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Molecular epidemiology of hospital-associated and community- acquired Clostridium difficile infection in a Swedish county order generic fildena on-line impotence remedy. Primary symptomless colonisation by Clostridium difficile and decreased risk of subsequent diarrhoea order fildena 100 mg amex erectile dysfunction protocol secret. Effect of antibiotic treatment on growth of and toxin production by Clostridium difficile in the cecal contents of mice. Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals. Asymptomatic carriage of Clostridium difficile and serum levels of IgG antibody against toxin A. Association between antibody response to toxin A and protection against recurrent Clostridium difficile diarrhoea. A common polymorphism in the interleukin 8 gene promoter is associated with Clostridium difficile diarrhea. Acquisition of Clostridium difficile and Clostridium difficile- associated diarrhea in hospitalized patients receiving tube feeding. Proton pump inhibitors and hospitalization for Clostridium difficile-associated disease: a population-based study. Risk of Clostridium difficile diarrhea among hospital inpatients prescribed proton pump inhibitors: cohort and case-control studies. Extraintestinal Clostridium difficile: 10 years’ experience at a tertiary-care hospital. Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of severe disease in North America and Europe. Molecular analysis of the pathogenicity locus and polymorphism in the putative negative regulator of toxin production (TcdC) among Clostridium difficile clinical isolates. Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile-associated diarrhea: a cohort study during an epidemic in Quebec. Fulminant Clostridium difficile: an underappreciated and increasing cause of death and complications. Conditions associated with leukocytosis in a tertiary care hospital, with particular attention to the role of infection caused by clostridium difficile. Recurrent Clostridium difficile diarrhea: characteristics of and risk factors for patients enrolled in a prospective, randomized, double-blinded trial. Pseudomembranous colitis: spectrum of imaging findings with clinical and pathologic correlation. Effective detection of toxigenic Clostridium difficile by a two- step algorithm including tests for antigen and cytotoxin. Prospective randomised trial of metronidazole versus vancomycin for Clostridium-difficile-associated diarrhoea and colitis. Tolevamer, a novel nonantibiotic polymer, compared with vancomycin in the treatment of mild to moderately severe Clostridium difficile-associated diarrhea. A comparison of vancomycin and metronidazole for the treatment of Clostridium difficile-associated diarrhea, stratified by disease severity. Adjunctive intracolonic vancomycin for severe Clostridium difficile colitis: case series and review of the literature. Treatment of antibiotic-associated Clostridium difficile colitis with oral vancomycin: comparison of two dosage regimens. Faecal metronidazole concentrations during oral and intravenous therapy for antibiotic associated colitis due to Clostridium difficile. Reassessment of Clostridium difficile susceptibility to metronidazole and vancomycin. Intravenous immunoglobulin for the treatment of severe, refractory, and recurrent Clostridium difficile diarrhea. Impact of emergency colectomy on survival of patients with fulminant Clostridium difficile colitis during an epidemic caused by a hypervirulent strain. Recurrence of symptoms in Clostridium difficile infection— relapse or reinfection? The role of the intestinal tract as a reservoir and source for transmission of nosocomial pathogens. Meta-analysis of probiotics for the prevention of antibiotic associated diarrhea and the treatment of Clostridium difficile disease. Cunha Infectious Disease Division, Winthrop-University Hospital, Mineola, New York, and State University of New York School of Medicine, Stony Brook, New York, U. Urosepsis is bacteremia from a urinary tract source, which is diagnosed by culturing the same organism from urine and blood. Community-acquired urosepsis occurs in non-leukopenic compromised hosts, those with preexisting renal disease, or those with anatomical abnormalities of the urinary tract. Nosocomial urosepsis may occur in normal as well as abnormal hosts