Dents Disease: Symptoms, Genetics, and Treatments

Dents Disease: Symptoms, Genetics, and Treatments Dents Disease Alessander Leyendecker Junior Clinical Aspects Dents disease is a recently characterized syndrome caused by a genetic mutation that leads to a renal tubular disorder and is characterized by manifestations of proximal tubule dysfunction. The proximal tubule is responsable for the reabsorption of sodium, potassium, calcium, glucose and low-molecular-weight proteins (like retinol binding protein and ÃŽ ±1 microglobulin and ÃŽ ²2 microglobulin) and for the secretion of ammonia, toxins, drugs and H+. Therefore, a proximal tubule dysfunction like Dents disease is characterized by low-molecular-weight proteinuria (excretion of low-molecular-weight proteins in the urine), hypercalcinuria (high concentration of calcium in the urine), nephocalcinosis (deposition of calcium salts in the renal parenchyma), nephrolithiasis (formation of crystalline aggregates that can develop anywhere along the urinary tract) and progressive renal failure. Low-molecular-weight proteinuria represents the most common symptom of Dents disease (Devuyst Thakker, 2010). Mapping: A higher disease severity in males and a lack of male to male transmission were identified by an analysis of 5 unrelated British families. The fact that females may show a milder phenotype suggests an X-linked recessive inheritance. The locus position on chromossome Xp11 was identified by linkage analysis of 2 3-generation families with Dent disease by Pook et al. (1993). Twenty X-linked polymorphic markers were used and the Linkage was established between Dents disease and the Xp1l 1 loci ARAFI (Z max = 5.42, 0 = 0.000), DXS426 (Z max = 3.61, 0 = 0.000), DXS255 (Z max = 5.48, 6 = 0.000) and DXS988 (Z max = 4.25, 0 = 0.045) to determine a locus order. In addition, DXS255 has presented a microdeletion in the affected members of one family, allowing the localization of Dents disease to Xp11.22 (Pook et al., 1993). Furthermore, another proximal renal tubular disorder associated with nephrolithiasis in a North American family and referred to as X-linked recessive nephrolithiasis has also been mapped to Xpl1.22. Suggesting that maybe there is one gene causing both X-linked recessive nephrolithiasis and Dents disease. Molecular Genetics: A study conducted by Fisher et al (1994) found a microdeletion in one Dent’s disease kindred, allowing the identification of the gene CLCN5 as a candidate. Furthermore, an investigation of 11 kindreds with renal tube disorders indentified 3 nonsense, 4 missense, 2 donor splice site mutations, 1 intragenic deletion and 1 microdeletion in CLCN5 gene (Llyod et al., 1996). Furthermore, Hoopes et al. (2005) indentified that some patients with Dents disease suffer from extra-renal symptoms such as cataract, mild intellectual impairment and hypotonia. Shared mutations in OCRL1 with the oculo-cerebrorenal syndrome of Lowe were identified in these patients. The presence of such extra-renal symptoms with mutations relating to Lowe syndrome is known as Dent disease 2. A research conducted by Bà ¶kenkamp et al. (2009) showed that low-molecular-weight proteinuria was a constant feature in all both Dent disease 1, Dent disease 2 and oculo-cerebrorenal syndrome of Lowe. However, there was a wide overlap in most of the other symptoms of the proximal tubulopathy. Nephrocalcinosis was observed more frequently in patients with Dents disease 1 than those with Dents disease 2 and Lowe syndrome; aminoaciduria, renal tubular acidosis, and renal failure was observed more frequently in patients with Lowe syndrome than patients with Dent-disease 1 and Dent disease disease 2. Genetics: All these findings have demonstrated that both Dent disease 1 and Dent