemostas 1985; 15: 389-94. * Pearson ES, Hartley HO. Biometrika tables for statisticians. Vol. 1. Cambridge: Cambridge University Press, 1966: 227. Pellegrini VD, Langhans MJ, Totterman S, Marder VJ, Francis CW. Embolic complications of calf thrombosis following total hip arthroplasty. J Arthroplasty 1993; 8: 449-57. Planes A, Vochelle N, Fagola M. Total hip replacement and deep vein thrombosis. J Bone Joint Surg [Br] 1990; 72-B: 9-13. Planes A, Vochelle N, Fagola M, et al. Efficacy and safety of a perioperative Enoxaparin regimen in total hip replacement under various anesthesias. J Surg 1991; 161: 525-31. Planes A, Vochelle N, Fagola M, et al. Once-daily dosing of Enoxaparin a low molecular weight heparin ; in prevention of deep vein thrombosis after total hip replacement. Acta Chir Scand Suppl 1990; 556: 108-15. Planes A, Vochelle N, Fagola M, Feret J, Bellaud M. Prevention of deep vein thrombosis after total hip replacement: the effect of low-molecular-weight heparin with spinal and general anaesthesia. J Bone Joint Surg [Br] 1991; 73-B: 418-22. Planes A, Vochelle N, Ferru J, et al. Enoxaparine, low molecular weight heparin: its use in prevention of deep venous thrombosis following total hip replacement. Haemostasis 1986; 16: 152-8. Planes A, Vochelle N, Mazas F, et al. Prevention of postoperative venous thrombosis: a randomized trial comparing unfractionated heparin with low molecular weight heparin in patients undergoing total hip replacement. Thromb Haemost 1988; 60: 407-10. Ritter MA, Hamilton CW. A comparative analysis of warfarin and lowdose heparin as thromboembolism prophylaxis in total hip replacement patients. Ann Surg 1975; 181: 896-901. Rocha E, Alfaro MJ, Paramo JA, Canadell JM. Preoperative identification of patients at high risk of deep venous thrombosis despite prophylaxis in total hip replacement. Thromb Haemost 1988; 59: 93-5. Rogers PH, Walsh PN, Marder VJ, et al. Controlled trial of low-dose heparin and sulfinpyrazone to prevent venous thromboembolism after operation on the hip. J Bone Joint Surg [Am] 1978; 60-A: 758-62. * Rosendaal FR. The emergence of a new species: the professional metaanalyst. J Clin Epidemiol 1994; 47: 1325-6. Rothermel JE, Wessinger JB, Stinchfield FE. Dextran 40 and thromboembolism in total hip replacement surgery. Arch Surg 1973; 106: 135-7. Sagar S, Maffei FH, Stamatakis JD, et al. Efficacy of low-dose heparin in prevention of extensive deep-vein thrombosis in patients undergoing total-hip replacement. Lancet 1976; I: 1151-4. Sakai DN, Amstutz HC. Prevention of thromboembolic phenomena. Clin Orthop 1976; 121: 108-12. Salvati EA, Lachiewicz P. Thromboembolism following total hipreplacement arthroplasty: the efficacy of dextran-aspirin and dextranwarfarin in prophylaxis. J Bone Joint Surg [Am] 1976; 58-A: 921-5 and sulindac.