due to the presence of stones, stents, or nephrostomy tubes (1–5). Urosepsis is accompanied by bacteremia with systemic symptoms with or without hypotension (6–8). Immune defects related to malignancy and/or chemotherapy do not diminish mucosal defenses, e. Catheter-associated bacteriuria in the hospital does not result in urosepsis in normal hosts. Urosepsis from urologic instrumentation/procedures may occur in normal or abnormal hosts (4,5,9–12) (Table 2). Because the uropathogens causing community-acquired versus nosocomially acquired urosepsis are dissimilar, different therapeutic approaches are required for community- acquired and nosocomially acquired urosepsis (5,9,11) (Table 3). The interaction between microorganisms and the host determines the systemic response rather than the origin of the infection. The clinical diagnostic approach is to identify systemic disorders or urinary tract abnormalities that predispose to urosepsis, i. Gram stain and culture of the urine with urinalysis plus blood cultures are the definitive diagnostic tests. Indwelling (short-term) Normal Low No antibiotics Remove Foley catheter as non-obstructed Foley soon as possible. Urosepsis due to cystitis in compromised hosts has no localizing signs (1,4,5) (Table 4). Table 4 Differential Diagnosis of Acute Cystitis, Rental Stone, Acute Pyelonephritis Clinical findings Acute cystitis Rental stone Acute pyelonephritis. Symptoms Abdominal pain Suprapubic discomfort Unilateral back pain Unilateral back pain Dysuria þ À þ. Urosepsis in Critical Care 291 Nosocomial urosepsis follows recent urologic instrumentation usually <72 hours. The diagnosis should be considered when a patient becomes septic after a urologic procedure. Patients presenting from the community with urosepsis often have stone or structural ureteral, bladder, or renal abnormality, acute prostatitis/prostatic abscess, or acute pyeloneph- ritis.

Patients with hypertrophic cardiomyopathy will have left ventricular hypertrophy and widespread deep cheap 150mg fildena free shipping male erectile dysfunction icd 9, broad Q waves buy cheap fildena 25 mg erectile dysfunction drugs forum. Symptoms are due to conduction via an accessory pathway and include tachypalpitations, light headedness, syncope, cardiopulmonary collapse, and sudden car- diac death. Life-threatening presentations are usually due the development of atrial fibril- lation or atrial flutter with 1:1 conduction, which can both precipitate ventricular fibrillation. Carvallo’s sign describes the increase in intensity of a tricuspid regurgitation murmur with inspiration. This occurs due to the increase in venous return during inspiration with falling pleural pressure. The Gallavardin effect occurs when the murmur of aortic stenosis is transmitted to the apex V. The Austin Flint murmur is a late diastolic murmur heard at the apex in aortic regurgita- tion. Atrial septal defects cause a mid-systolic murmur at the mid to upper left sternal border, with fixed splitting of S2. The ventricular rate in this situation is quite rapid, and cardiovascular collapse or ventricular fibrillation may result. The usual treatment is direct-current cardioversion, though quinidine may slow conduction through the bypass tract. Verapamil and propranolol have little effect on the bypass tract and may further depress ventricular function, which already is compromised by the rapid rate. Digoxin may accelerate conduction down the bypass tract and lead to ventricular fibrillation. As this patient de- scribes, claudication occurs with ambulation and is often described as a crampy to aching pain that is relieved with rest. Although lack of a palpable pulse sug- gests critical ischemia, it is not diagnostic. The narrowing most commonly occurs distal to the origin of the left subclavian artery, explaining the equal pressure in the arms and reduced pressure in the legs. Coarctations account for approxi- mately 7% of congenital cardiac abnormalities, occur more frequently (2×) in men than in women, and are associated with gonadal dysgenesis and bicuspid aortic valves. Adults will present with hypertension, manifestations of hypertension in the upper body (head- ache, epistaxis), or leg claudication. Physical examination reveals diminished and/or de- layed lower extremity pulses, enlarged collateral vessels in the upper body, or