NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
Walden University NURS 6501 ALTERATIONS IN CELLULAR PROCESSES – Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 ALTERATIONS IN CELLULAR PROCESSES assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 ALTERATIONS IN CELLULAR PROCESSES depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
The introduction for the Walden University NURS 6501 ALTERATIONS IN CELLULAR PROCESSES is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
After the introduction, move into the main part of the NURS 6501 ALTERATIONS IN CELLULAR PROCESSES assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
Role of Genetics
Genetics can play a huge role in many diseases. Addiction is no different. In fact, many studies have been done that show that genetics can influence addiction by as much as 60% (Arand, 2023). With addiction, genetics specifically affect inherited levels of dopamine, making people genetically predisposed to it (Arand, 2023).
Patient Presentation, Physiologic Response, and Cells involved
The patient may be partially in so much pain due to the lack of opioids working in their system. The patient received Naloxone in the field which reversed the effects of the substance they took. Another likely reason that the patient is suffering from pain in those areas is due to Rhabdomyolysis. According to McCane and Huether, Rhabdomyolysis can be a life-threatening condition in which contents of the muscle cell are released into circulation (2019). Substances can cause Rhabdomyolysis through prolonged immobilization or drug-induced energy demands, such as seizures, dystonic reactions, and hyperthermia (Bhai & Dimachkie, 2023). We do not know how long he had been down and do not know if he suffered from any seizures, but we can infer that it was likely one or multiple of these issues that caused the Rhabdomyolysis. In Rhabdomyolysis, damage to the muscle cells causes a disruption of the Sodium and Potassium pump within the cells (Torres et al, 2015). In normal, uninjured, muscle cells contain lower levels of intracellular Sodium and Calcium, and higher levels of Potassium (Torres et al, 2015). Depolarization of the muscle causes a surge of calcium to enter the cytoplasm, leading to contraction of the muscle (Torres et al, 2015). This is all dependent on ATP. In the injured muscle, there is a depletion of ATP, causing an increase of sodium and calcium in the cell, leading to an increase of water in the cell (Torres et al, 2015). Also, an elevated level of Calcium will cause activation of proteases and phospholipases, causing lysis of the cell’s membrane (Torres et al, 2015). If this sustains, it ultimately causes muscle necrosis (Torres et al, 2015). We also learned that he has high levels of potassium in his blood, showing further evidence that he does, in fact, have Rhabdomylosis. The EKG changes that we are seeing are directly related to the potassium levels in the blood. According to McCance and Huether, EKG changes of peaked T waves and a prolonged PR interval can be caused by high levels of potassium (2019). Some genetic factors that I would be curious about and may change my answer to the cause of the Rhabdomylisis would be if the patient had lipid, carbohydrate, or purine metabolism deficiencies, as these are some predispositions to Rhabdomylolysis (McCance & Huether, 2019).
This 16-year-old patient from NURS 6501 ALTERATIONS IN CELLULAR PROCESSES was presented to the PCP, and we diagnosed them with strep throat. The cells have gone through an extracellular matrix (McCance & Huether, 2019) and are now injured due to infection. The PCP prescribed the antibiotic to reverse the injury. The damage to the cell itself causes the patient to have a reddened pharynx and enlarged tonsils with white patches. The 16-year-old cells are also experiencing hypertrophy, causing an increase in size in the tonsils.
After this patient took two doses of amoxicillin 500mg, they experienced tongue and lips swelling, difficulty breathing, and audible wheezes. This patient is presenting with anaphylaxis. This is an IgE-mediated reaction. IgE antibodies are produced in the immune system. This is considered a type 1 hypersensitivity reaction. The binding of Fc receptors on mast cells and basophils to IgE triggers mast cells and creates an allergic reaction. Enzymes tryptase cause tissue damage, and TNF causes inflammation (Justiz-Vaillant & Zito, 2019).
Initially, when the patient was presented, they had no known drug allergies. The new drug allergy can connect to the infection, especially if it is recurrent. To verify that the amoxicillin allergy is a true allergy, the PCP can use an allergic test called a radioallergosorbent test (RAST) (Justiz-Vaillant & Zito, 2019).
The patient’s anaphylaxis is generalized and not systemic. A study showed that penicillin was reported for 40.7% of antibiotics causing anaphylaxis. In the same survey, it is said that the female gender is more likely to have drug-induced anaphylaxis. Patients with several comorbidities or other medications may also be at higher risk (Regateiro, Marques, & Gomes, 2020).
