Search

Shoaling behaviour is commonly displayed by fishes and is thought to reduce predation and increase foraging efficiency. Shoaling relies on coordination between individuals, with higher cohesion and alignment among individuals within a shoal providing greater net benefits of this behaviour. Whilst single species often shoal together in conspecific groups, mixed-species shoaling is frequently observed and has been identified as an important determinant of individual fitness for the multiple species involved. Despite their prevalence, the structure of mixed-species shoals and the mechanisms by which individuals gain protection from predators and enhance their foraging efficiency are not as well understood as for single-species shoals. In fact, mixed-species shoals may be less coordinated than single-species shoals, raising the intriguing question of why fishes form mixed-species shoals when this behaviour could be less beneficial than single-species shoaling. Here we used in situ stereo-video techniques to compare within and between shoal differences in cohesion and alignment, for mixed- and single-species shoals containing the tropical vagrant Indo pacific sergeant major damselfish, Abudefduf vaigiensis, in temperate waters. As expected, mixed-species shoals were less aligned than single-species shoals. However, within mixed-species shoals conspecifics were more cohesive and aligned than were heterospecifics, suggesting coordinated single-species subgroups formed within larger mixed-species shoals. The formation of subgroups may mitigate costs associated with differences between species, therefore enhancing benefits of mixed-species shoaling. As such, multiple levels of social structure may exist within mixed-species shoals that could facilitate growth and survival for vagrant A. vaigiensis in temperate regions. More broadly, this research highlights the importance of considering detailed internal structures of mixed-species shoals when trying to understand cost–benef

OBJECTIVE - Cardiovascular fitness (VO2max) and physical activity arc both related to risk of Metabolic disease. It is unclear, however, whether the metabolic effects of sedentary living are the same in fit and unfit individuals. The purpose of this study was, therefore, to describe the association between physical activity and the metabolic syndrome and to test whether fitness level modifies this relationship. RESEARCH DESIGN AND METHODS - physical activity Was measured objectively using individually calibrated heart rate against energy expenditure. VO2max was predicted front a submaximal exercise stress test. Fat mass and fat-free mass (FFM) were calculated using impedance biometry. A metabolic syndrome score was computed by summing the standardized values for obesity, hypertension, hyperglycemia, insulin resistance, hypertriglyceridemia, and the inverse level of HDL cholesterol and was expressed as a continuously distributed Outcome. To correct for exposure measurement cri-or, a random subsample (22\% of cohort) re-attended for three repeat measurements in the year following the first assessment. RESULTS - The relationship of VO2max (ml O-2 (.) kg(FFM)(-1) (.) min(-1)) and the metabolic syndrome score was of borderline significance after adjusting for age, sex, physical activity, and measurement error (beta = -0.58, P = 0.06). The magnitude of the association between physical activity (kJ (.) d(-1) (.) kg(FFM)(-1)) and the metabolic syndrome was more than three tunes greater than for VO(2ma)x (standardized beta = - 1,83, P = 0.0042). VO2max however, modified the relationship between physical activity energy expenditure and metabolic syndrome (P = 0 036). CONCLUSIONS - This study demonstrates a Strong inverse association between physical activity and metabolic syndrome, an association that is much steeper in unfit individuals. Thus, prevention of metabolic disease may be most effective In the subset of unfit inactive people.

The design of studies aimed at identifying the interaction between genetic and environmental determinants in disease risk is attracting increased attention. In this paper, we study the effect of errors on measuring exposures and the effect of assessing genotype at one locus on the association of a continuous outcome measure with continuous exposures and genotype. The estimation of misclassification errors in assessing genotypes from a separate study is proposed. If the exposure measurement error is substantial, then even relatively small errors in genotyping within limits that are often quoted can have an appreciable effect on interaction estimates. We, thus, consider a method for correcting the measurement errors when the interaction between the exposures and the genetic factor is significant. Finally, we present an epidemiological example to demonstrate the importance of correcting measurement errors. Copyright (C) 2004 John Wiley Sons, Ltd.

