Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spreading”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources
PubMed2006

Spread of the radial SNAP: a pitfall in the diagnosis of carpal tunnel syndrome using standard orthodromic sensory conduction study.

OBJECTIVE: To investigate the occurrence of the spread of the radial sensory nerve action potential (SNAP) among patients with carpal tunnel syndrome (CTS) during standard median orthodromic sensory conduction study (SCS) using index finger stimulation. METHODS: We prospectively examined 74 hands in 56 CTS patients. We stimulated the index finger using ring electrodes. SNAPs were recorded at wrist over median and radial nerves. RESULTS: A spread of radial SNAP was clearly identified over the median nerve despite its small amplitude, in 72/74 hands during stimulation of the base of the index finger. In hands with delayed median SNAP, two peaks were observed; however in hands with absence of genuine median SNAP, only one peak of the spread was noticed. The proximal interphalangeal joint (PIP) stimulation still elicited an identifiable spread in 47/74 hands. CONCLUSION: This spread phenomenon is a previously undescribed pitfall during the standard median orthodromic SCS, frequently occurring in CTS patients. SIGNIFICANCE: In severe CTS cases, one may make wrong conclusion of normal median sensory latency if unaware of this pitfall.

Action Potentials↗
PubMed2006

Do dialogues about concepts of pain reduce immigrant patients' reported spread of pain? A comparison between two consultation methods in primary care.

OBJECTIVES: Do dialogues about concepts of pain reduce the reported spread of pain more than the usual consultations? SETTING: A 4-week programme in primary care for immigrants on sick-leave, aged 16-45 years, containing daily exercises and randomised to either four interviews and dialogues about pain with a female doctor (group A) or the usual consultations with a male doctor (group B). METHODS: Two doctors made the first and the last evaluations (before and after the programme) containing diagnostics of tender-structure locations and depression (yes-no), and ratings of severity of psychosocial stressors. Anxiety about pain was noted (yes-no). The patients pointed to their painful areas and these were noted on pain drawings (0-18 fields). Median values were calculated, and non-parametric statistics were used to test for significant differences between groups and before-and-after values, and the correlation between the number of pain drawing fields and clinical variables. RESULTS: Forty-five persons participated in the whole programme, Group A (8 men, 15 women), group B (7 men, 15 women). Many of them needed an interpreter. Participants in group A had more tender-structure locations (two vs. one in group B). Nearly half had depression and two-thirds had serious psychosocial stressors. Almost all reported anxiety about pain at the start, but afterwards significantly fewer in group A (22 vs. 16, p < 0.05). In both groups, the number of pain drawing fields decreased significantly from, in median, eight to four (p < 0.001), particularly among the women (A: p < 0.05 vs. B: p < 0.01). Some very distressed participants reported more spread of pain than at the start. Reduced spread of pain was not significantly correlated to any clinical variable. CONCLUSIONS: Particularly the women in both consultation groups demonstrated much less spread of pain after treatment, despite similar clinical findings and less anxiety about pain in group A. The initially wide spread of pain may thus have been a way of communicating with the doctors.

Adolescent↗
PubMed2004

Hip-flexed postures do not affect local anaesthetic spread following induction of epidural analgesia for labour.

Hip-flexed postures enlarging the pelvic diameter are used to improve the obstetric course of labour. Although most investigations show that lateral and sitting positions do not affect the spread of epidural analgesia, the effect of recently introduced hip-flexed postures has yet to be confirmed. This prospective randomised study included 93 parturients. Ropivacaine 0.1% 12 mL plus sufentanil 0.5 micrograms/mL was administered epidurally over a period of 6 min in one of four postures: sitting, right hip-flexed left lateral position, left hip-flexed right lateral position and supine 30 degrees lateral tilt as a control group. Left and right cephalad and sacral epidural spread were measured every 2 min over a period of 30 min. Pain relief, motor blockade and maternal and fetal side effects were noted. The total epidural spread was 15+/-0.3 dermatomes and the upper level of thermo-algesic blockade T7-T8 (range T3 to T10) in all groups. There were no differences between groups in left or right total spread or upper level of epidural blockade, time to maximal block or pain relief. There was no motor block nor any maternal or fetal side effects. The power of the study (1 - beta) was 93%. We conclude that, for the three hip-flexed postures tested, position does not influence local anaesthetic spread or symmetry of thermo-algesic blockade after induction of obstetric epidural analgesia.

Adult↗
PubMed2006

Poly(ethylene oxide)s hydrophobically modified. Adsorption and spreading at the air-water interface.