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When I became Prime Minister, and the war broke out in all its hideous fury; when our own life and survival hung in the balance; I was already in a position to telegraph to the President on terms of an association which had become most intimate and, to me, most agreeable. This continued through all the ups and downs of the world struggle until Thursday last, when I received my last messages from him. These messages showed no falling off in his accustomed clear vision and vigour upon perplexing and complicated matters. I may mention that this correspondence which, of course, was greatly increased after the United States entry into the war, comprises to and fro between us, over 1700 messages. Many of these were lengthy messages, and the majority dealt with those more difficult points which come to be discussed upon the level of heads of Governments only after official solutions have not been reached at other stages. To this correspondence there must be added our nine meetings--at Argentia, three in Washington, at Casablanca, at Teheran, two at Quebec and, last of all, at Yalta, comprising in all about 120 days of close personal contact, during a great part of which I stayed with him at the White House or at his home at Hyde Park or in his retreat in the Blue Mountains, which he called Shangri-la. I conceived an admiration for him as a statesman, a man of affairs, and a war leader. I felt the utmost confidence in his upright, inspiring character and outlook, and a personal regard--affection I must say--for him beyond my power to express today. His love of his own country, his respect for its constitution, his power of gauging the tides and currents of its mobile public opinion, were always evident, but added to these were the beatings of that generous heart which was always stirred to anger and to action by spectacles of aggression and oppression by the strong against the weak. It is, indeed, a loss, a bitter loss to humanity that those heartbeats are stilled for ever. President Roosevelt's physical affliction lay heavily upon him. It was a marvel that he bore up against it through all the many years of tumult and storm. Not one man in ten millions, stricken and crippled as he was, would have attempted to plunge into a life of physical and mental exertion and of hard, ceaseless political controversy. Not one in ten millions would have tried, not one in a generation would have succeeded, not only
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33. Alfred North Whitehead, Religion in the Making, Lowell Institute Lectures New York: Macmillan, 1926 ; . 34. As quoted in Bernard Bergonzi, T.S. Eliot New York: Macmillan, 1972 ; , 162. 35. See `Theological Guidelines: Sources and Criteria, " The Book of Discipline of the United Methodist Church, 1988 Nashville: United Methodist Publishing House, 1988 ; , 80-89; see also the earlier formulation in The Book of Discipline of the United Methodist Church, 1972 Nashville: United Methodist Publishing House, 1972 ; , 75-79. The best study of this theological method is Donald A.D. Thorsen's The Wesleyan Quadrilateral: Scripture Tradition, Reason, and Experience as a Model of Evangelical Theology Grand Rapids: Francis Asbury Press, 1990 ; . 36. Stephen Hawking, A Brief History of Time New York: Bantam Books, 1988 ; . For the role of non rational elements in mathematics, believed by Hawking to be the highest form of rationality, see The Collected Works of Kurt Gdel, ed. Solomon Feferman et al. New York: Oxford University Press, 1986-date ; . Hawking does not represent New Light thinking for several reasons. First, he is an unrepentant modernist, an absolutist, and an advocate for the positivistic wing of s cience. Second, he despises mysticism or any movement of science into "meaning." Third, he is trying to prove or disprove God's existence, a rather arrogant pursuit in itself, solely by equation and evidence. 37. This is the analogy of Heinz R. Pagels who was executive director of the New York Academy of Sciences until his tragic death in a mountaineering accident. See his Perfect Symmetry: The Search for the Beginning of Time New York: Simon and Schuster, 1985 ; , 264. An excellent introduction to the phenomenon is Dennis Flanagan's chapter "Physics Seeks Its Holy Grail" in Flanagan's Version: A Spectator's Guide to Science on the Eve of the 21st Century New York: Alfred A. Knopf, 1988 ; , 30-61. For discussions of GUTs, see Perfect Symmetry, 267-84, and Mic hael Disney, The Hidden Universe New York: Macmillan, 1985 ; , 240-41. A dissenter to this attempt at unification is mathematician physicist astronomer biologist Freeman J. Dyson. His 1985 Gifford lectures, Infinite in All Directions New York: Harper and Row, 1988 ; , celebrate the diversity underlying the structure of the universe over the great unifying physical theories of Newton, Maxwell, Einstein or Hawking. 38. In two earlier publications I made tentative probings into this quadrilateral. See "Can a Mainstream Change Its Course?" in Liberal Protestantism: Realities and Possibilities ed. Robert S. Michaelson and Wade Clark Roof New York: Pilgrim Press, 1986 ; , 235-62; see also my `The Four Fundamentalisms of Oldline Protestantism, " Christian Century, 13 March 1985, 266-70. 39. Some reviewers have gone now to recommending certain books be read from back to front. See Robert Royal's comments about Robert J. Lifton and Eric Markusen's The Genocidal Mentality: Nazi Holocaust and Nuclear Threat New York: Basic Books, 1990 ; as found in First Things, January 1991, 55. 40. "I have taken as my patron saint St. Thomas of Didymus, who always insisted on an examination with his own hands, " are the words of Franois de Voltaire, the personifier and sulfinpyrazone.