reduced development of the lower extremities. There may be no murmur, a midsytolic mur- mur over the anterior chest and back, or an aortic murmur with a bicuspid valve. The clinical picture is not consistent with renal artery stenosis, pheochromocytoma, carcinoid, or Cushing’s syndrome. In patients with symptoms such as palpitations, the primary therapy should be patient reassurance. If this is unsuccess- ful, beta blockers can be helpful, especially in patients whose symptoms are more prominent during stressful situations and patients with hyperthyroidism. Therefore, in the case of left ventricular hypertrophy the negative deflection, or S wave, would be expected to be larger without an effect on the R wave. The symptoms are similar to those in this scenario but can also include neck pulsation, confusion, exertional dyspnea, dizziness, and syncope. Pacemaker twiddler’s syndrome occurs when the pulse generator of the pacemaker rotates in its subcutaneous pocket, leading to lead dis- lodgement and failure to sense or pace. A transthoracic echocardiogram should be obtained to assess for severity as well as the presence of ventricular thrombus. Presence of left ventricular thrombus would war- rant discussion of arrhythmogenic and embolic complications. Chest radiography may show an enlarged cardiac silhouette but will not be specific for the patient’s pathology. Without symp- toms of chest pain and a stable electrocardiogram, neither cardiac catheterization nor thrombolysis is indicated. It is unclear if atherosclerosis is the primary cause or a result of the same pathophysiologic mechanisms that lead to dilatation. Chronic infectious causes include syphilis and mycotic aneurysm from bacterial endocarditis. Chronic inflammatory states such as Takayasu’s arteritis, gi- ant cell arteritis, and seronegative spondyloarthropathies such as Reiter’s syndrome and ankylosing spondylitis are also associated with aneurysms. Troponin elevations are not known to be caused by pneumonia in the absence of myocardial necrosis. The sinus pacemaker is slow at the beginning of the tracing, accelerates during inspiration in the middle of the tracing, and then slows again during expiration. In atrial fibrillation there are no discernable conducting P waves and the rate is irregularly irregular. Correction of reversible etiologies is indicated since he is still able to generate enough pulse pressure to perfuse his vital organs. Although myocardial infarction due to right coronary artery disease can cause sinus bradycardia, there is no indication that this patient has any disease process other than his pulmonary infection. Temporary transvenous pacing is not indicated since the patient is well-perfused and reversible etiologies are yet to be corrected. In this patient, her body habitus is prohibitive in obtaining good windows for echocar- diography. Thus, a right heart catheterization is imperative for documenting pulmonary hypertension as well as for determining the cause. The right heart catheterization demon- strates an elevated mean arterial pressure, elevated left-ventricular end-diastolic pressure 214 V. In the presence of a normal cardiac output and an elevated left-ventricular ejection fraction, this is consistent with the diagnosis of diastolic heart failure. Systolic heart failure is associ- ated with similar indices on right heart catheterization, but left-ventricular function is de- pressed in systolic heart failure. The other causes listed as options are known causes of pulmonary hypertension but would not be expected to cause an increase in the left-ventric- ular end-diastolic pressure. Obstructive sleep apnea is usually associated only with mild ele- vations in pulmonary artery pressure. Both chronic thromboembolic disease and pulmonary arterial hypertension can cause severe ele- vations in the pulmonary arterial pressure but have a normal left atrial pressure. The magnitude of the shunt depends on the size of the defect, the diastolic properties of both ventricles, and the relative imped- ance of the pulmonary and systemic circulations. Defects of the sinus venosus type occur high in the atrial septum near the entry of the superior vena cava or lower near the ori- fice of the inferior vena cava and may be associated with anomalous connection of the right inferior pulmonary vein to the right atrium.

