Gene therapy Essay Example | Topics and Well Written Essays - 1250 words

Gene therapy - Essay Example Currently, research is going on for gene therapy by various approaches in different parts of the world for various diseases like combined immuno-deficiencies, hemophilia, Parkinson's disease, cancer and even HIV (Verma and Weitzman, 2005). Though gene therapy has been under research for the past 2 decades, no single gene therapy has been approve for clinical use. The main reason for this is safety concerns pertaining to gene therapy trials and treatment. In this essay, various strategies to increase the safety of gene therapy will be discussed through review of suitable literature. Safety issues related to gene therapy are mainly related to the methods employed in gene therapy. There are basically 2 methods of gene therapy and they are ex-vivo therapy and in-vivo therapy. In ex-vivo therapy, gene delivery is done in cells after being removed from the body (Hecht, 2004). The cells used thus are basically grown in the laboratory. The cells are than modified outside the body and then tr ansplanted back into the body. In some research trials, cells from blood or born marrow are taken out and cultured in a laboratory. Thereafter, the cells are exposed to the virus with the desired gene. The virus infects the cells and transfers the therapeutic genetic material into the nucleus of the cells. After this, the cells are injected into the patient’s body by vein. In in vivo therapy, gene delivery is done in the cells that are still in the body. The simplest method of introducing therapeutic genetic material into the cells is direct introduction into target cells. However, this method is not practical because it can be used only with certain tissues and requires large amounts of DNA. Other methods are there wherein the genes are delivered into cells by vectors like viruses or bacteria, by electroporation or tiny synthetic "envelopes" of fat molecules (Hecht, 2004). Of these, the most commonly used vector is virus. Vector is the carrier of the gene. Viruses are used a s vectors to deliver genetic material to the nucleus of the cell that contains its DNA. The natural ability of a virus to enter a cell is used for this purpose. The viruses used for gene therapy are retrovirus, adenovirus, adeno-associated virus and herpes simplex virus (Genetics Home Reference, 2008). While preparing the vectors for gene therapy, the DNA coding for a part or whole of the normal genes of the virus to be used as a carrier is removed and replaced with the treatment gene. The carriers are engineered in such a way that there ability to enter the cells is not lost but they cannot reproduce. Genes delivered by tiny synthetic "envelopes" of fat molecules enter the cell by cell membrane which has very high concentration of fat molecules. In electroporation, the genes are delivered into the cells by creating tiny openings in the cell membrane. This is done by using a bionic chip. The chip contains a single living cell embedded in a tiny silicon circuit (Hecht, 2004). Another method of gene therapy is where the therapeutic gene gets inside the target cell by chemically linking the DNA to a molecule that will bind to special cell receptors. After binding to these receptors, the DNA is engulfed by the cell membrane and passed into the interior of the target cell. However, this is less effective than the other methods (Genetics Home R

Minimalist visual artists and composers Essay Example | Topics and Well Written Essays - 500 words

Minimalist visual artists and composers - Essay Example The fact that music has more â€Å"space† in time that it has to occupy, along with the fact that the common chords used have emotional resonance means that minimalist music retains a more emotional intensity, while visual art remains more intellectual, as demonstrated by a comparison of Philip Glass’s â€Å"Einstein on the Beach† and John McCracken’s â€Å"Untitled Slab.† Einstein on the Beach begins with deconstructed common chords, before being overlaid by a female ensemble counting to six using the same chord. This is then quickly overlayed with a voice speaking quickly, words barely just too quick to catch any narrative out of (Glass). It then begins with an overlay of male voices singing harmonics and a different group of male voices counting to six using a different octave of the same chord. Each chord used is major, with harmonies communicating a combined sense of joy and loftiness. These musical elements, though deconstructed here, would still be recognizable even to a lay audience, and leave Glass’s music with a distinct emotional punch. McCracken’s work, â€Å"Untitled Slab,† is very different. This piece of work is a painting that resembles, in every element, a large black slab of marble, down to the sense of reflections in its black depth (McCracken). The fact that it looks so almost common place while being made with such distinct skill asks the viewer to engage with art critically; it demands the reader use their mind and think about art as a construct. This consciousness of art as art is common to minimalist visual art, and keeps the viewer at arm’s length, reducing the emotional punch that the art actually has. This means that minimalist visual art, while sharing many similarities with minimalist music, has a very different effect. Minimalist music retains a great deal of emotional punch, while visual art loses it to heightened intellectualism. These