A comparative study of spread and adsorbed monolayer of poly(ethylene oxide)s of different molecular weight hydrophobically modified with alkyl isocyanates of different length chain is reported. The modification of the polymer was carried out according to reported procedures. The polymers obtained were studied at the air-water interface by Langmuir isotherms for spread monolayers and by Gibbs isotherms for the adsorption process. Isotherms obtained are interpreted in terms of the hydrophobic and hydrophilic balance of the polymers. Limiting area per repeating unit (A(0)) and collapse pressure (pi(c)) from spread monolayers were obtained. Spread monolayers of the hydrophobically modified polymers show larger collapse pressure values than unmodified polymer monolayers. In the adsorption process the excess surface concentration Gamma(infinity), area per repeat unit sigma, and efficiency of the adsorption were determined. The values of the area occupied per repeat unit in adsorbed monolayer (sigma) were larger than those of the spread monolayer. The efficiency of the adsorption of poly(ethylene oxide)s increases with the hydrophobic modification and with the alkyl chain length.

Journal Article↗
PubMed2006

Viscous-gravity spreading of time-varying liquid drop volumes on solid surfaces.

Viscous-gravity spreading of liquid drops of time-dependent volume over a solid surface is considered. A self-similar solution for the drop configuration is obtained, in the case the liquid drop volume varies as a power-law function of time, along with the spreading laws in both cases of cylindrical and axisymmetric geometries. Results compare favorably with published experimental results and previous theoretical work. The limitations of the model are discussed, along with a comparison with viscous gravity spreading of oil on water. The validity of using approximate spreading laws is considered, and an approximate method is suggested to provide the dynamics of spreading in the general case where the drop volume does not necessarily vary as a power-law function of time.

Journal Article↗
PubMed2005

Quantitatively distinct requirements for signaling-competent cell spreading on engineered versus natural adhesion ligands.

To design synthetic microenvironments that elicit desired cell behaviors, we must better understand the molecular mechanisms by which cells interact with candidate biomaterials. Using cell lines with distinct alpha5beta1 integrin expression profiles, we demonstrate that this integrin mediates cell spreading on substrata coated with genetically engineered artificial extracellular matrix (aECM) proteins containing the RGD sequence (RGD-containing aECM protein [aRGD]) but lacking the PHSRN synergy site. Furthermore, aRGD-mediated adhesion stimulates an intracellular focal adhesion kinase (FAK) signal that is indicative of integrin tethering. Although both aRGD and the natural ECM protein fibronectin (FN) support alpha5beta1 integrin-mediated cell spreading, quantitative single-cell analysis revealed that aRGD-mediated spreading requires ten-fold greater threshold amount of integrin expression than FN-mediated spreading. Our analysis demonstrates that aRGD-based substrata mediate both biophysical (cell spreading) and biochemical (FAK signaling) events via the alpha5beta1 integrin, albeit with efficacy quantitatively distinct from that of natural ECM proteins that possess the full spectrum of adhesion and synergy domains.

Amino Acid Sequence↗
PubMed2004

The spread of cell death from impact damaged cartilage: lack of evidence for the role of nitric oxide and caspases.

UNLABELLED: Over 21 days in culture, cell death spreads, both radially and transversely, from loaded to surrounding cartilage. This spread was prevented by physical separation and separate culture post-impact. OBJECTIVE: One aim was to determine if nitric oxide (NO) is the intercellular signal mediating cell death. Another aim was to clarify the nature of the cell death, whether caspase mediated apoptosis or necrosis. DESIGN: Cyclic impacts were applied to the central 2 mm core of 4 mm canine articular cartilage discs. Post-impact culturing was for 21 days in the presence or absence of the iNOS inhibitor, L-NAME, or the broad-spectrum caspase inhibitor, Z-VAD FMK. Cell death was quantified using the TUNEL assay. Culture media were collected every 2 days for measurements of glycosaminoglycan (GAG) and NO release. RESULTS: Cell death spread from the loaded core into the surrounding ring over 21 days in culture. Although L-NAME significantly reduced nitrite release into the culture media of both loaded and control cartilage, the spread of cell death was not prevented. Neither was the spread of cell death prevented by Z-VAD FMK. CONCLUSIONS: These data indicate that NO is not acting as an intercellular signalling factor in this in vitro system and that the cell death post-impact is not caspase mediated.

Amino Acid Chloromethyl Ketones↗
PubMed2004

Spread of two linked social norms on complex interaction networks.

