What to do/not do before and in an Interview

What to do before an Interview

  1. Conduct Sufficient research about the company: This is valuable information that ensures that the interviewee is well versed with the company. It also makes it easy to answer the interview questions. Furthermore, it shows that the person is truly interested in the company.
  2. Rehearsal of the interview questions: one should prepare a list of questions that are most likely to be asked during the interview such as queries about the position that is being applied as well as questions about the company.
  3. Know what value one plans to add to the company: this is one of the most common questions during the interview. One should know the right answer to it beforehand.
  4. Perform web searches for previous interviews: Sites such as ‘brighter Monday’ may contain information about previous experiences of former interviewees.
  5. Ensure that one gets adequate sleep the night before: The benefits of a good night’s sleep are immense. Good sleep ensures that one is alert, looks good, and also feels good. Such qualities go along way when answering interview questions
  6. A good and healthy breakfast is crucial: This ensures that one is more focused and possesses the right energy levels for the interview
  7. Ensure that one is well-groomed: The image of an interviewee offers the first impression ever before the interview begins. Thus, the clothes should be smart and wrinkle-free.
  8. Besides being well groomed, one should brush their teeth and put on deodorant: This is to avoid bad smells that may put off the interview panel.
  9. Prepare the resume: It would be very unfortunate to show up at the interview without the resume. For this reason, the document and its copies should be prepared prior to the interview date a placed at a convenient place to avoid forgetting it
  10. Pay attention to references: Referees should be ready and solid meaning that upon being contacted, they should be in a position to give the right and helpful information about the interviewee.
  11. Know Personal strengths and make a list of them: This is because in most cases, the interview panel is interested to know points of strengths that one possesses.
  12. Carry a handkerchief: in addition to being hygienic, the interviewee might get nervous and sweaty. In such a case, this will help in wiping away the sweat
  13. Prepare thank you notes beforehand: this will make it easier to drop them off afterwards.
  14. Arrive early at the day of the interview: This ensures that one does not make the grave mistake of being late. It also ensures that one is fully prepared.

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What to do during an interview

  1. Greet the interviewers preferably by a handshake
  2. Wait for the interviewer to offer a seat instead of going ahead to sit immediately
  3. Eye contact is important when communicating with the interviewer
  4. When answering the questions, it is important to answer what is asked and avoid wandering off-topic
  5. Before answering a question, one should take some time. This shows that they are putting some thought into the answer.
  6. Be grammatically correct. Using some words such as yea instead of yes is not allowed
  7. One should take notes to show seriousness
  8. The interviewee should let the achievements speak for them
  9. Although an interview is a tense-moment. One should try and be calm and even more importantly, be themselves
  10. By starting with conversation topics that one is comfortable with, the interviewee can direct the direction of the interview to some extent which is an added advantage.
  11. Ensure that one asks questions such as the full description of the work as well as the expected pay.

What not to do during an Interview

  1. Be clear while answering the questions. This includes avoiding talking too fast and at an inaudible voice
  2. Don’t digress from your points answer questions directly.
  3. Don’t use words you don’t know the meaning of.
  4. Use the correct language that is English .Avoid use of slang language.
  5. Don’t give the employer any reason to think you will not perform well.
  6. Avoid being nervous you will probably will be, but it is best if you take a few seconds and clear your mind. If you find yourself being too nervous excuse yourself and go to the bathroom to get some air. Don’t take too long but it is better to collects your thoughts than to plow head when you can’t focus.
  7. Avoid being defensive since the interviewer will be asking technique

Questions and everyone has their weak spots.

  1. Don’t fidget since this might be something you have to practice but it is worth it.
  2. Don’t talk about your personal information so much in the interview.
  3. Avoid being arrogant be humble.
What to do after an interview
  1. Drop off your thank you note .Always thank your interviewer after you have left. Email them after you drop off your note. The more contact you have, the more you remain their mind over the other applicants.
  2. Create a list of items that you did well and that you would like to improve on. This can be the most effective things to do after an interview because it will allow you to improve for future interviews, or accesses general weakness that will be helpful in your career.
  3. Follow up appropriately. Sometimes the interviewer will tell you when they will notify you; other times it will be your responsibility to make the follow up

 

References

Barker, L. K., Moore, J. W., Olmi, D. J., & Rowsey, K. (2019). A Comparison of Immediate and Post-Session Feedback with Behavioral Skills Training to Improve Interview Skills in College Students. Journal of Organizational Behavior Management, 1-19.

