4,672 research outputs found

    Perancangan Sistem Informasi Pengelola Barang/Inventaris Di Jc Komp

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    Inventory information system is a system used to enter inventory data into the database, so that there are no errors in input, output data, and reporting based on the desired data. based on surveys and interviews with jc comp personnel, information was obtained that the existing system in the jc comp warehouse section is still manual. therefore, the system that will be created by the author is the result of a replication of the existing system in the jc comp warehouse section. in addition to the process of input and output of goods, this information system is also equipped with features for creating data reports, input and output of goods, and searching for goods data by item name. with the inventory information system is expected to be useful for the warehouse parts jc comp. By implementing this system in the jc comp warehouse, it is hoped that it can reduce errors that may occur. this system is also expected to further speed up the process of input, output, and report generation, which in turn will help the jc comp warehouseSistem Informasi Persediaan Barang adalah sebuah sistem yang digunakan untuk memasukkan data-data persediaan barang ke dalam database, sehinggga tidak terjadi kesalahan dalam input, output data, dan pembuatan laporan berdasarkan data yang diinginkan. Berdasarkan survey dan wawancara dengan bagian personalia Jc Komp, didapatkan informasi bahwa sistem yang ada dibagian gudang Jc Komp masih manual. Oleh karena itu, sistem yang akan dibuat oleh penulis adalah hasil replikasi dari sistem yang telah ada dibagian gudang Jc Comp. Selain proses input dan output barang, pada sistem informasi ini juga dilengkapi fitur pembuatan laporan data, input, dan output barang, dan pencarian data barang berdasarkan nama barang. Dengan adanya Sistem Informasi persediaan barang ini diharapkan dapat bermanfaat bagi bagian gudang Jc Komp. Dengan diterapkannya sistem ini pada bagian gudang Jc Comp, maka diharapkan dapat mengurangi kesalahan-kesalahan yang mungkin terjadi. Sistem ini juga diharapkan dapat lebih mempercepat proses input, output, dan pembuatan laporan yang pada akhirnya dapat membantu bagian gudang Jc Komp

    Amenable L-2-Theoretic Methods and Knot Concordance

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    We reveal new structures in the topological knot concordance group. As a key ingredient, we develop obstructions using L-2-theoretic methods for amenable groups in Strebel's class recently introduced by Orr and the author. Concerning (h)-solvable knots, which are defined in terms of certain Whitney towers of height h in bounding 4-manifolds, we show the following: for any n>1, there are (n)-solvable but non-(n. 5)-solvable (and therefore nonslice) knots, which are not detected by prior methods using Cochran-Orr-Teichner L-2-signature obstructions as well as Levine algebraic obstructions and Casson-Gordon invariants.X1197sciescopu

    Dynamics of Network Formation Processes in the Co-Author Model

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    This article studies the dynamics in the formation processes of a mutual consent network in game theory setting: the Co-Author Model. In this article, a limited observation is applied and analytical results are derived. Then, 2 parameters are varied: the number of individuals in the network and the initial probability of the links in the network in its initial state. A simulation result shows a finding that is consistent with an analytical result for a state of equilibrium while it also shows different possible equilibria.Dynamics, Network, Game Theory, Model,Simulation, Equilibrium, Complexity

    High-level polyomavirus JC viruria following long-term steroid therapy

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    CASE REPORT JC virus is a highly seroprevalent ubiquitous polyomavirus which is acquired at an early age through respiratory or oral route, Thereafter JCV establishes persistent, but mainly asymptomatic, infections in various tissues, including the genitourinary tract and brain Corresponding author Cristina Costa, MD S.C.D.U. Virologia Azienda Ospedaliero-Universitaria San Giovanni Battista di Torino Via Santena, 9 -10126 Torino E-mail: [email protected] increasing with age, with adult prevalence rate often between 15% and 60

    Engineering Framework to Utilize Miniaturized Charpy Type SE(B) Specimens to Predict Jc of Full Sized Specimens