NURS 6501 ALTERATIONS IN CELLULAR PROCESSES Reference:
Justiz-Vaillant, A. A., & Zito, P. M. (2019). Immediate hypersensitivity reactions Download Immediate hypersensitivity reactions. In StatPearls. Treasure Island, FL: StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
Regateiro, F. S., Marques, M. L., & Gomes, E. R. (2020). Drug-Induced Anaphylaxis: An Update on Epidemiology and Risk Factors. International Archives of Allergy and Immunology, 181(7), 481–487. https://doi.org/10.1159/000507445
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PSYCHOLOGICAL DISORDERS MODULE 6
Women’s and Men’s Health, Infections, and Hematologic Disorders
Sample Response for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
The Group A Streptococcus colonize and multiple in the lymph nodes such as the tonsils which causes the cervical adenopathy seen in the patient. The body’s response to the bacteria is the release of B cells and antibodies that cause inflammation in the targeted regions (Strep throat, 2020). The treatment administered Amoxicillin can cause an allergic reaction in patients as indicated by the swelling and difficulty breathing in the 16-year-old patient. Strep throat is a recurrent disease that can run in families and repeated treatments with Amoxicillin can cause the body to form antibodies to the antigen causing an allergic reaction response (Penicillin allergy, 2021). It is interesting that females are more susceptible to an allergic reaction to Penicillin however, males have a more severe reaction to the medication (Regateiro et al., 2020).
Reference
Penicillin allergy. (2021, September 21). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/penicillin-allergy/symptoms-causes/syc-20376222
Regateiro, F. S., Marques, M. L., & Gomes, E. R. (2020). Drug-Induced Anaphylaxis: An Update on Epidemiology and Risk Factors. International Archives of Allergy and Immunology, 181(7), 481–487. https://doi.org/10.1159/000507445
Strep throat. (2020). La Jolla Institute for Immunology. https://www.lji.org/diseases/strep-throat/
Sample Response for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
I was interesting to read in your post that the female gender is more likely to have drug-induced anaphylaxis. Anaphylaxis allergic reaction occur in women more frequently than men. Scientists are still trying to figure out why. According to the National Institutes of Allergy and Infectious Diseases they suggest that estrogen, a female hormone, may play a key role. They found that estrogen enhances the levels and activity of an enzyme lining the blood vessels, which in turn causes some of the severe allergic reactions. The enzyme increases the production of a substance called nitric oxide, which creates a drop-in blood pressure and allows fluid in blood vessels to leak into the tissues, resulting in swelling. Defiantly have to remind patients especially female patients that group A streptococcus is contagious and spreads through coughing, sneezing, sharing foods, drinks and can easily be picked from door doorknob or other surfaces (Elboray et al., 2018).
References:
Elboray, S. N., Little, P., Nehal, M., Marzouk, D., & Reda, M. (2018). Assessment of different clinical variables associated with group a streptococcal throat infection among children in primary care practice. Egypt J Commun Med, 36. https://ejcm.journals.ekb.eg/article_16335_48e8dfc4e4852dd9c7e7e1436ce43e9e.pdf
(2021). National Institute of Allergy and Infectious Diseases. Retrieved February 24, 2023
Sample Answer for NURS 6501 ALTERATIONS IN CELLULAR PROCESSES
Millions of Americans are estimated to be sickle cell trait carriers (Linder & McCance, 2019). I agree that sickle cell disease (SCD) is common in those with ancestors from Africa. However, it is a worldwide issue and can be found in those with ancestors such as “Mexican Americans, and white Americans, especially those whose families originally came from Turkey, Italy, Greece, Spain, and other Latin American or Mediterranean countries” (Texas Health and Human Services, n.d.). SCD is transmitted as an autosomal recessive disorder, and few clinical studies have examined how it affects the genders (Ceglie et al., 2019).
The SCD and sickle cell trait (HbAS) run throughout my family. Knowing if one has SCD or HbAS is essential because it can be passed down from parent to child. Typically, infants are tested for SCD during their neonatal screening (Linder & McCance, 2019). One is likely to inherit the disease when both parents are carriers. It is important to note that if both parents have HbAS, they have a one in four chance of having a child with SCD (Texas Health and Human Services, n.d.). If only one parent has HbAS, the child can not have SCD (Texas Health and Human Services, n.d.).