Hargie, O. (Ed.). (1997). The handbook of communication skills. Psychology Press.

Wiersma, U. J. (2016, December). The four stages of the employment interview. In Evidence-based HRM: a Global Forum for Empirical Scholarship. Emerald Group Publishing Limited.

AASP ethical codes

For your course project, you created a comprehensive sport psychology consultation plan for a specific team. Now that you have received feedback on the marketing presentation, assessment selections, and four performance enhancement interventions, you will write a 5–10-page paper reflecting on your experiences.

Incorporate the following in your reflection paper:

  • Describe changes that could be made to improve your completed presentations and interventions that would benefit the clients.
  • Explain the APA or AASP ethical codes that are used in your marketing presentation, assessment selections, and performance enhancement interventions.
  • Describe how approaches and consulting work might be different if applied to two differing populations other than the population of your selected Bulldogs team.
    • For example, female versus male athletes, professional versus amateur or youth athletes, diverse population versus the same population.
  • Describe how to distinguish between performance enhancement needs and other concerns that might need additional psychological services.

Use your textbook and articles from the course to support your claims.  Please review the scoring rubric to see how this assignment will be graded.

Assignment Requirements

  • Written communication: Written communication is free of errors that detract from the overall message.
  • APA formatting: Resources and citations are formatted according to APA current edition style and formatting.
  • Number of resources: A minimum of 3 resources used but can include the textbook and course materials.
  • Length of paper: 5–10 typed double-spaced pages, not including required cover sheet and reference page. No abstract required.
  • Font and font size: Times New Roman, 12 point.

Combination of agents targeting PI3K/AKT/mTOR and BCL2 pathways

AML Background

Acute myeloid leukemia (AML) is a disease characterized by abnormal proliferation and impaired differentiation of myeloid progenitors [1, 2]. This results in a buildup of leukemic cells in the bone marrow and the inhibition of normal hematopoiesis [3, 4]. AML is the most common type of acute leukemia in adults [1, 5]. It appears to be caused by mutations of key genes resulting in the deregulation and activation of cellular cascades that mediate pro-survival and anti-apoptotic responses [6-8]. The risk factors include exposure to benzene, ionizing radiation, and cytotoxic chemotherapy [9-11]. The 7+3 remission induction therapy with cytarabine and anthracycline has been the standard treatment strategy for AML [6, 12, 13]. This treatment is, however, challenging since it results in substantial toxicity and morbidity [6, 14, 15]. Elderly patients respond less satisfactory to the standard treatment partly due to cytogenetic abnormalities and an increased frequency of resistance mechanisms [1,3]. Younger patients have remission rates of 70-80% with most of them relapsing [1, 16, 17]. Hence, new therapeutic approaches are needed. Attractive targets include the signaling cascades that enhance proliferation, survival, and drug resistance of leukemic cells [3, 18, 19].

 

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BCL2 Pathway in AML

One of such targets that offer a potential therapeutic possibility is the anti-apoptotic proteins of the BCL-2 family [1, 20, 21]. These control the intrinsic pathway of apoptosis and are overexpressed in AML [22-24]. BCL-2, BCL-xL, and MCL-1 are the anti-apoptotic proteins while BAX and BAK effectors are pro-apoptotic [25, 26]. BAX and BAK are activated towards mitochondrial outer membrane permeabilization (MOMP) followed by caspase activation, leading to cell death [1, 27, 28]. BCL-2, BCL-xL, and MCL-1, which are highly expressed in patients with AML, hinder MOMP by binding pro-apoptotic proteins to their BH3 domain [29, 30].