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    AbstractThis paper introduces our experience of using miniature Charpy type SE(B) specimen in obtaining fracture toughness Jc of a material in the ductile to brittle transition temperature (DBTT) region. Width W x thickness B of 2 x 2 mm, 3 x 3 mm and 10 x 10 mm were chosen as miniature specimens and 25 x 25 mm were chosen as full sized specimen. 0.55% carbon steel JIS S55C, whose tensile to yield stress ratio σTS/σYS was equal to 1.8 was chosen as a material to simulate a degraded (embrittled) material in the DBTT region. Focus was placed on whether cleavage fracture could be predicted for these miniaturized specimens. Another focus was placed on whether the Jc of full sized specimen is predictable from the test results of the miniature sized specimens, in case cleavage fracture were observed. The results showed that the modified Ritch-Knott-Rice (RKR) failure criterion (which predicts the onset of cleavage fracture when the crack opening stress measured at 4 times the crack-tip opening displacement exceeds this σ22c) could predict whether cleavage fracture would occur or not. Another finding was that, in case cleavage fracture was observed though, the critical value σ22c in the modified RKR failure criterion was independent of specimen size, and thus, Jc of the full sized specimen is predictable from the miniature specimen test results, though M = (W-a)σYS/Jc was smaller than ASTM E1921 requirement of 30. Here, a and σYS are crack length and yield strength, respectively

