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PubMed1988

Maximum likelihood analysis of spike trains of interacting nerve cells.

Suppose that a neuron is firing spontaneously or that it is firing under the influence of other neurons. Suppose that the data available are the firing times of the neurons present. An "integrate several inputs and fire" model is developed and studied empirically. For the model a neuron's firing occurs when an internal state variable crosses a random threshold. This conceptual model leads to maximum likelihood estimates of internal quantities, such as the postsynaptic potentials of the measured influencing neurons, the membrane potential, the absolute threshold and also estimates of derived quantities such as the strength-duration curve and the recovery process of the threshold. The model's validity is examined via an estimate of the conditional firing probability. The approach appears useful for estimating biologically meaningful parameters, for examining hypotheses re these parameters, for understanding the connections present in neural networks and for aiding description and classification of neurons and synapses. Analyses are presented for a number of data sets collected for the sea hare, Aplysia californica, by J. P. Segundo. Both excitatory and inhibitory examples are provided. The computations were carried out via the Glim statistical package. An example of a Glim program realizing the work is presented in the Appendix.

Animals↗
PubMed1997

Modelling accelerated degradation data using Wiener diffusion with a time scale transformation.

Engineering degradation tests allow industry to assess the potential life span of long-life products that do not fail readily under accelerated conditions in life tests. A general statistical model is presented here for performance degradation of an item of equipment. The degradation process in the model is taken to be a Wiener diffusion process with a time scale transformation. The model incorporates Arrhenius extrapolation for high stress testing. The lifetime of an item is defined as the time until performance deteriorates to a specified failure threshold. The model can be used to predict the lifetime of an item or the extent of degradation of an item at a specified future time. Inference methods for the model parameters, based on accelerated degradation test data, are presented. The model and inference methods are illustrated with a case application involving self-regulating heating cables. The paper also discusses a number of practical issues encountered in applications.

Equipment Failure↗
PubMed2003

A gain-control model relating nulling results to the duration of dynamic motion aftereffects.

Strength of the motion aftereffect (MAE) is most often quantified by its duration, a high-variance and rather 'subjective' measure. With the help of an automatic gain-control model we quantitatively relate nulling-thresholds, adaptation strength, direction discrimination threshold, and duration of the dynamic MAE (dMAE). This shows how the nulling threshold, a more objective two-alternative forced-choice measure, relates to the same system property as MAE-durations. Two psychophysical experiments to test the model use moving random-pixel-arrays with an adjustable luminance signal-to-noise ratio. We measure MAE-duration as a function of adaptation strength and compare the results to the model prediction. We then do the same for nulling-thresholds. Model predictions are strongly supported by the psychophysical findings. In a third experiment we test formulae coupling nulling threshold, MAE-duration, and direction-discrimination thresholds, by measuring these quantities as a function of speed. For the medium-to-high speed range of these experiments we found that nulling thresholds increase and dMAE-durations decrease about linearly, whereas direction discrimination thresholds increase exponentially with speed. The model description then suggests that the motion-gain decreases, while the noise-gain and model's threshold increase with speed.

Adaptation, Physiological↗
PubMed2005

The seizure-related phenotype of brain-derived neurotrophic factor knockdown mice.

The present investigation focused on the seizure-related phenotype of mice lacking one allele of brain-derived neurotrophic factor. Thresholds for producing seizures in brain-derived neurotrophic factor wild-type and brain-derived neurotrophic factor heterozygous mice were compared in several seizure models, including thresholds for electrically-induced clonic, tonic-clonic and 6 Hz limbic seizures, as well as seizures induced chemically by kainate, pilocarpine and pentylenetetrazol. In addition, the rate of amygdala kindling, as well as pre- and post-kindling seizure thresholds was determined. Seizure thresholds for clonic and tonic-clonic electrically induced seizures did not differ between brain-derived neurotrophic factor wild-type and heterozygous mice. However, heterozygous mice had higher thresholds for 6 Hz limbic seizures compared with wild-type mice. Heterozygous mice also required larger doses of kainate to produce limbic seizures. Somewhat surprisingly, heterozygous mice required significantly lower doses of pilocarpine to produce limbic seizures. However, heterozygous mice required a higher dose of pentylenetetrazol to induce twitches, but not clonic seizures, compared with wild-type mice. In addition, heterozygous mice required more current to elicit focal afterdischarges in the amygdala both pre- and post-kindling than did wild-type mice, and, heterozygous mice kindled more slowly than wild-type mice. The present findings provide additional support for the hypothesis that brain-derived neurotrophic factor is involved not only in normal excitability, but may also be involved in abnormal excitability such as occurs in seizure disorders and epileptogenesis.

