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The reason for this is (A) b-Blocker (A) Epinephrine causes increased blood loss (B) a-Agonist during delicate surgery (C) Muscarinic agonist (B) Epinephrine causes swelling of the tissues generic arava 20mg without prescription symptoms 5 weeks 3 days, (D) Neuromuscular blocker making surgery more challenging (E) Dopamine agonist (C) Epinephrine is contraindicated in emer- gency surgery 17 buy discount arava 20mg on line treatment 7th feb. A 35-year-old woman presents to your office (D) Epinephrine causes vasoconstriction discount arava online visa symptoms xanax overdose, which for a regular check-up purchase arava 20 mg mastercard treatment resistant depression. Her only complaint is can lead to vascular ischemia in digits recurrent migraine headaches, which have (E) Epinephrine can cause hypotension when increased in frequency over the years. On exam- administered with sedative agents ination, her blood pressure is elevated at 54 Pharmacology 150/70. Dantrolene is the drug of choice to treat ma- sive therapy that is also used for prophylaxis of lignant hyperthermia caused by succinylcholine migraines. In contrast to propranolol, metoprolol receptors (A) Is used for the management of (E) Acts centrally to reduce fever hypertension (B) Has greater selectivity for b -adrenoceptors 24. A drug that acts at prejunctional a2-adreno- 2 (C) May be beneficial for the acute treatment of ceptors and is used to treat hypertension is migraine headache (A) Clonidine (D) Is less likely to precipitate bronchoconstric- (B) Methoxamine tion in patients with asthma (C) Metaproterenol (D) Dobutamine 19. Intravenous administration of epinephrine (E) Dopamine to a patient results in a severe decrease in dia- stolic pressure and an increase in cardiac output. Drug X causes an increase in blood pressure Which of the following drugs might the patient and a decrease in heart rate when administered have previously taken that could account for this to a patient intravenously. Drug X most (C) Phenylephrine likely is (D) Prazosin (A) Propranolol (B) Norepinephrine 20. Which of the following drugs is used to (C) Isoproterenol diagnose myasthenia gravis? Poisoning with an insecticide containing an (D) Edrophonium acetylcholinesterase inhibitor is best managed (E) Pralidoxime by administration of which one of the following agents? Pilocarpine reduces intraocular pressure in (A) Physostigmine patients with glaucoma because it (B) Bethanechol (A) Activates nicotinic cholinoceptors (C) Propranolol (B) Blocks muscarinic cholinoceptors (D) Pilocarpine (C) Selectively inhibits peripheral activity of (E) Atropine sympathetic ganglia (D) Inhibits acetylcholinesterase 27. Receptor actions of acetylcholine are mim- icked by nicotine at which one of the following 22. Muscarinic cholinoceptor agonists may (D) Cytochrome P450 cause vasodilation through the release of 3A (E) Acetylcholinesterase endothelial Chapter 2 Drugs Acting on the Autonomic Nervous System 55 (A) Histamine (C) Cardiac slowing induced by stimulation of (B) Norepinephrine the vagus nerve (C) Acetylcholine (D) Miosis induced by bright light (D) Nitric oxide 32. Emergency treatment of acute heart failure would be blocked by which one of the following is best managed with which of the following agents? Topical application of timolol to the eye would be expected to induce which of the 30. Phenylephrine is used to treat patients with nasal mucosa stuffiness because it causes vaso- 31. Neostigmine would be expected to reverse constriction by which one of the following conditions? Botulinum toxin blocks calcium-dependent exocytosis of acetylcholine from storage vesicles, producing paralysis. Common sources of botulinum toxin include canned home goods and, in cases of infant botulism, honey. Choline acetyltransferase is an enzyme catalyzing synthesis of acetylcholine from an acetate and choline. Enzyme acetylcholinesterase is responsible for catalyzing hydrolysis of acetylcholine. Acetylcholine synapses at the ganglia of many neurons and tissues, and this step is not blocked by botulinum toxin. Guanethidine blocks the release of norepinephrine from storage vesicles into the nerve terminals. Epinephrine, do- pamine, and serotonin release can be blocked by other agents (beyond the scope of this chap- ter), but not by guanethidine. Cocaine is a potent inhibitor of norepinephrine uptake, a process that normally terminates norepinephrine’s action. Oxidative deamination of norepinephrine