The combination of heart rate (HR) monitoring and movement registration may improve measurement precision of physical activity energy expenditure (PAEE). Previous attempts have used either regression methods, which do not take full advantage of synchronized data, or have not used movement data quantitatively. The objective of the study was to assess the precision of branched model estimates of PAEE by utilizing either individual calibration (IC) of HR and accelerometry or corresponding mean group calibration (GC) equations. In 12 men (20.6 - 25.2 kg/m(2)), IC and GC equations for physical activity intensity (PAI) were derived during treadmill walking and running for both HR ( Polar) and hip-acceleration [ Computer Science and Applications (CSA)]. HR and CSA were recorded minute by minute during 22 h of whole body calorimetry and converted into PAI in four different weightings (P1-4) of the HR vs. the CSA (1- P1-4) relationships: if CSA > x, we used the P1 weighting if HR > y, otherwise P-2. Similarly, if CSA less than or equal to x, we used P-3 if HR > z, otherwise P-4. PAEE was calculated for a 12.5-h nonsleeping period as the time integral of PAI. A priori, we assumed P-1 = 1, P-2 = P-3 = 0.5, P-4 = 0, x = 5 counts/min, y = walking/ running transition HR, and z = flex HR. These parameters were also estimated post hoc. Means +/- SD estimation errors of a priori models were - 4.4 +/- 29 and 3.5 +/- 20\% for IC and GC, respectively. Corresponding post hoc model errors were - 1.5 +/- 13 and 0.1 +/- 9.8\%, respectively. All branched models had lower errors ( P less than or equal to 0.035) than single-measure estimates of CSA ( less than or equal to - 45\%) and HR ( greater than or equal to 39\%), as well as their nonbranched combination ( greater than or equal to 25.7\%). In conclusion, combining HR and CSA by branched modeling improves estimates of PAEE. IC may be less crucial with this modeling technique.

Leptin is secreted by adipose tissue and acts upon receptors located in the hypothalamus to modify energy balance. Investigations of the relationship between leptin and physical activity energy expenditure (PAEE) at population level are scarce. The majority of studies addressing this topic are limited by their measurement of PAEE (i.e. questionnaires or ecological comparisons between rural and urban ethnic groups). To our knowledge, no studies have directly examined the relationship of objectively assessed PAEE and leptin in a large free-living population-based cohort. Therefore, we measured fasting plasma leptin and insulin concentrations, cardiorespiratory fitness ((V) over dot O-2max,O-pred), PAEE, and body composition in 758 Caucasian people (aged 40-65 yr). In sex-combined multiple regression analyses, leptin was significantly associated with PAEE (beta = -0.19, P = 0.0027), but not with (V) over dot O-2max,O-pred (beta = -0.0002, p = NS). The association between PAEE and leptin was significant in men when adjusted for percentage of body fat (beta = -0.28, P = 0.004) but not women (beta = -0.12, P = 0.18) but was significant in both men and women when adjusted for body mass index (men: beta = -0.28, P = 0.005; women: beta = -0.23, P = 0.01; combined: beta = -0.26, P = 0.00008). These data suggest the existence in this population of an independent inverse association between PAEE and fasting plasma leptin level.

Additive regression models have turned out to be useful statistical tools in the analysis of high-dimensional data. The attraction of such models is that the additive component can be estimated with the same optimal convergence rate as a one-dimensional nonparametric regression. However, this optimal property holds only when all the additive components have the same degree of "homogeneous" smoothness. In this paper, we propose a two-step wavelet thresholding estimation process in which the estimator is adaptive to different degrees of smoothness in different components and also adaptive to the "inhomogeneous" smoothness described by the Besov space. The estimator of an additive component constructed by the proposed procedure is shown to attain the one-dimensional optimal convergence rate even when the components have different degrees of "inhomogeneous" smoothness.

The wavelet threshold estimator of a regression function for the random design is constructed. The optimal uniform convergence rate of the estimator in a ball of Besov Space B-p, q(s) is probed under general assumptions. The adaptive wavelet threshold estimator with near-optimal convergence rate in a Aide range of Besov scale is also constructed. (C) 2001 Elsevier Science.