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Non-IgE-mediated reactions include hemolytic anemia buy fildena 50mg lowest price erectile dysfunction treatment operation, thrombocytopenia order fildena line erectile dysfunction doctors in south africa, acute interstitial nephritis, serum sickness, vasculitis, erythema multiforme, Stevens–Johnson syndrome, and toxic epidermal necrolysis. Toxicity is a consequence of administering a drug in quantities exceeding those capable of being physiologically “managed” by the host, and is generally due to either excessive dosing and/or impaired drug metabolism. Examples of toxicity caused by excessive dosing include penicillin-related neurotoxicity (e. Decreased drug metabolism or clearance may be due to impaired hepatic or renal function. For example, penicillin G neurotoxicity may be precipitated by aminoglycoside-induced renal failure. Side effects reflect the large number of adverse reactions that are neither immunologically mediated nor related to toxic levels of the drug. This review describes adverse reactions and important drug interactions involving antibiotics. It concentrates on those agents likely to be used in critical care and is not encyclopedic. This article only briefly discusses antiretroviral drugs and antibiotic dosing; it does not address issues specific to pregnant or pediatric patients. In the critical care setting, these reactions may be masked by underlying conditions or other therapies. While anaphylaxis can be precipitated by antigen–antibody complexes, it is usually IgE mediated. The binding of antibiotic epitopes to specific preformed IgE antibodies on the surface of mast cells results in the release of histamine and other mediators that lead to the aforementioned clinical presentations. Conversely, only 10% to 20% of patients who claim to have an allergy to penicillin are truly allergic as determined by skin testing (10). Fifty percent of patients with a positive skin test will have an immediate reaction when challenged with penicillins (11). Approximately 4% of patients with a history of penicillin allergy who test positive to penicillin will experience a reaction (only rarely anaphylaxis) when given a cephalosporin (12). First-generation cephalosporins and cefamandole share a side chain similar to the chain present in penicillin and amoxicillin, and there is an increased risk of allergic reactions to these cephalosporins in penicillin- allergic patients. Other second-generation and third-generation cephalosporins have differ- ent side chains than penicillin and amoxicillin; a recent meta-analysis found no increased risk of allergic reactions to these cephalosporins in penicillin-allergic patients when compared with patients without a penicillin allergy (13). While early studies concluded that there is an increased risk of reactions in penicillin-allergic patients given carbapenems, recent studies have demonstrated that administering meropenem and imipenem to these patients is safe (14–17). Aztreonam can be given safely to patients with a history of anaphylaxis to all b-lactams except ceftazidime (9). A cohort study of patients receiving oral erythromycin found a two-fold increased risk of sudden death in patients receiving this macrolide (19). Myocardial depression, hypotension, and sudden death have been reported with vancomycin use, generally in the setting of rapid administration in the perioperative period (20,21). Similarly, rapid administration of amphotericin B has been associated with ventricular fibrillation and asystole, especially in patients with renal dysfunction (22). Mechanisms include decreased glomerular filtration, acute tubular necrosis, interstitial nephritis, and crystallization of the drug within the tubules. With regard to antibiotics, the aminoglycosides Adverse Reactions to Antibiotics in Critical Care 545 and amphotericins are the prototypical classes associated with acute renal failure; the availability of drugs with similar spectrums of activity that are significantly less likely to cause acute renal failure is the major reason that use of these drugs has markedly declined in the last two decades. As with other antibiotic-associated adverse reactions, the likelihood of antimicrobial-induced nephrotoxicity is greater in patients with conditions or on medications that independently cause this complication. Depending upon the criteria used to define acute renal failure, aminoglycoside-induced nephrotoxicity occurs in 7% to >25% of patients who receive these drugs (24). It usually results from tubular epithelial cell damage and presents as acute tubular necrosis. When using a small change in serum creatinine as the criterion for renal dysfunction (22) one study found that gentamicin (26%) is more nephrotoxic than tobramycin (12%) and that nephrotoxicity usually becomes evident between 6 and 10 days after starting the aminoglycoside. Aminoglycoside-induced acute tubular necrosis is usually non-oliguric and completely reversible. However, occasional patients require temporary dialysis and a rare patient requires chronic dialysis. Factors that contribute to aminoglycoside-induced nephrotoxicity include dose, duration of treatment, use of other tubular toxins (26), and elevated trough aminoglycoside levels (25). Even