Sickle cell is “characterized by the presence of an atypical form of hemoglobin S (Hbs; sickle hemoglobin) within the erythrocytes.” (Linder & McCance, 2019). The beta chain of the hemoglobin is mutated and causes anemia (Linder & McCance, 2019). The cycle of malformation occurs when the RBC carries the malformed protein deoxygenate (Berkowitz, 2020). The genotypes for SCD include “homozygosity for the βS allele (HbS/S), heterozygosis for the βS allele and β-thalassemia (HbS/β), heterozygosity for the βS allele and some hemoglobin variants: HbS/C, HbS/D, HbS/Lepore-Boston” (Linder & McCance, 2019) (Ceglie et al., 2019). The disease is painful due to the effects on the hemoglobin.The cell’s sickling, occasional, and intermittent phenomenon causes pain because they clog small blood vessels (Berkowitz, 2020) (Linder & McCance, 2019). Sickling can be triggered by prolonged exposure to stressors such as “hypoxia, acidosis, decreased plasma osmolality, decreased plasma volume, and temperature” (Linder & McCance, 2019). The clogs can cause acute painful crises, ischemia, stroke, and renal ischemia (Berkowitz, 2020). Individuals with SCD have been known to have a yearly crisis that requires a hospital stay (Ceglie et al., 2019). The reduction of stressors can help reduce the amount of SCD attacks one can have. Treatments for crisis include non-steroidal anti-inflammatory drugs (NSAIDs), minor opioids (tramadol or codeine), and significant opioids (morphine) (Ceglie et al., 2019). As you mentioned, SCD can be hard on the patient and the family; therefore, connecting them with support groups can be helpful. Thank you for your post.
References
Berkowitz, A. (2020). Chapter 6. The Hematologic System. In A. Berkowitz, Clinical Pathophysiology Made Ridiculously Simply (p. 122). Miami: MedMaster .
Ceglie, G., Di Mauro, M., Tarissi De Jacobis, I., de Gennaro, F., Quaranta, M., Baronci, C., . . . Palumbo, G. (2019). Gender-Related Differences in Sickle Cell Disease in a Pediatric Cohort: A Single-Center Retrospective Study. Retrieved June 3, 2023, from National Library of Medicine National Center for Biotechnology Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906547/#:~:text=The%20incidence%20of%20sickle%20cell,as%20an%20autosomal%20recessive%20disorder.
Linder, L., & McCance, K. (2019). Chapter 31: Alterations of Hematologic Function in Children. In L. A. Linder, & K. L. McCance, Pathophysiology. The Biologic Basis for Disease in Adults and Children. Eighth Edition (pp. 1000- 1004). Canada: Elsevier.
Texas Health and Human Services. (n.d.). Sickle Cell Disease – So Your Baby Has The Sickle Cell Trait. Retrieved June 3, 2023, from Texas Health and Human Services: https://www.dshs.texas.gov/newborn-screening-program/sickle-cell-disease/sickle-cell-trait/sickle-cell-disease-so#:~:text=If%20only%20one%20parent%20has,of%20having%20sickle%20cell%20anemia.
Main Question Post
This patient is experiencing an anaphylactic allergic reaction to amoxicillin as evidenced by the rapid onset, swelling of lips and tongue, and wheezing with difficulty breathing. This scenario illustrates a type I IgE-mediated hypersensitivity reaction, necessitating previous exposure to this antigen. He may have been exposed and sensitized to this antibiotic in several ways. He likely received previous treatment with a penicillin antibiotic or, possibly though less likely, his sensitizing exposure was through foodstuffs where penicillin was used in manufacturing (Kulambil Padinjakara et al., 2008). Some communities and families alternately source foodstuffs (i.e., milk, meat, cheese) from non-commercial or unregulated sources. These could constitute an avenue for sensitization or chronic low-level exposure to penicillin leading to this allergic response. It would be reasonable to consider childhood exposure to antibiotics or possible genetic predisposition related to parental allergies.
According to McCance and Huether (2019), allergies are hereditary, and the likelihood of a child having an allergy doubles if both parents have the allergy. Notably, the first exposure to the antigen would have been without allergic symptoms, although antibodies were created, and the immune response has been prepared for second exposure since that time. A complex immune response is initiated upon reintroduction of the antigen, amoxicillin. Initially, a molecule of the antigen is captured by a dendritic cell which then presents the antigen molecule to a naive T-cell (Humeniuk et al., 2017, pp. 5). This interaction stimulates the production of cytokines, activation of intracellular pathways, and, ultimately, mast cell degranulation (McCance &Huether, 2019). Simultaneously, the released cytokines signal for B-cells to produce IgE antibodies immediately. The IgE attaches to the exterior of the mast cell and cross-links with the antigen leading to degranulation (Abbas et al., 2023). Several enzymes and mediators (i.e., prostaglandin, leukotrienes, platelet-activating factors) are released during degranulation (Justiz-Valillant & Zito, 2019, p.6). Although mast cell degranulation releases multiple biochemical mediators, the increase in histamine and inflammatory mediators in the bloodstream is what leads to the physical symptoms of an anaphylactic allergy the patient is exhibiting. According to McCance and Huether (20109), histamine’s effects are significant and systemic, causing bronchoconstriction, vasodilation, and increased vascular permeability. In this case, difficulty breathing and audible wheezing is due to bronchoconstriction, the direct effect of histamine acting on bronchial smooth muscle. The swelling of lips and tongue result from vasodilation and increased vascular permeability, related to histamine’s effect on vascular smooth muscle. Vasodilation allows increased blood flow to the area, while increased permeability allows plasma, cells, and fluid to move into the interstitium, causing swelling and edema (p.203, p.256). This fluid shift can significantly decrease circulating blood volume causing low blood pressure and circulatory collapse. If this patient’s presentation remained untreated, he would suffer respiratory failure, cardiovascular collapse, shock, and death.