The actual effect of ethylene on shoot gravitropic response has been controversial. To elucidate the role of ethylene in the modulation of shoot gravitropic response, Arabidopsis inflorescences and light-grown seedlings were pretreated with 0.1-10 muL L-1 of ethylene for either a long (12-48 h) or short term (0.5 h). When the gravicurvature was measured either in air or in ethylene, it was found that prolonged exposure to various levels of ethylene stimulated both inflorescence stem and hypocotyl gravicurvature in air, while the continued presence of ethylene immediately following reorientation of plant tissues inhibited gravicurvature of both tissues. Both stimulatory and inhibitory effects existed in inflorescence stems and hypocotyls when the plant tissues were exposed to a chosen concentration of ethylene. Stimulation by ethylene was stronger than its inhibition in inflorescence stems, while the reverse was true for the hypocotyls. Therefore, the continued presence of high levels of naturally produced ethylene in eto1-1 did not suppress the faster gravicurvature of inflorescence stems, whereas the removal of exogenously applied ethylene was necessary to observe faster gravicurvature of both the wild-type and eto1-1 hypocotyls. Both effects acted through the known ethylene receptor complex. These results strongly suggest that ethylene of a chosen concentration has opposing effects on the negative gravitropic responses of both inflorescence stems and hypocotyls. The ultimate negatively gravitropic behaviour of a plant tissue, when exposed to ethylene, depends on the dynamic interplay between these two opposing effects.

The fasting concentration of non-esterified fatty acids (NEFA) and the degree to which it declines during an oral glucose tolerance test are closely associated with insulin resistance and glucose intolerance. However, relatively few studies have described possible environmental determinants of NEFA concentrations. Physical activity is likely to be related to NEFA levels, but habitual activity level is difficult to quantify in epidemiological studies. In particular, it is unclear whether NEFA is more closely related to cardio-respiratory fitness or to habitual energy expenditure. In order to quantify these relationships, we analysed data from the Ely prospective population-based study in which 931 subjects underwent a glucose tolerance test with measurements of cardio-respiratory fitness and 4 d energy expenditure by heart-rate monitoring, a technique previously validated against whole-body calorimetry and doubly-labelled water. In order to estimate the latent variables of usual fitness and energy expenditure, a subset of 190 subjects underwent repeat testing on three further occasions over 1 year. In analyses adjusting only for age and sex, energy expenditure and cardio-respiratory fitness were both negatively correlated with the total area under the NEFA curve following the oral glucose load (standardised beta coefficients -0.030 and -0.039 respectively; both P<0.001) However, further adjustment for degree of obesity and bivariate measurement error suggested that the effect of energy expenditure was significantly greater than that for fitness (-0.047 and -0.005 respectively). These results suggest that the area under the NEFA curve in the oral glucose tolerance test, a measure of insulin sensitivity, is strongly associated with the habitual level of physical activity.

A test of the independence of two sets of variables is developed to have high power against a special family of dependence. In this each set of variables has the structure of a single factor model and the dependence is solely via the correlation gamma between the underlying latent variables. This is a model with only one nonzero canonical correlation. It is shown that a test based on the maximum likelihood estimate of gamma is appreciably more powerful than that based on r(1), the largest sample canonical correlation. If, however, the model is used, not just as a family of alternatives but as the basis for interpretation, and if substantial cross-correlation is present then the procedure is essentially equivalent to the use of r(1). (C) 2001 Academic Press.

Several methods for testing the difference between two group means of k independent populations are compared. Simulation shows that the likelihood ratio test with the Bartlett correction factor and the t test with appropriate degrees of freedom perform better, particularly when the sample size is small. However, the latter is very good for all configurations.

Background Previous studies have demonstrated an association between physical inactivity and hypertension, but the methods used to assess activity have been subjective and imprecise. Recently methods have become available allowing measurement of energy expenditure in free-living populations. Our aim was to employ these methods to assess the independent association between energy expenditure, cardio-respiratory fitness and blood pressure. Methods In a cross-sectional study of 775 people (45-70 years) participating in a continuing population-based cohort study, energy expenditure was assessed by 4 days of heart rate monitoring with individual calibration of the relationship between heart rate and energy expenditure, a method validated against doubly-labelled water and whole body calorimetry. Cardio-respiratory fitness was assessed in a sub-maximal test. To adjust for measurement error in the assessment of usual energy expenditure and fitness, 190 subjects repeated both tests on three further occasions at 4-monthly intervals. Results A highly significant linear trend in blood pressure was found across quintiles of the physical activity level, the ratio of total energy expenditure to basal metabolic rate. The differences in the mean systolic/diastolic blood pressure between the top and bottom quintile was 6.3/4.4 mmHg in men and 10.7/5.9 mmHg in women. These effects were independent of obesity and cardio-respiratory fitness. Correction for measurement error suggests that the true underlying relationship between usual energy expenditure and blood pressure is stronger still. Conclusions These findings are compatible with a strong association between usual energy expenditure and blood pressure and support public health strategies aimed at increasing overall energy expenditure.