    Endothelin system in human cardiovascular physiology and pathophysiology

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    The experiments presented here arose from an interest in endothelial function and, particularly, a wish to better understand the pharmacology and physiology of the endothelin (ET) system in human blood vessels in health, and the influence of cardiovascular disease on the ET system. This work followed from the discovery of ET-1 as a peptide endothelial mediator of vascular tone in 1988. Publications are grouped into sections representing different aspects of the work.Section 1 is concerned with exploring pharmacological responses to the ET family of peptides, the sarafotoxin analogue peptides, and ET antagonists, in human blood vessels in vivo. This was amongst the first work with ET-1 in humans, and certainly the first to use the sarafotoxins, ET receptor antagonists and ET converting enzyme (ECE) inhibitors. After characterisation of the pharmacological tools, it was possible to show clearly that endogenous ET-1 plays a physiological role in the control of peripheral resistance and blood pressure in healthy humans, suggesting important clinical applications for these agents. It was also shown that the ETA receptor is the major vasocontrictor receptor and that the major role in health of the ETB receptor is endothelium-dependent vasodilatation, enhancement of which may contribute to the beneficial clinical attributes of ETA receptor antagonism. In addition, local ET-1 infusion in the forearm circulation was shown to be a system whereby the clinical efficacy of systemically administered ET receptor antagonists could be modelled pharmacodynamicallySections 2-4 cover work confirming the substantial clinical utility of ET receptor antagonists and ECE inhibitors as vasodilators, particularly in essential hypertension, heart failure and renal failure. Other work, following congenital heart surgery, suggests that a cautious approach may be needed in some cases of pulmonary hypertension. Studies with neutral endopeptidase (NEP) inhibitors show unequivocally, but unexpectedly, that these agents are peripheral vasoconstrictors, and the evidence presented is consistent with this effect occurring because endogenously generated vascular ET-1 is an important substrate for NEP.Section 5 contains some miscellaneous but related studies, together with a series of review articles written from 1991-98 synthesising the literature at each stage and drawing conclusions about potential areas of major clinical interest in cardiovascular diseasePUBLICATIONS: • SECTION 1: CARDIOVASCULAR PHYSIOLOGY, Papers 1-19 • 1. Clarke JG, Benjamin N, Larkin SW, Webb DJ, Davies GJ, Maseri A. Endothelin is a potent long-lasting vasoconstrictor in men. Am J Physiol 1989;257:H2033-5. • 2. Cockcroft JR, Clarke JG, Webb DJ. The effect of intra-arterial endothelin on resting blood flow and sympathetically mediated vasoconstriction in the forearm of man. Br J Clin Pharmacol 1991;31:521-4. • 3. Waugh CJ, Dockrell MEC, Haynes WG, Olverman HJ, Williams BC, Webb DJ. The potassium channel opener BRL 38227 inhibits binding of [l25I]-labelled endothelin-1 to rat cardiac membranes. Biochem Biophys Res Commun 1992;185:630-5. • 4. Haynes WG, Webb DJ. Endothelium dependent modulation of responses to endothelin-1 in human veins. Clin Sci 1993;84:427-33. • 5. Dockrell MEC, Haynes WG, Williams BC, Webb DJ. Endothelin-1 and aggregation of human platelets in vitro. J Cardiovasc Pharmacol 1993;22(suppl 8), S204-6. • 6. Haynes WG, Webb DJ. Venoconstriction to endothelin-1 in humans: role of calcium and potassium channels. Am J Physiol 1993;265:H1676-81. • 7. Haynes WG, Webb DJ. Contribution of endogenous generation of endothelin-1 to basal vascular tone. Lancet 1994;344:852-4. • 8. Haynes WG, Strachan FE, Webb DJ. Endothelin ETA and ETb receptors cause vasoconstriction of human resistance and capacitance vessels in vivo. Circulation 1995;92:357-63. • 9. Strachan FE, Haynes WG, Webb DJ. Endothelium-dependent modulation of venoconstriction to sarafotoxin S6c in human veins in vivo. J Cardiovasc Pharmacol 1995;26(suppl. 3):S 180-2. • 10. Smith PJW, McQueen DS, Webb DJ. The effect of cooling on the contractile response to endothelin-1 in small arteries from humans. J Cardiovasc Pharmacol 1995;26(suppl3):S230-2. • 11. Plumpton C, Haynes WG, Webb DJ, Davenport AP. Phosphoramidon inhibition of the in vivo conversion of big endothelin-1 to endothelin-1 in the human forearm. Br J Pharmacol 1995; 116:1821-8. • 12. Haynes WG, Moffat S, Webb DJ. An investigation into the direct and indirect venoconstrictor effects of endothelin-1 and big endothelin-1 in man. Br J Clin Pharmacol 1995;40:307-11. • 13. Haynes WG, Ferro CJ, O'Kane KPJ, Somerville D, Lomax CC, Webb DJ. Systemic endothelin receptor blockade decreases peripheral vascular resistance and blood pressure in humans. Circulation 1996;93:1860-70. • 14. Dockrell MEC, Webb DJ, Williams BC. Activation of the endothelin B receptor causes a dose-dependent accumulation of cyclic GMP in human platelets. Blood Coag Fibrinolysis 1996;7:178-80. • 15. Plumpton C, Ferro CJ, Haynes WG, Webb DJ, Davenport AP. The increase in human plasma immunoreactive endothelin but not big endothelin-1 or its C-terminal fragment induced by systemic administration of the endothelin antagonist TAK-044. Br J Pharmacol 1996;119:311-4. • 16. Haynes WG, Hand MH, Dockrell MEC, Eadington DW, Lee MR, Benjamin N, Webb DJ. Physiological role of nitric oxide in regulation of renal function in