disease 2 are a X-linked recessive inherited condition, caused by mutations in the OCRL1 (Dent disease 2) or CLCN5 (Dent disease 1) genes. These genes are located on chromosome Xp11.22 (Dent disease 1) and Xq25 (Dent disease 2). Mutation in CLCN5 are responsible for about 60% of the cases of Dent disease and mutation in OCRL are responsible for about 15% of the cases of Dent disease (Hoopes et al., 2004). So, nearly 25% of the cases of Dent disease do not have a known disease-causing mutation in OCRL or CLCN5, implying another genetic heterogeneity. Due to the fact that Dents disease is a X-linked recessive disorder, the disease is generally found in males only. Females carriers may show a milder phenotype. Furthermore, the disease may be present in early childhood (Devuyst Thakker, 2010). To date around 250 families with Dent-1 disease and about 50 patients with Dent-2 disease have been reported (Ludwig, Levtchenko Bà ¶kenkamp, 2014). The diagnosis of Dents disease is always difficult due to the wide variability of clinical presentation and, occasionally, lack of family history. Therefore, the disorder is likely underdiagnosed and the prevalence of this disease in the population is still unknown. More than 200 Dents disease 1 patients withCLCN5defects have been described with several different disease-causing mutations all over the gene. The types of mutations includes missense (44%) and nonsense (26%) mutations, small deletions/insertions (15%) and splice defects (11%), with a few hotspots, usually affecting arginine codons. Large insertions/deletions can be detected in around 4%of the patients. However, OCRLmutations in Dents disease 2 patients are not uniformly distributed. Missense mutations are usually found in exons 8–15 while nonsense or frameshift mutations very often affect exons (Ludwig, Levtchenko Bà ¶kenkamp, 2014). CLCN5 encodes the electrogenic Clà ¢Ã‚ Ã‚ »/H+ exchanger ClC-5. OCRL1 encodes a phosphatidylinositol bisphosphate (PIPà ¢Ã¢â‚¬Å¡Ã¢â‚¬Å¡) 5-phosphatase and mutations are also linked to the Lowe Syndrome. Mutations in any of these genes can culminate in the lack or dysfunction of these important proteins and result in the phenothype of Dents disease. Pathophysiology: The ability to reabsorb low-molecular-weight proteins and albumin that are ultrafiltered by the glomerulus are characteristics of the epithelial cells covering the proximal tubule portions of the nephron. This ability involves a process called receptor-mediated endocytosis. In the receptor-mediated endocytosis the particle to be endocytosed binds to specific receptor proteins concentrated at certain locations in the plasma membrane. Several types of receptors participate in the receptor-mediated endocytosis. These sites form a small depression in the plasma membrane that is covered by clathrin (a type of fibrous protein). After the binding of a ligand to plasma membrane-spanning receptors, a signal is sent through the membrane, leading to membrane coating, accumulation of the ligands into coated pits, and formation of a membrane invagination. The receptor and its ligand are then opsonized in clathrin-coated vesicles. The clathrin confers stability to the vesicle that are being transp orted into the cell. In the cytoplasm the vesicle loses its clathrin coverage and individual vesicles fuse to early endosomes. The acidification of endosomes by proton pumps ATP-dependent leads to the dissociation of the protein-receptor complex. This process allows the endosomes to fuse with the lysosomes through late endosomes. This acidification is reached by ATP-mediated transport of cytosolic H+ through the V-ATPase and demand an equal Cl conductance to preserve electroneutrality. It has been theorized that the H+ gradient can be neutralized