In this paper, we study the spread of social norms, such as rules and customs that are components of human cultures. We consider the spread of two social norms, which are linked through individual behaviors. Spreading social norms depend not only on the social network structure, but also on the learning system. We consider four social network structures: (1) complete mixing, in which each individual interacts with the others at random, (2) lattice, in which each individual interacts with its neighbors with some probability and with the others at random, (3) power-law network, in which a few influential people have more social contacts than the others, and (4) random graph network, in which the number of contacts follows a Poisson distribution. Using the lattice model, we also investigate the effect of the small-world phenomenon on the dynamics of social norms. In our models, each individual learns a social norm by trial and error (individual learning) and also imitates the other's social norm (social learning). We investigate how social network structure and learning systems affect the spread of two linked social norms. Our main results are: (1) Social learning does not lead to coexistence of social norms. Individual learning produces coexistence, and the dynamics of coexistence depend on which social norms are learned individually. (2) Social norms spread fastest in the power-law network model, followed by the random graph model, the complete mixing model, the two-dimensional lattice model and the one-dimensional lattice. (3) We see a "small world effect" in the one-dimensional model, but not in two dimensions.

Computer Simulation↗
PubMed2005

Malaria transmission intensity and the rate of spread of chloroquine resistant Plasmodium falciparum: Why have theoretical models generated conflicting results?

The rate at which falciparum resistant malaria spreads in different transmission settings is still a controversial subject. We have assessed the spread of mutant Plasmodium falciparum parasites in six Ugandan populations with varying prevalence of chloroquine resistance (CQR), malaria transmission intensity, multiplicity of parasite clones and prevalence of CQ use. For each population, we have determined the wild and mutant allele frequency at codons 76 and 86 of the pfcrt and pfmdr1 genes, respectively. The highest frequency (median = 16.3%, range: 0.0-70.4%) of infections with two pure mutants (no wild genotype in either gene), adjusted for clone multiplicity, was observed at the extremes of malaria transmission intensity. The wild/mutant (W/M) allele ratio (an index for tracking the progression of CQR) was less than one in all sites (median = 0.51, range: 0.09-0.98) for the pfcrt-76 gene, while it was greater than one in two of six sites (median = 0.75, range: 0.4-1.6) for the pfmdr1-86 gene, suggesting that the pfcrt-76 mutants were the predominant parasites at all sites. Furthermore, the pfmdr1-86 W/M allele ratio was consistently higher than that of the pfcrt-76. The spread of mutations linked to CQR in P. falciparum commences with the pfcrt-76 gene mutations, followed later by the pfmdr1-86 gene mutations that modulate higher CQR. Such spread occurs faster at the extremes of the transmission spectrum and could explain why mathematical models have previously generated conflicting results with respect to malaria transmission intensity and spread of CQR.

Alleles↗
PubMed2005

Isocaloric substitution of plant sterol-enriched fat spread for carbohydrate-rich foods in a low-fat, fibre-rich diet decreases plasma low-density lipoprotein cholesterol and increases high-density lipoprotein concentrations.

BACKGROUND AND AIM: The aim of the study was to determine the effects on plasma cholesterol of replacing a plant sterol-enriched fat spread with carbohydrate-rich foods relative to a diet high in saturated fat. METHODS AND RESULTS: Twenty-nine men and women, from the general community, with mean age (SD) 48 (14)y, body mass index 29.0 (6.2)kg/m(2), and plasma total cholesterol concentration 6.48 (0.97)mmol/L completed the randomised, crossover dietary intervention. There were three diets: New Zealand diet (NZ diet) high in total (34%kJ) and saturated (15%kJ) fat, a cholesterol-lowering fibre-rich diet reduced in total (30%kJ) and saturated fat (8%kJ) but including a plant sterol spread (PS diet), and the same cholesterol-lowering diet with the plant sterol spread isocalorically replaced with carbohydrate (CHO diet); total fat, 26%kJ; saturated fat 7%kJ. All foods were provided and each diet was followed for four weeks. Mean (SD) plasma low-density lipoprotein cholesterol concentration declined from 4.68 (0.91)mmol/L on the high saturated fat diet to 4.12 (0.83)mmol/L (P<0.001) on the carbohydrate diet and 3.76 (0.84)mmol/L (P<0.001) on the plant sterol diet. The 20% decrease on the plant sterol diet was significantly greater (P<0.001) than the 12% decrease on the carbohydrate diet. Relative to the NZ diet, mean (95% CI) plasma high-density lipoprotein cholesterol concentration changed by -0.11 (-0.16, -0.06)mmol/L on the CHO diet but was not different at the end of the PS diet, -0.03 (-0.09, 0.02). CONCLUSION: Including a plant sterol-enriched fat spread in a cholesterol-lowering diet produces a more favourable plasma lipid profile than the same diet made lower in total and saturated fat by replacing the spread with carbohydrate-rich foods.

