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We investigated the reproducibility of measurements of maximal voluntary torque and maximal voluntary activation using twitch interpolation. On 5 days, each of 5 subjects performed 10 maximal voluntary isometric contractions of their elbow flexors. Single supramaximal stimuli were delivered over biceps brachii at the measured peak torque during each effort, and in the relaxed muscle 5 s later. A voluntary activation score was calculated from the size of twitches evoked by the stimuli (resolution < 0.15 Nm). Although all subjects were able to drive the stimulated elbow flexor muscles maximally in some trials, they did not do so in 75% of all contractions. Maximal voluntary torques did not vary significantly within a subject between sessions. There were consistent differences in the level of maximal voluntary activation between subjects (P < 0.01), but no differences in voluntary activation within an individual across days in 4 of 5 subjects. Failure to drive the stimulated elbow flexor muscles maximally was not associated with inadvertent co-contraction of the antagonist muscles.

BACKGROUND--To increase the sensitivity of measurements of maximal inspiratory pressure (MIP) as a test of inspiratory muscle strength and endurance, software was developed to correct for variation in lung volume. METHODS--Using a body plethysmograph to determine absolute lung volume during each manoeuvre, values for MIP were expressed as a percentage of the pressure "expected" from the unfatigued MIP/lung volume relation in each subject. RESULTS--The method reduced the variance in peak and average pressure during a series of 18 MIP manoeuvres of 10 seconds duration separated by rest intervals of 10 seconds. CONCLUSIONS--The correlation between average pressure and contraction number was improved significantly by the MIP/lung volume correction. This simple correction has many applications in measurements of the MIP.

The family support needs of parents with an intellectual disability (ID) are relatively unknown. This paper reviewed two types of intervention for parents with ID: those designed to strengthen social relationships and those teaching parenting skills. A literature search was conducted using electronic databases and a limited number of evaluative studies were found. The evidence for interventions aimed at strengthening social relationships was inconclusive; although positive changes were observed, there were limitations in study design which restricted the generalizability of the results. The evidence for parental skills teaching suggested that behavioural based interventions are more effective than less intensive forms such as lesson booklets and the provision of normal services, although these studies also had limitations. There is a need for further large scale controlled studies in this area to provide clearer evidence and to explore additional factors relating to child, parent and family which may impact on outcomes.

Respiratory pacing has advanced the long-term management of respiratory failure secondary to neurological disorders. It has an established role in curtailing invasive mechanical ventilation after upper motor neuron lesions such as spinal cord injury. There is increasing interest to expand the application of intramuscular diaphragm pacing to amyotrophic lateral sclerosis (ALS), a progressive and fatal neurodegenerative disease. Although diaphragm pacing has been offered to ALS patients, evidence-based data to determine its benefits remain lacking. The limited current literature indicates progression of respiratory dysfunction in ALS patients despite diaphragm pacing. The data from clinical trials are inadequate to substantiate its survival and sleep benefits. Its advantages over non-invasive mechanical ventilation have not been directly investigated. Furthermore, there are cautions for ALS patients to consider when opting for diaphragm pacing. Progressive degeneration of the phrenic motor neurons in classic ALS will interrupt the transmission of pacer signals to sustain diaphragm contractions. Pacing protocols that are safe for other neurological conditions may be detrimental for ALS, at least as suggested by transgenic animal models. Issues inherent to the device warrant expert intervention in implanted patients. At present, clinical effectiveness and long-term safety concerns about diaphragm pacing in ALS remain to be addressed.

BACKGROUND--Although psychological distress predicts mortality in asthma, an underlying physiological link has not been shown. This study examined relations between impaired voluntary drive to breathe and measures of mood states. METHODS--The level of maximal voluntary activation of the diaphragm and elbow flexors was measured in a previous study using a sensitive modification of the twitch interpolation technique in 11 asthmatic and 10 control subjects. In this study psychological distress was assessed using the Profile of Mood States questionnaire and measures of distress were compared with the muscle voluntary activation results. RESULTS--For the asthmatic subjects, depressed mood increased the risk of impaired maximal voluntary activation of the diaphragm by 3.5 times (95% CI 1.09 to 11.3). No such association was observed in control subjects. CONCLUSIONS--These results suggest that depressed mood may predispose an asthmatic patient to impaired voluntary activation of the diaphragm. Such individuals would be at increased risk of rapidly developing ventilatory failure if faced with severe airway narrowing.

BACKGROUND--Clinical tests of diaphragmatic strength are limited by the wide normal variation in maximal pressure which result, in part, from changes in diaphragmatic length. During relaxation at different lung volumes diaphragmatic length (LDI) can be estimated from the length of the zone of apposition (LZapp) and the transverse diameter of the rib cage (DRC). A study was carried out in two subjects using sequential digital radiography at six frames/second to determine whether these relations apply during maximal respiratory efforts which distort the rib cage and diaphragm. METHODS--The length of the anteroposterior contour of the diaphragm and DRC were determined by curve fitting. LZapp was measured with a millimetre rule. RESULTS--A significant correlation was found between LDI and LZapp during both maximal inspiratory and expulsive manoeuvres (R2 = 0.88 and 0.52). LDI was estimated from the measurements of LZapp and DRC using a multiple regression equation derived from measurements during static relaxation. Despite the complex dynamic events at the onset of these "static" manoeuvres, actual LDI correlated strongly with derived LDI using all data for the two manoeuvres in each subject (R2 = 0.95 and 0.84). Measurements with ultrasonography (12 cm linear probe) and magnetometers confirmed the changes in LZapp and DRC during inspiratory and expulsive efforts. CONCLUSIONS--Non-invasive measurements of LZapp and DRC can be used to derive an accurate estimate of diaphragmatic length under dynamic conditions.

SUMMARYCadmium and lead concentrations were compared in tissues of cutlassfish, Trichiurus lepturus L., its intestinal nematode Hysterothylacium sp. type MB larvae, and in water from the same location in the Sea of Oman. Metal accumulation in hosts, parasites and sea water was measured by ICP-OES. Hysterothylacium larvae from the intestinal lumen and visceral cavity showed much higher metal concentrations than in host tissues or sea water. Statistical analyses revealed no significant differences in metal accumulation between infected and uninfected hosts. Cadmium concentration in the host muscle was lower than in intestine, liver and gonad tissues. The mean concentrations of lead and cadmium in nematodes were 289·03 and 81·5 times higher than in host intestine, 188·4 and 225 times higher than in host muscle, 108·6 and 65·3 times higher than in host gonads, 70·5 and 19·5 times higher than in host liver and 3351 and 148 times higher than in sea water. The results show the value of this and possibly related nematodes as bioindicators of heavy metals and their potential use in environmental studies.