in nerve termi- nals and the effector cells describes the action of monoamine oxidase, which is targeted by cer- tain antidepressant medications. Inhibition of metabolism of norepinephrine in nerve terminals describes catechol-O-methyltransferase, which is found in nerve and other effector cells. Poten- tiation of tyrosine dehydroxylase would, in fact, cause excessive amounts of norepinephrine to accumulate; however, this enzyme is not affected by cocaine. Norepinephrine release can be blocked, not promoted, by agents such as bretylium and guanethidine. Passage of sodium via ligand- gated ion channel is manifested by nicotinic acetylcholine receptors. Activation of Gq-protein resulting in increase of phosphatidylinositol and calcium mobilization refers to the mechanism of action of muscarinic receptors type M1 and M3, as well as a1-adrenoceptors. Activation of Gq-protein resulting in increase of phosphatidylinositol and calcium mobilization refers to mechanism of action of M2-cholinoceptors and a2-adrenoceptors. Finally, binding to l-receptors in the specific areas of the brain describes the action of opioid agents. Bethanechol is a type of muscarinic receptor agonist that is used clinically to ameliorate urinary retention. Nicotinic blockers such as trimethaphan are rarely used in clinical practice because of the lack of selectivity. Acetylcholinesterase reactivator pralidoxime has to be given within 30 minutes of exposure to insecticide because of the effects of ‘‘aging’’ (i. Physostigmine is a cholines- terase inhibitor that is occasionally used in atropine or scopolamine poisoning. Pancuronium is a nondepolarizing inhibitor of acetylcholine that is used for muscle paralysis. Oxybutynin acts by binding to muscarinic receptors located on the detrusor muscle of the bladder, suppressing involuntary contraction of the muscle. Acetylcholinesterase inhibitors such as edrophonium are used for myasthenia gravis. Benztropine, an antimuscarinic agent, is used as an adjunct for treatment of Parkinson disease. Reserpine is a norepinephrine uptake inhibitor occasionally used for treat- ment of hypertension. It acts by antagonizing musca- rinic receptors in bronchial smooth muscle, thereby causing bronchodilation. Succinylcholine is a depolarizing neuromuscular blocker that is used in rapid- sequence intubation, as well as other procedures. It quickly relaxes all muscles in the body, allowing a prompt intubation to prevent the reflux of gastric contents into the trachea. Neostigmine is an indirect-acting cholinergic agonist used for treatment of myasthenia gravis and reversal of neuromuscular blockade. Homatropine is an antimuscarinic agent used for induction of mydriasis for ophthal- mologic examinations. Pralidoxime is an acetylcholinesterase reactivator used for organophos- phate poisoning. Ephedrine acts indirectly to release norepinephrine from nerve terminals, causing effects similar to those of catecholamines, including elevated blood pressure. An example of an indirect-acting cho- linergic agonist is edrophonium, which is used for diagnosis of myasthenia gravis.
None of these scholars buy arava toronto medications kosher for passover, however 20 mg arava visa treatment definition math, have satisfactorily solved the problem of this apparently ‘double-faced’ religiosity (see below) generic arava 10mg with mastercard medications causing thrombocytopenia. References to On the Sacred Disease follow the division into chapters and sections of H cheap arava 20 mg overnight delivery treatment skin cancer. On the Sacred Disease 47 as Jeanne Ducatillon has claimed,8 that the statements of the ﬁrst chapter actually reveal an authentic religious conviction, we are obliged to deﬁne as accurately as possible how this conviction is related to the concept of the divine as an immanent natural law and of its workings as natural processes. But we must also consider the possibility (which Ducatillon appears to have overlooked) that the accusations of the ﬁrst chapter are no more than rhetorical or occasional arguments pour besoin de la cause which need not imply the author’s personal involvement, seeing that many of these statements have an obviously hypothetical character. Yet such a hypothetical argument does reﬂect my opinion on the logical connection between the premise and the conclusion, since it shows what I believe to be a valid or a non-valid conclusion from a given premise (a premise which I need not be- lieve to be true). Thus the argument reﬂects my