Glucose intolerance and diabetes mellitus are associated with physical inactivity, but it is unclear whether preventive interventions should aim at increasing overall energy expenditure or increasing participation in vigorous, fitness-enhancing activities. Studies aimed at separating and quantifying the effects of these two dimensions of physical activity should use well-validated measurement instruments and employ a study design in which the bivariate error structure of these instruments is determined. In the Isle of Ely Study (Cambridgeshire, United Kingdom), 775 individuals aged 45-70 years in 1994-1997 completed a glucose tolerance test and assessment of 4-day physical activity level (total energy expenditure/basal metabolic rate) by heart rate monitoring, a technique that has been validated against doubly labeled water and whole-body calorimetry. Cardiorespiratory fitness (maximum oxygen uptake (VO2max) per kg)) was measured in a submaximal test. To correct for measurement error, the authors had 190 individuals repeat both tests on three occasions at 4-month intervals. Two-hour glucose level was negatively correlated with physical activity level (men: r = -0.22, p < 0.001; women: r = -0.11, p < 0.05) and VO2max per kg (men: r = -0.18, p < 0.01; women: r = -0.19, p < 0.001) and was positively correlated with age and obesity. The model incorporating bivariate adjustment for measurement error showed that energy expenditure had a major effect on glucose tolerance, but there was less of an effect for cardiorespiratory fitness. These data provide support for public health strategies aimed at increasing overall energy expenditure.

It is becoming standard practice in epidemiology to adjust relative risk estimates to remove the bias caused by non-differential errors in the exposure measurement. Estimation of the correction factor is often based on a validation study incorporating repeated measures of exposure, which are assumed to be independent. This assumption is difficult to verify and often likely to be false. We examine the effect of departures from this assumption on the correction factor estimate, and explore the design of validation studies using two or even three different types of measurement of exposure, where assumption of independence between the measures may be more realistic. The value of good biomarker measures of exposure is demonstrated even if they are feasible to use only in a validation study. Copyright (C) 1999 John Wiley & Sons, Ltd.

The bias in relative risk estimates caused by errors in measurement of the relevant exposure is being increasingly recognized in epidemiology. Estimation of the necessary correction factor to remove this bias for univariate exposure has been considered in an earlier paper. We consider here the multivariate situation in which non-differential errors in measurement can lead to incorrect identification of the variable most closely associated with disease. Estimation of the necessary correction factor when the true exposure is unobservable necessarily requires assumptions. We explore the robustness of the estimation to departures from a range of assumptions. The value of good biomarkers is demonstrated. We present a bivariate example in which failure to take account of measurement error leads to the incorrect exposure being identified as the important determinant of disease risk. Copyright (C) 1999 John Wiley & Sons, Ltd.

Systemic corticosteroids prescribed for treatment of pulmonary diseases in preterm, very low birth weight infants caused severe suppression of the hypothalamic-pituitary- adrenal axis and produced serious physiological and metabolic disturbances. However, the effect of inhaled corticosteroids on their pituitary-adrenal functions is not known. We prospectively evaluate the pituitary-adrenal function using the human CRH stimulation test in a cohort of very low birth weight infants at risk for hypothalamic-pituitary-adrenal axis suppression in a double blind, randomized pilot study designed for assessing the efficacy and adverse effects of inhaled fluticasone propionate in newborn preterm infants who required mechanical ventilation for treatment of respiratory distress syndrome. Twenty-five preterm (<32 gestational weeks), very low birth weight (<1500 g) infants were randomized to receive inhaled fluticasone propionate (n = 13) or a placebo inhaler (n = 12). The medication was given every 12 h (fluticasone propionate, 1,000 mu g/day) for 14 days. All surviving infants had their pituitary-adrenal functions assessed by human CRH test on the following morning immediately after completion of the 2-week course. All basal (0 min) and poststimulation (15, 30, and 60 min) plasma ACTH and serum cortisol concentrations were significantly suppressed in the inhaled fluticasone group compared to their corresponding levels in the placebo group [basal plasma ACTH concentrations (F = 6.0; P = 0.02), post;stimulation plasma ACTH concentrations (F > 8.6; P < 0.01), basal serum cortisol concentrations (F = 5.6; P = 0.03), and poststimulation serum cortisol concentrations (F > 15.6; P < 0.001)]. This is the first study in very low birth weight infants that demonstrates unequivocally that cumulative high dose inhaled corticosteroids can induce moderately severe suppression of both the pituitary and adrenal glands. The systemic bioactivity is probably associated with pulmonary vascular abso

It is known that ratios of regression coefficients have an interpretation more stable under model perturbation than regression coefficients themselves. This is explored in more detail for a special case of linear and log linear regression.