Background Adult socioeconomic position (SEP) is one of the most frequently hypothesised indirect pathways between childhood SEP and adult health. However, few studies that explore the indirect associations between childhood SEP and adult health systematically investigate the mediating role of multiple individual measures of adult SEP for different health outcomes. We examine the potential mediating role of individual measures of adult SEP in the associations of childhood SEP with self-rated health, self-reported mental health, current smoking status and binge drinking in adulthood. Methods Data came from 10,010 adults aged 25-64 years at Wave 3 of the Survey of Family, Income and Employment in New Zealand. The associations between childhood SEP (assessed using retrospective information on parental occupation) and self-rated health, self-reported psychological distress, current smoking status and binge drinking were determined using logistic regression. Models were adjusted individually for the mediating effects of education, household income, labour market activity and area deprivation. Results Respondents from a lower childhood SEP had a greater odds of being a current smoker (OR 1.70 95% CI 1.42-2.03), reporting poorer health (OR 1.82 95% CI 1.39-2.38) or higher psychological distress (OR 1.60 95% CI 1.20-2.14) compared to those from a higher childhood SEP. Two-thirds to three quarters of the association of childhood SEP with current smoking (78%), and psychological distress (66%) and over half the association with poor self-rated health (55%) was explained by educational attainment. Other adult socioeconomic measures had much smaller mediating effects. Conclusions This study suggests that the association between childhood SEP and self-rated health, psychological distress and current smoking in adulthood is largely explained through an indirect socioeconomic pathway involving education. However, household income, area deprivation and labour market activity are still likely to be important as they are intermediaries in turn, in the socioeconomic pathway between education and health.

Background Reducing health inequalities requires interventions that work as well, if not better, among disadvantaged populations. The aim of this study was to determine if the effects of price discounts and tailored nutrition education on supermarket food purchases (percentage energy from saturated fat and healthy foods purchased) vary by ethnicity, household income and education. Method A 2×2 factorial trial of 1104 New Zealand shoppers randomised to receive a 12.5% discount on healthier foods and/or tailored nutrition education (or no intervention) for 6 months. Results There was no overall association of price discounts or nutrition education with percentage energy from saturated fat, or nutrition education with healthy food purchasing. There was an association of price discounts with healthy food purchasing (0.79 kg/week increase; 95% CI 0.43 to 1.16) that varied by ethnicity (p=0.04): European/other 1.02 kg/week (n=755; 95% CI 0.60 to 1.43); Pacific 1.20 kg/week (n=101; 95% CI 0.06 to 2.34); Māori −0.15 kg/week (n=248; 95% CI −1.10 to 0.80). This association of price discounts with healthy food purchasing did not vary by household income or education. Conclusions While a statistically significant variation by ethnicity in the effect of price discounts on food purchasing was found, the authors caution against a causal interpretation due to likely biases (eg, attrition) that differentially affected Māori and Pacific people. The study highlights the challenges in generating valid evidence by social groups for public health interventions. The null findings for tailored nutritional education across all social groups suggest that structural interventions (such as price) may be more effective.

We studied the short-term effect of oral doses of quinine and quinidine on the renal clearance of amantadine in healthy young (age range, 27 to 39 years) and older (age range, 60 to 72 years) adults of both genders in a three-limbed randomized crossover study. Renal clearance of amantadine (13.2 +/- 5.8 L/hr) was significantly inhibited by quinine (9.7 +/- 4.8 L/hr) and quinidine (8.9 +/- 4.0 L/hr) only in male subjects and was not associated with age. The chiral selectivity for the renal clearance of quinidine over quinine was confirmed and extended with the suggestion of both age- and gender-associated changes on the renal clearance ratio for these two diastereomeric drugs. These data support the continued use of amantadine for studies on the renal elimination of organic cationic drugs.

Maximal voluntary drive to the diaphragm and a non-respiratory muscle group (elbow flexors) was compared in 10 control subjects and 11 asthmatics who were studied when well. The degree of voluntary activation during repeated attempted maximal quasi-static efforts was determined using the twitch interpolation technique in the absence of contractile fatigue under both control conditions and following bronchial challenge with histamine. Diaphragm activation was assessed using bilateral phrenic stimulation at the normal resting end-expiratory lung volume after exhalation from TLC. Asthmatic subjects showed lower and more variable voluntary activation than control subjects for both diaphragm (82.0% +/- 18.4 [SD], vs 87.8% +/- 12.0, P0.01) and elbow flexors (91.3% +/- 7.6 vs 95.8% +/- 4.1, P0.01). Histamine challenge decreased FEV1 in asthmatic subjects to 50% of the initial value, but had no significant effect on voluntary activation in either subject group. The decreased voluntary drive to the diaphragm observed in some asthmatic subjects may predispose to rapid development of ventilatory failure during severe airway narrowing.

The purpose of this study was to determine whether there is a risk profile for predicting or preventing shoulder dystocia and whether any of the obstetric maneuvers to disimpact a shoulder reduce the likelihood of permanent injury.A retrospective analysis of 14,297 parturients with 12,532 vaginal deliveries and 1765 cesarean sections (12.4%) from January 1986 through June 1990 was performed. A total of 204 maternal and infant charts, related to shoulder dystocia or neonatal injury, were reviewed in depth for age, parity, episiotomy, type of delivery, hemorrhage, maternal obesity, diabetes, weight gain, fetal weight, sex, and Apgar scores. In addition, the type of maneuver or combination thereof used to relieve the dystocia, type of injury to the infant, and follow-up of the injury were reviewed.The 185 coded episodes of shoulder dystocia represent 1.4% of all vaginal deliveries (12,532). There were 42 injuries recorded: 14 fractured clavicles and 28 brachial plexus injuries. An additional 19 patients, not coded for shoulder dystocia, sustained 14 fractured clavicles and five brachial plexus injuries. All but one of the brachial plexus injuries resolved by 6 months. The occurrence of shoulder dystocia increased in direct relationship to the birth weight and becomes significant in newborns over 4000 gm (p0.01). The occurrence of a previous large infant was also a significant risk factor (p0.01). Diabetes and midforceps delivery become significant factors only in the presence of a large fetus. Obesity, multiparity, postdate pregnancy, use of oxytocin, low forceps delivery, episiotomy, and type of anesthesia were unrelated to shoulder dystocia. No delivery method was without injury.This study clearly indicates that most of the traditional risk factors for shoulder dystocia have no predictive value, shoulder dystocia itself is an unpredictable event, and infants at risk for permanent injury are virtually impossible to predict. In addition, no delivery method in shoulder dystocia was superior to another with respect to injury. Thus no protocol should serve to substitute for clinical judgment.

