Norma Jean Mortensen Baker Was Born To Her Mother Gladys Mortensen On

Norma Jean Mortensen Baker was born to her mother Gladys Mortensen on June 1st, 1926 at 9:30 am in Los Angeles, California. Gladys was divorced from her husband, C. Stanley Gifford and separated from her husband Ed Mortensen. Ed Mortensen was who Gladys put on Norma Jean's birth certificate as her father but it is still in question if he was her father of if it was her first husband Jack Baker who was her father. Gladys had two other kids from another marriage. She had them in her first marriage to Jack Baker. They were married when she was sixteen in 1917. The kids names were Hermitt Jack and Berneice. They went to live with their father's family in Kentucky after their divorce in 1921. Hermitt reportedly died of Tuberculosis in the early 20's, but Gladys reported both of them dead when Norma Jean was born. Gladys later reunited in the 60's when Berneice in the 60's when Berneice became Gladys legal guardian. After Norma Jean was born Gladys decided she couldn't afford her and so she sent her to live with a mail carrier and his wife, Albert and Ida Bolender. Norma Jean spent her first years with the Bolenders. They were very religious. They boarded children at their property. It was two acres. They tried to adopt her but Gladys always rejected. Her Grandmother live across the street from the Bolenders. Her name was Della Hogan Monroe Grainger. She would take Norma Jean to her house for visits often. Later in life Marilyn said that she awoke in the night fighting for her lifer because her grandmother was holding a pillow over her face. Many people say she couldn't remember this happening because she was only a year old then. Another time Della tried to ?rescue? Norma Jean. She tired breaking the Bolenders door down. She had to be taken away by the police and she was put in an asylum on August 4, 1927, where she died 3 weeks later from a heart attack during a manic seizure. Norma Jean's situation was very confusing for her. She got weekend visits from Gladys. Norma Jean never called her her mama though. She didn't know Gladys was really her mother until Ida Bolender pointed it out to her. She had always called the Bolenders mom and dad until Ida corrected her. There was another kid there named Lester. He got away with away with calling them mom and dad because he had been adopted by them. Yet, they called Norma Jean and Lester ?twins? which only confused Norma Jean even more. Gladys started spending more time with her daughter and she took her to work with her occasionally. She was five when she saw pictures of the father for the first time. ?I felt so excited I almost fell off my chair...That was my first happy time.? (Marilyn by: Kathy Rooks-Denes, copyright 1993, pg. 19). In 1934 Norma Jean was brought to lice with her mom and an English couple. They urged her out of the religious shell she was in and got her into singing and dancing and the movies. Gladys worked two jobs. She tried to provide a good family life for her daughter but in 1935 Gladys was taken away on away on a stretcher. She was put in the same mental hospital her mom had died in and was diagnosed with paranoid schizophrenia. She would stay in the hospital almost the rest of her life. Her mother would never allow her to be adopted out so she lived in 12 different families, 10 of them foster parents, when she wasn't in a Los Angeles orphaninge. At age 16 Norma Jean was forced into a marriage to 20 year old Jim Dougherty. She didn't want to marry him. She thought she was way too young but she was forced to do so anyways. ?I had six mothers weeping when I marched down the aisle? (Marilyn pg. 25) Gladys wasn't there though even though she wasn't in a hospital at the time. They didn't take a honeymoon and Jim went to work the next day like their marriage wasn't any big deal. ?It was like being retired to a zoo. The effect marriage had on me was to increase my lack of interest in sex...Actually our marriage was a sort of friendship with sexual privileges, (which) brought me neither pain nor happiness.? (Marilyn pg. 26) She wanted a baby but he talked her out

The Outsiders- by SE Hinton Why Gangs Portrayed in this Novel are Real

The Outsiders- by SE Hinton Why Gangs Portrayed in this Novel are Real Gangs. This is what is portrayed in SE Hinton's novel, The Outsiders. Two different gangs from opposite ends of the social ladder clash in this epic novel of social tension between two rival groups, the Socs and the Greasers. The main character, 14-year-old Ponyboy, is a Greaser who lives under the cycle of poverty and endless pressure from the Socs. They are the upper class Westside crowd who are accepted in society. The Greasers, in contrast, struggle to put food on the table and are social outcasts. SE Hinton has mentioned about gangs several times in her novel. But what really defines a gang? According to some, it is, "A group of young people who spend time together for social reasons." While others define gangs as, "A group of people who work together for some criminal or antisocial purpose." Although these are the most popular ones, it does not mean there aren't more definitions, as it is an ever evolving phenomenon.Gangs of New YorkIn the Outsiders, many different gangs are de picted. This led me to believe that the gangs are very real in this tale. The main reason behind this is the fact they give three main characteristics of a gang. They are; the fear they instill on the general public, the marked territory, and rivalry between other gangs.The fear they instill on the general public is there for reputation purposes. If you're an established person with a reputation to protect, none of the very many below you will question your authority. The fear the community has for the Greasers, as well as the Socs, was evident when Ponyboy stated that, "One day the Socs are a menace to society, the next they are the greatest contributions." On the other hand, Greasers were always known as a peril to...