patients with peak and trough levels within recommended ranges can develop nephrotoxicity. Meta-analyses (27,28) and prospective evaluation (29) have demonstrated that once a day dosing of an aminoglycoside in immunocompetent adults with normal renal function is effective treatment for infections caused by gram-negative bacilli (employing bacteriologic cure as an end point) and is less toxic than traditional multiple daily dosing. Vancomycin can also cause renal tubular injury; the larger vancomycin doses currently recommended for treatment of pneumonia and bacteremia are associated with an increased incidence of nephrotoxicity (30). Until recently, amphotericin B was the drug of choice for severe fungal infections due to Candida or Aspergillus. Amphotericin B can affect the renal tubules, renal blood flow, or glomerular function; renal dysfunction is seen in at least 60% to 80% of patients who receive this drug (31). However, renal dysfunction is usually transient, and few patients suffer serious long-term renal sequelae. Rarely, irreversible renal failure develops when the agent is used in high doses for prolonged periods (32). Risk factors for amphotericin B toxicity include abnormal baseline renal function, daily and total drug dose, and concurrent use of other nephrotoxic agents (e. However, some studies have not found that other drugs enhance amphotericin B-induced nephrotoxicity (22). Reversing sodium depletion and optimizing volume status prior to infusing the drug can decrease the risk of amphotericin B-induced nephrotoxicity (31,34). Liposomal preparations of amphotericin B are associated with a lower risk of nephro- toxicity compared with the parent compound. Methicillin was the first antibiotic shown to be associated with interstitial nephritis (35); nephritis can also be caused by numerous other b-lactams (36), usually following prolonged and/or high-dose therapy. Historically, renal failure was believed to be acute in onset and associated with fever, chills, rash, and arthralgias. However, the presentation of antibiotic-induced interstitial nephritis can be variable, and it should be suspected in any patient on a potentially offending agent who develops acute renal dysfunction. Urinary eosinophilia supports the diagnosis, but is present in less than half of the patients. Discontinuation of the offending agent generally reverses the process and permanent sequelae are unusual. Sulfonamides, acyclovir, and ciprofloxacin can crystallize in the renal tubules causing acute renal failure (37).

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Quest Diagnostics has licensed the heteroduplex tracking technology used in SensiTrop test and is developing a validated test based on this purchase fildena with amex erectile dysfunction treatment miami. There are a number of pharmacogenetic determinants of antiretroviral drug exposure buy cheap fildena 100 mg impotence drug, toxicity, and activity. Several prospective clinical trials and cohort studies have identified a number of associations between human genetic variants, drug metabolism and toxicity. ViroSeq’s high throughput processing provides an integrated system from sample preparation to the final interpretive resistance report to aid in treatment decisions. While such testing is rou- tine in Western countries and used repeatedly over the course of treatment to see if interventions are effective it is unavailable to many people in the developing world, especially in rural areas. Accordingly, combination therapies have been used to address the rapidly evolving virus. Both approaches share the requirement for a considerable increase in the number of protease mutations to lead to clinical resistance, thereby increasing the genetic barrier. Most reports on drug resistance deal with subtype B infections in developed countries. The addition of new drugs to the existing therapeutic arsenal will improve treatment options and clinical pros- pects particularly for those patients failing current drug regimens based primarily on combinations of reverse transcriptase and protease inhibitors. The large number of therapy options makes it difficult to select an optimal ther- apy, particularly in patients that develop resistance to some drugs. Universal Free E-Book Store Personalized Management of Viral Infections 399 1 2 3 Patient Viral load measurement Genome sequencing 4a 4b 4c Via rule-based system Via mutation table Via statistical model 5 Resistance profile 6 7 Additional information on patient Therapy prediction engine 9 8 Manual therapy selection Therapy ranking Fig. In the case of anticipated therapy change the viral genome is sequenced from the patient’s blood serum (3). Interpretations of the viral genome sequence is effected either manually using a mutation table (4a), or via a rules-based system (4b), or with a statistical model derived from clinical resistance data (4c). The interpretation results in a resistance profile (5) that is quali- tative in the first two cases and quantitative when using statistical models. In doing so, additional information on the patient is also taken into account (patient history, habits, drug side effects, etc. Therapy prediction engines (7) can assist this process by a quantitative analysis that yields a list of therapies