Anti-apoptotic proteins frustrate treatment options by reducing responsiveness to chemotherapy induction and facilitating treatment refractoriness [31-33]. Potential treatment strategies aimed at inhibiting BCL-2 family proteins portray high in vitro and in vivo efficacy [31]. Among the promising treatments is ABT-737 with impressive pre-clinical activity [31, 34]. This BH3 mimetic Bcl-2/Bcl-xL inhibitor is effective against hematological malignancies [31, 35]. However, ABT-737’s weak interaction with Mcl-1 and Bfl-1/A1 reduces its cytotoxicity in cancers [31,36]. Also, by up-regulating Mcl-1, cells that were initially sensitive to ABT-737 develop resistance [31, 37, 38]. Hence, pharmacological modulation of Mcl-1 is necessary for determining ABT-737-induced cytotoxicity [39].

PI3K/AKT/mTOR in AML.

Other signal transduction pathways have been identified as driving features of Leukemia [31]. Among these is the Phosphoinositide 3-Kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway [31,40,41]. mTOR signaling pathway has been found to negatively affect patient outcomes [31,42-44]. It contributes to the activation of Akt which in turn directly influences the transcription of Bcl-2 family genes responsible for regulating apoptosis [31,45,46]. Selective blockade of mTOR activity shows promise in disrupting pro and anti-apoptotic protein balance, hence, promoting leukemic cell death [31, 47, 48]. The inhibition of mTOR signaling also enhances the sensitivity of AML blasts to cytotoxic agents, hence, better response to chemotherapy [3, 49]. Through clinical studies, allosteric mTOR inhibition using rapamycin and everolimus has been shown to impair leukemia-initiating cells (LICs) function [3, 50].

Conclusion

Overall, the inhibition of BCL-2 family proteins and P13’K/AKT/mTOR pathways has potent effects associated with the survival of leukemia cells and decreased cell proliferation. Therefore, this offers a potential future approach for the treatment of AML. However, clinical trials of single targeted agents have faced challenges resulting from severe toxicity and build-up of resistance. A strategy to curb these challenges involves a synergistic combination of targeted agents.

References

1.Airiau K, Prouzet-Mauléon V, Rousseau B, Pigneux A, Jeanneteau M, Giraudon M, Allou K, Dubus P, Belloc F, Mahon FX. Synergistic cooperation between ABT-263 and MEK1/2 inhibitor: effect on apoptosis and proliferation of acute myeloid leukemia cells. Oncotarget. 2015; 7: 845-59.

https://doi.org/10.18632/oncotarget.6417

2.Kumar CC. Genetic abnormalities and challenges in the treatment of acute myeloid leukemia. Genes & cancer. 2011; 2: 95-107.

https://doi.org/10.1177/1947601911408076

3.Chiarini F, Lonetti A, Teti G, Orsini E, Bressanin D, Cappellini A, Ricci F, Tazzari PL, Ognibene A, Falconi M, Pagliaro P,Iacobucci I, Martinelli G,…& Martelli AM. A combination of temsirolimus, an allosteric mTOR inhibitor, with clofarabine as a new therapeutic option for patients with acute myeloid leukemia. Oncotarget. 2012; 3: 1615-28.

https://doi.org/10.18632/oncotarget.762

4.Passegué E, Jamieson CH, Ailles LE, Weissman IL. Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics?. Proceedings of the National Academy of Sciences. 2003;100: 11842-9.

5.De Kouchkovsky I, Abdul-Hay M. Acute myeloid leukemia: a comprehensive review and 2016 update. Blood cancer journal. 2016; 6: e441.

https://doi.org/10.1038/bcj.2016.50

6.Altman JK, Sassano A, Platanias LC. Targeting mTOR for the treatment of AML. New agents and new directions. Oncotarget. Oncortarget. 2011; 2: 510-17.

https://doi.org/10.18632/oncotarget.290

7.Castelli G, Pelosi E, Testa U. Emerging therapies for acute myelogenus leukemia patients targeting apoptosis and mitochondrial metabolism. Cancers. 2019; 11: 260.

https://doi.org/10.3390/cancers11020260

8.Grafone T, Palmisano M, Nicci C, Storti S. An overview on the role of FLT3-tyrosine kinase receptor in acute myeloid leukemia: biology and treatment. Oncology reviews. 2012;6: e8.

https://doi.org/10.4081/oncol.2012.e8

9.Estey E, Döhner H. Acute myeloid leukaemia. The Lancet. 2006; 368:1894-907.