sense of ‘logic’ or ‘necessity’ and the presuppositions underlying the stringency of my argument. One might object that our apparent problem is not genuine, and that there is nothing strange about intellectuals participating in traditional cul- tic activities such as prayer and sacriﬁce, while at the same time holding ‘advanced’ religious or theological ideas which seem inconsistent with the presuppositions underlying these cultic practices. It is probably this hypothetical character which has led most interpreters to refrain from bringing these statements to bear on the discussion of the writer’s theological ideas (e. Norenberg (¨ 1968) 69 also claims that the sections 41–6 are put into the mouth of the magicians, although later on (74–6) he suddenly takes them seriously as reﬂecting the author’s own opinion. However, his own ‘hypothetical’ remarks there on the ‘moral signiﬁcance’ of the divine remain inconclusive and partly contradict his earlier views on the divinity of nature. As will become clear in the course of this chapter, I do not believe that ‘the divine’ (to theion) mentioned in 1. His remarks reﬂect, indeed, a genuine belief in the Divine, but, as perhaps in the case of a Socrates or a Euripides, it is not simply a belief in the gods as traditionally and popularly conceived. At least three questions are important: (i) To what extent did intellectuals try to harmonise their own theological conceptions with traditional beliefs and, if they did, then for what 48 Hippocratic Corpus and Diocles of Carystus does not concern a discrepancy between religious theory and religious prac- tice or between theology and cult, but a tension between different ideas in one and the same text. For there is a difference between intellectuals simply participating (from habit or under social pressure) in cultic actions, and intellectuals, such as the author of On the Sacred Disease, making explicit statements and deﬁnitions about what they believe should be the right way of approaching the gods. Moreover, the author’s assertions not only con- cern cult and ritual, but also characteristics of the divine and the way in which it manifests itself within human experience. Therefore the problem deserves to be considered, and we must try to ﬁnd out how these two sets of religious opinions are related to each other. I shall ﬁrst deal with the statements on the divine character of the disease and consider whether these admit of being extrapolated into a ‘theology’. This will for a substantial part consist in an attempt to evaluate and clarify the interpretative debate on the author’s claim that ‘all diseases are divine and all are human’. Then I shall deal with the statements in his chapter 1 and relate these to the assertions about the divine character of the disease. Finally I shall summarise my conclusions concerning the religious notions which can, with some degree of certainty, be attributed to the author of On the Sacred Disease. On the one hand it is often stated that there was no institutionalised orthodoxy in ancient Greece and no sacred books with authorised interpretations and that, consequently, many different religious beliefs were tolerated (see Lloyd (1979) 10–15). On the other hand it cannot be denied that at the end of the ﬁfth century (in Attica at least) a growing intolerance manifests itself, e. In this respect it is signiﬁcant that it is the author of On the Sacred Disease himself who accuses his opponents of impiety and atheism (1. On all these matters see Bryant (1986); Dover (1975); Fahr (1969); Guthrie (1969) vol. Miller (1953) 9–15), though I shall say something about this in the course of my comments on interpretation (1). On the Sacred Disease 49 intend to offer a new one, but I believe that the debate would beneﬁt from recognising that these interpretations are different and incompatible, and from acknowledging the presuppositions underlying both views. My second a priori remark is that the use of terminological oppositions such as ‘rational versus irrational’ and ‘natural versus supernatural’ in order to deﬁne the meaning of theios and anthropinos¯ is confusing rather than illuminating. The two interpretations are as follows: (1) A disease is divine in virtue of being caused by factors ( prophasies;on this term see below) which are themselves divine: the climatic factors heat, cold and winds. These can, on this view, be called divine because they are beyond human control (the author accepting aporos, ‘hopeless’, ‘impossible to resolve’, as