Detecting Autoantibodies in Human Sera Samples using ELISA

Detecting Autoantibodies in Human Sera Samples using ELISA Introduction Autoimmunity is a series of immune responses that is made against an organisms own cells and tissues due to inability to recognise own cells and tissues as self (Mandal, 2014). Diseases can arise as a result of autoimmunity. This includes lupus (SLE). Lupus (SLE) arises because of immunological mechanisms. With tolerance to antigens is lost and production of autoreactive lymphocytes the process of autoantibody is produced. Continuous production of autoantibodies from autoantibody producing cells results in formation of immune complexes. (Bolland and Ravetch, 2000). There are many factors which influence the susceptibility and development of lupus (SLE). These include hormonal, environmental, and genetic factors (Lisnevskaia et al, 2014). Genes involved in lupus (SLE) include MHC loci, tumor necrosis factor alpha, components of the complement factor and the mannose binding protein (Tsao and Grossman, 2001). Environmental triggers have influence on expression for lupus (SLE) such as vi tamin D deficiency. Vitamin D has an important role in order for the immune system to function properly because receptors of vitamin D are found in the cells of the immune system such as T lymphocytes, monocytes and dendritic cells. Also reduced vitamin D intake due to photosensitivity is associated with lupus (SLE). Thus, deficiency in vitamin D has a major consequence for the immune system and can create autoimmune diseases (Albishri et al, 2015). Hormones have a role in acting as chemical messengers in the immune response (Csaba, 2014). These chemical signals produced from hormones are disrupted especially between the brain and target cells which is an important factor in lupus (SLE) (Pick, n.d.). Because of this disrupted balance of hormone production certain hormones are more prevalent which cause lupus (SLE). High estrogen concentrations have been linked to lupus (SLE) due to it causing autoimmunity and with patients having a fast conversion of androgens to estrogens. Patients with joint pains are linked with lupus (SLE) and also have a high concentration of estrogen (Lupusinternational.com, n.d.). Diagnosis of lupus (SLE) include the lupus band test which detects for the presence of antinuclear antibodies. This is done using immunofluorescence. By looking at the florescence pattern the type of antibody can be detected. For a person to be positive for lupus (SLE) IgG and other complement depositions will be found at the dermoepidermal junction. To be specific there will be a bandlike deposit along the epidermal basement membrane due to the presence of IgG. Also a bandlike deposit will be present in the nucleus of the epidermal cells. A high concentration of anti-dsDNA antibody from titers also shows the presence of SLE due to anti-dsDNA antibody having a high specificity for SLE (Gill et al, 2003). Diagnosis can also be made using the SLICC criteria. For a patient to have SLE, at least four criterions need to be met including one clinical criterion (Petr i et al, 2012). There is currently no cure for SLE but a number of treatments are available. Prognosis for SLE has improved significantly since the 1950s with people diagnosed it living for less than five years. Now ninety percent of people with SLE live over ten years. The effect of SLE is more evident in men and children than in women. Causes of early death has been due to failure of organs and infections. Because of improved survival rate other factors have come in to play for the death of SLE patients. Cardiovascular disease is one factor and it is important to prevent this from being developed (Doria et al, 2006).       The ELISA test is a diagnostic test used to measure the concentration of certain antibodies or antigens present in a sample from a disease patient. ELISA is unique due to the separation of specific and non-specific interactions during serial binding to the multiwell plate. At the end of ELISA, a coloured product is produced that is associated with the amount of antibody or antigen present in the solution sample (Bio-Rad, n.d.). The first step of ELISA is coating, where a layer of antigen or antibody is adsorbed to the wells on the plate. After coating, blocking and detection are the next steps. Several washes are needed between each ELISA step to remove unbound materials. During this process excess liquid is removed in order to prevent dilution of the solutions added in the next stage (Bio-Rad, n.d.). For detection of SLE in the patient, the patients serum sample undergoes the ELISA test to detect the concentration of anti-dsDNA-antibodies which is specific for patients with SLE. A h igh concentration of anti-dsDNA-antibodies will indicate that the patient has SLE (Wigand et al, 1997). The aim of this experiment is to measure the concentration of anti-dsDNA-antibody present in both of the serum samples using the ELISA test by binding to the complimentary antigen double stranded DNA in the wells. The samples come from a female patient known to be suffering