https://doi.org/10.1016/S0140-6736(06)69780-8

10.Sill H, Olipitz W, Zebisch A, Schulz E, Wölfler A. Therapyrelated myeloid neoplasms: pathobiology and clinical characteristics. British journal of pharmacology. 2011; 162: 792-805.

https://doi.org/10.1111/j.1476-5381.2010.01100.x

11.Belson M, Kingsley B, Holmes A. Risk factors for acute leukemia in children: a review. Environmental health perspectives. 2007; 115: 138-45.

https://doi.org/10.1289/ehp.9023

12.Chen KT, Gilabert-Oriol R, Bally MB, Leung AW. Recent Treatment Advances and the Role of Nanotechnology, Combination Products, and Immunotherapy in Changing the Therapeutic Landscape of Acute Myeloid Leukemia. Pharmaceutical research. 2019; 36: 125.

13.Murphy T, Yee KW. Cytarabine and daunorubicin for the treatment of acute myeloid leukemia. Expert opinion on pharmacotherapy. 2017; 18: 1765-80.

https://doi.org/10.1080/14656566.2017.1391216

14.Getz KD, Sung L, Ky B, Gerbing RB, Leger KJ, Leahy AB, Sack L, Woods WG, Alonzo T, Gamis A, Aplenc R. Occurrence of treatment-related cardiotoxicity and its impact on outcomes among children treated in the AAML0531 clinical trial: a report from the Children’s Oncology Group. Journal of Clinical Oncology. 2019; 37:12.

https://doi.org/10.1200/JCO.18.00313

15.Kohrt HE, Coutre SE. Optimizing therapy for acute myeloid leukemia. Journal of the National Comprehensive Cancer Network. 2008; 6:1003-16.

https://doi.org/10.6004/jnccn.2008.0076

16.Kiyoi H, Yamaguchi H, Maeda Y, Yamauchi T. JSH Practical Guidelines for Hematological Malignancies, 2018: I. Leukemia-1. Acute myeloid leukemia (AML). International Journal of Hematology. 2020: 111; 1-9.

https://doi.org/10.1007/s12185-020-02856-3

17.Kantarjian H. Acute myeloid leukemia—major progress over four decades and glimpses into the future. American journal of hematology. 2016; 91: 131-45.

https://doi.org/10.1002/ajh.24246

18.Huang K, Sun Z, Ding B, Jiang X, Wang Z, Zhu Y, Meng F. Suppressing Hedgehog signaling reverses drug resistance of refractory acute myeloid leukemia. OncoTargets and therapy. 2019; 12: 7477.

https://doi.org/10.2147/OTT.S216628

19.Yang X, Xu X, Liu Y, Gong A, Wang D, Liao X, Zhu H. Advances in Acute Myeloid Leukemia Stem Cells. InAdvances in Hematologic Malignancies. 2019.

 https://doi.org/10.5772/intechopen.84263

20.Tzifi F, Economopoulou C, Gourgiotis D, Ardavanis A, Papageorgiou S, Scorilas A. The role of BCL2 family of apoptosis regulator proteins in acute and chronic leukemias. Advances in hematology. 2012; 2012: 524308.

https://doi.org/10.1155/2012/524308

21.Campos ED, Pinto R. Targeted therapy with a selective BCL-2 inhibitor in older patients with acute myeloid leukemia. Hematology, transfusion and cell therapy. 2019; 41: 169-77.

http://doi.org/10.1016/j.htct.2018.09.001

22.Adams JM, Cory S. Bcl-2-regulated apoptosis: mechanism and therapeutic potential. Current opinion in immunology. 2007; 19: 488-96.

https://doi.org/10.1016/j.coi.2007.05.004

23.Kalkavan H, Green DR. MOMP, cell suicide as a BCL-2 family business. Cell Death & Differentiation. 2018; 25: 46-55.