Features of Goodpastures Syndrome

Features of Goodpastures Syndrome Introduction Goodpastures syndrome, a rare autoimmune disease is characterized by anti-GBM (anti-glomerular basement membrane) antibodies attacking glomerular and alveolar basement membranes of the kidneys and lungs respectively. It was first reported by Dr. Ernest William Goodpasture in 1919 and first used by Stanton and Tange in 1957 in their case studies involving nine patients with the pulmonary-renal syndrome. [1, 2] Clinical Features   Ã‚   The onset of this disease ranges from the ages of 20-30 and 60-70 especially in young men in their late twenties or in men and women over sixty years of age study. [3] The diagnostic techniques involved in detection of Goodpastures syndrome include i) urine analysis that detects kidney damage by presence of high number of red blood cells or protein in the urine sample ii) blood tests showing the presence of anti-GBM antibodies iii) x-rays that can show anomalies in lung anatomy or iv) biopsies that involve imaging of a kidney tissue sample to demonstrate glomeruli characterised by crescent-shaped structures and lines of antibodies attached to the GBM. [4] While Goodpastures syndrome constitutes the representation of clinical features like rapidly progressive glomerulonephritis (RPGN) and pulmonary hemorrhage from any cause, Goodpasture disease also includes the presence of anti-GBM antibodies in addition to the other characteristics. The term anti-GBM disease constitutes a patient with the typical autoantibodies, irrespective of clinical symptoms and characteristic features. [1,5] The clinical manifestations associated with Goodpastures syndrome include acute renal failure resulting from rapidly progressive glomerulonephritis along with pulmonary hemorrhage that might prove fatal. The symptoms in relation to it consist of bleeding of lungs, kidney failure, hematuria, proteinuria, general malaise, fatigue, and weight loss. [1,6,7,8,9] The exact etiology of this syndrome is not known however there seem to be genetic and environmental risk factors. The factors being i) exposure to organic solvents or hydrocarbons ii) smoking and drugs iii) infection iv) exposure to metal particulate matter v) lymphocyte-depletion therapy. [1,5,10] The characteristic pathology in individuals experiencing the Goodpastures Syndrome can be detected by immunofluorescence staining technique of the IgG on the GBM that shows smooth diffuse linear patterns. [11] Hemodialysis, plasma exchange, cyclophosphamide drugs and immunosuppressive agents like methylprednisolone pulse therapy or oral administration of prednisolone are possible treatments for Goodpastures syndrome. [12,13,14] Basic Cellular and Molecular Mechanisms The localization of immunoglobulin IgG deposits at sites of inflammation within the pulmonary and renal basement membranes shows Goodpastures syndrome (a form of the anti-GBM disease) to be an antibody-mediated autoimmune disease. The pathogenic role of these antibodies has been confirmed by  transplantation of circulating or kidney-eluted anti-GBM antibodies to Rhesus monkey or human kidney allografts that result in the development of the disease.  A type II hypersensitivity reaction occurs when antibodies are targeted against extracellular matrix (ECM) specific antigens. [15]   The hypersensitivity response affects all organs in the body of which collagen is a constituent but the alveolar and glomerular basement membranes are more prone to the effect. This discrepancy is a result of increased accessibility of epitopes (antigen molecules facilitating attachment to a matching antibody) linked to overexpression of ÃŽÂ ±3 collagen chains in the respective basement membranes allowing access and formation of antibodies. [16] While ÃŽÂ ±3NC1 antibodies are the most common in patients with Goodpastures syndrome, ÃŽÂ ±5NC1 antibodies are less prevalent. Sometimes antineutrophil cytoplasmic antibody [ANCA] can also be present. [5,17] The disorder develops antibodies that target ÃŽÂ ±3 chain of basement membrane collagen (type IV collagen) present in alveoli in lungs and in the glomeruli that form the filtering units of the kidneys within the nephrons. These structures contain the basement membrane with collagen as its essential component that differentiates the epithelia from the underlying tissue. The conformational epitopes of the Goodpasture antigen are localized within 2 regions in the carboxyl terminal, noncollagenous (NC1) domain of a type IV collagen chain, ÃŽÂ ±3(IV)NC1. [1, 5, 18]. Upon interaction of the anti-GBM antibodies with the conformational epitope of the GBM glycoproteins, the complement pathway of the immune system gets activated. This results in infiltration by polymorphonuclear leukocytes (PMNs) and monocytes. The severely damaged GBM induces reflux of fibrinogen into the Bowman space, fibrinogen polymerizes to fibrin through the proliferation of procoagulant factors from activated mono cytes, leading to a crescent formation.[19] Goodpastures syndrome is linked with specific HLA types. Both positive (HLA-DR15) and negative (HLA-DR7) associations are defined and being used to develop an understanding of antigen presentation, tolerance and autoimmunity. [20,21,22] Recent Developments Recent developments like the plasmapheresis technique, steroidal drugs, and immunosuppressive therapy have drastically ameliorated the course of the medical condition in comparison to yesteryears, in which Goodpasture syndrome was deemed fatal. [23] Zhao et al., demonstrate the significant role of ÃŽÂ ±5NC1-specific antibodies in pathogenesis of Goodpastures disease and also re-confirm ÃŽÂ ±345 collagen IV molecule as the original GP autoantigen. [17] The invention of a drug, now patented, with its active element containing boron  that constitutes inhibitors of arginase activity has claimed remedial effects in the pathological state of Goodpastures