Alleles↗
PubMed2006

What are the risks from medical X-rays and other low dose radiation?

The magnitude of the risks from low doses of radiation is one of the central questions in radiological protection. It is particularly relevant when discussing the justification and optimization of diagnostic medical exposures. Medical X-rays can undoubtedly confer substantial benefits in the healthcare of patients, but not without exposing them to effective doses ranging from a few microsieverts to a few tens of millisieverts. Do we have any evidence that these levels of exposure result in significant health risks to patients? The current consensus held by national and international radiological protection organizations is that, for these comparatively low doses, the most appropriate risk model is one in which the risk of radiation-induced cancer and hereditary disease is assumed to increase linearly with increasing radiation dose, with no threshold (the so-called linear no threshold (LNT) model). However, the LNT hypothesis has been challenged both by those who believe that low doses of radiation are more damaging than the hypothesis predicts and by those who believe that they are less harmful, and possibly even beneficial (often referred to as hormesis). This article reviews the evidence for and against both the LNT hypothesis and hormesis, and explains why the general scientific consensus is currently in favour of the LNT model as the most appropriate dose-response relationship for radiation protection purposes at low doses. Finally, the impact of the LNT model on the assessment of the risks from medical X-rays and how this affects the justification and optimization of such exposures is discussed.

Dose-Response Relationship, Radiation↗
PubMed2006

Development of interaction measures based on adaptive non-linear time series analysis of biomedical signals.

An important feature of interaction between two signal components is the direction of the interaction. Recently, different methods have been developed and applied for detecting the direction of interactions. Besides frequency-dependent methods, Granger causality is a well-known frequency-independent approach. One popular linear approach is based on autoregressive modeling of the underlying process and evaluates prediction errors under different past assumptions. In the present study, this linear concept is extended to self-exciting threshold autoregressive models, which cover a wider class of processes. An approach for the definition of a state-dependent Granger causality is given and applied to simulated data.

Algorithms↗
PubMed2000

Prediction of vesico-ureteric reflux in childhood urinary tract infection: a multivariate approach.

UNLABELLED: In this study, independent predictors obtained from patient history, physical examination and laboratory results for vesico-ureteric reflux (VUR) in children of 0-5 y with a first urinary tract infection (UTI) were assessed and the added value of renal ultrasound (US) investigated. Information was collected from children visiting the paediatric outpatient department with a first proven UTI, defined as a urine monoculture with > or = 10(5) organism/ml, with clinical symptoms and possible white cell count > or = 20 per high-power field of spun fresh urine. Children with neurologic bladder dysfunction were excluded. VUR was determined by voiding cystourethrography (VCUG) and graded from I to V. The diagnostic value of predictors was judged using multivariate logistic modelling with the area under the receiver operating characteristic (ROC area). A risk score was derived based on the regression coefficients of the independent predictors in the logistic model. In 140 children (51 boys and 89 girls) VUR was diagnosed in 37. Independent predictors for VUR were male gender, age, family history for uropathology, serum C-reactive protein level (CRP) and dilatation of the urinary tract on US. The ROC area of this model was 0.78 (95% CI: 0.69-0.87). This prediction model identified 12% (95% CI: 7-18) of the patients without VUR without missing one case of VUR. If we used VUR > or = grade 3 as a threshold, the model assessed VUR to be absent in 34% (95% CI: 26-42). CONCLUSION: A prediction rule based on age, gender, family history, CRP and US results is useful in assessing the probability of VUR in the individual child with a first UTI and may help the physician to make decisions about performing additional imaging techniques. Prospective validation of the model in future patients, however, will be necessary before applying the rule in practice.

Age Factors↗
PubMed1998

Mouse embryos do not wait for the MBT: chromatin and RNA polymerase remodeling in genome activation at the onset of development.

In Xenopus and Drosophila embryos, activation of the zygotic genome occurs after a series of rapid nuclear divisions in which DNA replication occupies most of the cell cycle. In these organisms, it has been proposed that zygotic transcription does not begin until a threshold nucleocytoplasmic ratio has been obtained in which repressive factors are titrated out and interphase becomes long enough to allow synthesis of transcripts. In mammalian embryos, however, a model of threshold nucleocytoplasmic ratios does not seem to apply, as beginning with the 1-cell stage, there are regulated cell cycles with the expression of zygotic transcripts during the cleavage period. By taking advantage of the slower kinetics at the onset of mouse development, we have characterized changes in chromatin structure and the basal transcription machinery throughout the transition from transcriptional incompetence, to minor activation of the zygotic genome during the 1-cell stage, and through major genome activation at the 2-cell stage. Further maturation of chromatin structure continues through subsequent cleavage cycles as a foundation for the first cellular differentiations in the blastocyst. The epigenetic chromatin modifications that occur during the cleavage period may have long range and inheritable effects and are undoubtedly important in the ability of the mammalian oocyte to remodel previously defined nuclear structures and cell fates.