24.Zhou JD, Zhang TJ, Xu ZJ, Gu Y, Ma JC, Li XX, Guo H, Wen XM, Zhang W, Yang L, Liu XH. BCL2 overexpression: clinical implication and biological insights in acute myeloid leukemia. Diagnostic pathology. 2019; 14: 68.

https://doi.org/10.1186/s13000-019-0841-1

25.Davids MS, Letai A. Targeting the B-cell lymphoma/leukemia 2 family in cancer. Journal of clinical oncology. 2012; 30: 3127.

https://doi.org/10.1200/JCO.2011.37.0981

26.Eichhorn JM, Alford SE, Sakurikar N, Chambers TC. Molecular analysis of functional redundancy among anti-apoptotic Bcl-2 proteins and its role in cancer cell survival. Experimental cell research. 2014; 322: 415-24.

https://doi.org/10.1016/j.yexcr.2014.02.010

27.Kale J, Osterlund EJ, Andrews DW. BCL-2 family proteins: changing partners in the dance towards death. Cell Death & Differentiation. 2018; 25: 65-80.

28.Suhaili SH, Karimian H, Stellato M, Lee TH, Aguilar MI. Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization. Biophysical reviews. 2017; 9: 443-57.

https://doi.org/10.1007/s12551-017-0308-0

29.Kang MH, Reynolds CP. Bcl-2 inhibitors: targeting mitochondrial apoptotic pathways in cancer therapy. Clinical cancer research. 2009; 15: 1126-32.

https://doi.org/10.1021/acs.jnatprod.5b01137

30.Campbell KJ, Tait SW. Targeting BCL-2 regulated apoptosis in cancer. Open biology. 2018; 8: 180002.

https://doi.org/10.1098/rsob.180002

31.Iacovelli S, Ricciardi MR, Allegretti M, Mirabilii S, Licchetta R, Bergamo P, Rinaldo C, Zeuner A, Foà R, Milella M, McCubrey JA, Martelli AM, Tafuri A. Co-targeting of Bcl-2 and mTOR pathway triggers synergistic apoptosis in BH3 mimetics resistant acute lymphoblastic leukemia. Oncotarget. 2015; 6: 32089-103.

https://doi.org/10.18632/oncotarget.5156

32.García-Aranda M, Pérez-Ruiz E, Redondo M. Bcl-2 inhibition to overcome resistance to chemo-and immunotherapy. International journal of molecular sciences. 2018; 19: 3950.

https://doi.org/10.3390/ijms19123950

33.Andreeff M, Jiang S, Zhang X, Konopleva M, Estrov Z, Snell VE, Xie Z, Okcu MF, Sanchez-Williams G, Dong J, Estey EH. Expression of Bcl-2-related genes in normal and AML progenitors: changes induced by chemotherapy and retinoic acid. Leukemia. 1999; 13: 1881-92.

https://doi.org/10.1038/sj.leu.2401573

34.Baev DV, Krawczyk J, Szegezdi E. The BH3-mimetic ABT-737 effectively kills acute myeloid leukemia initiating cells. Leukemia research reports. 2014; 3: 79-82.

https://doi.org/10.1016/j.lrr.2014.06.001

35.Timucin AC, Basaga H, Kutuk O. Selective targeting of antiapoptotic BCL2 proteins in cancer. Medicinal research reviews. 2019; 39: 146-75.

https://doi.org/10.1002/med.21516

36.Mazumder S, Choudhary GS, Al-harbi S, Almasan A. Mcl-1 Phosphorylation defines ABT-737 resistance that can be overcome by increased NOXA expression in leukemic B cells. Cancer research. 2012; 72: 3069-79.

https://doi.org/10.1158/0008-5472.CAN-11-4106

37.Stamelos VA, Redman CW, Richardson A. Understanding sensitivity to BH3 mimetics: ABT-737 as a case study to foresee the complexities of personalized medicine. Journal of molecular signaling. 2012; 7: 12.

38.Quinn BA, Dash R, Azab B, Sarkar S, Das SK, Kumar S, Oyesanya RA, Dasgupta S, Dent P, Grant S, Rahmani M. Targeting Mcl-1 for the therapy of cancer. Expert opinion on investigational drugs. 2011; 20: 1397-411.

https://doi.org/10.1517/13543784.2011.609167

39.Pan R, Ruvolo VR, Wei J, Konopleva M, Reed JC, Pellecchia M, Andreeff M, Ruvolo PP. Inhibition of Mcl-1 with the pan–Bcl-2 family inhibitor (–) BI97D6 overcomes ABT-737 resistance in acute myeloid leukemia. Blood, The Journal of the American Society of Hematology. 2015; 126: 363-72.