There is substantial evidence that lower socioeconomic position (SEP) is associated with poorer mental health outcomes. However, uncertainties exist about the origins of socioeconomic gradients in mental health problems and the relative contributions of both childhood and adult SEP. In this study we assess the association of childhood SEP with psychological distress in adulthood and investigate how much of this association is mediated by adult SEP. Data for this cross-sectional analysis came from Wave 3 of the Survey of Family, Income and Employment (SoFIE) in New Zealand (n=14,470). Childhood SEP was measured using parental occupation recalled at age 10. Non-specific psychological distress was assessed using the Kessler 10 scale (K10). Adult SEP was measured using five socioeconomic indicators (area deprivation, household income, wealth, labour market activity, education). The association of childhood SEP with psychological distress before and after controlling for confounders and adult SEP indicators was determined using logistic regression with the K10 dichotomised at low/moderate versus high/very high. Sensitivity analyses included birth cohort and sex. There was a weak inverse relationship between increasing proportion of psychological distress with lower childhood SEP. Adjusted for age, sex and ethnicity, respondents with low compared to high childhood SEP had 1.35 greater odds of reporting high psychological distress (95% CI 1.13-1.60). Adjustment for adult mediating SEP variables led to a 77% reduction in the excess odds ratio to 1.08 (95% CI 0.90-1.29). The relationship did not significantly differ by birth cohort or sex. This finding is consistent with the current evidence that socioeconomic circumstances in adulthood are important determinants of inequalities in adult mental health and mediate much of the association of childhood SEP with adult psychological distress.

Visual recognition of cyanosis is an important clinical activity. While pulse oximetry is almost universal in the hospital environment, there are circumstances where it is not available or may be unreliable. Cyanosis recognition is affected by lighting colour. In addition, there is, mainly anecdotal, evidence that people with greater colour vision deficiencies (CVDs) have particular difficulty and there is no effective lighting strategy to assist in the observation. The change of blood colour with oxygenation has been shown to lie close to the direction of colour confusions made by congenital red-green dichromats. The important sites of observation are lips, nail beds and palm creases. 10 subjects who were known to be chronically hypoxaemic were recruited from the chronic respiratory program. Their blood oxygen saturation (SpO(2)) varied from 84% to 96% pre-exercise, and 61-84% post-exercise. Ten normal subjects were recruited whose SpO(2) was 99% or 100%. The spectral radiances of lips, nail beds and palm creases were measured using a telespectroradiometer and compared with the spectral radiances of a white tile of known spectral reflectances measured in the same location. This is a non-contact method of measurement, avoiding the blanching caused by pressure of contact methods. The spectral reflectances were calculated, and the chromaticities calculated for a Planckian radiator T = 4000K. Measurements on lips yielded the most consistent results. The colour changes pre- and post-exercise and compared with normal colour lie generally along a deutan confusion line. These results show the direction of the colour change and confirm the, previously anecdotal, difficulties in detecting cyanosis by observers with CVDs.

The reflex mechanism of the short-latency inhibitory reflex to transient loading of human inspiratory muscles is unresolved. Muscle afferents mediate this reflex, but they may act via pontomedullary inspiratory centers, other bulbar networks, or spinal circuits. We hypothesized that altered chemical drive to breathe would alter the initial inhibitory reflex if the neural pathways involve inspiratory medullary centers. Inspiration was transiently loaded in 11 subjects during spontaneous hypercapnic hyperpnea and matched voluntary hyperventilation. Electromyographic activity was recorded bilaterally from scalene muscles with surface electrodes. The latencies of the initial inhibitory response (IR) onset (32 ± 0.7 and 38 ± 1 ms for spontaneous and voluntary conditions respectively, P < 0.001) and subsequent excitatory response (ER) onset (80 ± 2.9 and 78 ± 2.6 ms, respectively, P = 0.46) and the normalized sizes of IR (65 ± 2 and 67 ± 3%, respectively, P = 0.50) and ER (51 ± 8 and 69 ± 6%, respectively, P = 0.005) were measured. Mean end-tidal Pco2 was 43 ± 1.5 Torr with dead space ventilation and was 14 ± 0.6 Torr with matched voluntary hyperventilation ( P < 0.001). A mean minute volume >30 liters was achieved in both conditions. The absence of significant difference in the size of the IR suggested that the IR reflex arc does not transit the brain stem inspiratory centers and that the reflex may be integrated at a spinal level. In voluntary hyperventilation, an initial excitation occurred more frequently and, consequently, the IR onset latency was significantly longer. The size of the later ER was also greater during voluntary hyperventilation, which is consistent with it being mediated via longer, presumably cortical, pathways, which are influenced by voluntary drive.

1. The maximal voluntary pressure generated by the diaphragm (transdiaphragmatic pressure, Pdi) is about 50% greater during maximal expulsive efforts than during maximal inspiratory efforts against a closed airway. However, these pressures cannot be increased by interpolated phrenic stimuli in trained subjects. This suggests that variable neural drive is not responsible for the difference in voluntary pressure. To investigate whether dynamic changes in diaphragm length during inspiratory and expulsive efforts could account for this difference, we used digital sequential radiography at 6 frames per second. 2. During the development of peak Pdi in inspiratory efforts, total diaphragm length decreased by about 20% in the antero-posterior and lateral projections. During maximal expulsive efforts (with glottis open), the diaphragm shortened slightly in the early stage of pressure development but then lengthened due to contraction of abdominal muscles before peak pressure was achieved. 3. Given that force increases when a contracting muscle is lengthened (expulsive effort) and decreases during shortening (inspiratory effort), this study provides a definitive explanation for the difference in maximal voluntary pressure between pure inspiratory and expulsive efforts.

BACKGROUND: This study investigated whether the inspiratory muscles are susceptible to fatigue during acute airway narrowing because of increased airway resistance and hyperinflation. METHODS: Asthmatic subjects performed up to four series (on separate days) of 18 maximal static inspiratory efforts of 10 seconds' duration with 10 second rest intervals (50% duty cycle; total duration six minutes): at functional residual capacity (FRC) (control); after histamine induced bronchoconstriction, which decreased forced expiratory volume in one second (FEV1) to a mean of 55% (SD 11%) of the initial value; at a voluntarily increased lung volume (initial volume held at 140% control); and after inhalation of histamine at a voluntarily increased lung volume. RESULTS: For the group of subjects the mean (SD) maximal inspiratory pressure (MIP) in the control experiments was 114 (22) cmH2O and the initial volume was 3.5 (1.2) 1. After histamine inhalation the initial lung volume for contractions increased to 118% (5%) of the control volume. In the high lung volume experiments initial volumes were 140% (12%) of the control (volume without histamine) and 140% (15%) (with histamine). The relation between MIP and initial absolute lung volume was determined for each subject before fatigue developed. When the inspiratory pressures for each contraction in the endurance test were normalised to the pressure expected for that lung volume, no significant differences were found between the four experimental conditions for MIP, or between pressures sustained over the 18 contractions. CONCLUSIONS: Histamine induced bronchoconstriction and hyperinflation had no detectable effect on inspiratory muscle strength or endurance in these asthmatic subjects.