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2. Camu W, Khoris J, Salachas F, Rouleau G, Meininger V, and the French Motor Neuron Group Study. Genetics of ALS: clinical consequences. J Neurol Sci. 1999; 165 suppl 1 ; : S21-S26. 3. Spencer PS, Nunn PB, Hugon J, et al. Guam amyotrophic lateral sclerosisparkinsonism-dementia linked to a plant excitant neurotoxin. Science. 1987; 237: 517-522. Cox PA, Sacks OW. Cycad neurotoxins, consumption of flying foxes, and ALSPDC disease in Guam. Neurology. 2002; 58: 956-959. Kuzuhara S, Kokubo Y, Sasaki R, et al. Familial amyotrophic lateral sclerosis and parkinsonism-dementia complex of the Kii Peninsula of Japan: clinical and neuropathological study and tau analysis. Ann Neurol. 2001; 49: 501-511. Poorkaj P, Tsuang D, Wijsman E, et al. Tau as a susceptibility gene for amyotrophic lateral sclerosis-parkinsonism dementia complex of Guam. Arch Neurol. 2001; 58: 1871-1878. Howlett WP, Brubaker GR, Mlingi N, Rosling H. Konzo, an epidemic upper motor neuron disease studied in Tanzania. Brain. 1990; 113: 223-235. Ludolph AC, Spencer PS. Toxic models of upper motor neuron disease. J Neurol Sci. 1996; 139 suppl ; : 53-59. 9. Hochberg FH, Bryan JA, Whelan MA. Clustering of amyotrophic lateral sclerosis [letter]. Lancet. 1974; 1: 34. Melmed C, Krieger C. A cluster of amyotrophic lateral sclerosis. Arch Neurol. 1982; 39: 595-596. Hyser CL, Kissel JT, Mendell JR. Three cases of amyotrophic lateral sclerosis in a common occupational environment. J Neurol. 1987; 234: 443-444. Chad D, Mitsumoto H, Adelman LS, et al. Conjugal motor neuron disease. Neurology. 1982; 32: 306-307. Paolino E, Granieri E, Tola MR, Rosati G. Conjugal amyotrophic lateral sclerosis [letter]. Ann Neurol. 1983; 14: 699. Maloo JC, Radhakrishnan K, Poddar SK, Thacker AK. Conjugal motor neuron disease. J Assoc Physicians India. 1987; 35: 303-304. Cornblath DR, Kurland LT, Boylan KB, Morrison L, Radhakrishnan K, Montgomery M. Conjugal amyotrophic lateral sclerosis: report of a young married couple. Neurology. 1993; 43: 2378-2380. Camu W, Cadilhac J, Billiard M. Conjugal amyotrophic lateral sclerosis: a report on two couples from southern France. Neurology. 1994; 44: 547-548. Poloni M, Micheli A, Facchetti D, Mai R, Ceriani F, Cattalini C. Conjugal amyotrophic lateral sclerosis: toxic clustering or change? Ital J Neurol Sci. 1997; 18: 109-112. Rachele MG, Mascia V, Tacconi P, Dessi N, Marrosu F, Giagheddu M. Conjugal amyotrophic lateral sclerosis: a report on a couple from Sardinia, Italy. Ital J Neurol Sci. 1998; 19: 97-100. Brooks BR. El Escorial World Federation of Neurology criteria for the diagnosis of amyotrophic lateral sclerosis: subcommittee on Motor Neuron Diseases Amyotrophic Lateral Sclerosis of the World Federation of Neurology Research Group on Neuromuscular Diseases and the El Escorial "Clinical limits of amyotrophic lateral sclerosis" workshop contributors. J Neurol Sci. 1994; 124 suppl ; : 96-107. 20. Mitsumoto H, Hanson MR, Chad DA. Amyotrophic lateral sclerosis: recent advances in pathogenesis and therapeutic trials. Arch Neurol. 1988; 45: 189202. Preux PM, Druet-Cabanet M, Couratier P, et al. Estimation of the amyotrophic lateral sclerosis incidence by capture-recapture method in the Limousin region of France. J Clin Epidemiol. 2000; 53: 1025-1029. Durrleman S, Alperovitch A. Increasing trend in ALS in France and elsewhere: are the changes real? Neurology. 1989; 39: 768-773. Berger MM, Kopp N, Vital C, Redl B, Aymard M, Lina B. Detection and cellular localization of enterovirus RNA sequences in spinal cord of patients with ALS. Neurology. 2000; 54: 20-25. MacGowan DJ, Scelsa SN, Waldron M. An ALS-like syndrome with new HIV infection and complete response to antiretroviral therapy. Neurology. 2001; 57: 1094-1097 and tacrine.
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