by the C1C-5 action. In theory, ClC-5 provides an electrical shunt to neutralize the H+ gradient. Therefore, the vesicular acidification should be impaired by the loss of the endosomal Cl conductance mediated by ClC-5, resulting in the dysfunction of proximal tubule cells. To confirm this hypothesis, Piwon et al. (2000) created two distinct strains of ClC-5 knock-out (KO) mice which both have symptoms of the main characteristics of Dentâ₠¬â„¢s disease including manifestations of proximal tubule dysfunction like low-molecular-weight proteinuria. A reduced acidification of early endosomes in ClC-5-deficient mice have been demonstrated by in vitro experiments. However, ClC-5 is a 2Cl/H+ exchanger and not just a Cl channel, so the importance of this exchange activity for Dent’s disease was still unknown and needed to be assessed. In order to investigate this relevant question, Novarino et al. (2010) created a knock-in (KI) mouse presenting a point mutation in a important glutamate residue which transforms the exchanger into an uncoupled Cl channel that should help the endosomal acidification. The conventional ClC-5 KO mouse was subsequently compared with the KI mice. Acidification of the renal endosomes from wild-type and KI mice was regular, but greatly impaired in KO mice. Nevertheless, the same symptoms were indentified in both KI and KO mice, despite normal endosomal acidification and patients with Dentâ€⠄¢s disease, including low-molecular-weight proteinuria, hypercalciuria and hyperphosphaturia. Moreover, both the KI and KO mouse presented impaired proximal tubule endocytosis, indicating that proximal tubule dysfunction in Dent’s disease may happen in spite of the regular acidification of the endosomes. These findings indicate a function for a diminished endosomal Cl accumulation in Dent’s disease. Diagnosis: The clinical diagnosis of Dent’s disease is grounded on the presence of low-molecular-weight proteinuria, hypercalciuria, and at least one of the following characteristics: kidney stones, hematuria, nephrocalcinosis, renal insufficiency or hypophosphataemia (Hoopes et al., 2004). The clinical diagnosis can also be supported by nephrolithiasis and/or history of X-linked inheritance of renal Fanconi syndrome. The diagnosis can be confirmed by the recognition of mutation in both CLCN5 or OCRL1 by sequence analysis. Sequence analysis of affected males allows the identification of whole-gene deletions, multiexonic and exonic due to the lack of amplification is this case. Confirmation may also require deletion/duplication studies. It is imperative to previously identify the disease-causing mutation in the family when conducting a carrier test for at-risk relatives. The diagnosis of Dent disease 2, related with OCRL1 mutations, is more common than a diagnosis of Lowe syndrome when th ere are an absence of clinical symptoms and lack of severe intellectual deficit. Treatment: The reduction of hypercalciuria, prevention of nephrocalcinosis and kidney stones, and retardate the evolution of chronic kidney disease (nephrolithiasis) are the objectives of the current treatment. Thiazide diuretics in doses higher than 0.4 mg/kg/day have reducted urinary calcium excretion by more than 40% in males with Dent disease (Raja et al., 2002). However, side effects like hypokalemia, volume depletion, and cramping often occur. Similarly, we need to be cautious due to the fact that an increased hypercalciuria can result from the treatment of rickets with vitamin D. Furthermore, recent studies has been shown that a high citrate diet can slow the progression of chronic kidney disease in CLCN5 knockout mice (Cebotaru et al., 2005) and can be efficiently used to treat Dent disease. Genetic Counseling: The two types of Dent’s