https://doi.org/10.1182/blood-2014-10-604975

40.Nepstad I, Hatfield KJ, Grønningsæter IS, Reikvam H. The PI3K-Akt-mTOR Signaling Pathway in Human Acute Myeloid Leukemia (AML) Cells. International Journal of Molecular Sciences. 2020; 21: 2907.

https://doi.org/10.3390/ijms21082907

41.Martelli AM, Tazzari PL, Evangelisti C, Chiarini F, Blalock WL, Billi AM, Manzoli L, McCubrey JA, Cocco L. Targeting the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin module for acute myelogenous leukemia therapy: from bench to bedside. Current medicinal chemistry. 2007; 14: 2009-23.

https://doi.org/10.2174/092986707781368423

42.Carneiro BA, Kaplan JB, Altman JK, Giles FJ, Platanias LC. Targeting mTOR signaling pathways and related negative feedback loops for the treatment of acute myeloid leukemia. Cancer biology & therapy. 2015; 16: 648-56.

https://doi.org/10.1080/15384047.2015.1026510

43.Mirabilii S, Ricciardi MR, Piedimonte M, Gianfelici V, Bianchi MP, Tafuri A. Biological aspects of mTOR in leukemia. International journal of molecular sciences. 2018; 19: 2396.

https://doi.org/10.3390/ijms19082396

44.Fransecky L, Mochmann LH, Baldus CD. Outlook on PI3K/AKT/mTOR inhibition in acute leukemia. Molecular and cellular therapies. 2015; 3: 2.

45.Altomare D, R Khaled A. Homeostasis and the importance for a balance between AKT/mTOR activity and intracellular signaling. Current medicinal chemistry. 2012; 19: 3748-62.

https://doi.org/10.2174/092986712801661130

46.Manning BD, Toker A. AKT/PKB signaling: navigating the network. Cell. 2017; 169: 381-405.

http://doi.org/10.1016/j.cell.2017.04.001

47.Vachhani P, Bose P, Rahmani M, Grant S. Rational combination of dual PI3K/mTOR blockade and Bcl-2/-xL inhibition in AML. Physiological genomics. 2014; 46: 448-56.

https://doi.org/10.1152/physiolgenomics.00173.2013

48.Kumar D, Das B, Sen R, Kundu P, Manna A, Sarkar A, Chowdhury C, Chatterjee M, Das P. Andrographolide analogue induces apoptosis and autophagy mediated cell death in U937 cells by inhibition of PI3K/Akt/mTOR pathway. PLoS One. 2015; 10.

https://doi.org/10.1371/journal.pone.0139657

49.Perl AE, Kasner MT, Tsai DE, Vogl DT, Loren AW, Schuster SJ, Porter DL, Stadtmauer EA, Goldstein SC, Frey NV, Nasta SD, Hexner EO, Dierov JK,…& Luger SM. A phase I study of the mammalian target of rapamycin inhibitor sirolimus and MEC chemotherapy in relapsed and refractory acute myelogenous leukemia. Clinical Cancer Research. 2009;15: 6732-9.

https://doi.org/10.1158/1078-0432.CCR-09-0842

50.Tan P, Tiong S, Fleming S, Pomilio G, Cummings N, Droogleever M, McManus J, Schwarer A, Catalano J, Patil S, Avery S. The mTOR inhibitor everolimus in combination with azacitidine in patients with relapsed/refractory acute myeloid leukemia: a phase Ib/II study. Oncotarget. 2017; 8: 52269.

https://doi.org/10.18632/oncotarget.13699

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Quality And Cost

 

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Quality assessment is being adapted as a method for buyers, patients, and providers to evaluate healthcare expenditure. To this end, substantial advancements have been made towards the science of quality assessment over the past years. However, several challenges continue to be addressed so that quality assessment can achieve its ability as a counterforce to the demands of cost containment. Some of the obstacles encountered during the quality assessment include; Detecting and balancing the rival standpoints of the key participant in the healthcare system and coming up with a culpability framework. Also launching the finest criteria by which the performance of the healthcare will be compared to, picking routine reporting indicators, conflicts between financial and non-financial motivations and quality care goals, and developing information systems required for quality monitoring.