Anish Kapoor Exhibition Review Essay Example | Topics and Well Written Essays - 750 words

Anish Kapoor Exhibition Review - Essay Example Anish Kapoor: Memory suggests the sequences in which human perception arises through the principle of memory. â€Å"Memory,† a site-specific installation which contrives to fill Guggenheim’s enormous gallery space, becomes an investigation of scale, volume, color and materiality and consequently experiments on the limitations or restrictions of space and place. The exterior shell of this massive egg-shaped sculpture secures itself tightly against the peripheries of the gallery walls and ceiling, and down again to the floor. The eight millimeter thick Cor-Ten steel material chosen by Kapoor allows the form to achieve an apparent weightlessness although in reality, the sculpture is sits heavily at twenty-four tons. The illusion of lightness is realized through the construction of complex structural engineering that is specifically designed to be experienced through a series of partial and spatially separated views. Hence, Memory’s charm lies in its inaccessibility, preventing itself from revealing its true form. Memory is conceived as a new kind of experience as something that cannot be experienced at once but is rather understood through a series of separate, meaningful fragments. No one sees the whole thing at once as a result of the use of gallery space. Each visible segment is only seen after the viewer has experienced other unrelated elements of the museum and we are reminded that our memory in part, works in a similar fashion. The exhibit’s presentation invites us to daydream and reconstruct a mental image through the process of gestalt. In that sense, Kapoor considers the ways in which people feel and think about space, how they form attachments to their environment, and how feelings about space and place are affected by the sense of time. Memory is a critical understanding of how we are rooted to place and space. He extends his observation regarding the directionality of the different viewpoints

Who was to blame for the banking crisis Essay Example | Topics and Well Written Essays - 2500 words

Who was to blame for the banking crisis - Essay Example After the Great Depression of 1930 the world economy faced a dangerous financial crisis. It all began when sky rocket property prices in the United States started decreasing and this impact soon spread all over the financial sector. The Global Financial Crisis initiated in July 2007 with the credit crunch when US investors lost confidence in the investment of mortgage property. This all compelled US investors to inject a large portion of capital into the financial market. By September 2008 the crisis got worse and hit all stock markets globally and made the market volatile. The consumers started losing confidence in properties and the stock market and were in a position of fear what could be lying ahead of them (Broman, 2012). The banking industry has seen many fiscal crises in the past, the notable one of them being the one that started in the 1930. Since then many countries have seen ups and downs when it comes to their banking industry. The most recent one of them being that in 2007; which changed the perspective of many investors and regulators. It all took one Lehman Brothers to go bankrupt for the Wall Street crisis panic to spread worldwide and affect other countries, developing or developed. The causes were smaller in person and unimportant but together, they caused huge economies to collapse and endure great loss. The reasons were as followed: On a general note, the global financial crisis began developed its roots in 2007, July, when the US investors started to lose confidence in the values of subprime mortgages, resulting in a liquidity crisis. This lead to the US federal bank adding a notable sum of capital into the financial market but nevertheless, the issue persisted such that by 2008, the stock markets around the world became seriously volatile and subsequently crashed. The Global market braced them for they feared the impending doom that approached them. Questions pertaining to the liquidity of banks, a fall in the availability of

Occupational Behaviour Assignment Example | Topics and Well Written Essays - 2500 words