Syndrome. [24] A recently developed, patented prophylaxis for glomerulonephritis resulting from Goodpastures syndrome comprises of administration of a therapeutically effective amount of an IL-6 antibody that binds with or regulates the expression or activity of a mammalian IL-6 polypeptide. [25] Conclusions Goodpastures Syndrome is an autoimmune disease characterized by anti-GBM antibodies attacking glomerular and alveolar basement membranes. The innate immune response comprises of (i) cell death; (ii) polymorphonuclear cell releasing neutrophils, basophils, eosinophils, antigens and monocytes to infiltrate the glomerulus. The adaptive immune response triggers the classical pathway of complement activated by antigen-antibody complex formation, and type II hypersensitivity reaction. Here antigens are targeted against cell- specific and tissue specific antigens (chiefly the connective tissue). Unanswered Questions Currently, there is a lot of research focusing on deciphering the causative agents of the harmful antibodies that lead to the development of Goodpastures syndrome. Evidence from this research can lead to novel drug discovery, eventually leading to a potential definitive cure for Goodpastures syndrome. [17] The exact the genetic determinants that constitute the etiology of Goodpastures syndrome are yet to be found. Bibliography Salama AD, Pusey CD. Goodpasture syndrome and other antiglomerular basement membrane diseases. In: Gilbert SJ, Weiner DE, eds. National Kidney Foundations Primer on Kidney Diseases. 6th ed. Philadelphia, PA: Elsevier Saunders; 2014: chap 21. Benoit, F. L., D. B. Rulon, G. B. Theil, P. D. Doolan, and R. H. Watten. Goodpastures syndrome: a clinicopathologic entity. The American journal of medicine 37, no. 3 (1964): 424-444. Hudson B, Tryggvason K, Sundaramoorthy M, Neilson E. Alport syndrome, goodpasture syndrome, and type IV Collagen. New Engl J Med 2003; 348:2543-56. Fervenza, Fernando C. Goodpasture Syndrome | NIDDK National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/kidney-disease/glomerular-diseases/goodpasture-syndrome (accessed March 1, 2017). Phelps RG, Turner AN. Anti-glomerular basement membrane disease and Goodpasture disease. In: Johnson RJ, Feehally J, Floege J, eds. Comprehensive Clinical Nephrology. 5th ed. Philadelphia, PA: Elsevier Saunders; 2015: chap 24. Lahmer T, Heemann U. Anti-glomerular basement membrane antibody disease: a rare autoimmune disorder affecting the kidney and the lung. Autoimmun Rev 2012;12:169-73. Pedchenko V, Bondar O, Fogo AB, Vanacore R, Voziyan P, Kitching AR, et al. Molecular architecture of the Goodpasture autoantigen in anti-GBM nephritis. N Engl J Med2010;363:343-54. Salant David J. Goodpastures disease new secrets revealed. N Engl J Med 2010; 363:388-91. Dammacco F, Battaglia S, Gesualdo L, Racanelli V. Goodpastures disease: a report of ten cases and a review of the literature. Autoimmun Rev 2013;12:1101-8. Jones, Joanne L., Sara AJ Thompson, Priscilla Loh, Jessica L. Davies, Orla C. Tuohy, Allison J. Curry, Laura Azzopardi et al. Human autoimmunity after lymphocyte depletion is caused by homeostatic T-cell proliferation. Proceedings of the National Academy of Sciences 110, no. 50 (2013): 20200-20205. MD, Edward. Renal Pathology http://library.med.utah.edu/WebPath/RENAHTML/RENAL093.html (accessed March 1, 2017). Greco, Antonio, Maria Ida Rizzo, Armando De Virgilio, Andrea Gallo, Massimo Fusconi, Giulio Pagliuca, Salvatore Martellucci, Rosaria Turchetta, Lucia Longo, and Marco De Vincentiis. Goodpastures syndrome: a clinical update. Autoimmunity reviews 14, no. 3 (2015): 246-253. Bolton, W. Kline. Goodpastures syndrome. Kidney international 50, no. 5 (1996): 1753-1766. Johnson, John P., Walter Whitman, William A. Briggs, and Curtis B. Wilson. Plasmapheresis and immunosuppressive agents in anti-basement25] membrane antibody-induced Goodpastures syndrome. The American journal of medicine 64, no. 2 (1978): 354-359. Rutgers A, Meyers KEC, Canziani G, Kalluri R, Lin J, Madaio MP. High affinity of anti-GBM antibodies from Goodpasture and transplanted Alport patients to 3 (IV) NC1 collagen. Kidney Int. 2000;58:115-122. Kelly, Patrick T., and Edward F. Haponik. Goodpasture syndrome: molecular and clinical advances. Medicine 73, no. 4 (1994): 171-185. Zhao J, Cui Z, Yang R, et al. Anti-glomerular basement membrane autoantibodies against different target antigens are associated with disease severity. Kidney Int 2009; 76:1108. Borza, Dorin-Bogdan, Eric G. Neilson, and Billy G. Hudson. Pathogenesis of Goodpasture syndrome: a molecular perspective. In Seminars in nephrology, vol. 23, no. 6, pp. 522-531. WB Saunders, 2003. Morita, Takashi, Yasunosuke Suzuki, and Jacob Churg. Structure and development of the glomerular crescent. The American journal of pathology 72, no. 3 (1973): 349. Phelps, Richard G., and Andrew J. Rees. The HLA complex in Goodpastures disease: a model for analyzing susceptibility to autoimmunity. Kidney international 56, no. 5 (1999): 1638-1653. Phelps, Richard G., Victoria Jones, A. Neil Turner, and Andrew J. Rees. Properties of HLA class II molecules divergently associated with Goodpastures disease. International immunology 12, no. 8 (2000): 1135-1143. Turner AN, Rees AJ. Anti-glomerular basement membrane disease (Chapter 3.11). In: Cameron SDAM, Grunfeld JP, Kerr DNS, Ritz E, eds Oxford Textbook of Nephrology, 2nd edn. Oxford University Press, Oxford, 1997 Shah MK, Hugghins SY. Characteristics and outcomes of patients with Goodpastures syndrome. South Med J 2002;95:1411-8. Van Zandt, Michael, Adam Golebiowski, Min Koo Ji, Darren Whitehouse, Todd Ryder, and Raymond Paul Beckett. Inhibitors of arginase and their therapeutic applications. U.S. Patent 9,266,908, issued February 23, 2016. Marshall, Diane, and Stevan Shaw. Method for the treatment of glomerulonephritis by administering an IL-6 antibody. U.S. Patent 9,321,837, issued April 26, 2016.