Objectives: A prospective study comparing the efficiacy and side-effects of oral sulindac with intravenous indomethacin in clinically stable preterm infants (<1750 g) requiring non-invasive closure of haemodynamically significant patent ductus arteriosus. Methodology: As maturity and birthweight are the two major determinants of ductal closure, infants were matched as closely as possible for these parameters. An eligible patient was first assigned to the sulindac group and a subsequent patient with similar gestational age (+/-1 week) and birthweight (+/- 100 g) to the previously recruited infant would automatically receive indomethacin. A total of eight infants were enrolled in each group, Results: The ductus arteriosus was successfully closed in all eight infants receiving indomethacin, and in seven of eight infants receiving sulindac. No significant differences were found with regards to the ductal size between the two groups at diagnosis or on each of the consecutive days of treatment (P>0.25). More renal adverse effects were encountered in the indomethacin group. Significant differences in changes from baseline value for urine output, plasma sodium, urea and creatinine concentrations were noted at 24, 48 and 72 h after commencement of treatment between the two groups (P<0.05). All the parameters returned to normal or pre-treatment levels 48 h after stopping therapy. Unexpectedly, severe gastrointestinal complications were encountered in the sulindac group. Conclusions: Sulindac is capable of promoting ductal constriction in clinically stable preterm infants without compromising the renal function. The spectrum of gastrointestinal complications observed in sulindac treated infants were similar to those described for indomethacin. The use of sulindac for ductal closure in the preterm infant should remain experimental.

Antenatal corticosteroids have been widely used for the prevention of respiratory distress syndrome in preterm neonates, yet little is known about their effects on the hypothalamic-pituitary-adrenal axis in these infants. We prospectively evaluated pituitary-adrenal function in 61 preterm (<32 gestational weeks), very low birth weight (<1500 g) infants on days 7 and 14 of life using the human CRH stimulation test. The baseline and poststimulation plasma ACTH and serum cortisol concentrations did not differ significantly between infants whose mothers received no antenatal corticosteroids, and those whose mothers received 1-2 doses or >2 doses (mean 7.2 doses) of prenatal dexamethasone (P = > 0.12). The number of doses of dexamethasone and the time intervals between the last dose of drug and delivery did not significantly affect the pituitary-adrenal responsiveness on days 7 and 14 of life. Among infants who did not require mechanical ventilation at the time of the human CRH test, significantly higher plasma ACTH (P < 0.014) and lower serum cortisol concentrations (P < 0.02) were found on day 14 than on day 7. In contrast, none of the poststimulation hormone concentrations were significantly different in ventilated infants between days 7 and 14. The relationship between the blood hormone concentrations in each time epoch (day 7 and day 14) and possible confounding factors including gestational and postconceptional age, birth weight, sex, Apgar scores, mode of delivery, single or higher order births, and mode of ventilation were determined. Plasma ACTH concentrations on day 7 were found to be significantly higher in ventilated than in nonventilated infants (P = 0.006). However, none of the aforementioned factors correlated significantly with plasma ACTH concentrations on day 13. Serum cortisol concentrations on day 7 were significantly higher in infants of greater gestational age (P = 0.039) and birth weight (P = 0.013), with lower Apgar scores at 1 and 5 min (P = 0.02

To evaluate the pituitary-adrenal reserve and to standardize the methodology of performing the human CRH (hCRH) stimulation test, we performed the hCRH test on 14 preterm (<32 gestational weeks), very low birth weight infants, who did not receive antenatal or postnatal corticosteroid treatment, on days 7 and 14 of life. Blood samples were obtained 0 (baseline), 15, 30, and 60 min after an iv dose of hCRH (1 mu g/kg). The plasma ACTH concentration rose from a basal value of 5.7 +/- 0.6 pmol/L (mean +/- SEM) to 11.9 +/- 2.1 pmol/L (P < 0.005), 9.2 +/- 1.2 pmol/L (P < 0.005), and 7.7 +/- 0.8 pmol/L (P < 0.005) at 15, 30, and 60 min, respectively. The corresponding rises in serum cortisol fi om a basal concentration of 396 +/- 67 nmol/L were 509 +/- 71 nmol/L (P < 0.0001), 647 +/- 62 nmol/L (P < 0.0001), and 578 +/- 60 nmol/L (P < 0.0001). The plasma ACTH concentration consistently peaked early at 15 min; whereas the maximum cortisol response occurred 30 min post-hCRH stimulation. No significant differences were detected between the hCRH tests performed on days 7 and 14 (P > 0.15). Mechanical ventilation, infant gender, and mode of delivery did not significantly influence the hormonal responses (P > 0.25). We have defined in this study the pattern, the magnitude of the pituitary-adrenal response, and the timing of the peak concentrations of plasma ACTH and serum cortisol in relation to a standard iv dose of hCRH. The hCRH test in very low birth weight infants appears to be safe and reproducible, and produces a pituitary-adrenal response comparable to that seen in older children and adults, indicating that pituitary-adrenal function is mature at these early stages of gestation.