ranked by their likelihood of success (8) (Source: Lengauer et al. Additionally, by examining patient samples taken at different time points, it is also possible to determine how previously rare mutations became more common. However, short-read approaches lose the linkage relationship between the mutations although they can detect multiple mutations, but not whether they were all in one strain or housed among a few strains circulating in the patient. Reads longer than 10 kilobases are common, and efforts are being made to further increase the average read length. Knowing which mutations are present and their phasing information can help clinicians decide upon a drug treatment regimen for the patient. Different drugs might be needed to target a virus strain with two mutations as compared to two strains with one mutation each. The combination test is performed from the same blood sample and the results are in one report. The patient virus is also sequenced, with the genotypic data provided alongside the susceptibility results. Finally, it measures the ability of the viral protease and reverse transcriptase to drive replication – known as replication capacity, one component of viral fitness. Further studies on the development of newer molecular methods for a better management of chronic hepa- titis B will minimize morbidity (Chakravarty 2012 ). With the increasing progress in nucleic acid technologies, investigation of viral genetic biomarkers may be integrated in clinical diagnostic routine. It is offered as a web-based deci- sion support tool to assist physicians to optimize and individualize the treatment schedule of patients with chronic hepatitis B. The complications of chronic hepatitis C, including cirrhosis and hepatocellular carci- noma, are expected to increase dramatically world-wide over the next 10–20 years. Liver biopsy provides valuable information about the baseline severity and subsequent progression of hepatitis C. Severe fibrosis or cirrhosis on the pre-treatment liver biopsy is associ- ated with decreased response rates. Response rates to currently approved therapies also vary by genotype, with genotype 2 and 3 patients enjoying a 76 % response rate to the current standard of care while patients with genotype 1a and 1b have only a 46 % response to the current standard of care. In addition to limited efficacy, treatment is often poorly tolerated because of side effects that prevent some patients from completing therapy. For these reasons, identification of a biomarker of response to treatment is a high priority. Poor response rate across Hispanics of all nationalities indicates that strategies to improve the sustained virologic response in Latinos are needed. Almost 80 % of those with the favorable response genotype eradicated the virus, while only about 30 % with the less favorable response genotype did so. Because the genotype leading to better response is in substantially greater frequency in European than African popu- lations, this genetic polymorphism also explains approximately half of the differ- ence in response rates between African-Americans and patients of European ancestry. Unexpectedly though, the authors reported that the C alleles actually appeared to be linked to higher rather than lower baseline viral loads. Genotype non-1 and a low viral load are the most sig- nificant pre-treatment indicators of sustained virologic response. Covarying positions were common and linked together into networks that differed by response to therapy. Using this analysis to detect patterns within the networks, the authors could predict the outcome of therapy with >95 % coverage and 100 % accuracy, raising the possibility of a prognostic test to reduce therapeutic failures. Furthermore, the hub positions in the networks are attractive antiviral tar- gets to suppress evolution of resistant variants. Lab21 is developing proprietary new assays to monitor the emergence of these genotypic variants. A high-throughput “massively parallel sequencing” approach followed by individual genotyping has been used to identify new, highly sensitive genetic predictors of drug response (Smith et al. Compared with previous results, the genetic variants identified through this analysis were shown to predict failure to respond with high sensitivity and specificity. By predicting which patients are unlikely to respond to the standard treatment, clinicians would be able to make an informed choice about which patients should be offered newly emerging therapies. Roche Diagnostics is partnering with three Spanish entities, including two research institutes and the software developer Advance Biological Laboratories Universal Free E-Book Store Personalized Management of Fungal Infections 405 Therapy Edge Spain to develop personalized antiviral treatment strategies for patients with chronic hepatitis C or B. Other partners include the Vall d’Hebron Institute of Research and the Networking Biomedical Research Centre in Liver and Digestive Diseases, which is comprised of eight research groups. Roche will use its 454 sequencing systems and bioinformatics analysis, coupled with other genetic and molecular analysis techniques, to apply massively parallel sequencing in developing personalized antiviral treatments for chronic sufferers.