1. This study used a sensitive modification of the twitch interpolation technique to compare the extent of voluntary neural drive to the diaphragm and the elbow flexors during fatigue. For the diaphragm both inspiratory and expulsive efforts were tested, and fatigue was induced by expulsive efforts which were either maximal voluntary contractions (MVCs, 10 s duration, 50% duty cycle) or submaximal contractions (50% MVC, 3 s duration, 60% duty cycle). 2. Over the series of thirty MVCs peak elbow torque declined to 57.9 +/- 3.0% (mean +/- S.E.M.) of the initial value while maximal inspiratory pressure declined to 78.7 +/- 7.3% (P < 0.05). For the diaphragm the relative decline in voluntary peak inspiratory (and expulsive) force was similar to the decline in twitch responses to single and twin (10 ms interval) stimuli. However, for the elbow flexors the decline in twitch force was disproportionately greater than the decline in maximal voluntary force. The decline in twitch force for the diaphragm could not be attributed to failure at the neuromuscular junction. 3. At the start of the exercise, twitch potentiation (following three brief MVCs) was significantly less for the diaphragm than for the elbow flexors (20% versus 61%, P < 0.01). 4. In the unfatigued state maximal voluntary efforts by subjects activated 98.4 +/- 0.4% of the stimulated elbow flexors compared with 95.0 +/- 1.5% of the diaphragm (P < 0.05). During the exercise period there was a progressive failure in the ability to activate the limb muscle ('central fatigue'; voluntary drive declined from 98.4 +/- 0.4 to 86.8 +/- 2.2%, P < 0.01) whereas the decline in voluntary activation during inspiratory contractions was not significant (from 95.0 +/- 15 to 91.5 +/- 2.5%). 5. Voluntary activation during attempted maximal efforts was less complete for both muscles when stimuli were delivered without warning. The index of voluntary activation for unwarned stimuli was lower for the diaphragm (performing expulsive efforts, 81.0 +/- 2.8%) than for the limb muscle (89.9 +/- 1.5%, P < 0.01). 6. During repeated submaximal expulsive efforts we confirmed that subjects develop a marked inability to contract the diaphragm voluntarily, but when the diaphragm performed inspiratory manoeuvres at the same level of contractile fatigue, the index of voluntary drive was greater than 94%. 7. In conclusion, when tested with inspiratory efforts the diaphragm developed less central fatigue than the limb muscle over the same exercise period.(ABSTRACT TRUNCATED AT 400 WORDS)

The objective of this study was to determine the probabilities of specific morbid events or death among patients with end-stage renal disease (ESRD) treated by hemodialysis. A prospective cohort study was performed between March 1988 and September 1989 in 18 hemodialysis centers in 13 Canadian cities, representing about one third of the hemodialysis population in Canada. The inception cohort consisted of 496 patients entering hemodialysis who had survived 1 month. The few new hemodialysis patients who received erythropoietin (EPO) in the last 3 months of the study were excluded. Survival curves were compared using the Cox proportional hazards regression model. Older age and history of cardiovascular disease were independently associated with a greater probability of death. Age and history of cardiovascular disease were also associated with a greater probability of nonfatal circulatory events (myocardial infarction, angina requiring hospitalization, or stroke), while a serum albumin level less than or equal to 30 g/ L (3.0 g dL) was associated with an increased probability of pulmonary edema. The probability of surviving 12 months without receiving a blood transfusion was 47.2% for males and 27.5% for females. The incidence of non-A, non-13 hepatitis, as estimated by unexplained elevations in serum aspartate aminotransferase (AST) values, was not different between patients receiving and not receiving blood transfusions. The probability of hospitalization for any cause was greater for patients with grafts for vascular access than for those with fistulae, for those with a history of cardiovascular disease, for those with a serum albumin level less than or equal to 30 g/L, and for those with renal disease due to diabetes or vascular disease. Hospitalization due to circulatory disease was more likely among those with a history of cardiovascular disease and among those with a lower serum albumin level. Hospitalization for infectious disease was more likely among those with a lower serum albumin level and less likely among those with a fistula for vascular access. Among all patients receiving hemodialysis treatment for more than 6 months, there were 14.8 hospital days per year. The probability of any infection other than local access infection was greater for subjects with a prosthetic graft than for those with a fistula, for those with a serum albumin level less than or equal to 30 g/L, and for aboriginal compared with nonaboriginal people. The factors associated with septicemia were type of vascular access, serum albumin level, and race. For pneumonia, the relative risk was greater for those with a low serum albumin level. The probabilities of thrombosis or local access infection were determined among 347 hemodialysis patients with either a fistula or polytetrafluoroethylene (PTFE) graft as a first permanent vascular access. Follow-up commenced with the first successful use of the access. The probability of an access infection by 12 months was 5.5% for fistulae and 19.7% for grafts. The probability of graft thrombosis requiring surgical correction by 12 months was greater among subjects with grafts and those with a serum albumin value less than or equal to 30 g/L. For those with a serum albumin level less than or equal to 30 g/L, the probability of thrombosis was 18.4% for fistulae and 39.9% for grafts. For those with a serum albumin level greater than 30 g/L, the probabilities were 14.4% and 32.3%.

Inspiratory muscles are uniquely adapted for endurance, but their function is compromised in chronic obstructive pulmonary disease (COPD) due to increased loads, reduced mechanical advantage, and increased ventilatory requirements. The hyperinflation of COPD reduces the flow and pressure-generating capacity of the diaphragm. This is compensated by a threefold increase in neural drive, adaptations of the chest wall and diaphragm shape to accommodate the increased volume, and adaptations of muscle fibers to preserve strength and increase endurance. Paradoxical indrawing of the lower costal margin during inspiration in severe COPD (Hoover's sign) correlates with high inspiratory drive and severe airflow obstruction rather than contraction of radially oriented diaphragm fibers. The inspiratory muscles remain highly resistant to fatigue in patients with COPD, and the ultimate development of ventilatory failure is associated with insufficient central drive. Sleep is associated with reduced respiratory drive and impairments of lung and chest wall function, which are exaggerated in COPD patients. Profound hypoxemia and hypercapnia can occur in rapid eye movement sleep and contribute to the development of cor pulmonale. Inspiratory muscles adapt to chronic loading with an increased proportion of slow, fatigue-resistant fiber types, increased oxidative capacity, and reduced fiber cross-sectional area, but the capacity of the diaphragm to increase ventilation in exercise is compromised in COPD. In COPD, neural drive to the diaphragm increases to near maximal levels in exercise, but it does not develop peripheral muscle fatigue. The improvement in exercise capacity and dyspnea following lung volume reduction surgery is associated with a substantial reduction in neural drive to the inspiratory muscles.

An error has been found in the computation of the C parameter defined in Eq. (44), which led to its overestimation by a factor 2(1/4). The correct values for C are 9.2, 9.7, and 9.3 for the multi-interferometer, H1 and L1 analyses, respectively. None of the upper limits presented in the article were affected.

High-precision variational calculations using multiple basis sets in Hylleraas coordinates are presented for the 1s22s 2S state of lithium. The variational bound of -7.478 060 326(10) a.u. for the nonrelativistic energy is in good agreement with our revised experimental value of -7.47 806 034(20) a.u., thereby resolving a long-standing disrepancy. Two-electron calculations of the QED corrections are extended to three-electron systems and compared with other results. The comparison for Li-like ions up to U89+ suggests a simple interpretation for the ''screening of the Lamb shift'' recently calculated by Cheng, Johnson, and Sapirstein [Phys. Rev. Lett. 66, 2960 (1991)]. © 1991 The American Physical Society.