disease are X-linked. Therefore, men are affected more harshly. The father of an affected man will not have the disease or will he be a carrier of the mutation. The probability of transmitting the disease allele in each pregnancy is 50% if the mother of the proband is a carrier. Males who inherit the mutation will be affected and females who inherit the mutation will be carriers and will generally not be strongly affected. Affected men pass the disease-causing mutation to all of their daughters (who become carriers) and none of their sons. It is possible to conduct carrier testing for at-risk female relatives and prenatal testing for pregnancies at increased. Word count: 1673 References Blanchard A, Vargas-Poussou R, Peyrard S, Mogenet A, Baudouin V, Boudailliez B, Charbit M, Deschesnes G, Ezzhair N, Loirat C, Macher MA, Niaudet P, Azizi M: Effect of hydrochlorothiazide on urinary calcium excretion in Dent disease: an uncontrolled trial. Am J Kidney Dis 2008, 52:1084-1095. Bà ¶kenkamp A, Bà ¶ckenhauer D, Cheong HI, Hoppe B, Tasic V, Unwin R, Ludwig M. (2009). Dent-2 disease: A mild variant of Lowe Syndrome. J. Pediatr, 155, pp. 94-99, ISSN 0022-3476 Cebotaru V, Kaul S, Devuyst O, Cai H, Racusen L, Guggino WB, Guggino SE: High citrate diet delays progression of renal insufficiency in the ClC-5 knockout mouse model of Dent’s disease. Kidney Int 2005, 68:642-652. Devuyst, O., Thakker, R. V. (2010). Dent’s disease. Orphanet Journal of Rare Diseases. Fisher, S. E., Black, G. C., Lloyd, S. E., Hatchwell, E., Wrong, O., Thakker, R. V., Craig, I. W. (1994). Isolation and partial characterization of a chloride channel gene which is expressed in kidney and is a candidate for Dents disease (an X-linked hereditary nephrolithiasis). Human molecular genetics, 3(11), 2053-2060. Hara-Chikuma M, Wang Y, Guggino SE, Guggino WB, Verkman AS: Impaired acidification in early endosomes of ClC-5 deficient proximal tubule. Biochem Biophys Res Commun 2005, 329:941-946. Hoopes, R. R., Raja, K. M., Koich, A., Hueber, P., Reid, R., Knohl, S. J., Scheinman, S. J. (2004). Evidence for genetic heterogeneity in Dents disease.Kidney international,65(5), 1615-1620. Hoopes RR Jr, Shrimpton AE, Knohl SJ, Hueber P, Hoppe B, Matyus J, Simckes A, Tasic V, Toenshoff B, Suchy SF, Nussbaum RL, Scheinman SJ. Dent Disease with mutations in OCRL1. Am J Hum Genet. 2005;76:260–267. doi: 10.1086/427887. Ludwig, M., Levtchenko, E., Bà ¶kenkamp, A. (2014). Clinical utility gene card for: Dent disease (Dent-1 and Dent-2).European Journal of Human Genetics. Lloyd, S. E., Pearce, S. H., Fisher, S. E., Steinmeyer, K., Schwappach, B., Scheinman, S. J., Thakker, R. V. (1996). A common molecular basis for three inherited kidney stone diseases. Nature, 379(6564), 445-449. Novarino G, Weinert S, Rickheit G, Jentsch TJ: Endosomal chloride-proton exchange rather than chloride conductance is crucial for renal endocytosis. Science 2010, 328:1398-1401. Pagon, R. A., Adam, M. P., Bird, T. D., Dolan, C. R., Fong, C. T., Stephens, K., Rossetti, S. (2012). Dent Disease. Piwon N, Gunther W, Schwake M, Bà ¶sl MR, Jentsch TJ: ClC-5 Cl-channel disruption impairs endocytosis in a mouse model for Dent’s disease. Nature 2000, 408:369-373. Pook, M. A., Wrong, O., Wooding, C., Norden, A. G. W., Feest, T. G., Thakker, R. V. Dents disease, a renal Fanconi syndrome with nephrocalcinosis and kidney stones, is associated with a microdeletion involving DXS255 and maps to Xp11.22. Hum. Molec. Genet. 2: 2129-2134, 1993. Raja KA, Schurman S, DMello R G, Blowey D, Goodyer P, Van Why S, Ploutz-Snyder RJ, Asplin J, Scheinman SJ. Responsiveness of hypercalciuria to thiazide in Dents disease. J Am Soc Nephrol. 2002;13:2938–44 Wrong.O.M., Norden.A.G.W. and Feest.T.G. (1990) Quart. J. Med. 77, 1086-1087.