from SLE. Sample A was obtained when she was feeling relatively well and sample B was collected on the day of the practical. By comparing the yellow colour intensity at the end of the ELISA test for both samples and compared to the controls and using the standard curve the concentration of anti-dsDNA antibodies can be obtained and correlated to the relevant SLE prognosis level. An assay result above the laboratory reference range for the anti-dsDNA-antibody at a particular prognosis level will show that the patient is positive for SLE and the level of SLE prognosis. Based on the level of SLE prognosis suitable treatments will be given to the patient. Results On each strip the first three wells were labelled the positive controls, the next three labels were measured the negative controls and the remaining wells were labelled sample A and B (three for each sample). In the first stage 50 µl of purified antigen was added to each well of the microplate strip. The strip was incubated for two minutes at room temperature to allow time for the antigen to bind to each plastic well. A layer of antigens was present in each well once incubation had finished. After incubation the wells were washed using a wash buffer to remove excess liquid. In stage three 100 µl of blocking buffer was added into each well and incubated for two minutes to remove unbound sites. The wells were washed again to remove excess liquid. In the next step 50 µl of the positive controls, negative controls and the test autosera samples were loaded into the relevant wells. The strip was then incubated for 10 minutes at room temperature. After incubation for 10 minutes the we lls were washed to remove the unbound antibodies. Once the wash was done 50 µl of secondary antibody was added to the wells. Then the wells were incubated for 5 minutes at room temperature. The washing procedure was repeated again to remove any unbound secondary antibodies. In stage nine 50 µl of the HRP enzyme substrate was added to the wells. The strip was incubated for 5 minutes at room temperature. This allowed sufficient time for the HRP enzyme which is conjugated to secondary antibodies to metabolise the TBT substrate. The metabolisation of the TBT substrate produced a blue-coloured product. Each well turned blue fairly quickly during the incubation and the final strip is shown in figure 1. The intensity for the positive control was six, negative control was zero, and sample A and sample B was five. Figure 1. The micro plate strip showing the blue-coloured product after the enzyme substrate was added and then incubated for 5 minutes. For the final stage of the ELISA test the reaction was stopped by adding 50 µl of stop solution, (10% (v/v) phosphoric acid/ddH2O) into the wells. The blue solution turned yellow on addition of the stop solution. This is seen in figure 2. The intensity for the positive control was six, negative control was zero, sample A was one and sample B was two. Figure 2. The micro plate strip showing the yellow-coloured product after the addition of the stop buffer to the blue-coloured product. Absorbance measurements were obtained using a plate reader for the controls and samples. The absorbance relates to the concentration of anti-dsDNA antibodies present in the samples. The data is shown in table 1. Table 1. The absorbance data for the controls and samples. +ive controls -ive controls Sample 1 Sample 2 1 2 3 Avg 1 2 3 Avg 1 2 3 Avg 1 2 3 Avg 0.660 0.717 0.655 0.677 0.063 0.053 0.084 0.067 0.139 0.139 0.141 0.140 0.287 0.255 0.236 0.259 Discussion The antigen that coated the wells of the microplate strip was double stranded DNA. Two epitopes were present. During the reaction when the control and the autosera samples are loaded, the antibodies present are being detected which is complementary to the antigens coated in the wells. The antibodies need to be diluted using a blocking buffer for prevention of non-specific binding of proteins in the antiserum on the well specifically the solid phase. The antibodies in the serum will bind to the complementary antigens during incubation. Any unbound antibodies are removed by washing. After this, secondary antibodies are added in order to detect the primary antibodies. During incubation the secondary antibodies binds to the primary antibodies (Vlab.amrita.edu, 2011). Looking at figure 1, in the positive control samples, the intensity of the blue coloured product was six due to a known amount of anti-dsDNA antibodies present in the sample. This is used to show the procedure is working. The negative control had a blue colour intensity of zero due to no antibodies present in the sample. The intensities of both sample A and B were similar on the scale of five. From figure 2, looking at the positive control sample the intensity of the yellow coloured product is five due to the high amount of known antibodies present which a patient with SLE should have. The mean absorbance value from table 1 for sample 1 is lower than sample 2 which correlates to the colour intensity which is lower than sample 2. This means that sample 1 is from the patient when she was