Occupational Behaviour - Assignment Example utor to why Netflix continues to outperform competition and achieve substantially-high ratings from consumers who appear satisfied with its customer service practices. Based on careful analysis of the firm, its high pay structures and autonomous working environments are missing metrics to determine whether these policies are the genuine catalyst for organisational success and performance. Some research findings have discovered that pay systems are not always effective for achieving long-run job performance and that there are risks to providing too much autonomy. Based on all research and investigation into theory of organisational behaviour and even human psychology, as well as business theory, it is recommended to implement a 360 degree feedback appraisal system at Netflix and engage in the management-by-objectives ideology. These practices will give the firm a new ability to accurately measure true job performance and determine whether there is substantial return on investment for having such liberal HR policies. In order to maintain its reputation as a world class provider of superior customer service, Netflix seeks to hire only the most talented and motivated employees. HR-related perks include generous pay packages, seemingly unlimited vacation opportunities, a reduction of work rules and policies and considerable job role autonomy in order to attract and retain these high performers. This would, theoretically, provide considerable socio-psychological benefits that make employees more committed and motivated to achieve organisational goals. However, there is a potential plethora of problems with providing employees with perks such as the aforementioned to achieve job role performance. First, the case study did not indicate that Netflix has established a metrics system that would measure performance appropriately; a method of ensuring return on investment for these HR activities. Whilst Netflix believes that this will create a culture of commitment for the