This Symposium includes 15 presentations and an editorial review dealing with prorenin activation and function. It comes 20 years after prorenin was first reported in various contexts and attracted attention because of its connection with renin–angiotensin, its high concentration relative to renin in the blood, and its presence in extrarenal, as well as renal, tissues. Intriguing changes in plasma prorenin have been reported after treatment with antihypertensive and other drugs, following various physiological stimuli, and in pathophysiological states such as Wilms' tumor, Bartter's syndrome, and diabetic nephropathy. Lately, very high prorenin concentrations have been found in human and animal ocular fluid, ovarian follicular fluid, and in association with angiogenesis and microangiopathy. High circulating prorenin concentrations and fulminant hypertension have been reported in rats harbouring the mouse Ren-2 gene. However, what prorenin does in all these extrarenal fluids, tissues, and conditions is not well understood. Among the reasons for this lack of understanding are the difficulties in measuring prorenin and in establishing good animal models. We have not answered the critical question as to whether prorenin itself is bioactive like a hormone, and if so, what its action(s) might be. Nor have we established the main alternative, i.e., whether the function of prorenin is indirect, through renin–angiotensin, be it in the circulation or in the extrarenal tissues. This Symposium provides only partial methodological advances and answers, but we hope it will stimulate the breakthrough work needed to supply more complete answers.Key words: hormonal function, renin–angiotensin, hypertension.

This study was designed to compare the recovery from fatigue of human inspiratory and limb muscles using repeated maximal static contractions. Series of 18 maximal contractions of 10 sec duration were performed with a duty cycle of 50% for maximal inspiratory efforts (against a shutter at FRC), and with duty cycles of 5%, 10%, 20% and 50% for the elbow flexors in repeated studies on 6 subjects. The peak inspiratory pressure at the end of the series declined to 86.7% +/- 5.3% (mean +/- S.D.) of its initial value: maximal force of the elbow flexors declined to 83.5% +/- 7.0% (5% duty cycle), 80.0% +/- 5.5% (10% duty cycle), 70.0% +/- 9.3% (20% duty cycle), and 66.4% +/- 8.0% (50% duty cycle). Thus, the elbow flexors required approximately a 10-fold reduction in duty cycle to maintain over a series of contractions a force generating capacity comparable to that of the diaphragm. A small degree of 'central' fatigue developed progressively during all series of contractions but did not correlate with duty cycle. Fatigue-induced changes in twitch contraction properties varied with changes in duty cycle. Our major conclusions are that the human diaphragm has a marked capacity to recover from fatigue and that this may have been underestimated in previous studies from this and other laboratories.

The purpose of this study was to determine the biological effects of the elastic modulus of the femoral stem in canine hip arthroplasty. Cementless total hip arthroplasty was performed in 12 dogs, six had a low elastic modulus polyacetal resin stem and six had a high modulus stainless steel stem. The components were otherwise similar. At six and 12 months after operation, radiographic and histomorphometric analysis showed that those with steel implants had more cortical porosity than did the other group (p less than 0.01). We suggest that the elastic modulus of the implant is an important factor in controlling cortical bone resorption. A low modulus femoral prosthesis can significantly decrease bone resorption which might otherwise eventually lead to implant failure.

Panic attacks are common in chronic obstructive pulmonary disease (COPD), and the prevalence of panic disorder is at least 10 times higher than in the general population. In the current study, we examined resistive load perception in patients with COPD with and without panic attacks.We tested competing hypotheses, based on conflicting results of earlier studies, that those patients with COPD with panic attacks or panic disorder would show either heightened or blunted perception of dyspnea as the magnitude of inspiratory resistive loads increased.We compared 20 patients with COPD with panic attacks or panic disorder, 20 patients without panic, and 20 healthy, age-matched subjects using an inspiratory resistive load-testing protocol.We administered a diagnostic interview for panic attacks and panic disorder. We measured perceived dyspnea in response to increasing inspiratory resistive loads (modified Borg scale) and several respiratory variables. Dyspnea ratings increased linearly for all groups as the size of resistive loads increased. No significant differences were found between groups on the respiratory variables. Patients with COPD with panic attacks or panic disorder rated their level of dyspnea significantly higher than did other subjects.Patients with COPD with panic attacks showed heightened sensitivity to inspiratory loads. The result reinforces the influence of psychological factors on symptom perception in this disease.

Loading of inspiratory muscles produces a profound short-latency inhibitory response (IR) of the electromyogram (EMG), followed by an excitatory response (ER). Duration of IR correlates positively with the apnoea hypopnoea index in obstructive sleep apnoea (OSA) patients, for whom measurement of this reflex may allow the assessment of a physiological response to therapy. To test the reliability of reflex measurement, we studied 11 human subjects on 4 separate days. Inspiration was transiently occluded during 2 sets of 30 trials on each day. Scalene muscle EMG was rectified and averaged. Ten parameters (4 latencies and 6 EMG sizes) were measured. Reproducibility was analysed by ANOVA, intraclass correlation coefficient (ICC) and coefficient of variation (CV). The mean ICC was 0.56 (range 0.30-0.76) and the mean CV was 25% (range 6.7-48%). These results show good measurement reliability. The abnormalities seen in disease are significantly larger than these CVs. The reflex response to airway occlusion may be assessed reliably using our method.

This paper was published online on 3 August 2007 with a formatting error in the fifty-first affiliation in the author list.The affiliation should read as ‘‘University of Western Australia, Crawley, WA 6009, Australia.’’ The affiliation has beencorrected as of 4 March 2008. The affiliation is incorrect in the printed version of the journal.

This paper was published online on 29 October 2007 with a formatting error in the fiftieth affiliation in the author list. The affiliation should read as ‘‘University of Western Australia, Crawley, WA 6009, Australia.’’ The affiliation has been corrected as of 4 March 2008. The affiliation is incorrect in the printed version of the journal.

This paper was published online on 9 July 2007 with a formatting error in the fiftieth affiliation in the author list. The affiliation should read as ‘‘University of Western Australia, Crawley, WA 6009, Australia.’’ The affiliation has been corrected as of 4 March 2008. The affiliation is incorrect in the printed version of the journal.