feeling relatively well due to a very low amount of anti-dsDNA antibodies present. Sample 2 has a higher absorbance value than sample 1 with a colour intensity which is also higher at two. Because of t his result sample 2 comes from the patient when she was feeling unwell. Also this level of intensity shows that the patient has a low level for SLE because of low level detection. The experiment was successful because the results obtained were precise and accurate. The only issue during the experiment was that the intensity of the blue-coloured product was the same for both sample A and B when the enzyme substrate was added. Sample 1 had the lowest concentration of anti-DNA antibodies whereas sample 2 had the higher concentration of anti-dsDNA antibodies. This is because of the colour intensity of the final product where sample 1 is low and sample 2 is higher. The mean absorbance value for sample A is 0.14. The laboratory reference range value for sample A is -0.02. Based on the laboratory reference value this means that when the patient was feeling relatively well she was negative towards SLE. The mean absorbance for sample B is 0.26. The laboratory reference value for sample B is 0.13. The absorbance value is higher than the reference value meaning it is positive for a disease prognosis level which is a low level. This means that the patient is mainly disease free but with periods where low disease activity occurs. ELISA is a procedure used to measure the concentration of antigen present in the sample. The estimate of the analyte concentration is as a result from the construction of a standard curve. The standard curve is constructed from the making of several serial dilutions of a known concentration of the analyte across the range of concentrations close to the expected unknown concentration. The unknown samples concentration is derived by interpolation which needs a standard curve which has been properly generated (Natarajan and Remick, 2008). As the intensity yellow colour in the end result has a value of only two we can say that the patient has a very low level of anti-dsDNA present which means the disease is likely to be calm but with a few periods of low disease activity (Kirkbride, 2015). These low disease activities include cutaneous manifestations, musculoskeletal manifestations and serositis which can be treated with nonsteroidal anti-inflammatory drugs (NSAIDS) or immunosuppression medications which have a low potency on top of the already taken hydroxychloroquine and corticosteroids (Mosca et al, 2001). Bibliography Albishri, J., Alsubai, K. and Alsubai, H. (2015). Vitamin D in systemic lupus erythematosis. World journal of pharmacy and pharmaceutical sciences, 5(1), pp.455-462. Bio-Rad. (n.d.). ELISA Procedure | Bio-Rad. [online] Available at: https://www.bio-rad-antibodies.com/elisa-procedure.html [Accessed 19 Dec. 2016]. Bio-Rad. (n.d.). What is ELISA? An Introduction to ELISA | Bio-Rad. [Online] Available at: https://www.bio-rad-antibodies.com/an-introduction-to-elisa.html [Accessed 19 Dec. 2016]. Bolland, S. and Ravetch, J. (2000). Spontaneous Autoimmune Disease in FcÃŽÂ ³RIIB-Deficient Mice Results from Strain-Specific Epistasis. Immunity, 13(2), pp.277-285. Csaba, G. (2014). Hormones in the immune system and their possible role. A critical review. Acta Microbiologica et Immunologica Hungarica, 61(3), pp.241-260. Doria, A., Iaccarino, L., Ghirardello, A., Zampieri, S., Arienti, S., Sarzi-Puttini, P., Atzeni, F., Piccoli, A. and Todesco, S. (2006). Long-Term Prognosis and Causes of Death in Systemic Lupus Erythematosus. The American Journal of Medicine, 119(8), pp.700-706. Gill, J., Quisel, A., Rocca, P. and Walters, D. (2003). Diagnosis of systemic lupus erythematosus. American Family Physician, 68(11), pp.2179-2186. Kirkbride, G. (2015). Understanding Laboratory Tests and Results for Systemic Lupus Erythematosus (SLE). [Online] Hospital for Special Surgery. Available at: https://www.hss.edu/conditions_understanding-laboratory-tests-and-results-for-systemic-lupus-erythematosus.asp [Accessed 20 Dec. 2016]. Lisnevskaia, L., Murphy, G. and Isenberg, D. (2014). Systemic lupus erythematosus. The Lancet, 384(9957), pp.1878-1888. Lupusinternational.com. (n.d.). Hormones and SLE Lupus International. [Online] Available at: http://www.lupusinternational.com/Living-With-Lupus/Pregnancy-and-Lupus-/Hormones-and-SLE.aspx [Accessed 19 Dec. 2016]. Mandal, A. (2014). What is Autoimmunity?. [Online] News-Medical.net. Available at: http://www.news-medical.net/health/What-is-Autoimmunity.aspx [Accessed 16 Dec. 2016]. Mosca, M., Ruiz-Irastorza, G., Khamashta, M. and Hughes, G. (2001). Treatment of systemic lupus erythematosus. International Immunopharmacology, 1(6), pp.1065-1075. Natarajan, S. and Remick, D. (2008). The ELISA Standard Save: Calculation of sample concentrations in assays with a failed standard curve. Journal of Immunological Methods, 336(2), pp.242-245. Petri, M., Orbai, A., Alarcà ³n, G., Gordon, C., Merrill, J., Fortin, P., Bruce, I., Isenberg, D., Wallace, D., Nived, O., Sturfelt, G., Ramsey-Goldman, R., Bae, S., Hanly, J., Sà ¡nchez-Guerrero, J., Clarke, A., Aranow, C., Manzi, S., Urowitz, M., Gladman, D., Kalunian, K., Costner, M., Werth, V., Zoma, A., Bernatsky, S., Ruiz-Irastorza, G., Khamashta, M., Jacobsen, S., Buyon, J., Maddison, P., Dooley, M., van Vollenhoven, R., Ginzler, E., Stoll, T., Peschken, C., Jorizzo, J., Callen, J., Lim, S., Fessler, B., Inanc, M., Kamen, D., Rahman, A., Steinsson, K., Franks, A., Sigler, L., Hameed, S., Fang, H., Pham, N., Brey, R., Weisman, M., McGwin, G. and Magder, L. (2012). Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. Arthritis Rheumatism, 64(8), pp.2677-2686. Pick, M. (n.d.). Lupus And Hormones | Women to Women. [Online] Womentowomen.com. Available at: https://www.womentowomen.com/inflammation/lupus-and-hormones/ [Accessed 19 Dec. 2016]. Tsao, B. and Grossman, J. (2001). Genetics and systemic lupus erythematosus. Current Rheumatology Reports, 3(3), pp.183-190. Vlab.amrita.edu. (2011). INDIRECT Elisa (Theory) : Immunology Virtual Lab I : Biotechnology and Biomedical Engineering : Amrita Vishwa Vidyapeetham Virtual Lab. [Online] Available at: http://vlab.amrita.edu/?sub=3brch=69sim=721cnt=1 [Accessed 20 Dec. 2016]. Wigand, R., Gottschalk, R., Falkenbach, A., Matthias, T., Kaltwasser, J. and Hoelzer, D. (1997). Detection of dsDNA antibodies in diagnosis of systemic lupus erythematosuscomparative studies of diagnostic effectiveness of 3 ELISA methods with different antigens and a Crithidia luciliae immunofluorescence test. Zeitschrift fur Rheumatologie, 56(2), pp.53-62.

Essay on 1983 Essay

Different dictionaries provide a number of meanings to the word fool. Firstly, the word fool perhaps implies â€Å"a silly person†, â€Å"a dumb† or even a â€Å"dunderhead†. Apart from these negative connotations to the word fool, the term could also mean, â€Å"a professional in counterfeiting folly to draw entertainment for others, a clown, or a jester†. Besides, a fool could a character in a script of other literal work that is created and manipulated to feature a fool. In Twelfth Night by William Shakespeare, there are several unconventional fools other than the clown Feste. Feste and the cauldron of fools in the play dexterously combine their unusual traits and wits to stimulate other characters into their charade eliciting their own form of foolery. This paper explores the role of the fool in William Shakespeare play, Twelfth Night. To begin with, Feste plays a significant role in the Twelfth Night by William Shakespeare in the Illyrian society. He features a transcendental ringleader capable of trouncing conventional social hierarchies and leading them in his own views and interests, aside from the intense criticism of his environment. Feste’s significance in the play is well embedded in his ability to socialize and interact with the nobles and the common with equal ease. In the play, Feste is an employed clown of Olivia’s late father. Therefore, he is an â€Å"official fool† implying that he is permitted to speak the truth to people surrounding him (Act I. Scene V). This role reflects Feste and truthful fool in this Illyrian society, even though he mirrors a critic of his environment. William Shakespeare also injects humor in the play through the characters and mannerism of Feste. For instance, Feste emerges as a conventional fool when he clad as the curate, Sir Topaz. He goes on to visit the imprisoned Malvolio incarnated as Sir Topaz in the company of like fools, Sir Toby and Maria. Shakespeare exerts a shower of humor and wit in the play through the Feste’s charade. Feste humorously abuses the unawares Malvolio of the disguise calling him a â€Å"Satan† and a â€Å"lunatic† (Act IV. Scene II). In a punning twist and turns of words, the in-disguise Feste cum Sir Topaz wittingly confuses Malvolio bringing out the fool in the latter. Incidentally, Malvolio featured as an intentional ruin to people’s pleasure in the play. Therefore, Feste’s folly dawns an acceptable and just behavior among the audience in light of his condemnable actions. Feste represents a genius with words character in the play. He has a knack for witty repartee and word play. Indeed, this justifies Cesario’s description of Feste as the â€Å"wise fellow to play the fool† (3.1.14). Besides, Feste’s penchant for excellent sizing up situations is dramatic and significant in the play. He points out other character’s folly drawing a couple of bucks and a laugh. For instance, Feste’s shrewd description of â€Å"the greedy and drunk† Sir Toby in an honest and humorous mockery justifies to the Elizabethan audience his legitimacy as a licensed fool. Notwithstanding, this folly acts offers an honest insight to the audience of the concealed and dark secrets and aspects of a character in the play. Source document

Adult Antisocial Behavior