Effect of temperature on rate of reaction :: GCSE Chemistry Coursework Investigation

Effect of temperature on rate of reaction Aim: To find out if the temperature increases the rate of reaction of two chemicals. Prediction: My prediction is that the higher the temperature is the faster the rate of the reaction will be. Equipment: Hot water, thermometer, flask, cold water, stopwatch, tissue paper, paper with ‘X’ marked on it, safety glasses, measuring cylinder, large beaker, sodium thiosulphate, hydrochloric acid. Method: The experiment has to be done five times for the five different temperatures of the sodium thiosulphate. The temperatures are: 20 °C, 30 °C, 40 °C, 50 °C and 60 °C To start the experiments fill the flask with 50cm ³ of sodium thiosulphate into the large beaker. Fill the large beaker up with the water of right temperature that is required for the experiment. Put the thermometer into the flask with sodium thiosulphate and check the temperature is right for the experiment. If the water is too cold, in the large beaker pour in some more hot water or if it is too hot pour in some cold water to reach the required temperature for the sodium thiosulphate. Once the sodium thiosulphate is the right temperature, take it out of the water, wipe the bottom of the flask with tissue paper and place it onto the piece of paper with ‘X’ marked on it. Now measure 5cm ³ of hydrochloric acid in the measuring cylinder. Then pour the hydrochloric acid into the sodium thiosulphate, at this moment start timing with the stopwatch and keep timing until you cannot see the ‘X’ mark through the liquid. Make sure you wear safety glasses and handle the acid carefully. Fair Test: To make this investigation fair you have to make sure you use the same concentration of hydrochloric acid for all experiments. You also have to make sure you use the same amount of hydrochloric acid and sodium thiosulphate for all the experiments. Also make sure you time the experiments accurately. Observation: My observation was that when the temperature of the sodium thiosulphate was higher the solution turned cloudy quicker. Results: -------------------------------------------- Temperature ( °C) Time for cross to disappear (minutes) 20 2.49 30 1.