Central Giant Cell Granuloma in Eight Year Old Patient

Central Giant Cell Granuloma in Eight Year Old Patient INTRODUCTION Central giant cell granuloma (CGCG) is a benign aggressive destructive osteolytic lesion of osteoclastic origin1 that ocur in the mandible and maxilla and accounts for approximately 7% of all benign tumours of jaws2. The world health organization (WHO) has defined CGCG as an intraosseous non-neoplastic lesion, consisting of cellular fibrous tissues that contain multiple haemorrhage multinucleated giant cells, and, occasionally trabeculae of woven bone3. The nature of CGCG is still controversial. Jaffe was hypothesized that this is a reactive and self curing lesion and included the terminology giant cell reperative granuloma. Later, the neoplastic hypothesis was raised to explain the aggressive subtype4. Recently, both reperative and neoplastic assumptions are true, so that CGCG lesions are patially reactive and partially neoplastic4. CGCG is an uncommon lesion that occurs in young adults before the age of 30 years with a female preponderance5. There was a peak incidence for males between the age of 10-14 years and for females between 15-19 years of age6. It is more common in the anterior mandible than in the maxilla. Histological characteristics are highly cellular, fibroblastic stroma with plump, spindle- shaped cells with a high mitotic rate; the vascular density is high. The multinucleated giant cells are prominent throughout the fibroblastic stroma but are not necessarily abundant. They are often located most numerously around of haemorrahge6. Clinically, CGCG shows a wide variety behavior that is ranging from a non-aggressive, asymptomatic (indolent) and slow growing lesions to an aggressive, large, expansive lesion with rapid growth and aggressive sign and symptoms. Choung et al.7were the first described between the differences aggressive and non- aggressive lesions based on signs and symptoms and histological features. Aggressive lesions are characterized by one or more of the following features: pain, paresthesia, root resorption, rapid growth, cortical perforation, and a high recurrence rate after surgical curretage. Radiogically, the lesion appears as a radiolucent area and it can be unilocular or multilocular with either well-defined or can be ill-defined margins8. Multiple lesions are rare and are often associated with a syndrome (i.e. Noonansyndorme, neurofibromatosistype I ) or with cherubism6. The radiological and histological apperances of CGCG are not pathognomatic, and therefore further examination such as blood tests, including calcitonin, phosphate, parathyroid hormone and alkaline phosphate levels must be performed to confirm the diagnosis and to exclude hyperparathyroidism8. One of the treatment choice for CGCG is curratege with or without adjuvant therapy, i.e. liquid nitrogen, cryosurgery, peripheral ostectomy and Carnoy’s solution and another treatment modality is aggressive en- bloc resection, resulting in varying degrees of deformity5. It results in serious mutilation of the jaw and face. Loss of teeth and of dental germs in young patients is also often unavoidable9. In growing patients, to preserve both aesthetic and functional necessity non-surgical methods such as intralesional injections with corticosteroids, IFN-ÃŽ ± 2a and systemic dose of calcitonin are increasingly used by clinicans. These alternative therapeutic strategies come in useful for large aggressive lesions to cure or reduce the size and thus minimize the need for extensive surgical resection that can result in functional and aesthetic deficits in young patients. Calcitonin therapy for CGCG was first announced by Harris in 1993 and since then several case reports have been published of successful treatment of this lesion using different types of calcitonin and different strategies of administration5. In this report a patient is presented with massive aggressive CGCG who were treated with salmon calcitonin, as a single treatment modality, after initial treatment with intralesional steroid had failed. CASE REPORT An 8- year- old male patient complaining of a tender/ non-tender swelling on the left mandibular molar area was referred to the oral and maxillofacial surgery service at the Selcuk University, Faculty of Dentistry, in 2010. There was neither medical history nor trauma. Physical examination †¦Ã¢â‚¬ ¦.cm, lymphadenopathy, Radiographically, in the left mandibular molar area a diffuse radiolucency†¦Ã¢â‚¬ ¦ Based on clinical and radiological findings pre-diagnosis of CGCG was made and laboratory investigations were required to eliminate hyperparathyroidism (brown tumors) before treatment. Parathyroid hormone levels were found in normal reference ranges. Additionally low level of haemoglobin and high level of creatinin and phosphate were examined. An incisional biopsy was performed under local anesthesia. Histologically diagnosis of the lesion was proved as CGCG. Because of the patient’s age and dental development conservative therapy was preferred. Intralesional steroid injections of a solution of Kenacort-A (10 mg/ml triamcinolone aqueous suspension, Bristol-Myers Squibb S.p.A, Loc.ta Fontana del Ceraso, Angani, Italy) were performed during 1 year but there was no resolution in the lesion. After initial steroid treatment was failed authors decided using intranasal (systemic) calcitonin treatment. Miacalcic ® 200 IU/day nasal spray (Novartis Pharmaceuticals Corporation, East Hanover, New Jersey, USA) (calcitonin-salmon) was preferred and performed 2 yearlong. Luckily any side effect was seen and the patient was showed exceptionally good cooperation to treatment and. During systemic calcitonin therapy clinicians must be on the alert about some side effect such as bloating or swelling of the face, arms, hands, lower legs, or feet, chills, cough, difficulty with breathing, difficulty with swallowing, dizziness, fever, itching, joint pain, muscle aches and pains, nausea or vomiting, nervousness, puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue, skin rash, sweating, tightness in the chest, tingling of the hands or feet, trembling or shaking of the legs, arms, hands or feet, trouble sleeping, unusual weight gain or loss. Following calcitonin therapy there was a decrease in tumor size that was observed clinically. Preserving the teeth and growing jaw bone for natural mastication and facial aesthetic the tumor was not decided to operate. The patient has a three- year follow up and has any clinical or radiological sign or symptoms. DISCUSSION CGCG is an uncommon lesion that occurs more frequently in females. In most cases it appears before the age of 30 years. Mandibular lesion is more often than the maxillary lesion with a ratio 2:1. In the mandible the anterior and posterior regions are equally affected while in the maxilla, the anterior region is usually affected.(ant. Mu post. Mu) The clinical behavior of CGCG ranges from a slow growing asymptomatic swelling to an aggressive lesion that presents pain, local bone destruction, root resorption or tooth displacement. Some authors have classified CGCG into two types, based on clinical and radiographic features. The first is non-aggressive CGCG, which is characterized by slow, almost asymptomatic growth that does not perforate the cortical bone or induce root resorption and has a low tendency to recur. The second is aggressive CGCG, which is characterized by pain, rapid growth, expansion, and perforation of the cortical bone, radicular resorption and high tendency to recur. Histologically, CGCG is characterized by the presence of multinucleated giant cells (MGC) in background composed of mononucleated stromal cells (MSC) with ovoid or spindle-shaped mesenchymal nuclei. The giant cells are typically seen in a hemorrhagic field containing numerous poorly defined vascular channels, which may be quite prominent. A patchy distribution of cellular elements is one feature that helps differentiate CGCG fromtrue giant cell tumors. In aggressive lesions, Ficarra et al. reported more numerous giant cells in CGCG and Nougeria et al. showed that in aggressive lesions