humans. Am J Physiol 1997;272:F364-71. • 17. Ferro CJ, Haynes WG, Johnston NR, Lomax CC, Newby DE, Webb DJ. The peptide endothelin receptor antagonist, TAK-044, produces sustained inhibition of endothelin1 mediated arteriolar vasoconstriction. Br J Clin Pharmacol 1997;44:377-383. • 18. Verhaar MC, Strachan FE, Newby DE, Cruden NL, Koomans HA, Rabelink TJ, Webb DJ. Endothelin-A receptor antagonist-mediated vasodilatation is attenuated by inhibition of nitric oxide synthesis and by endothelin-B receptor blockade. Circulation 1998;97:752-6. • 19. Strachan FE, Spratt JC, Wilkinson IB, Gray GA, Johnston NR, Webb DJ. Systemic blockade of the endothelin-B receptor increases peripheral vascular resistance in healthy men. Hypertension 1999;33:581-5. • SECTION 2: HYPERTENSION AND RENAL DYSFUNCTION Papers 20-24 | 20. Haynes WG, Hand MF, Johnstone HA, Padfield PL, Webb DJ. Direct and sympathetically mediated venoconstriction in essential hypertension: enhanced responses to endothelin-1. J Clin Invest 1994;94:1359-64. • 2 1. Sturrock NDC, Lang CC, MacFarlane LJ, Dockrell MEC, Ryan M, Webb DJ, Struthers AD. Serial changes in blood pressure, renal function, endothelin and lipoprotein (a) during the first 9 days of cyclosporin therapy in males. J Hypertens 1995;13:667-73. • 22. Hand MF, Haynes WG, Johnstone HA, Anderton JL, Webb DJ. Erythropoietin enhances vascular responsiveness to norepinephrine in renal failure. Kidney Int 1995;48:806-13. • 23. Ferro CJ, Spratt JCS, Haynes WG, Webb DJ. Inhibition of neutral endopeptidase causes vasoconstriction of human resistance vessels in vivo. Circulation 1998;97:2323-30. • 24. Hand MH, Haynes WG, Webb DJ. Reduced endogenous endothelin-1-mediated vascular tone in chronic renal failure. Kidney Int 1999;55:613-20. • SECTION 3 | ISCHAEMIC HEART DISEASE Papers 25-27 | 25. Wieczorek I, Haynes WG, Webb DJ, Ludlam CA, Fox KAA. Raised plasma endothelin in unstable angina and non-Q wave myocardial infarction: relation to cardiovascular outcome. Br Heart J 1994;72:436-41. • 26. Flaynes WG, Hamer DW, Robertson CE, Webb DJ. Plasma endothelin following cardiac arrest: differences between survivors and non-survivors. Resuscitation 1994;27:117-22. • 27. Newby DE, Flint LL, Fox KAA, Boon NA, Webb DJ. Reduced responsiveness to endothelin-1 in peripheral resistance vessels of patients with syndrome X. J Am Coll Cardiol 1998;31:1585-90. • SECTION 4 | HEART FAILURE AND PULMONARY HYPERTENSION Papers 28-30 | 28. Davidson NC, Coutie WJ, Webb DJ, Struthers AD. Hormonal and renal differences between low dose and high dose angiotensin converting enzyme inhibitor treatment in patients with chronic heart failure. Heart 1996;75:576-81. • 29. Love MP, Haynes WG, Gray GA, Webb DJ, McMurray JJV. Vasodilator effects of endothelin-converting enzyme inhibition and endothelin ETA receptor blockade in chronic heart failure patients treated with ACE inhibitors. Circulation 1996;94:2131-7. • 30. Prendergast B, Newby DE, Wilson LE, Webb DJ, Mankad PS. Early therapeutic experience with the endothelin antagonist, BQ-123, in pulmonary hypertension after congenital heart surgery. Heart 1999;82:505-8 • SECTION 5 | MISCELLANEOUS TOPICS AND REVIEWS Papers 31-34 and 35-46 | 31. Sanai L, Haynes WG, McKenzie A, Grant IS, Webb DJ. Endothelin production in sepsis and the adult respiratory distress syndrome. Intens Care Med 1996;22:52-6. • 32. Mickley EJ, Gray GA, Webb DJ. Activation of endothelin ETa receptors masks the constrictor role of endothelin ETg receptors in rat isolated small esenteric arteries. Br J Pharmacol 1997;120:1376-82. • 33. McEwan PE, Valdenaire O, Sutherland L, Webb DJ, Gray GA. A non-radioactive method for localization of endothelin receptor mRNA in situ. J Cardiovasc Pharmacol 1998;31(suppl l):S443-6. • 34. Smith PJW, Ferro CJ, McQueen DS, Webb DJ. Functional studies in small arteries do not support a primary role for endothelin in the pathogenesis of Raynaud's disease. J Cardiovasc Pharmacol 1998;31(suppl l):S473-6. • 35. Webb DJ. Endothelin receptors cloned, endothelin converting enzyme characterised and pathophysiology explored. TiPS 1991;12:43-6. • 36. Haynes WG, Webb DJ. The endothelin family of peptides: local hormones with diverse roles in health and disease. Clin Sci 1993;84:485-500. • 37. Haynes WG, Davenport AP, Webb DJ. Endothelin: progress in pharmacology and physiology. TiPS 1993;14:225-8. • 38. Kennedy RL, Haynes WG, Webb DJ. Endothelins as regulators of growth and function in endocrine tissues. Clin Endocrinol 1993;39:259-65. • 39. Webb DJ, Haynes WG. Endothelins come of age. Lancet 1993;342:1439-40. • 40. Webb DJ. Evidence for endothelin-1-mediated vasoconstriction in severe chronic heart failure: endothelin antagonism in heart failure. Circulation 1995;92:3372. • 41. Ferro CJ, Webb DJ. The clinical potential of endothelin receptor antagonists in cardiovascular medicine. Drugs 1996;51:12-27. • 42. Gray GA, Webb DJ. The endothelin system and its potential as a therapeutic target in cardiovascular disease. Pharmacol Ther 1996;72:109-48. • 43. Newby DN, Webb DJ. The endothelin system in cardiovascular disease: discovery to drug development in under a decade. BMJ 1997;314:531-2. • 44. Webb DJ. Endothelin: from molecule to man [BPS Research Prize Lecture]. Br J Clin Pharmacol 1997;44:9-20. • Webb DJ, Monge JC, Rabelink A, Yanagisawa M. Endothelin: new discoveries and rapid progress in the clinic. Trends Pharmacol Sci 1998;19:5-8. • 46. Haynes WG, Webb DJ. Endothelin as a regulator of cardiovascular function in health and disease. J Hypertens 1998;16:1081-98