a proper associate of theios,cf. These factors can be called human because they (or at least some of them) are capable of being controlled, or in any case inﬂuenced, by human agency. The governing connotations of theios 12 This is not to suggest that the oppositions ‘rational–irrational’ and ‘natural–supernatural’ are used by modern scholars as if they were equivalent, but rather to avoid the anachronistic associations these terms conjure up. One of these reasons, he says, may be the ‘hopelessness’ (por©h) with which the disease confronted them. But he proceeds to show that this only applies to a cognitive ‘hopelessness’ (por©h toÓ m ginÛskein); as for the therapeutic aspect, he says, these people claim to be ‘well provided’ with means to cure (eÎporoi) rather than ‘hopeless’ (poroi). Apparently the author accepts aporos as a justiﬁed associate of theios, but he points out that these people are actually not aporoi at all. By showing that the disease is caused by ‘human’ factors as well (which are in their turn inﬂuenced by the divine factors mentioned) the author demonstrates that in his account a disease can be both divine and human (i. These connotations, in fact, also led the Presocratic philosophers to apply the word to their ultimate principles. It is rather that just as the other diseases have a nature from which they arise, likewise this one has a nature and a cause. Each of these arguments may be questioned: repetition of this kind is quite frequent in On the Sacred Disease (e. Besides, after the opening sentence (perª t¦v ¬r¦v noÅsou kaleomnhv æde cei) it is more reasonable to expect an exposition of what the author believes than the rejection of what other people believe. On the Sacred Disease 51 kaª ¡l©ou kaª pneumtwn metaballomnwn te kaª oÉdpote tremiz»ntwn. This disease which is called sacred arises from the same causes as the others, from the things that come and go away and from cold and sun and winds that change and never rest. These things are divine, so that one ought not to separate this disease and regard it as being more divine than the others; it is rather that all are divine and all are human, and each of them has a nature and a power of its own, and none is hopeless or impossible to deal with. The ﬁrst interpretation is mainly based upon the remark ‘these things are divine’ (taÓta d’stª qe±a, 18. The author derives the divinity of the disease from the divinity of its causes, the climatic factors whose inﬂuence has been discussed in 10. And since these factors are – as the author claims – the causes of all diseases, all diseases are equally divine, so that none of them should be distinguished from the others as being more divine. It is not stated explicitly in either of these passages in what sense they are human,17 but it has been suggested that diseases are caused (or at least determined in their development) by human factors as well. For these reasons, for instance, the brain (¾ gkf- alov) is not mentioned in chapter 18, although the writer had stated ear- lier (3. But in the author’s view all diseases are both divine and human: the explanandum is not that all diseases are human, but in what sense all diseases are divine as well. Among the ‘human’ factors determining the disease we should probably also reckon the individual’s constitution (phlegmatic or choleric: 2. A difﬁculty of this view is that not all of these factors seem to be accessible to human control or even inﬂuence, so that this connotation of anthropinos¯ seems hardly applicable here. Yet perhaps another association of the opposition theios– anthropinos¯ has prompted the author to use it here, namely the contrast ‘universal–particular’, which also seems to govern the use of theios in the Hippocratic treatise On the Nature of the Woman.
All these patients underwent preliminary examination with X rays purchase genuine arava symptoms diabetes, computer assisted tomography and fibrobronchoscopy order 20mg arava mastercard symptoms 7dpiui, with biopsy and histological verification purchase arava 20mg with amex symptoms colon cancer. Negative findings were recorded in three patients treated with chemotherapy arava 20 mg lowest price medicine 94, which exerts an inhibitory effect on the accumulation of radiopharmaceuticals. Its accumulation in viable myocardium correlates with regional myocardial perfusion and itisproportional to the regional blood flow as well . Recently, therehas been some increaseinthevolume ofpublications on itsapplica tion outside the field