Animals↗
PubMed1982

Model for simulating cyclic variations in focal epileptogenic excitability.

During 0.2 to 1.0 Hz stimulation of an epileptogenic focus, the phenomenon of cyclic spike driving (CSD) occurs, wherein 20- to 40-sec active periods, in which each stimulus triggers an all-or-none interictal event (IE), alternate with quiet periods of similar duration, in which IE are not triggered. CSD was simulated by a model in which individual IE are followed by biphasic response functions which sum linearly to produce long-term oscillations of epileptogenic excitability relative to the IE triggering threshold. The model successfully simulates all of the major characteristics of experimentally induced CSD, including the effects of manipulating stimulus parameters. Results of the simulation provide clues as to the time course of mechanisms which control epileptogenic triggerability.

Action Potentials↗
PubMed1993

Renal tubule Na,K-ATPase polarity in glucocorticoid-induced polycystic kidney disease.

Cyst formation in polycystic kidney disease (PKD) involves proliferation of cyst lining epithelial and changes in trans-epithelial fluid and electrolyte transport. In vitro studies have suggested that mislocation of Na,K-ATPase to the apical tubular surface may be an important component of cyst fluid transport. We undertook in vivo studies of Na,K-ATPase location using the "threshold" murine model of glucocorticoid-induced PKD (GIPKD). Using histological, immunohistochemical, and densitometric techniques, we compared cyst formation and the cellular location of Na,K-ATPase in suckling C3H (low threshold for GIPKD) and DBA (high threshold) mice given an inducing dose of 200 mg/kg methylprednisolone acetate. As expected, C3H mice demonstrated greater cyst formation as measured by proportion of section area occupied by the tubule lumen (26.7% vs 15.5%; p < 0.001). Cyst formation was associated with increased Na,K-ATPase staining and increased apical Na,K-ATPase location. MPA treatment in C3H mice resulted in apical staining that exceeded basolateral staining (35.3% of reference window vs 29.8%; p < 0.001). The relatively GIPKD-resistant DBA mice did not show such change in Na,K-ATPase location. These immunohistochemical studies suggest a role for Na,K-ATPase in renal cyst formation.

Animals↗
PubMed1999

Methods for detecting and estimating population threshold concentrations for air pollution-related mortality with exposure measurement error.

The association between daily fluctuations in ambient particulate matter and daily variations in nonaccidental mortality have been extensively investigated. Although it is now widely recognized that such an association exists, the form of the concentration-response model is still in question. Linear, no threshold and linear threshold models have been most commonly examined. In this paper we considered methods to detect and estimate threshold concentrations using time series data of daily mortality rates and air pollution concentrations. Because exposure is measured with error, we also considered the influence of measurement error in distinguishing between these two completing model specifications. The methods were illustrated on a 15-year daily time series of nonaccidental mortality and particulate air pollution data in Toronto, Canada. Nonparametric smoothed representations of the association between mortality and air pollution were adequate to graphically distinguish between these two forms. Weighted nonlinear regression methods for relative risk models were adequate to give nearly unbiased estimates of threshold concentrations even under conditions of extreme exposure measurement error. The uncertainty in the threshold estimates increased with the degree of exposure error. Regression models incorporating threshold concentrations could be clearly distinguished from linear relative risk models in the presence of exposure measurement error. The assumption of a linear model given that a threshold model was the correct form usually resulted in overestimates in the number of averted premature deaths, except for low threshold concentrations and large measurement error.

Air Pollutants↗
PubMed1993

Risk assessment in immunotoxicology. II. Relationships between immune and host resistance tests.

