Light as a source of error in estimates of water potential by vapor equilibration.
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A linear model for the errors of the 'spleen colony' assay for haemopoietic stem cells has been derived. The components emerging from the model are interpreted and practical recommendations given for interpreting measurements made with this assay. The model permits correction for the effect of overlapping colonies and gives average errors for single measurements of the number of CFU-s. More reliable and more precise information can be obtained using this model. The spleen colony technique detects a population of immature precursor cells designated as CFU-s (Till & McCulloch, 1961). The relative error of measurement is often large when compared with the changes in the phenomena studied. Consequently a better knowledge of the errors of this technique is highly desirable. This paper should be regarded as an extension of the previous analysis of Till (1972). The theory for the errors of the spleen colony technique was applied to 905 determinations of the CFU-s numbers performed on random-bred mice. Data from random-bred mice rather than those from inbred mice have been used because the error components can be expected to be larger and, consequently, more easily detectable. The model of errors has also been validated using data published by Till (1972) and has subsequently been applied to data from several inbred mice strains (Znojil & Necas, 1988).
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The effects of assuming (i) that testicular tissue shrinks equally regardless of species or treatment at fixing and processing, (ii) that all Leydig cells in a given testis have spherical nuclei of identical size, and (iii) that testicular volume (i.e. the reference volume) is constant regardless of species or treatment, on the estimation of Leydig cell numbers in mammalian testes were investigated. This was accomplished by comparing the results of stereological analyses of Leydig cell numerical density and Leydig cell number in control testes of hamster, guinea-pig, and rat and in atrophied testes of hamster, and rat, obtained via the disector method which is unbiased with respect to the particle shape under study, and the Floderus equation which assumes that the particles under study are identical spheres. In control hamster, and also in guinea-pig, the effects of the three assumptions on the estimates of Leydig cell number per testis were negligible, because in these two treatment groups, the total shrinkage of testis tissue at fixing and processing (ST%) was low, Leydig cell nuclear profiles were circular in section, and the average volume of a testis was close to unity (i.e. 1 cm3). By contrast, in hamsters, and rats with atrophied testes, these assumptions produced incorrect estimates in Leydig cell number per testis, because the ST% was high, the majority of Leydig cell nuclear profiles were pleomorphic, and the average volume of a testis was lower than control. In summary, this study documents that the assumptions of equal shrinkage in testis tissue at fixing and processing, a constant testicular reference volume, and spheroidal shape of Leydig cell nuclei may contribute significant errors in estimates of Leydig cell number in mammalian testes. The magnitude of the errors introduced by these assumptions depends upon the species and the experimental treatment.
BACKGROUND: Physiological data obtained with the pulmonary artery catheter (PAC) are susceptible to errors in measurement and interpretation. Little attention has been paid to the relevance of errors in hemodynamic measurements performed in the intensive care unit (ICU). The aim of this study was to assess the errors related to the technical aspects (zeroing and reference level) and actual measurement (curve interpretation) of the pulmonary artery occlusion pressure (PAOP). METHODS: Forty-seven participants in a special ICU training program and 22 ICU nurses were tested without pre-announcement. All participants had previously been exposed to the clinical use of the method. The first task was to set up a pressure measurement system for PAC (zeroing and reference level) and the second to measure the PAOP. RESULTS: The median difference from the reference mid-axillary zero level was - 3 cm (-8 to + 9 cm) for physicians and -1 cm (-5 to + 1 cm) for nurses. The median difference from the reference PAOP was 0 mmHg (-3 to 5 mmHg) for physicians and 1 mmHg (-1 to 15 mmHg) for nurses. When PAOP values were adjusted for the differences from the reference transducer level, the median differences from the reference PAOP values were 2 mmHg (-6 to 9 mmHg) for physicians and 2 mmHg (-6 to 16 mmHg) for nurses. CONCLUSIONS: Measurement of the PAOP is susceptible to substantial error as a result of practical mistakes. Comparison of results between ICUs or practitioners is therefore not possible.
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While the quantity of evidence relating behaviour and coronary heart disease is great, the quality is variable. It is possible to discern two broad categories of research error, the methodological and the conceptual, to account for this. The former may be corrected by sufficiently careful study design: the latter may require a complete re-examination of hypotheses. An alternative conceptual model is proposed in which three components (a) a surfeit of adversity in the absence of support, (b) consequent arousal and activation of the cardiovascular system, and (c) the coexistence of one or more of a well documented set of organic risk factors, allow the integrated and systematic testing of hypotheses relating behaviour and coronary heart disease. The authors are presently employing this conceptual model in the investigation of a number of such hypotheses.
The diagnosis of venous leakage as a cause of impotence, based on failure to induce an artificial erection by means of rapid saline infusion alone, may be invalid. Our recent experience with 2 men whose impotence was subsequently found to be psychogenic in nature suggests that saline erection cavernosometry should routinely incorporate the intracavernosal administration of papaverine, in order to avoid a falsely positive diagnosis of venous leakage.
Published studies show that among identical twins, lower birthweight is associated with lower adult intelligence. However, no such relation between birthweight and adult IQ exists among fraternal twins. A likely explanation for the association between birthweight and intelligence among identical twins is the identical twin transfusion syndrome which occurs only between some monochorionic identical twin pairs. The IQ scores from separated identical twins were reanalysed to explore the consequences of identical twin transfusion syndrome for IQ resemblance and heritability. Among 129 published cases of identical twin pairs reared apart, 76 pairs contained some birthweight information. The 76 pairs were separated into three classes: 23 pairs in which there was clear evidence of a substantial birthweight differences (indicating the probable existence of the identical twin transfusion syndrome), 27 pairs in which the information on birthweight was ambiguous (?), and 26 pairs in which there was clear evidence that the twins were similar in birthweight. The reanalyses showed: (1) birthweight differences are positively associated with IQ differences in the total sample of separated identical twins; (2) within the group of 23 twin pairs who showed large birthweight differences, there was a positive relation between birthweight differences and IQ differences; (3) when heritability of IQ is estimated for those twins who do not suffer large birthweight differences, the resemblance (and thus, h2/b) of the separated identical twins' IG is 0-95. Given that the average reliability of the individual IQ test is around 0-95, these data suggest that genetic factors and errors of measurement cause the individual differences in IQ among human beings. Because of the identical twin transfusion syndrome, previous studies of MZ twins have underestimated the effect of genetic factors on IQ. An analysis of the IQs for heavier and lighter birthweight twins suggests that the main effect of the identical twin transfusion syndrome is to lower the IQ of the lighter birthweight twin, rather than to raise the IQ of the more fortunate partner or to influence the IQ of both members. This reanalysis suggests that postnatal cultural and social environment produce little of the total phenotypic variation in IQ found in the normal population. In the future, investigators who use twin studies to estimated heritability must ascertain whether their identical twin pairs suffered from the identical twin transfusion syndrome. Accurate estimates of heritability can only be obtained using identical twins who do not suffer from placental circulation problems. Most likely, the identical twin transfusion syndrome produces anoxia and brain damage during early prenatal development in the smaller identical twin. The anoxia is caused by a lowering of the haemoglobin content of the smaller twin by 35% or more.
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Two patients are presented in whom ultrasonic cephalometry suggested intrauterine fetal growth retardation. The respective newborn infants were normally grown and had dolichocephaly with a normal head circumference. Dolichocephaly should be considered when cephalometry alone suggests a diagnosis of placental insufficiency.
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