    Aging and physical fitness are more important than obesity in determining exercise-induced generation of GH

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    Exercise is a potent stimulus for GH secretion. Aging and obesity are associated with a diminution of GH secretion. We wanted to determine whether age or fat mass is more important in regulating the GH response to exercise. Four groups of healthy men were studied: seven lean young men [age, &lt;40 yr; body mass index (BMI), &lt;25 kg/m2], six overweight young men (age, &lt;40 yr; BMI, &gt;27.5), seven lean older men (age, &gt;60 yr; BMI, &lt;25), and 6 overweight older men (age, 60 yr; BMI, &gt;27.5). The men performed a maximal exercise test. GH secretion was higher in the younger men than in the older men. Peak GH was higher in the older lean men than in the older overweight men. There was no difference between the young groups. Fitness correlated negatively with age and positively with peak GH. In young men, there was no relation between BMI, bioimpedance, or leptin and GH secretion. In contrast, in older men there was an inverse correlation between measures of fat mass and GH secretion. Age and physical fitness are more important than body fat in regulating exercise-induced GH secretion. These findings have important clinical implications if we are to prevent the frailty and morbidity associated with aging. <br/

    The Australian Incident Monitoring Study in Intensive Care: AIMS-ICU. The development and evaluation of an incident reporting system in intensive care

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    Publisher's copy made available with the permission of the publisher © 1996 Australian Society of AnaesthetistsIntensive care units are complex, dynamic patient management environments. Incidents and accidents can be caused by human error, by problems inherent in complex systems, or by a combination of these. Study objectives were to develop and evaluate an incident reporting system. A report form was designed eliciting a description of the incident, contextual information and contributing factors. Staff group sessions using open-ended questions, observations in the workplace and a review of earlier narratives were used to develop the report form. Three intensive care units participated in a two-month evaluation study. Feedback questionnaires were used to assess staff attitudes and understanding, project design and organization. These demonstrated a positive attitude and good understanding by more than 90% participants. Errors in communication, technique, problem recognition and charting were the predisposing factors most commonly chosen in the 128 incidents reported. It was concluded that incident monitoring may be a suitable technique for improving patient safety in intensive care.U. Beckman, L.F. West, G.J. Groombridge, I. Baldwin, G.K. Hart, D.G. Clayton, R.K. Webb, W.B. Runcima
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