An interrelationship between atrial natriuretic peptide (ANP) and the renin-angiotensin system has been established. Both of these hormonal systems are modulated by sodium balance. The role of the beta-adrenoceptor in the regulation of release of ANP is not clear. We therefore undertook a study to examine changes in atrial-specific granule number and plasma ANP level following beta-adrenoceptor blockade in rats on low and high sodium intakes. A low-sodium diet, as compared with a high-sodium diet, elevated right and left atrial-specific granule number (right atria 54.6 +/- 8.7 vs. 42.3 +/- 5.7; left atria 47.7 +/- 7.7 vs. 30.6 +/- 3.4 granules/unit area) and plasma renin activity (28 +/- 3.7 vs. 5.4 +/- 0.8 ng AI/ml/hr). Plasma ANP levels were lower in the low-sodium animals (98 +/- 34 vs. 345 +/- 38 pg/ml). When treated with the nonspecific beta-adrenoceptor blocker propranolol, the elevated plasma renin activity and atrial-specific granule number in rats on a low sodium intake were significantly less. Neither of these parameters changed in rats on a high sodium intake. Conversely, propranolol treatment resulted in lower plasma ANP levels in rats with high sodium intake. The already-suppressed plasma ANP level in rats on a low-sodium diet was unaltered with beta-adrenoceptor blockade. The results suggest that dietary sodium intake is an important determinant of the response of atrial-specific granule number and plasma ANP levels following beta-adrenoceptor blockade with propranolol.

To determine the role of arterial O2 content on the mechanism of muscle O2 utilization, we studied the effect of 2, 11, and 20% carboxyhemoglobin (COHb) on O2 uptake (VO2), and CO2 output (VCO2) kinetics in response to 6 min of constant moderate- and heavy-intensity cycle exercise in 10 subjects. Increased COHb did not affect resting heart rate, VO2 or VCO2. Also, the COHb did not affect the asymptotic VO2 in response to exercise. However, VO2 and VCO2 kinetics were affected differently. The time constant (TC) of VO2 significantly increased with increased COHb for both moderate and heavy work intensities. VO2 TC was positively correlated with blood lactate. In contrast, VCO2 TC was negatively correlated with increased COHb for the moderate but unchanged for the heavy work intensity. The gas exchange ratio reflected a smaller increase in CO2 stores and faster VCO2 kinetics relative to VO2 with increased COHb. These changes can be explained by compensatory cardiac output (heart rate) increase in response to reduced arterial O2 content. The selective slowing of VO2 kinetics, with decreased blood O2 content and increased cardiac output, suggests that O2 is diffusion limited at the levels of exercise studied.

1. This study used three techniques (bilateral phrenic nerve stimulation, motor cortex stimulation and quantitative electromyography) to assess the degree of activation of the diaphragm, intercostal-accessory muscles and abdominal muscles during postural tasks and respiratory manoeuvres. They included maximal inspiratory and expulsive efforts. 2. Bilateral phrenic nerve stimuli at supramaximal levels produced an average change in transdiaphragmatic pressure (Pdi) of 28 cmH2O during relaxation. During maximal inspiratory or expulsive efforts, all subjects were able to activate the diaphragm fully at functional residual capacity as judged by the failure of stimuli delivered during the voluntary efforts to increase Pdi. Peak voluntary Pdi was about 30% less for inspiratory than expulsive manoeuvres. 3. By contrast, transcranial activation of motor cortical output to the diaphragm and abdominal muscles produced an increment in abdominal pressure of 25 +/- 7 cmH2O during maximal voluntary expulsive efforts. Given the lack of response to phrenic nerve stimulation at similar voluntary pressures, this suggests that abdominal muscles, and not the diaphragm, fail to generate their full contractile force during maximal voluntary expulsive manoeuvres. 4. Motor cortical stimulation during weak inspiratory efforts produced a small reduction in oesophageal pressure (i.e. increase in net inspiratory force) of 7-14 cmH2O. This response could not be extinguished during maximal voluntary inspiratory efforts in two of three subjects. This occurred despite the cortical co-activation of 'antagonist' muscles in the chest wall and abdomen, and passive transmission of pressure from the abdominal to thoracic compartments. 5. Integrated electromyographic activity (EMG) recorded from abdominal muscles (rectus abdominis, external oblique) was greater during trunk flexion than during maximal expulsive efforts. Similarly, integrated EMG of the intercostal-accessory muscles (sternomastoid, scalenes, parasternal intercostals) was greater during tasks requiring head and/or neck flexion than during the maximal inspiratory efforts. 6. These data show that the diaphragm can be fully activated by the central nervous system during voluntary respiratory tasks but that other agonist 'respiratory' muscles need not be activated fully. Given the complex actions of 'inseries' respiratory muscles revealed here, it is argued that differences in the transdiaphragmatic pressure during various postural and respiratory tasks do not necessarily imply variation in the level of diaphragmatic neural drive.

In the summer of 1987 the then Home Secretary, Douglas Hurd, delivered the Police Foundation Lecture (Hurd, 1987). He resurrected a topic which ‘most people, police, lawyers and public alike thought had been dead and buried these last ten years' (Morton, 1987). The so-called right to or of silence, left intact by the Royal Commission on Criminal Procedure (1981), was on the agenda for criminal justice reform again, resuming the position it held with the publication of what Zander (1985) called ‘the ill-fated and notorious eleventh report of that prestigious Committee' (Criminal Law Revision Committee, 1972).

We evaluated maximal O2 uptake (VO2max), the metabolic acidosis threshold determined by the V-slope analysis [plot of CO2 output (VCO2) as a function of oxygen uptake (VO2)], the ratio of increase in VO2 to work rate increment (delta VO2/delta WR), the upper slope (S2) of the V-slope analysis, and the VO2 for work below and above the metabolic acidosis threshold to determine whether the changes in O2 transport caused by increased carboxyhemoglobin (HbCO) affected these parameters and variables. Ten normal subjects (aged 32.8 +/- 7.1 yr) performed symptom-limited incremental exercise tests in a ramp pattern on a cycle ergometer while breathing air and air with added carbon monoxide to cause HbCO to be approximately 11% and 20%. VO2max decreased by 11.6 and 19.3%, the metabolic acidosis threshold decreased by 11.9 and 19.6%, delta VO2/delta WR decreased by 8.9 and 14.0%, and S2 increased by 13.6 and 21.8% when HbCO was increased to 11 and 20%, respectively. Most importantly, VO2 was unchanged related to work rate below the metabolic acidosis threshold during the tests with increased HbCO but was reduced at the work rates above the metabolic acidosis threshold. These findings are consistent with the concept that the metabolic acidosis threshold is synonymous with an anaerobic threshold, i.e., the latter demarcating the VO2 above which the contracting muscles are not adequately supplied with O2 but below which they are.

The International Prospective Primary Prevention Study in Hypertension (IPPPSH) compared a β-blocker-containing vs. a non-β-blocker-containing antihypertensive regimen in 6,357 moderate-severe hypertensive men and women treated over 3-5 years. Blood pressure (BP) control was comparable with either regimen

A rapid method for the determination of the fat content of foodstuffs by transmittance infrared spectrometry is described. Fat is extracted with a chloroform-methanol (2:1) solvent containing an apolar methylsilicone oil as an internal standard. After partitioning of both components into the chloroform layer, the areas of a strong absorption band at 5·72 μm representing carbonyl ester stretching of the fat and that of a strong band in the internal standard at 7·88 μm due to CH 3 Si stretching are recorded. Fat content is estimated from the band area ratio (fat/internal standard) using suitable calibration plots. The calibration strategy used is discussed in some detail. The method was tested on a diverse range of foodstuffs including dairy products, processed meats, biscuit and cakes, chocolate, salad dressings, etc., and the results obtained were generally in good agreement with those given by standard reference methods.