MGCs are usually more numerous, larger and uniformly scattered throughout the lesion. Flanagan et al. were the first to demonstrate that giant cells in CGCGs are osteoclasts through osteoclast- specific monoclonal antibodies staining. This report was provide in vitro reaction of giant cells to calcitonin and showed the behavior of giant cells in cortical bone excavation typical of osteoclasts. It has been demonstrated that giant cells express calcitonin receptors. Calcitonin therapy is based on these findings. It is though those giant cells are directly inhibited in their function by calcitonin. Others, however, debate that CGCGs develop from mononuclear precursor cells and, as such, are part of the granulocyte/macrophage lineage or are primarily of fibrotic origin. Although giant cells are the most prominent histopathological feature of CGCGs, the focus of interest has shifted to the role of the mononuclear cells. Recent studies have shown that mononuclear cells, rather than the giant cells are proliferating compartment responsible for the biological activity of the lesion. de Lange et al. reported that the giant cells of CGCG are derived from subset of mononuclear phagocytes. These mononuclear precursor cells differentiate into mature giant- cells under the influence of RANKL expressing, proliferating, spindle shaped (osteoblastlike) stromal cells. Nougeria et al. designed a study to determine receptors of MGCs and find out their origin. This study showed, positive immunohistochemical expression of receptor activator of nuclear factor –kB (RANK), tartrate- resistant acid phosphatase (TRAP), vitronectin receptor (VNR) and calcitonin receptor and these findings have suggested on osteoclastic phenotype for MGCs. The presence of CD68 glycoprotein and alpha-1-antichymotrypsin has suggested that MGCs have a macrophage/hystiocyte origin. In the light of these findings aim of the treatment of CGCGs should include both inhibit osteoclastic activity of the lesion and inhibit the differentiation of macrophage/ hystiocyte precursors into osteoblast like cells. Traditional treatment for CGCGs is surgical curettage. Some authors proposed excision via curettage for treatment of CGCGs and the overall recurrence rate has been reported to range from 16 % to 49 %. A higher incidence of recurrence was found in aggressive CGCG and younger patients, especially males. In growing patients, aggressive surgical approaches may result in facial deformities and patients may lose some of tooth germs. Eisenbud et al. indicate that surgical curettage with peripheral osteotomy is still not the safest treatment for CGCGs especially in aggressive lesions. The functional and aesthetic alterations as well as the psychological consequences caused by the surgical treatment of CGCG have encouraged researchers to look for effective alternative therapeutic strategies. Alternative therapeutic options for CGCGs are systemic calcitonin intralesional injection of corticosteroids and IFN-ÃŽ ±. Calcitonin has been administered as a nosespray and as subcutaneous daily injections. Recently only nosespray form is available. This hormone increases the influx of calcium into the bones, functions as an antagonist to parathyroid hormone, and inhibits osteoclastic bone resorption. Calcitonin has also been hypothesized to directly inhibit giant cells. In 1993 Harris was first reported total remission of CGCGs in 4 patients. On the contrary Kaban et al (1999) observed a significant growth following calcitonin therapy. Response of patients to calcitonin therapy is variable. Many factors can contribute to the various responses to calcitonin which have been reported in the literature. The different types of calcitonin (human, salmon) and the different types of administration (subcutaneous injections, nasal spray) are some of these factors. With regard to the efficacy of calcitonin therapy, 3 phenomena have been recognized: Primary resistance or primary non-response is noted. There is the so-called plateau phenomenon, denoting that the alkaline phosphates serum levels cannot be lowered beyond a certain point, irrespective of the calcitonin dose. The third potential problem is secondary resistance, also called the escape phenomenon. Patients who initially react well to calcitonin show a diminished reaction after some time. Increased activity of osteoclasts through loss of calcitonin receptors is the more likely explanation for this phenomenon. Intralesional corticosteroids injection for CGCGs treatment was first reported by Jacoway et al. (1988). This method hypothesized that the extracellular production of bone- resorption- mediating lysosomal proteases by giant cells in inhibited by steroids which also induce apoptosis of the osteoclast- like cells. In English literature, complete remission results from intralesional administration of corticosteroids in insufficient and the number of patients is very small. Especially, in large cases intralesional corticosteroid therapy may not be effective and may not provide of reduction in size. No reports in which the effectiveness of intralesional corticosteroid injection for CGCG is described separately for the aggressive type and non- aggressive type are available. Nougeria et al. indicated that MGCs may be similar to osteoclasts and macrophages/hystiocytes and that CGCG can be prompted to respond to calcitonin or intralesional glucocorticoid as shown in the literature. They reported the expression of glucocorticoid and calcitonin receptors in CGCG before and after treatment with intralesional injection of steroids. They concluded that glucocorticoid receptor expression in the MGCs was higher in patients with a good response. The difference in calcitonin reseptor expression was not statistically significant between the aggressive and non- aggressive lesions and between the patients with a good response and with a modatare/negative response to treatment. Although aggressive CGCG had higher calcitonin receptor expression no significant difference in calcitonin receptor expression in different clinical forms of CGCG was found in this study. The treatment response was determined using previously described scores. In which four criteria were conside red: stabilization or regression of the lesion size evaluated clinically and in follow-up radiographs; the absence of sumptoms; increased radio-opacity in radiographs, representing peripheral and/or central calcification of the lesion, increased difficulty in solution infiltrating the lesion during the sequence of applications. If a case provided all of these, the response was determined to be good; providing two or three criteria was determined to be moderate; and providing one criteria or no criteria implied a negative response to treatment. Another alternative therapeutic agent is IFN-ÃŽ ±, it has angiogenic potential and it is a mediator in differentiation from mesenchymall cells to osteoblasts thus leading to an increase in bone apposition. Similar to corticosteroids IFN-ÃŽ ± is also capable of stopping rapid growth of their lesions and reducing their size, but it still necessary to use additional surgery to eliminate the lesion. In the literature only one case report was showed complete remission with IFN-ÃŽ ± therapy. Several reports suggest that IFN-ÃŽ ± administered as a monotherapy for aggressive CGCGs is useful for inhibiting the rapid growth of lesions and for reducing their size. Total remission of lesion cannot be achieved, because IFN-ÃŽ ± has no direct inhibiting effect on proliferating tumor cells and additional surgery is probably still required to eliminate lesions. Therefore, the effectiveness of monotherapy with IFN-ÃŽ ± is still questionable. CGCG is found predominantly in young adults. Surgical treatment of these patients might have resulted in physical and psychological disorders, such as developmental disorder of the mandible, dysfunction of mastication, and facial deformities, non- surgical treatment with systemic calcitonin administration which is a minimally invasive procedure and less costly and should be considered the first choice for treatment of CGCG in young patients.