Several methods have been used to measure health care quality. These include; assessing the appropriateness of an intervention which indicates the effectiveness of the intervention, examining the level at which care given parallels health guidelines and standards and practice profiling which relates the patterns of cost. Also, there are quality processes among providers by already established standards, and Process assessment in which interpersonal health care quality can be evaluated by consumer ratings which consist of both received care and its satisfaction (MClellan, 2013).

Baldrige Excellence Framework for Health Care helps organizations in assessing their management performance. This framework acknowledges goals such as customer satisfaction and employees involvement. Through customer satisfaction, quality can be achieved without increasing cost. This is possible in the following ways; reducing quality issues that arise due to consumer dissatisfaction, reducing cost without compromising service quality and rising customer expectations by providing services which they view as being of high value (Nolan & Bisognano 2006)

References

MClellan, M. B. (2013). Improving Health Care Quality: The Path Forward. Center for Health Policy (ed.). Brookings Institution: http://www. brookings. Edu/research/testimony/2013/06/26-improving-health-care-quality-mcclellan: Congressional Testimony

Nolan, T., & Bisognano, M. (2006). Finding the balance between quality and cost: what’s the answer to improving the value of health care? One group believes hospitals could take a lesson from Japanese quality expert Noriaki Kano. Healthcare Financial Management60(4), 66-73.

 

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IOM future of nursing

 

Reflection Paper

The IOM future of nursing recommendation number 4 requires a proportional increase of nurses with bachelor’s degree to 80% by 2020. I see myself fitting in this recommendation because being a student today makes me part of this recommendation. Currently, this recommendation motivates me to actively focus on obtaining my bachelor’s degree in nursing, which equips me with a lot of knowledge that can help in performing nursing duties to the best levels. Additionally, I am focused on convincing my colleagues in my social circuit to undertake higher education which will help in achieving this recommendation. I support this recommendation because it is aimed at improving my skills and services to meet the demand of increased patients’ population. Moreover, this increment will assist in making the nursing work accessible and manageable (Blegen, Goode, Park, Vaughn, & Spetz, 2013).

The number of nurses with a doctorate is recommended to increase to 80% by 2020. This is a challenge for me because am currently not done with my bachelor’s degree and yet the year 2020 is around the corner. Moreover, the number of people with a doctorate in nursing is less than 1% which suggests a shortfall for nurses and crippled workforce supply chain (portal 2011). Also, few numbers of nurses with doctorate makes me feel the insufficiency in qualified academic and clinical nurse faculty to help me undertake my doctorate. Thus, I don’t feel my fitness in this recommendation.

Recommendation number six requires that nurses engage in long-life learning. I see myself fitting in this recommendation because it recommends that I don’t stop at my degree level but should continue with my education. This is important because a degree does not provide me with all I need to know in my entire career. This recommendation is designed to equip me with continued competence and advanced education which provides sufficient and necessary skills to provide quality care. As a nurse, it provides with the opportunity to strengthen my academic pathways in both baccalaureate degree entry and completion levels. Moreover, the suggestion that faculties partner with healthcare organizations to establish and prioritize competence to update the curricula regularly will ensure that I am ready to tackle the current and future health needs of the population (Altman, Butler,& Shern 2016).

 

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Increasing my level of education will equip me with necessary and sufficient skills that are required in my career field. This will reduce competition because a limited number of people have acquired these education levels. Acquiring higher education equips me with the theoretical knowledge and analytical skills which enable me to compete better in the job market. Moreover, it helps me develop a speed of learning and the ability to learn in depth.

Increasing my level of education will provide me with a managerial role and help me to get promoted from a bedside nurse. This is exciting because it will be challenging than what am used to and will help me learn much and grow professionally. Also, it is essential for me as I am interested in moving up my career ladder and provide a better and higher level of quality care. This will also enable me to meet the increased and more complex demands of today’s patients (American Association of Colleges of Nursing, 2012).

 

References

Altman, S. H., Butler, A. S., & Shern, L. (Eds.). (2016). Assessing progress on the Institute of Medicine report The Future of Nursing. National Academies Press.

American Association of Colleges of Nursing, & American Association of Colleges of Nursing. (2012). Fact sheet: The impact of education on nursing practice. Retrieved June1, 2012.

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