B. Abbott, R. Abbott, R. Adhikari, J. Agresti, P. Ajith, B. Allen, R. Amin, S. B. Anderson, W. G. Anderson, M. Arain, M. Araya, H. Armandula, M. Ashley, S. Aston, P. Aufmuth, C. Aulbert, S. Babak, S. Ballmer, H. Bantilan, B. C. Barish, C. Barker, D. Barker, B. Barr, P. Barriga, M. A. Barton, K. Bayer, K. Belczynski, J. Betzwieser, P. T. Beyersdorf, B. Bhawal, I. A. Bilenko, G. Billingsley, R. Biswas, E. Black, K. Blackburn, L. Blackburn, D. Blair, B. Bland, J. Bogenstahl, L. Bogue, R. Bork, V. Boschi, S. Bose, P. R. Brady, V. B. Braginsky, J. E. Brau, M. Brinkmann, A. Brooks, D. A. Brown, A. Bullington, A. Bunkowski, A. Buonanno, M. Burgamy, O. Burmeister, D. Busby, R. L. Byer, L. Cadonati, G. Cagnoli, J. B. Camp, J. Cannizzo, K. Cannon, C. A. Cantley, J. Cao, L. Cardenas, M. M. Casey, G. Castaldi, C. Cepeda, E. Chalkey, P. Charlton, S. Chatterji, S. Chelkowski, Y. Chen, F. Chiadini, D. Chin, E. Chin, J. Chow, N. Christensen, J. Clark, P. Cochrane, T. Cokelaer, C. N. Colacino, R. Coldwell, R. Conte, D. Cook, T. Corbitt, D. Coward, D. Coyne, J. D. E. Creighton, T. D. Creighton, R. P. Croce, D. R. M. Crooks, A. M. Cruise, A. Cumming, J. Dalrymple, E. D’Ambrosio, K. Danzmann, G. Davies, D. DeBra, J. Degallaix, M. Degree, T. Demma, V. Dergachev, S. Desai, R. DeSalvo, S. Dhurandhar, M. Diaz, J. Dickson, A. Di Credico, G. Diederichs, A. Dietz, E. E. Doomes, R. W. P. Drever, J.-C. Dumas, R. J. Dupuis, J. G. Dwyer, P. Ehrens, E. Espinoza, T. Etzel, M. Evans, T. Evans, S. Fairhurst, Y. Fan, D. Fazi, M. M. Fejer, L. S. Finn, V. Fiumara, N. Fotopoulos, A. Franzen, K. Y. Franzen, A. Freise, R. Frey, T. Fricke, P. Fritschel, V. V. Frolov, M. Fyffe, V. Galdi, J. Garofoli, I. Gholami, J. A. Giaime, S. Giampanis, K. D. Giardina, K. Goda, E. Goetz, L. Goggin, G. Gonzalez, S. Gossler, A. Grant, S. Gras, C. Gray, M. Gray, J. Greenhalgh, A. M. Gretarsson, R. Grosso, H. Grote, S. Grunewald, M. Guenther, R. Gustafson, B. Hage, W. O. Hamilton, D. Hammer, C. Hanna, J. Hanson, J. Harms, G. Harry, E. Harstad, T. Hayler, J. Heefner, I. S. Heng, A. Heptonstall, M. Heurs, M. Hewitson, S. Hild, E. Hirose, D. Hoak, D. Hosken, J. Hough, E. Howell, D. Hoyland, S. H. Huttner, D. Ingram, E. Innerhofer, M. Ito, Y. Itoh, A. Ivanov, D. Jackrel, B. Johnson, W. W. Johnson, D. I. Jones, G. Jones, R. Jones, L. Ju, P. Kalmus, V. Kalogera, D. Kasprzyk, E. Katsavounidis, K. Kawabe, S. Kawamura, F. Kawazoe, W. Kells, D. G. Keppel, F. Ya. Khalili, C. Kim, P. King, J. S. Kissel, S. Klimenko, K. Kokeyama, V. Kondrashov, R. K. Kopparapu, D. Kozak, B. Krishnan, P. Kwee, P. K. Lam, M. Landry, B. Lantz, A. Lazzarini, B. Lee, M. Lei, J. Leiner, V. Leonhardt, I. Leonor, K. Libbrecht, P. Lindquist, N. A. Lockerbie, M. Longo, M. Lormand, M. Lubinski, H. Luck, B. Machenschalk, M. MacInnis, M. Mageswaran, K. Mailand, M. Malec, V. Mandic, S. Marano, S. Marka, J. Markowitz, E. Maros, I. Martin, J. N. Marx, K. Mason, L. Matone, V. Matta, N. Mavalvala, R. McCarthy, B. J. McCaulley, D. E. McClelland, S. C. McGuire, M. McHugh, K. McKenzie, J. W. C. McNabb, S. McWilliams, T. Meier, A. Melissinos, G. Mendell, R. A. Mercer, S. Meshkov, E. Messaritaki, C. J. Messenger, D. Meyers, E. Mikhailov, P. Miller, S. Mitra, V. P. Mitrofanov, G. Mitselmakher, R. Mittleman, O. Miyakawa, S. Mohanty, V. Moody, G. Moreno, K. Mossavi, C. MowLowry, A. Moylan, D. Mudge, G. Mueller, S. Mukherjee, H. Muller-Ebhardt, J. Munch, P. Murray, E. Myers, J. Myers, T. Nash, G. Newton, A. Nishizawa, K. Numata, B. O’Reilly, R. O’Shaughnessy, D. J. Ottaway, H. Overmier, B. J. Owen, H.-J. Paik, Y. Pan, M. A. Papa, V. Parameshwaraiah, P. Patel, M. Pedraza, S. Penn, V. Pierro, I. M. Pinto, M. Pitkin, H. Pletsch, M. V. Plissi, F. Postiglione, R. Prix, V. Quetschke, F. Raab, D. Rabeling, H. Radkins, R. Rahkola, N. Rainer, M. Rakhmanov, M. Ramsuder, K. Rawlins, S. Ray-Majumder, V. Re, H. Rehbein, S. Reid, D. H. Reitze, L. Ribichini, R. Riesen, K. Riles, B. Rivera, N. A. Robertson, C. Robinson, E. L. Robinson, S. Roddy, A. Rodriguez, A. M. Rogan, J. Rollins, J. D. Romano, J. Romie, R. Route, S. Rowan, A. Rudiger, L. Ruet, P. Russell, K. Ryan, S. Sakata, M. Samidi, L. Sancho de la Jordana, V. Sandberg, V. Sannibale, S. Saraf, P. Sarin, B. S. Sathyaprakash, S. Sato, P. R. Saulson, R. Savage, P. Savov, S. Schediwy, R. Schilling, R. Schnabel, R. Schofield, B. F. Schutz, P. Schwinberg, S. M. Scott, A. C. Searle, B. Sears, F. Seifert, D. Sellers, A. S. Sengupta, P. Shawhan, D. H. Shoemaker, A. Sibley, J. A. Sidles, X. Siemens, D. Sigg, S. Sinha, A. M. Sintes, B. J. J. Slagmolen, J. Slutsky, J. R. Smith, M. R. Smith, K. Somiya, K. A. Strain, D. M. Strom, A. Stuver, T. Z. Summerscales, K.-X. Sun, M. Sung, P. J. Sutton, H. Takahashi, D. B. Tanner, M. Tarallo, R. Taylor, R. Taylor, J. Thacker, K. A. Thorne, K. S. Thorne, A. Thuring, K. V. Tokmakov, C. Torres, C. Torrie, G. Traylor, M. Trias, W. Tyler, D. Ugolini, C. Ungarelli, K. Urbanek, H. Vahlbruch, M. Vallisneri, C. Van Den Broeck, M. Varvella, S. Vass, A. Vecchio, J. Veitch, P. Veitch, A. Villar, C. Vorvick, S. P. Vyachanin, S. J. Waldman, L. Wallace, H. Ward, R. Ward, K. Watts, J. Weaver, D. Webber, A. Weber, A. Weidner, M. Weinert, A. Weinstein, R. Weiss, S. Wen, K. Wette, J. T. Whelan, D. M. Whitbeck, S. E. Whitcomb, B. F. Whiting, C. Wilkinson, P. A. Willems, L. Williams, B. Willke, I. Wilmut, W. Winkler, C. C. Wipf, S. Wise, A. G. Wiseman, G. Woan, D. Woods, R. Wooley, J. Worden, W. Wu, I. Yakushin, H. Yamamoto, Z. Yan, S. Yoshida, N. Yunes, M. Zanolin, J. Zhang, L. Zhang, PHYSICAL REVIEW D 77, 069904(E) (2008)