of cardiology, i. They were dividedaccord ing to theirdiagnosis and histological findings, as follows: — Group I. Patients with primary lung cancer: planocellular carcinoma — 16 patients; adenocarcinoma — 4 patients; small cell carcinoma — 5 patients. Control of patients with: pulmonary echinococcosis — 8 patients; pulmonary cysts — 2 patients. Figure 1presentstheexaminationresultsforafemale, 55 yearsofage, who was complainingforsixmonths ofchestpain,cough, shortnessofbreathduring exertion, fatigue, and loss ofweight and appetite. An intensive accumulation was found in the upperpulmonary fieldofherleftlung (Fig. In the sagittal, coronal and transversal scans, increased tracer uptake was visualized. These two patients have undergone preliminary treatmentwith chemotherapy and radiotherapy. Ten patient controls— withpulmonary echinococcosis(eightpatients)andpulmonary cysts(two patients) — were alsoexamined. Inthesecases,theindexofinclusiondecreaseswithvaluesthataretypical of those in the control group. Both chemotherapy and radiotherapy inhibit radio pharmaceutical uptake in the focus of the malignant tumour. Intensive uptake isa resultoftheenhanced metabolic activityofgrowing tumour cells. Itisaccumulated in their mitochondria and cytoplasm on the basis of generated membrane potential and increasedpassivediffusion [6-8]. It may be helpful in identifying mediastinal lymph node involvement and has a potential role in staging bronchial carcinoma. Ithas been used for tumour imaging  and has been reported as being highly successful in the evaluation of several tumours. The patientpopulation included 13 males and 1female with an age rangeof40-80 years (mean age: 61. Of the patients, six had squamous cell carcinoma, four adenocarcinoma, two small cellcarcinoma and two anaplastic large cellcarci noma (TableI). One patient who had received radiotherapy and developed local recur rence two months before the study was also included. Final histological diagnosis of bronchogenic carcinoma was achieved through bronchoscopic biopsy. The images were examined for focal uptake in the tumour and hilar and mediastinal lymph nodes. Itmay be help ful in identifying mediastinal lymph node involvement, and has a potential role in staging bronchial carcinoma. Fifty-seven patients were suspected to have recurrent colorectal adenocarcinoma with prior staging ranging from Duke’s B1-C2, while another six patients were suspected of primary colorectal cancer. High sensitivity in the detection of locoregional recurrence and liver métastasés was found in the study. Single photon emission computed tomography was clearly superior to planar imaging in detecting small lesions and locating them. According to our national cancer statistics, colorectal cancer is among thetoptenleadingtypesofcancer. The majority ofpatientshad lymph node involvement atthe time of surgery; as a result, diseases frequently recurred. The developmentofdiagnostictoolsfortheearlydetectionofrecurrentcolorectalcancer as well as monitoring results of treatment are obviously needed. The hospital’sethicalcommittee approved the study ofthesepatients and informed consent was obtained from allpatients. Scintigraphic techniques Whole body images, anterior and posterior projections, were obtained at 10 min, 4 h and 24 h post-injection. A low energy general purpose collimator was used and 1000 000 counts were acquired. The tomographic images were acquired at 128 x 128 pixels of 30 sper view and 64 views per 360°, giving 20 000-40 000 counts per view. Visual analysis ofthe studies was done by two experienced nuclear medicine physicians. Planarimages were evaluatedand conclusionswere expressed as ‘nega tive, suspect or positive’. Of 57 patients, 48 cases were proved to have recurrentdiseases and 9 cases were ina remission state. All serawere senttothe Division ofNuclear Medicine, Johann Wolfgang Goethe University Medical Centre, Frankfurt/Main, Germany. The overallaccuracy rateindiagnosisis84%, witha very highpositivepredictivevalue (97%), butpoor negativepredictivevalue (50%). Only three cases of bone métastasés and five cases of lymph node métastasés were found inthesepatients;therefore, diagnosticefficacywas notevaluateddue to smallsample size. Lung, bone and other lesions were not evaluated because the number of lesions was too small. Our study also exhibited high positive and negative predictive values for the detection of locoregional recurrence and liver métastasés, which is similar to other reports . However, lung