High dose dexamethasone is frequently used for the treatment of neonatal respiratory conditions and to facilitate weaning from mechanical ventilation in preterm, very low birth weight infants. However, very little is known about the severity, site, and duration of steroid-induced hypothalamic-pituitary-adrenal axis suppression in this category of patients. Twenty-three preterm, very low birth weight infants who received a full 3-week dose-tapering course of dexamethasone were prospectively studied, with a human CRH stimulation test performed at three different times: before the start of steroid treatment (week 0), immediately after the course (week 3), and 4 weeks after stopping dexa methasone (week 7). Plasma ACTH and serum cortisol concentrations were measured at 0 (baseline), 15, 30, and 60 min. Immediately after the steroid course (week 3), both basal and poststimulation plasma ACTH and serum cortisol concentrations were markedly suppressed. The hormone concentrations at 0, 15, 30, and 60 min in week 3 were significantly lower than their corresponding levels in week 0 (P < 0.0001 for both ACTH and cortisol) and week 7 (P < 0.0001 and P < 0.005 for ACTH and cortisol, respectively). In contrast, when the hormone levels in week 7 were compared to their corresponding concentrations in week 0, only the 60 min serum cortisol concentration in week 7 was significantly lower (P = 0.02). The currently used dosage of dexamethasone caused severe pituitary-adrenal suppression immediately after treatment, but substantial recovery of the endocrine axis was observed 4 weeks after discontinuation of therapy. Although the recovery appeared to be earlier with the pituitary center, both pituitary and adrenal glands were capable of mounting a biochemically adequate response to exogenous human CRH stimulation at this stage. Steroid replacement therapy may be desirable at a time of stress in the immediate posttreatment period, but it would seem unnecessary 1 month after stopping dexam

We describe an exposure of varicella tester virus in our neonatal intensive-care unit and the emergency procedures instituted to prevent an outbreak. Fifty-seven infants and 129 staff members were exposed but none developed chickenpox. The measures included rapid identification of varicella antibody status in all neonates and those staff members with uncertain history of varicella infection; cohorting of exposed infants according to immune status; and prompt administration of varicella tester immunoglobulin to susceptible patients. The recommendations of the American Academy of Pediatrics did not accurately predict the immune status of preterm infants, as only one of the eight susceptible infants would have qualified for immunoglobulin prophylaxis if their guidelines had been followed. Mass screening of all exposed infants using the varicella tester enzyme linked immunosorbent assay (ELISA) test was the only reliable means of determining the immune status. Of the four risk factors evaluated for the prediction of antibody status: gestational age, postnatal age, birthweight and episodes of blood transfusion, only postnatal age was found to independently predict the immune status of our patients. Because varicella tester susceptible staff members are difficult to identify on the basis of history, we suggest that prospective screening of staff in high-risk units be undertaken and vaccination with live varicella vaccine be offered to susceptibles.

In an earlier work, Wong [1] had developed a SAS program SLOPE for the analysis of biological assays in complete randomization design based on slope ratio method. In this paper, we discuss how to develop SAS programs to handle the statistical analysis for parallel line assays and assays based on quantal responses. These programs are capable of checking the statistical validity of an assay and estimating the potencies of test preparations relative to a standard.

SAS is a powerful statistical package but it does not cover all analyses that a user may require particularly in a specialized area such as biological assay. A SAS program SLOPE has been developed for the analysis of biological assays in complete randomization based on the slope ratio method. The program is capable of checking the statistical validity of an assay and estimating the potencies of test preparations relative to a standard. It calculates potencies and their corresponding confidence intervals for a group of bioassays where each assay has equal number of preparations. It also allows the user to produce scatter plots of response by dose.