A prospective longitudinal survey for sleeping disease (SD) was carried out over a 20 wkperiod on a caged freshwater population of farmed rainbow trout Oncorhynchus mkyiss . Pancreas,heart and red and white skeletal muscle were examined histologically and the presence and severityof lesions recorded. Sera were tested for viraemia with Salmonid Alphavirus (SAV) and for virus neu-tralizing (VN) antibodies. Viraemia was detected for 4 wk, beginning at Week 6 and with a peakprevalence of 57.9% at Week 7. Clinical signs and mortalities appeared at Week 8. Total mortality inthe study cage from Week 6 onward was 6.3%, but other cages at the site had mortality levels of upto 47.2%. VN antibodies were first detected at Week 9, with seroprevalence increasing to 80% by theend of the study (Week 20). Geometric mean antibody titres peaked at 1/89.4 at Week 17. Histologi-cal lesions were first detected at Week 7 (pancreas only), before increasing in prevalence and sever-ity to peak at Weeks 9 and 10. The majority of lesions were resolved by Week 15.KEY WORDS: Sleeping disease · Rainbow trout · Longitudinal survey · Antibody · Viraemia ·Histopathology

STUDY OBJECTIVES The human inspiratory muscles respond to a brief occlusion of the upper airway during inspiration with a profound short-latency reflex inhibition. This inhibition contrasts with the excitatory stretch reflex of limb muscles and may protect the airway from aspiration. It was postulated that this reflex would be altered in subjects with obstructive sleep apnea (OSA) who have repetitive upper airway occlusion. DESIGN Subjects underwent overnight polysomnography, as well as muscle reflex studies. For the reflex studies (performed during wakefulness), occlusions lasting 250 milliseconds were delivered during inspiration. Surface electromyogram was recorded over the scalenes, parasternal intercostals, and chest wall (overlying diaphragm). SETTING Research and sleep laboratories. PARTICIPANTS Nineteen subjects with untreated OSA (9 moderate and 10 severe) and 9 healthy control subjects. MEASUREMENTS AND RESULTS In the subjects with severe OSA, the duration of the inhibition was prolonged by at least 25% compared with control subjects. The peak of the inhibitory response for scalenes occurred significantly later for subjects with severe OSA than for control subjects (by 76 +/- 5 ms vs 60 +/- 3 ms [mean +/- SEM], respectively). Onset latencies of the later excitatory response were delayed for scalenes, parasternal intercostals, and chest wall recordings (eg, scalenes: 105 +/- 9 ms for subjects with severe OSA vs 83 +/- 5 ms for control subjects). CONCLUSIONS The latency of peak inhibition and duration of inhibition were positively correlated with the respiratory disturbance index for all muscle groups. These changes may reflect adaptation in central respiratory paths due to repetitive loading during sleep.

The authors report a patient with amyotrophic lateral sclerosis (ALS) who showed a lessening of deterioration in respiratory muscle strength during treatment with hyperimmune goat serum (HGS) (Aimspro). Respiratory function tests (RFTs) were measured by established protocols, and all measurements were expressed as a percentage of normal predicted values. The rate of decline was calculated by linear regression analysis. Respiratory muscle strength decline was less during 13 months of treatment with HGS (mean 1.3% per month, range 0.8-1.7%) compared to the preceding 13 months (mean 2.3% per month, range 1.2-3.1%), while a greater decline would be expected with disease progression. Comparison with similarly affected patients in the literature suggest that a decline of 4-5% per month of predicted values may be expected during the treatment phase.

Severe flooding may become more frequent due to global warming. A historical cohort study was conducted by telephone interview for new episodes of illness in all age groups, and for psychological distress in adults, following severe river flooding on 12 October 2000 in the town of Lewes in Southern England. Two hundred and twenty-seven residents of 103 flooded households and 240 residents of 104 non-flooded households in the same postal district were recruited by random selection of addresses from a post flooding survey and a commercial database respectively. Having been flooded was associated with earache (RR 2.2 [1.1,4.1] p = 0.02), and a significant increase in risk of gastroenteritis with depth of flooding (RR 1.7 [0.9,3.0] p = 0.09, p for trend by flood depth = 0.04). Adults had a four-times higher risk of psychological distress defined as a score ofor = 4 in response to the 12-item General Health Questionnaire (GHQ-12) (RR 4.1 [2.6, 6.4] p0.0005, p for trend by flood depth = 0.01). Associations between flooding and new episodes of physical illness in adults diminished after adjustment for psychological distress. Flooding remained highly significantly associated with psychological distress after adjustment for physical illnesses. Psychological distress may explain some of the excess physical illness reported by flooded adults and possibly by children as well. Policies to promote population resilience to flooding where flood prevention has failed must include practical support for flood victims and provision of appropriate psychological support. Associations with physical illnesses affirm the need for advice and assistance with individual, household and environmental hygiene and access to medical services.