William Shakespeares Othello Essay -- William Shakespeare Othello Ess

William Shakespeare's Othello Every artist needs a subject to draw inspiration from—an idea to develop into a masterpiece. Leonardo da Vinci had Madame Lisa to portray in paint. The Beach Boys had Rhonda to render in rhyme. And William Shakespeare had one of one hundred stories written by Giraldi Cinthio to help him create his masterpiece, Othello. Each artist creates his own interpretation from his source. Shakespeare transformed the core of Cinthio’s story into a tragedy. A tragedy is drama which depicts â€Å"a public struggle between larger-than-life protagonists and universal forces† (Glossary 175). A tragedy also involves a â€Å"hero’s suffering and his consequent moments of tragic insight or knowledge† (McJannet 1). Each subtle change, which Shakespeare adapts from his source, serves to turn an ordinary tale into an extraordinary tragedy. The changes Shakespeare makes create a â€Å"larger-than-life protagonist.† In Cinthio’s work, the Ensign falls in love with Disdemona. The Ensign tries every means available to woo her, yet he fails in every attempt. The Ensign â€Å"imagined that the cause of his ill success was that Disdemona loved the Captain of the troop† (Cinthio 137). As a result, â€Å"the love which [the Ensign] had borne the lady now changed into the bitterest hate, and†¦he devoted all his thought to plot the death of the Captain of the troop and to divert the affection of the Moor from Disdemona† (Cinthio 137). Cinthio’s plot does not center on Othello, it is powered by Disdemona. Shakespeare makes a key change when creating his play. Shakespeare makes Othello the clear protagonist. Iago’s plotting revolves around Othello. Not only does Othello pass Iago over for a rightly deserved position, but â€Å"it is thought a... ...Michelangelo did with a chisel, so Shakespeare does with a pen. Shakespeare took Cinthio’s idea of a Moor. Shakespeare chipped away parts, and patched them back together, in a reconfiguration from his own mind’s eye. Shakespeare creates a tragic flaw, and from this a tragic error occurs. Shakespeare creates an impressive protagonist amid a fateful world. Within this tragic world, the fatal manipulation of Othello is brought to light. In short, Shakespeare turns a tale into a tragedy and a story into a masterpiece. Works Cited: Cinthio, Giraldi. Hecatommithi. Trans. J. E. Taylor. Ed. Alvin Kernan. New York: New American Library, 1998. (134-146). Glossary. (170-175). McJannet, Dr. Linda. â€Å"Short Paper: Shakespeare and Cinthio.† Spring, 2006. (1-2). Shakespeare, William. Othello. Ed. Alvin Kernan. New York: New American Library, 1998. (2-128).

Distribution Plan Essay

The distribution and delivery section of LEAPh Incorporation aims to satisfy and create values for the customers in which the company operates. The distinguishing characteristics of the business will be the combination of management experience, sales and distribution experience, high quality, innovative products and exceptional customer service. In particular, the Leading Philippines Incorporation will do a full service distribution servicing the customers in the market with a fulfilling assistance. In addition, the LEAPh Inc. will have an exclusive contract to distribute a new, groundbreaking product that would enable the company to gain immediate access to a majority of the potential customer base. The LEAPh Inc. intends to become a recognized distributor of one of a kind Digital Single-Lens Reflex Camera (DSLR) in the Philippines and become an internationally known locale brand. Leading Philippines Inc. plans to develop strong relationships with key customers so that the company will be viewed as an indispensable partner, rather than just another manufacturer. The company will work closely with each customer to recommend product assortment unique for their retail base, appropriate stocking levels, pricing and display assortments, as well as promotional ideas and material to increase sales. The LEAPh will seek out and work with the retailers that represent to deliver the most innovative and exciting products possible to the customers that will be served. In order for the products to be received by the customers, the LEAPh will be going to distribute the cameras through sales representatives and through retail stores as well. The company will be using a three level distribution channel. In a three level channel structure, the retailers serve as intermediaries between the consumers and the manufacturer which is the LEAPh. Retailers order products directly from the manufacturer, and then sell those products directly to the consumers. This will enable the company to stay in touch with the retailers up to the end users of the products and understand their tastes, preferences and tendencies. This will also help the company to minimize the total distribution costs for the given products. MANUFACTURER RETAILERS CUSTOMERS Leading Philippines Inc. Department Stores Customers The intermediaries which are the retailer’s outlets provide several benefits to both manufacturers and consumers. It will improve