For some variables proven fildena 100 mg impotence cures, the goal is to have as low a raw score as possible (for example fildena 25 mg with amex erectile dysfunction psychological causes treatment, errors on a test). Only when the underlying raw score distribution is normal will its z-distribution be normal. Whether the standard deviation in the raw scores is 10 or 100, it is still one standard deviation, which transforms into an amount in z-scores of 1. Now you can see why z-scores are so useful: All normal z-distributions are similar, so a particular z-score will convey the same information in every distribution. There- fore, the way to interpret the individual scores from any normally distributed variable is to envision a z-distribution similar to Figure 6. Then, for example, if we know that z is 0, we know that the corresponding raw score is at the mean (and at the median and mode). Therefore, approximately 68% of the scores on any nor- mal distribution will be between the z-scores at ;1. Likewise, any other z-score will always be in the same relative location, so if z is 1. But, if z is 13, then, like Biff’s, the raw score is one of the highest possible scores in the upper tail of the distribution, having a low frequency, a low relative frequency and a very high percentile. As you’ll see in the following sections, in addition to describing relative standing as above, z distributions have two additional uses: (1) comparing scores from different distributions and (2) computing the relative frequency of scores. Say that Cleo received a grade of 38 on her statistics quiz and a grade of 45 on her English paper. These scores reflect different kinds of tasks, so it’s like comparing apples to oranges. Then we can compare Cleo’s relative standing in English to her relative standing in statistics, so we are no longer comparing apples and oranges. Note: The z-transformation equates or standardizes different distributions, so z-scores are often referred to as standard scores. Thus, Cleo did relatively better in statistics because she is farther above the statistics mean than she is above the English mean. Another student, Attila, obtained raw scores that produced z 522 in statistics and z 521 in English. His z-score of 21 in English is rel- atively better, because it is less distance below the mean. However, z-scores always increment by one standard deviation, whether it equals 5 points in statistics or 10 points in English. Therefore, the spacing of the z-scores is the same for the two classes and so they are comparable. Now we can see that Cleo scored better in statistics than in English but that Attila scored better in English than in statistics. Recall that relative frequency is the proportion of time that a score occurs, and that rel- ative frequency can be computed using the proportion of the total area under the curve. We can use the z-distribution to determine relative frequency because, as we’ve seen, when raw scores produce the same z-score they are at the same location on their distri- butions. By being at the same location, a z-score delineates the same proportion of the curve, cutting off the same “slice” of the distribution every time. Thus, the relative fre- quency at particular z-scores will be the same on all normal z-distributions. For example, 50% of the raw scores on a normal curve are to the left of the mean, and scores to the left of the mean produce negative z-scores. Having determined the relative frequency of the z-scores, we work backwards to identify the corresponding raw scores. In the English distribution, students having negative z-scores have raw scores between 10 and 40, so the relative frequency of these scores is. Similarly, approximately 68% of the scores always fall between the z-scores of 11 and 21. Working backwards to the raw scores we see that sta- tistics grades between 25 and 35 constitute approximately 68% of the statistics distribution, and English grades between 30 and 50 constitute approximately 68% of the English distribution. The same will be true for a distribution of running speeds, a distribution of personality test scores, or for any normal distribution. We can also use z-scores to determine the relative frequency of scores in any other portion of a distribution. The Standard Normal Curve Because all normal z-distributions are similar, we don’t need to draw a different z-distribution for every set of raw scores. Instead, we envision one standard curve that, in fact, is called the standard normal curve. The standard normal curve is a perfect normal z-distribution that serves as our model of any approximately normal z-distribu- tion. It is used in this way: Most data produce only an approximately normal distribu- tion, producing a roughly normal z-distribution. However, to simplify things, we operate as if the z-distribution always fits one, perfect normal curve, which is the stan- dard normal curve. We use this curve to first determine the relative frequency of partic- ular z-scores. Then, as we did above, we work backwards to determine the relative frequency of the corresponding raw scores. This is the relative frequency we would expect, if our data formed a perfect normal distribution. Usually, this provides a reason- ably accurate description of our data, although how accurate we are depends on how closely the data conform to the true normal curve. Therefore, the standard normal curve is most accurate when (1) we have a large sample (or population) of (2) interval or ratio scores that (3) come close to forming a normal distribution. The first step is to find the relative frequency of the z-scores and for that we look at the area under the standard normal curve. Statisticians have already determined the pro- portion of the area under various parts of the normal curve, as shown in Figure 6. The numbers above the X axis indicate the proportion of the total area between the z-scores. The numbers below the X axis indicate the proportion of the total area between the mean and the z-score. The range is roughly between zs of ;3, a distance of six times the standard deviation. If the range is six times the standard deviation, then the stan- dard deviation is one-sixth of the range. Most often we begin with a particular raw score in mind and then compute its z-score (using our original z-score formula).

By H. Vibald. Northeastern University.

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