Ethical Principals for Protecting Research Participants Essay

Participating in a research study is an opportunity for people to contribute to the advancement of healthcare practice or other measures. Researchers typically collect data from a population of people that share common characteristics that make them appropriate subjects for the area being studied. In order to assure that participants are adequately protected, a set of ethical principles should be adhered to by all research facilitators. â€Å"The Belmont Report articulates three primary ethical principles on which standards of ethical conduct in research are based: beneficence, respect for human dignity, and justice† (Beck & Polit, 2006). The principle of beneficence serves to minimize harm to participants, maximize the benefits of the study, and protect the participant from any form of exploitation. â€Å"In research with humans, harm and discomfort can take many forms: they can be physical, emotional, social, or financial† (Beck & Polit, 2006). Facilitators of any research study must be conscious of this and use strategies to alleviate potential of such harm. Ethical researchers must be prepared to terminate their study if any evidence of distress on the participants is discovered. Another duty that researchers face is to protect participants from exploitation. â€Å"Involvement in a study should not place participants at a disadvantage or expose them to situations that they have not been prepared† (Beck & Polit, 2006). In summary, participants must feel secure that the information they provide will not be used against them in any fashion. The second ethical principle addressed by The Belmont Report is the respect for human dignity. Study participants have the right to self-determination, or the capability to control their own activities. This right encompasses the ability to ask questions, refuse to provide information, or even withdraw from a study without consequences. The entitlement of self-determination also includes the freedom from being coerced into participating in a study, such as an economically disadvantaged person being offered a large stipend to participate. This may be seen as placing this individual under undue pressure to participate in the study. The principle of the respect for human dignity also includes the right to full disclosure. This allows a person to make informed, voluntary decisions regarding the study they are participating in. â€Å"Full disclosure means that the researcher has fully described the nature of the study, the person’s right to refuse participation, the researcher’s responsibilities, and the likely risks and benefits that would be incurred† (Beck & Polit, 2006). The last ethical principle delivered in The Belmont Report pertains to justice. This principle ensures participants’ rights to fair treatment and the right to privacy. Justice promotes duties to neither neglect nor discriminate against individuals. â€Å"The principle of justice imposes particular obligations toward individuals who are unable to protect their own interests to ensure they are not exploited for the advancement of knowledge† (Beck & Polit, 2006). Researchers must also acknowledge the participants’ right to privacy. They must ensure that their research is minimally intrusive and the participants’ privacy is respected throughout the study. People that partake in a study should expect that any information they provide will be kept in strict confidence. There are designated procedures in place to ensure participants’ satisfaction of a study upon completion. One such task is the risk/benefit assessment. â€Å"Such an assessment is designed to determine whether the benefits of participating in a study are in line with the costs, be they financial, physical, emotional, or social† (Beck & Polit, 2006). Researchers can also offer a debriefing session after data collection is complete. This allows participants to ask questions or air complaints pertaining to the study. Researchers can demonstrate their interest in study participants by offering to share findings with them once the data has been analyzed. Lastly, facilitators should refer participants to appropriate health or psychological services as deemed necessary. Bibliography Beck, C. and Polit, D. (2006.) Essentials of Nursing Research: Methods, Appraisal, and Utilization. (6th ed.) Philadelphia: Lippincott, Williams, and Wilkins.