The Antisocial Personal Disorder or APD is recognized to be a psychological mental health problem and is deemed to cause certain kinds of behavior in an individual.   Although the effect of this mental illness in a person would greatly vary, the disorder is said to result to violent tendencies, like destructive behavior even committing crimes like rape or murder.There are of course interventions that can be applied to suppress its impacts on children and adult, and there are early warning signs that can be detected that signals personal affliction of the ailment. (McCord and Tremblay, 1992) The inability to prevent this disorder from early childhood can result to the sustaining of the disorder until adulthood, which can lead to violent outcomes.   The antisocial disorder can be more common that what is usually perceived, as there are cases when people would be mild psychopaths – those who have violent tendencies, but not as threatening as full-blown psychopaths. (Kantor, 2 006)   How the disorder can affect an individual can be wide and varied, and the capacity for treatment can also be ranged.The prevalent and general feature of the APD is the individual’s indifference or ignorance of other people, and the pattern of such behavior is consistent and sustained, often resulting to violence.   Diagnosis would be dependent of the people surrounding the individual – those who witness his/her behavior – and the childhood history of one’s conduct and attitudes.   (Lykken, 1995)The occurrence of the antisocial personality disorder is higher in males than in females, with 3% and 1% respectively, of the population diagnosed as having the mental disorder.   (Wolman, 1999) Several symptoms serves as red flags that indicate affliction, and these attitudinal indicators can vary widely among individuals.   It would be the consistency of the dysfunctional behavior that would determine if the person is indeed antisocial.The indivi dual’s inability to feel remorse or guilt after committing repetitive dysfunctional attitude would be a strong indicator of antisocial disorder.One of the markers of the antisocial disorder is the constant resort to deceit and manipulation of a person.   Acts of violence and crime are committed without regard for others or care for the law or any other implications or ramifications.   Violating the rights of others is a known characteristic of APD, as with the tendency to lie or steal.   Disregard for others and difficulty to make and maintain friends is common in antisocial individuals.They can also be susceptible to alcoholism, drug dependency, or any other substance abuse, and can be prone to committing acts of violence.  Ã‚   People with the antisocial behavior disorder can experience extreme difficulties in relating with others, or maintaining relationships, as they have little regard for the emotional and physical well-being of others.Other characteristics that would show consistent dysfunctional behavior in terms of the persons capacity to socialize can be an indicator of the disorder.The etiological background of the APD finds some connection to genetics, as the disorder is argued to be something inherited or passed over from parents, although the relationship would only refer to higher probability of occurrence and not the actual genetic transmission of the disorder.   Ultimately, the behavior of the person would be shaped by his/her social environment.The family of the individual with APD can be a strong cause for the development and progression of the disorder.   For one, individuals with fathers that are alcoholics or sociopaths can be said to be more prone to developing the disorder; also, it can cause somatization disorder in females. (Kantor, 2006)Another probable cause of antisocial disorder is the lack of maternal care or a mother, in the first years of the life of the child.   Parents of individuals with the disorder are usually lenient and do not show consistent effort to discipline the child.   Also, these parents displays unbecoming attitude, like alcoholism or abuse, which can impact on the behavior of the child.   Improper rearing can distort the emotional and mental development of a child, and therefore lead to antisocial behavior in adulthood. The Macdonald triad – pyromania, bedwetting, and animal cruelty – is identified by scholars to be a sign of antisocial disorder in people below 18, which can easily be sustained until adulthood. (Heginbotham, 2000)But the true cause of antisocial behavior in adults can be difficult to pinpoint, are prediction and tracing is quite complex and tedious; but the above indicators are noted to be the common characteristics of adults diagnosed with the disorder.In our society, the antisocial behavior disorder is estimated to be found in a certain percentage of the population- with males having more propensities for acquiring the mental diseas e.   Studies show that 5.8% of males are under a lifetime risk of being antisocial, which is significantly higher than the female risk rate. (Wolman, 1999)   For the females, the lifetime risk factor can be present in 1.2% of the population.   Actual prevalence the mental disorder is similarly higher in males, with 3% of the population said to be antisocial, which equates to almost 10 million in the United States. (Wolman, 1999)   The females have a 1% rate of antisocial behavior.Environments where violent is prevalent, like penitentiaries and prisons, are noted to have 75% of the population diagnosed as being antisocial.   