We have reported on the design and content of a screening battery using a "tier" approach for detecting potential immunotoxic compounds in mice (Luster et al., Fundam. Appl. Toxicol., 10, 2-19, 1988). The data base generated from these studies, which consists of over 50 selected compounds, has been collected and analyzed in an attempt to improve future testing strategies and provide information to aid in developing future quantitative risk assessment for immunotoxicity. In a recent study it was shown that as few as two or three immune parameters were needed to predict immunotoxicants in mice (Luster et al., Fundam. Appl. Toxicol., 18, 200-210, 1992). In particular, enumeration of lymphocyte populations and quantitation of the T-dependent antibody response were particularly beneficial. Furthermore, commonly employed apical measures (e.g., leukocyte counts, lymphoid organ weights) were fairly insensitive. The present analyses focus on the use of this data base to develop statistical models that examine the qualitative and quantitative relationship(s) between the immune function and host resistance tests. The conclusion derived from these analyses are: (1) A good correlation exists between changes in the immune tests and altered host resistance in that there were no instances where host resistance was altered without affecting an immune test(s). However, in some instances immune changes occurred without corresponding changes in host resistance. (2) No single immune test could be identified which was fully predictive for altered host resistance, although most assays were relatively good indicators (i.e., > 70%). Several others, such as proliferative response to lipopolysaccharide and leukocyte counts, were found to be relatively poor indicators for host resistance changes. (3) The ability to resist infectious agent challenge is dependent upon the degrees of immunosuppression and the quantity of infectious agent administered. (4) Logistic and standard regression modeling using one extensive chemical data set from the immunosuppressive agent, cyclophosphamide, indicated that most immune function-host resistance relationships followed linear rather than linear-quadratic (threshold-like) models. For most of the relationships this could not be confirmed using a large chemical data set and, thus, a more mechanistically based approach for modeling will need to be developed. (5) Using this limited data set, methods were developed for modeling the precise quantitative relationships between changes in selected immune tests and host resistance tests.

Animals↗
PubMed1985

[Narcolepsy].

First described as a separate entity by Gelineau in 1880 and later considered as a symptom, narcolepsy has eventually been recognized as a disease on clinical and polygraphic grounds. Its prevalence stays between 0.04 and 0.06 percent. Age at onset varies from 5 to 50 with a peak in the second decade. Clinical symptoms include excessive daytime somnolence, overwhelming daytime sleep episodes, attacks of cataplexy, hypnagogic hallucinations, sleep paralysis and disturbed nocturnal sleep; sleep onset REM episodes are the main polygraphic feature. Natural history varies with the different symptoms. Excessive daytime somnolence never subsides completely. Cataplexy may disappear spontaneously. Hypnagogic hallucinations and sleep paralysis are not present in all patients and tend to be more transitory. A positive diagnosis of narcolepsy requires a minimum of one major symptom, daytime sleep episodes or cataplexy, together with documented sleep onset REM episodes. Prolonged polygraphic recordings or multiple sleep latency test are of special interest in difficult cases. Clinical variants can be grouped under three headings, incomplete, symptomatic and associated narcolepsies. The etiology of narcolepsy is not well understood. However the discovery of natural animal models of narcolepsy, mainly dogs, has prompted genetic, pharmacological and biochemical studies. The breeding of narcoleptic canine colonies has led to the evidence of a possible autosomal recessive model of inheritance in some species. Pharmacological and neurochemical analysis has shown an imbalance between monoaminergic and cholinergic mechanism. In man, extensive family studies suggest either a two-threshold multifactorial model of inheritance or a dominant mode of inheritance and immunologic studies have recently shown a strong association between HLA-DR2 and narcolepsy. Assays of CSF biogenic amines suggest a decreased bioavailability of dopamine to explain sleepiness and an imbalance between monoamines and acetylcholine to explain cataplexy. A disturbance of circadian rhythms has not been evidenced in narcoleptics. Treatment is still purely symptomatic. Amphetamines and tricyclic antidepressants have been extensively used. However they are not free of side-effects hence the need for alternative treatments.

Adolescent↗
PubMed1997

Further studies of phonation threshold pressure in a physical model of the vocal fold mucosa.

This paper reports results of further experimentation on a previously developed physical model of the vocal-fold mucosa [Titze et al., J. Acoust. Soc. Am. 97, 3080-3084 (1995)]. The effects of vocal-fold thickness, epithelial membrane thickness, and prephonatory glottal geometry on phonation threshold pressure were studied. Phonation threshold pressures in the range of 0.13 to 0.34 kPa were observed for an 11-mm-thick vocal fold with a 70-micron-thick "epithelial" membrane for different "mucosal" fluid viscosities. Higher threshold pressure was always obtained for thinner vocal folds and thicker membranes. In another set of experiments, lowest offset threshold pressure was obtained for a rectangular or a near-rectangular prephonatory glottis (with a glottal convergence angle within about +/- 3 degrees). It ranged from 0.07 to 0.23 kPa for different glottal half-widths between 2.0 and 6.0 mm. The threshold for more convergent or divergent glottal geometries was consistently higher. This finding only partially agrees with previous analytical work which predicts a lowest threshold for a divergent glottis. The discrepancy between theory and data is likely to be associated with flow separation from a divergent glottis.