métastasés were poorly detected, as shown by this and another study . Thus, a combination of these two modes would yield very high sensitivity and specificity in the diagnosis of the disease. The problems encountered in this study include high contrast in the heart, which may result in a high false negative rate in detecting lung métastasés, and non specific accumulation of activity in the large bowel, especially in the caecum and the ascending colon, which occasionally caused difficulty in interpreting the findings. Clinical results in the detection of colorectal carcinomas and recurrences, Scand. Seventy-two patients (40 with infection, 17 with colorectal carcinoma and 15 with malignant melanoma) with 135 known lesions were studied using radiolabelled antibodies. False negative results were mainly related to localization in organs with physiologically high count rates, such as kidneys, the urinary bladder, liver, stomach and the cardiac blood pool. False positive results were probably caused by normal tissue expressing the antigen. The planar method offers the advantage of an easier procedure, and is better suited for whole body studies. The combination of both studies seems to be promising for the early detec tion of tumoral and infection sites, providing a higher detection rate and a considerable increase in information. Moreover, while the mortality from cardiovascular disease is decreasing, cancer mortality is increasing steadily.
The regression equation works like this: The slope indicates the direction in which the Ys change as X increases and the rate at which they change order 10mg arava mastercard medications blood thinners. The Y intercept indicates the starting point from which the Y scores begin to change quality arava 10 mg medicine you cant take with grapefruit. Thus discount arava 20 mg overnight delivery symptoms xanax is prescribed for, together purchase cheap arava line medicine pills, the slope and intercept describe how, starting at a particular Y score, the Y scores tend to change by a specific amount as the X scores increase. As an example, say that we have developed a test to identify (predict) those indi- viduals who will be good or bad workers at a factory that makes “widgets. The predictor (X) variable is participants’ scores on the widget test, and the criterion (Y) variable is the number of widgets they produced. This is a very strong, positive linear relationship, and so the test will be what researchers call “a good predictor” of widget-making. The numerator of the formula for b is the same as the numerator in the formula for r, and the denominator of the formula for b is the left-hand quantity in the denominator of the formula for r. This positive slope indicates a positive relationship, which fits with the positive r of 1. Had the rela- tionship been negative, the formula would have produced a negative number here. Computing the Y Intercept The formula for the Y intercept of the linear regression line is a 5 Y 2 1b21X2 First, multiply the mean of all X scores times the slope of the regression line. Describing the Linear Regression Equation Once you have computed the Y intercept and the slope, rewrite the regression equation, substituting the computed values for a and b. Plotting the Regression Line We use the finished regression equation to plot our linear regression line. To draw a line, we need at least two data points, so choose a low and high X score, insert each into the regression equation, and compute the Y¿ for that X. Therefore, we also use the finished regression equation to predict anyone’s Y score if we know their X score. In fact, computing any Y¿ using the equation is the equivalent of going to the graph and traveling vertically from the X score up to the regression line and then left to the value of Y¿ on the Y axis. We can compute Y¿ for any value of X that falls within the range of Xs in our data, even if it’s a score not found in the original sample: No one scored an X of 1. Our regression equa- tion is based only on widget test scores between 1 and 4, so we shouldn’t predict a Y for an X of, for example, 6. This is because we can’t be sure what the nature of the relationship is at 6—maybe it’s curvilinear or has a steeper slope. Putting all of this together, the preceding computations are summarized in Table 8. Substitute the values of a and b into the formula for the regression equation: Y¿ 5 1b21X2 1 a 5. The components of the regression equation to To use X to predict Y in these scores, compute