References
Abbas, M., Moussa, M., & Akel, H. (2023). Type I hypersensitivity reaction. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK560561/Links to an external site.
Humeniuk, P., Dubiela, P., & Hoffmann-Sommergruber, K. (2017). Dendritic cells and their role in allergy: Uptake, proteolytic processing and presentation of allergens. International Journal of Molecular Sciences, 18(7), 1491. https://doi.org/10.3390/ijms18071491Links to an external site.
Justiz-Vaillant, A. A., & Zito, P. M. (2019). Immediate hypersensitivity reactions. In StatPearls. StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513315/Links to an external site.
Kulambil Padinjakara, R.,N., Ashawesh, K., & Patel, V. (2008). Allergic reaction to blue cheese: serendipity or actual causation? The New Zealand Medical Journal (Online), 121(1283), 102-4. https://www.proquest.com/scholarly-journals/allergic-reaction-blue-cheese-serendipity-actual/docview/1034247049/se-2Links to an external site.
McCance K. L. & Huether S. E. (2019). Pathophysiology : the biologic basis for disease in adults and children (Eighth). Elsevier.
NURS 6501 WEEK 2 CASE STUDY ANALYSIS
Case Study Analysis
This paper examines a case study of a 49-year-old male patient. The patient has rheumatoid arthritis. He has come to the clinic with a chief complaint of fever. The patient currently uses medications, including atorvastatin 40 mg at night, methotrexate 10 mg every Friday morning, and prednisone 5 mg. He reports a fever for about a week and admits to sweats and chills. He also has hemoptysis, fatigue, and chest pain. The patient works as a grain inspector at a large farm cooperative. An extensive work-up led to the client being diagnosed with invasive aspergillosis. Therefore, the purpose of this essay is to examine the reasons for the client presenting with the above symptoms, genes associated with the development of the disease, the immunosuppression process, and its effect on the body systems.
Why the Patient Presented with the Described Symptoms
The patient developed the above symptoms because of the combination of the prolonged use of immunosuppressive drugs and environmental exposures from his occupation. Methotrexate and prednisone are two drugs that increase the risk of immunosuppression when used over a long period. Corticosteroids such as prednisone work by inhibiting the body’s inflammatory responses. They also repress the activity of key immunomodulatory transcription factors such as NF-kB and AP-1 factors, which play a crucial role in strengthening the body’s immune systems (Luo et al., 2021). Prolonged use of these drugs weakens the immunity, which predisposes patients to opportunistic infections, including invasive aspergillosis.
The patient in the case study has also been using methotrexate. Methotrexate is a drug that inhibits dihydrofolate reductase, an enzyme involved in the reduction of folate to tetrahydrofolate. The effects of methotrexate include suppression of the immune responses and inflammatory processes. Methotrexate suppresses the immune system through processes such as inhibition of pyrimidine and purine syntheses and the blockage of transmethylation reactions. These inhibitions cause the release of adenosine, uncoupling of nitric oxide synthase, and inhibition of NF-kB signaling, JAK-STAT signaling, and regulation of long noncoding RNAs (Valer et al., 2021). The changes cause immunosuppression, hence, the increased risk of opportunistic infections.
The immunosuppression from the use of corticosteroids and methotrexate, coupled with environmental exposure to Aspergillus bacteria caused invasive Aspergillosis. The patient in the case study reports that he works as a grain inspector at a large farm cooperative. His workplace could have predisposed him to Aspergillus, a fungus that causes Aspergillosis in immunocompromised individuals. The fungus causes three types of bronchopulmonary aspergillosis, including invasive, chronic, and allergic aspergillosis (Fosses Vuong et al., 2024). Patients with invasive aspergillosis experience symptoms, including fever, dyspnea, hemoptysis, increased sputum production, and pleuritic chest pain.