This clearly shows that individuals with the antisocial disorder are more likely to commit crimes and be penalized.The treatment of the antisocial behavior would necessitate the mapping of the behavior of the person in able to determine the appropriate therapy or treatment that would be applied.   Although treatment and various social techniques is so mething that is available to people with the disorder, psychologists would claim that conduct disorders would be something that can be resistant to treatment.Treatments of adults with the disorder is especially difficult, can no scientific evidence would prove that certain treatment indeed works.   Therapy and communication training is children can be a more effective tool, as it would prevent development of the behavior.   Exposing a person to social environments and cultivating positive relationships, like a good classroom setting, or more importantly, as healthy family life, can be a long-term deterrent to antisocial behavior.In conclusion, antisocial behavior is a mental disorder that can lead a person to commit acts of violence – how violent it would be can vary to a wide extent – from domestic violence to theft to heinous crimes like rape, murder, and homicide.The absence of remorse or any signs of guilt is cause by APD, and this type of emotional behavior wo uld cause the individual to continuously exhibit dysfunctions in their behavior.   The antisocial disorder is something that can start from early childhood and can be developed to psychopath behavior until adulthood.   Although genetic relationship can also be found, it is basically caused by the environment and situation of a person during his formative years of childhood, which can have massive impacts on behavior later in life.   Individuals with the APD are difficult to interact with, usually always in solitude, irritable, moody, deceptive and manipulative.The disorder can occur in a small percentage of the population, and the prospect for cure or repression can be more effective if intervention would start from the onset of detection, or preferably, from childhood.ReferencesBlack, Donald. (2000). Bad Boys, Bad Men: Confronting Antisocial Personality Disorder. C. Lindon Larson. United Kingdom: Oxford University Press.Brain, Christine. (2002). Advanced Psychology: Applicati ons, Issues and Perspectives. United Kingdom: Nelson Thornes.Heginbotham, Christopher. (2000). Philosophy, Psychiatry, and Psychotherapy: Personal Identity in Mental Disorder. England: Ashgate.Kantor, Martin. (2006). The Psychopathy of Everyday Life: How Antisocial Personality Disorder Affects All of Us. United States: Praeger Publishers.Larsen, Randy, and David Buss. (2008). Personality Psychology: Domains of Knowledge about Human Nature. Boston: McGraw Hill.

Analysis Of The Article The Trade Deficit Isn t A...

In the US News article â€Å"The Trade Deficit Isn’t a Scorecard, and Cutting It Won’t Make America Great Again† by Neil Irwin, economics and politics meet as presidential candidate Donald Trump’s economic policy is scrutinized. Part of Trump’s plan to make America great again is to eliminate the trade deficit (Neil, 2016); Irwin disagrees. Irwin argues that the trade deficit is not bad at all because it allows the United States to have lower interest rates, which spur foreign investment. Additionally, Irwin counteracts Trump’s theory that a trade deficit means fewer jobs and therefore a declining economy. Irwin argues that the trade deficit does not mean a declining economy, but rather, it is what is done with the money flowing into the US†¦show more content†¦Trade is how goods or services are exchanged between countries. An exchange is broken down into two categories: imports and exports. Imports are goods and services coming into a country; whereas, goods and services flowing out of a country are exports. When different countries trade with each other, they develop a trade deficit, a trade surplus, or a trade balance. A trade deficit is when the value of imports exceeds the value of exports, and a trade surplus is when the value of exports exceeds the value of imports. A trade balance is when imports and exports are traded at equal rates/amounts. While it is ideal to have free trade, which is trade without any restrictions upon it, it is not that simple. Instead, there are tariffs and quotas that prevent free trade. Tariffs are taxes on imports, and quotas are a limit on the quantity of a good that can be imported during a given time period. Tariffs and quotas exist because governments may prefer that their products be sold nationally more than another country’s products to help their own economy. Their own economy is helped because more jobs can be given to that country’s workers instead of a nother country’s workers. While quotas and tariffs may help boost a country’s economy, free trade allows for reduced prices, less inefficiencies, and increased consumption worldwide. With tariffs, the supply curve remains level as the price level never changes due to the extra-tax upon imported items. It should be