Euthanasia Background Essay

* What’s Euthanasia? * The Pro-Life Alliance defines it as: ‘Any action or omission intended to end the life of a patient on the grounds that his or her life is not worth living.’ * The Voluntary Euthanasia Society looks to the word’s Greek origins – ‘eu’ and ‘thanatos,’ which together mean ‘a good death’ – and say a modern definition is: ‘A good death brought about by a doctor providing drugs or an injection to bring a peaceful end to the dying process.’ * Three classes of euthanasia can be identified — passive euthanasia, physician-assisted suicide and active euthanasia — although not all groups would acknowledge them as valid terms.† * What is physician-assisted suicide/physician aid in dying? * It is descriptively accurate and carries with it no misleading connotations. * Other contributors to this volume prefer the synonymous term physician-assisted suicide because it is technically accurate, and still others prefer physician aid in dying because it is relatively neutral. * Although suicide can be considered heroic or rational depending on setting and philosophical orientation, in much American writing it is conflated with mental illness, and the term suggests the tragic self-destruction of a person who is not thinking clearly or acting rationally. Pros: * Everyone has the right to die * The right of a competent, terminally ill person to avoid excruciating pain and embrace a timely and dignified death bears the sanction of history and is implicit in the concept of ordered liberty. * The exercise of this right is as central to personal autonomy and bodily integrity as rights safeguarded by this Court’s decisions relating to marriage, family relationships, procreation, contraception, child rearing and the refusal or termination of life-saving medical treatment. * In particular, this Court’s recent decisions concerning the right to refuse medical treatment and the right to abortion instruct that a mentally competent, terminally ill person has a protected liberty interest in choosing to end intolerable suffering by bringing about his or her own death. * Patient suffering should be able to end their life. * At the Hemlock Society they get calls daily from desperate people who are looking for someone like Jack Kevorkian to end their lives, which have lost all quality. * Americans should enjoy a right guaranteed in the European Declaration of Human Rights — the right not to be forced to suffer. * It should be considered as much of a crime to make someone live that with justification does not wish to continue as it is to take life without consent. * What about palliative (end-of-life) care? * The evidence for the emotional impact of assisted dying on physicians shows that euthanasia and assisted suicide are a far cry from being ‘easier options for the caregiver’ than palliative care, as some critics of Dutch practice have suggested. * We wish to take a strong stand against the separation and opposition between euthanasia and assisted suicide, on the one hand, and palliative care, on the other, that such critics have implied. There is no ‘either-or’ with respect to these options. * Every appropriate palliative option available must be discussed with the patient and, if reasonable, tried before a request for assisted death can be accepted. * What about living wills? * Living wills can be used to refuse extraordinary, life-prolonging care and are effective in providing clear and convincing evidence that may be necessary under state statutes to refuse care after one becomes terminally ill. * A recent Pennsylvania case shows the power a living will can have. In that case, a Bucks County man was not given a feeding tube, even though his wife requested he receive one, because his living will, executed seven years prior, clearly stated that he did ‘not want tube feeding or any other artificial invasive form of nutrition. * A living will provides clear and convincing evidence of one’s wishes regarding end-of-life care. * Healthcare * Even though the various elements that make up the American healthcare system are becoming more circumspect in ensuring that money is not wasted. * The cap that marks a zero-sum healthcare system is largely absent in the United States. * Considering the way we finance healthcare in the United States, it would be hard to make a case that there is a financial imperative compelling us to adopt physician-assisted suicide in an effort to save money so that others could benefit. Cons: * There will be a slippery slope to legalized murder. * In a society as obsessed with the costs of health care and the principle of utility, the dangers of the slippery slope†¦ are far from fantasy. * Assisted suicide is a half-way house, a stop on the way to other forms of direct euthanasia, for example, for incompetent patients by advance directive or suicide in the elderly. So, too, is voluntary euthanasia a half-way house to involuntary and nonvoluntary euthanasia. * If terminating life is a benefit, the reasoning goes, why should euthanasia be limited only to those who can give consent? Why need we ask for consent? * The Hippocratic Oath and Prohibition of Killing would make it impossible. * The prohibition against killing patients†¦ stands as the first promise of self-restraint sworn to in the Hippocratic Oath, as medicine’s primary taboo: ‘I will neither give a deadly drug to anybody if asked for it, nor will I make a suggestion to this effect’. * In forswearing the giving of poison when asked for it, the Hippocratic physician rejects the view that the patient’s choice for death can make killing him right. * For the physician, at least, human life in living bodies commands respect and reverence–by its very nature. As its respectability does not depend upon human agreement or patient consent, revocation of one’s consent to live does not deprive one’s living body of respectability. * The deepest ethical principle restraining the physician’s power is not the autonomy or freedom of the patient; neither is it his own compassion or good intention. Rather, it is the dignity and mysterious power of human life itself, and therefore, also what the Oath calls the purity and holiness of life and art to which he has sworn devotion.† * There is also Government involvement in end-of-life decisions. * Cases like Schiavo’s touch on basic constitutional rights, such as the right to live and the right to due process, and consequently there could very well be a legitimate role for the federal government to play. * There’s a precedent–as a result of the highly publicized deaths of infants with disabilities in the 1980s, the federal government enacted ‘Baby Doe Legislation,’ which would withhold federal funds from hospitals that withhold lifesaving treatment from newborns based on the expectation of disability. * The medical community has to have restrictions on what it may do to people with disabilities – we’ve already seen what some members of that community are willing to do when no restrictions are in place.Healthcare spending implications will shut it down. * There would be healthcare spending implications. * Savings to governments could become a consideration. * Drugs for assisted suicide cost about $35 to $45, making them far less expensive than providing medical care. * This could fill the void from cutbacks for treatment and care with the ‘treatment’ of death.† * Social groups would also be at risk. * It must be recognized that assisted suicide and euthanasia will be practiced through the prism of social inequality and prejudice that characterizes the delivery of services in all segments of society, including health care. * Those who will be most vulnerable to abuse, error, or indifference are the poor, minorities, and those who are least educated and least empowered. * This risk does not reflect a judgment that physicians are more prejudiced or influenced by race and class than the rest of society – only that they are not exempt from the prejudices manifest in other areas of our collective life.