Genes That May be Associated with the Development of the Disease
Invasive aspergillosis has genetic predispositions. Studies have revealed the presence of specific genes increases the risk of an individual being affected by the disease. The research by Cb et al. (2020) demonstrated a strong association between polymorphisms within CX3CR1 and ART2 genes and the risk of invasive aspergillosis. Carriers of CX3CR1rs9823718, CX3CR1rs7631529A, and ARNT2rs137421G alleles had an increased risk of developing invasive aspergillosis (Cb et al., 2020). In another research, the C allele of IL10rs1800896 was linked with an increased risk of invasive aspergillosis in 36 patients out of 357 patients enrolled in the study (Tanpaibule et al., 2020). Tanpaibule et al. (2020) asserted in their study that epigenetic events such as those leading to DNA methylation alter gene expression, histone modification, and interaction between genotypes, environment, and microbes, which increase the risk of invasive aspergillosis in patients. Furthermore, the authors argue that deficiency in the PTX3 gene, downregulation of CD50 and CD80 molecules, and variations in STAT1 and STAT3 genes increase the risk of invasive aspergillosis (Tanpaibule et al., 2020).
Process of Immunosuppression and the Effect it has on Body Systems
Immunosuppression refers to the reduced ability of the body’s immune system to respond to foreign antigens. The process of immunosuppression begins with the body’s exposure to substances or environments that kill immune effector cells. The exposure also inhibits the intracellular pathways that are involved in antigen recognition and activation of immune responses. Factors such as exposure to oncogenic viruses, ionizing and ultraviolet radiation, infections, including HIV, use of some medications, and infection by parasites can cause immunosuppression. Immunosuppression affects the ability of the body’s systems to defend themselves against foreign antigens. The risk of opportunistic infections and cancer development in immunosuppressed individuals is high. In some cases, the mortality rate is high among immunocompromised patients (Rice, 2019). Immunosuppression also affects the ability of the body systems to recover from an infection. As a result, immunosuppressed patients are likely to stay longer in the hospital as compared to those with normal immunity.
Conclusion
In summary, the patient developed the described symptoms due to the combined effects of immunosuppression and environmental exposure to opportunistic infections. Several genes play a role in the development of invasive aspergillosis in immunocompromised individuals. Immunosuppression develops from an individual’s exposure to factors that lower the body’s immunity to respond to foreign antigens. Immunosuppression has adverse patient and health outcomes.
References
Cb, L., M, M.-B., Jm, S.-M., J, B., C, C., J, S., M, L., J, S.-C., Lm, C., L, A.-F., Ma, L.-N., L, F., Jm, A., L, P., E, L.-F., M, A.-R., L, P., Sm, G., M, L., … J, S. (2020). Polymorphisms within the ARNT2 and CX3CR1 genes are associated with the risk of developing invasive Aspergillosis. Infection and Immunity, 88(4). https://doi.org/10.1128/IAI.00882-19
Fosses Vuong, M., Hollingshead, C. M., & Waymack, J. R. (2024). Aspergillosis. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK482241/
Luo, J., Beattie, J. A., Fuentes, P., Rizvi, H., Egger, J. V., Kern, J. A., Leung, D. Y. M., Lacouture, M. E., Kris, M. G., Gambarin, M., Santomasso, B. D., Faleck, D. M., & Hellmann, M. D. (2021). Beyond Steroids: Immunosuppressants in steroid-refractory or resistant immune-related adverse events. Journal of Thoracic Oncology, 16(10), 1759–1764. https://doi.org/10.1016/j.jtho.2021.06.024
Rice, J. M. (2019). Immunosuppression. In R. A. Baan, B. W. Stewart, & K. Straif (Eds.), Tumour Site Concordance and Mechanisms of Carcinogenesis. International Agency for Research on Cancer. http://www.ncbi.nlm.nih.gov/books/NBK570319/
Tanpaibule, T., Jinawath, N., Taweewongsounton, A., Niparuck, P., & Rotjanapan, P. (2020). Genetic risk surveillance for invasive aspergillosis in hematology patients: a prospective observational study. Infectious Diseases and Therapy, 9(4), 807–821. https://doi.org/10.1007/s40121-020-00331-4
Valer, J. B., Curra, M., Gabriel, A. de F., Schmidt, T. R., Ferreira, M. B. C., Roesler, R., Evangelista, J. M. C., Martins, M. A. T., Gregianin, L., & Martins, M. D. (2021). Oral mucositis in childhood cancer patients receiving high-dose methotrexate: Prevalence, relationship with other toxicities and methotrexate elimination. International Journal of Paediatric Dentistry, 31(2), 238–246. https://doi.org/10.1111/ipd.12718