first are the ______ and ______. Compute b for the following scores: X Y X Y 1 1 2 2 3 3 4 Compute b: ©X 5 12, ©Y 5 25, ©X2 5 28, 4. To describe the amount of prediction error we expect when predicting unknown scores, we first determine how well we can predict the actual Y scores in our sample: We pretend we don’t know the scores, predict them, and then compare the predicted Y¿ scores to the actual Y scores. The error in a single prediction is the amount that a participant’s Y score differs from the corresponding predicted Y¿ score: In symbols this is Y 2 Y¿, and it is literally the dif- ference between the score a participant got and the score we predict he or she got. The predictions for some participants will be closer to their actual Y scores than for others, so we would like to compute something like the average error across all predictions. To find the average error, we first compute Y¿ for everyone in the sample and sub- tract their Y¿ from their actual Y score. Statisticians equate errors with deviations, so Describing Errors in Prediction 169 Y 2 Y¿ equals the amount that Y deviates from Y¿. To get the average error, we would like to simply sum these deviations and then find the average, but we cannot. Therefore, the Ys are equally spread out around their Y¿ scores, in the same way that previously we saw that Xs are spread out around their X. Because of this, like with the mean, the positive and nega- tive deviations with Y will cancel out, always producing a sum equal to zero. The sum of the squared deviations of Y 2 Y¿ is not necessarily zero, so neither is the average squared deviation. Computing the Variance of the Y Scores Around Y9 The variance of the Y scores around Y¿ is the average squared difference between the actual Y scores and their corresponding predicted Y¿ scores. The S2 indicates sample variance or error, and the subscript Y¿ indi- Y¿ cates that it is the error associated with using Y¿ to predict Y scores. The formula that defines the variance of the Y scores around Y¿ is ©1Y 2 Y¿ 22 S2 5 Y¿ N Like other definitional formulas we’ve seen, this formula is important because it shows the core calculation involved: We subtract the Y¿ predicted for each participant from his or her actual Y score giving us a measure of our error. The answer is one way to measure roughly the “average” amount of error we have when we use linear regression to predict Y scores. Note: Among the approaches we might use, the regression procedures described in this chapter produce the smallest error in predictions possible, thereby producing the smallest sum of squared deviations possible. In the defining formula, we can replace Y¿ with the formulas for finding Y¿ (for finding a, b, and so on). Among all of these formulas we’ll find the com- ponents for the following computational formula. The computational formula for the variance of the Y scores around Y9 is S2 5 S2 11 2 r22 Y¿ Y Much better! Therefore, finish the computations of S2 using the formula at the begin- Y ning of this chapter. Although this variance is a legitimate way to compute the error in our predictions, it is only somewhat like the “average” error, because of the usual problems when interpreting variance. First, squaring each difference between Y and Y¿ produces an unrealistically large number, inflating our error. Second, squaring produces error that is measured in squared units, so our predictions above are off by 2. To distinguish the standard deviation found in regression, we call it the standard error of the estimate. Computing the Standard Error of the Estimate The standard error of the estimate is similar to a standard deviation of the Y scores around their Y¿ scores. It is the clearest way to describe the “average error” when using Y¿ to predict Y scores. By computing the square root, the answer is a more realistic number and we are no longer dealing with a squared variable. The core calcu- lation, however, is still to find the error between participants’ actual Y scores and their predicted Y¿ scores, and this is as close as we will come to computing the “average error” in our predictions. Then we find the square root of the quantity 1 2 r2 and then multiply it times the standard deviation of all Y scores. Therefore, we conclude that when using the regression equation to predict the number of widgets produced per hour based on a per- son’s widget test score, when we are wrong, we will be wrong by an “average” of about 1.
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