Humans↗
PubMed2000

Section 4--bioeffects in tissues with gas bodies. American Institute of Ultrasound in Medicine.

Several animal models have exhibited thresholds for petechial hemorrhage in lung within the current output of diagnostic ultrasound systems. In addition, thresholds for damage in the mouse intestine due to diagnostic pulses of ultrasound have been explored. The implications for human lung and intestinal exposure to clinical diagnostic ultrasound have not yet been determined. In this section, the data supporting the thresholds of petechial hemorrhage in these organ systems and the morphological observations will be reviewed. The potential mechanical mechanisms of damage to these organs due to diagnostic ultrasound also will be reviewed. Special attention will be given to the occurrence of inertial cavitation both in vitro and in vivo. The effects of ultrasound parameters, age, and species on the threshold for damage in animal models will be explored.

Age Factors↗
PubMed2004

Towards a unifying basis of auditory thresholds: the effects of hearing loss on temporal integration reconsidered.

For signal detection and identification, the auditory system needs to integrate sound over time. It is frequently assumed that the quantity ultimately integrated is sound intensity and that the integrator is located centrally. However, we have recently shown that absolute thresholds are much better specified as the temporal integral of the pressure envelope than of intensity, and we proposed that the integrator resides in the auditory pathway's first synapse. We also suggested a physiologically plausible mechanism for its operation, which was ultimately derived from the specific rate of temporal integration, i.e., the decrease of threshold sound pressure levels with increasing duration. In listeners with sensorineural hearing losses, that rate seems reduced, but it is not fully understood why. Here we propose that in such listeners there may be an elevation in the baseline above which sound pressure is effective in driving the system, in addition to a reduction in sensitivity. We test this simple model using thresholds of cats to stimuli of differently shaped temporal envelopes and durations obtained before and after hearing loss. We show that thresholds, specified as the temporal integral of the effective pressure envelope, i.e., the envelope of the pressure exceeding the elevated baseline, behave almost exactly as the lower thresholds, specified as the temporal integral of the total pressure envelope before hearing loss. Thus, the mechanism of temporal integration is likely unchanged after hearing loss, but the effective portion of the stimulus is. Our model constitutes a successful alternative to the model currently favored to account for altered temporal integration in listeners with sensorineural hearing losses, viz., reduced peripheral compression. Our model does not seem to be at variance with physiological observations and it also qualitatively accounts for a number of phenomena observed in such listeners with suprathreshold stimuli.

Animals↗
PubMed1994

Response of the magnocellular system in rats to hypovolemia and cholecystokinin during pregnancy and lactation.

To define changes in the magnocellular neuroendocrine system during lactation and pregnancy, we compared plasma levels of oxytocin (OT) and vasopressin (VP) after polyethylene glycol (PEG)-induced hypovolemia and cholecystokinin (CCK) stimulation. Conscious virgin, pregnant (day 20), and lactating (day 6) Sprague-Dawley rats were injected with either PEG (70-600 mg/ml; 35 or 70 ml/kg sc), CCK (100 micrograms/ml; 4 ml/kg ip), or vehicle and decapitated 4 h (PEG) or 5 min (CCK) later. Changes in thresholds for release of hormone and the responsiveness (slopes relating [hormone] to blood volume depletion or to plasma osmolality) of the OT and VP systems were determined using an iterative nonlinear threshold regression model. After PEG, plasma osmolality increased coincident with a decrease in blood volume, with both stimuli contributing to the rise in plasma VP and OT. Compared with virgin rats, neither the threshold nor the responsiveness of the VP system was altered by the combined stimulus, whereas the oxytocinergic system of pregnant rats was more responsive to osmotic component. Lactating rats, however, had a higher threshold for VP release and an apparent elevation of the OT threshold beyond 25% volume depletion. Regardless of the reproductive state, the threshold for VP release was always lower than that for OT. Intraperitoneal CCK elevated plasma [OT] in each reproductive state, although the response in lactating animals was attenuated. In virgin and lactating rats, plasma levels of VP also increased slightly but significantly in response to CCK. During gestation when cardiovascular volume is expanded, both the VP and OT neuroendocrine systems were reset, enabling secretion of both hormones in response to hypovolemia with hypertonicity. During lactation, both neuroendocrine systems are reset such that greater changes in fluid balance are needed to stimulate hormone release. Regardless of the reproductive state, the threshold for VP release was always lower than that for OT, indicative of preferential release of VP with less than a 5% (virgin, pregnant) or a 20% (lactating) loss in blood volume.

Animals↗