Pushing Paper Can Be Fun Essay

A large city government was putting on a number of seminars for managers of various departments throughout the city. At one of these sessions the topic discussed was motivation—how to motivate public servants to do a good job. The plight of a police captain became the central focus of the discussion: I’ve got a real problem with my officers. They come on the force as young, inexperienced rookies, and we send them out on the street, either in cars or on a beat. They seem to like the contact they have with the public, the action involved in crime prevention, and the apprehension of criminals. They also like helping people out at fires, accidents, and other emergencies. The problem occurs when they get back to the station. They hate to do the paperwork, and because they dislike it, the job is frequently put off or done inadequately. This lack of attention hurts us later on when we get to court. We need clear, factual reports. They must be highly detailed and unambiguous. As soon as one part of a report is shown to be inadequate or incorrect, the rest of the report is suspect. Poor reporting probably causes us to lose more cases than any other factor. I just don’t know how to motivate them to do a better job. We’re in a budget crunch, and I have absolutely no financial rewards at my disposal. In fact, we’ll probably have to lay some people off in the near future. It’s hard for me to make the job interesting and challenging because it isn’t- it’s boring, routine paperwork, and there isn’t much you can do about it. Finally, I can’t say to them that their promotions will hinge on the excellence of their paperwork. First of all, they know it’s not true. If their performance is adequate, most are more likely to get promoted just by staying on the force a certain number of years than for some specific outstanding act. Second, they were trained to do the job they do out in the streets, not to fill out forms. All through their careers the arrests and interventions are what get noticed. Some people have suggested a number of things, like using conviction records as a performance criterion. However, we know that’s not fair—too many other things are involved. Bad paperwork increases the chance that you lose in court, but good paper work doesn’t necessarily mean you’ll win. We tried setting up team competitions based on the excellence of the reports, but the officers caught on to that pretty quickly. No one was getting any type of reward for winning the competition, and they figured why they should bust a  gut when there was no payoff. I just don’t know what to do.