the efficiency of the company; make a better assortment of products, the reutilization of transactions, and easier searching for goods as well as customers. The use of this level of distribution will also aid the search processes of both the buyers and sellers. Producers are searching to determine their customers’ needs, while customers are searching for certain products and services. A degree of uncertainty in both search processes can be reduced by using this channel of distribution. For example, consumers are more likely to find what they are looking for when they shop at retail institutions organized by separate lines of trade, such as grocery, hardware, and clothing store. In addition, producers can make some of their commonly used products more widely available by placing them in many different retail outlets, so that consumers are more likely to find them at the right time. The company will be implementing an individualized customer service which will provide the customers with what they want, when and how they want it with the help of the retailers. This fully integrated program for the customers will help the company to increase its sales through innovations of the products, creating promotions, advertising, custom marketing material and the word of mouth from its customers. In this way, the company has the full control over the distribution of the products as well. Here are the methods that will be used in this level of channel distribution of the products from Leading Philippines Inc.: †¢ Selling of products through the leading retail outlets and department stores nationwide. †¢ Selling the products by the orders that are received by telephone, email and fax which is also known as telemarketing. ( Made possible by advertising the products through websites) This stage of distribution channel will also be use in order for the products to be widely available in all leading department stores and retailer’s shops nationwide. And to optimize the product launch as well. The LEAPh will employ an intensive distribution to the customers so that the products could be distributed from as many department stores and retailers ‘outlets as possible to provide a location convenience for its consumers. It will also increase the sales of the company, and provide wider customer recognition. By communicating and building relationships with the members at each step in the channel, there should be a proper communication throughout the channel and every member in the channel should contribute for a healthy relationship. Transparency should be maintained throughout the channel.

Selling organs on the black market - 1081 Words

Selling Organs on the Black Market Every teenager wants to own the newest iPhone or iPad but to save up for those working at the local McDonald’s it would take some time. But in China, you can get it just by selling a kidney. In face according to a BBC news article dated April 6, 2012 five people were arrested for convincing a teenager to sell his kidney in an online chat room for the equivalent of $3,000. The teenager is now suffering from kidney failure, and just for a couple of new toys. The New York Times states on June 29, 2012 that only 10% of the global needs for organ transplantation are being met. The UK Telegraph of May 28, 2012 states that experts are saying that a rise in diabetes and other diseases has led to the†¦show more content†¦There is only one country that allows the legal buying and selling of organs, Iran allows people to sell and buy kidneys under the state regulated surveillance of two non-profit organizations but Iranians are not allowe d to sell kidneys to non-citizens. Now that we have discussed both the problems and the causes of the black market organ trade, let’s focus on two possible solutions we could implement. First we well discuss a possible opt out policy, and then we will look at enforcing and implementing laws. Let’s begin with a possible solution is to activate an opt out policy in each state. Richard Brodsky wants to change the way the New York organ donation system works. He believes that this system could help increase organ and tissue donations. The proposal would require that people be automatically added to the state donor registry unless they opt out when they get a driver’s licenses or state identification card. Richard says his bill has sparked a lot of interest but that he knows both individuals and religious groups have raised concerns. Mary baily a member of the Hastings Center, stated that it’s easy to see this would not go over well with Americans at a t ime when many are pushing against government control on a variety of other issues. UCLA professor and medical doctor, Gabriel Danovitch testified before the U.S. House of Foreign Affairs in 2012 that there are several things the U.S. government can do. He begins by stating that the National organShow MoreRelatedThe Ethical And Medical Controversy1413 Words   |  6 PagesThe argument regarding the selling of organs on the black market has been an ethical and medical controversy for decades. 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