Adult↗
PubMed2004

The combined use of cholesterol-lowering drugs and cholesterol-lowering bread spreads: health behavior data from Finland.

BACKGROUND: Cholesterol-lowering drugs may metabolically interact with cholesterol-lowering bread spreads. This study analyses the prevalence of use of drugs, bread spreads or the combination of both in people aware of their high/elevated cholesterol level, and compares users of the three therapies on health behavior and demographics. METHODS: Participants (9581, 25-74 years) from The National FINRISK 2002 Study filled out a questionnaire on demographics and health (related) issues. Blood samples, blood pressure, body weight and height were measured. RESULTS: Of those who reported to have a high cholesterol level (31% of the study population), 19% used cholesterol-lowering drugs, 11% used cholesterol-lowering bread spreads and 5% combined both therapies. On a population level, only 1% jointly used a drug and bread spread therapy. The combination was used by especially highly educated people and those having a healthy diet. CONCLUSION: Combining a cholesterol-lowering drug with a bread spread regimen is relatively rare, even among those being aware of their high cholesterol levels. The combined usage was most frequent among 'the better off'. Public health risks of a metabolic interaction between both therapies may not be of major importance yet, but future follow-up is recommended.

Adult↗
PubMed2000

Effects of clomethiazole on spreading depression in the rat hippocampal slice.

Clomethiazole is neuroprotective in a variety of animal models of ischaemic stroke, but the mechanism is unclear. This study examined whether clomethiazole is able to modify spreading depression elicited in rat hippocampal slices. When spreading depression was induced by superfusion with high K(+) medium (50 mM), clomethiazole at 100 microM reduced its duration. Both the amplitude and duration of spreading depression were reduced at 200 microM. Clomethiazole at 200 microM tended to reduce the amplitude of the K(+)-induced shift in direct current (DC) potential but this was not statistically significant. When a pair of K(+) pulses were presented, 30 min apart, the second produced a smaller DC potential than the first. Clomethiazole at 200 microM increased the size of the ratio of these responses. Superfusion with a hypoxic solution induced spreading depression observed as a shift in the DC field potential. The amplitude of this was decreased significantly by clomethiazole at 200 microM. With intracellular recordings, the effects of clomethiazole were quantified by measuring the time from the peak K(+)-induced depolarisation to the recovery of membrane potential following the period of hyperpolarisation. Clomethiazole did not reduce this period significantly. It is concluded that clomethiazole can reduce some forms of spreading depression, but only at the higher concentrations tested. It is unlikely that this effect contributes to its neuroprotective properties.

Action Potentials↗
PubMed2003

Syndecan-1-mediated cell spreading requires signaling by alphavbeta3 integrins in human breast carcinoma cells.

Syndecans are cell surface heparan sulfate proteoglycans with regulatory roles in cell adhesion, proliferation, and differentiation [Annu. Rev. Biochem. 68 (1999) 729]. While the syndecan heparan sulfate chains are essential for matrix binding, less is known about the signaling role of their core proteins. To mimic syndecan-specific adhesion, MDA-MB-231 mammary carcinoma cells were plated on antibodies against syndecan-4 or syndecan-1. While cells adherent via syndecan-4 spread, cells adherent via syndecan-1 do not. However, cells adherent via syndecan-1 can be induced to spread by Mn(2+), suggesting that activation of a beta(1) or beta(3) integrin partner is required. Surprisingly, pretreatment of cells with a function-activating beta(1) antibody does not induce spreading, whereas function-blocking beta(1) integrin antibodies do, suggesting involvement of a beta(1)-to-beta(3) integrin cross-talk. Indeed, blockade of beta(1) integrin activation induces alpha(v)beta(3) integrin activation detectable by soluble fibrinogen binding. Spreading in response to syndecan-1 is independent of integrin-ligand binding. Furthermore, competition with soluble murine syndecan-1 ectodomain, which does not disrupt cell adhesion, nonetheless blocks the spreading mechanism. These data suggest that the ectodomain of the syndecan-1 core protein directly participates in the formation of a signaling complex that signals in cooperation with alpha(v)beta(3) integrins; signaling via this complex is negatively regulated by beta(1) integrins.

Breast Neoplasms↗
PubMed2001

Randomised controlled trial of use by hypercholesterolaemic patients of a vegetable oil sterol-enriched fat spread.

Plant sterols may be a useful additive therapy in the treatment of hypercholesterolaemic patients. The purpose of this study was to determine the effect of a fat spread enriched with vegetable oil sterols on plasma lipid, lipoprotein and apolipoprotein concentrations. A randomised double blind placebo-controlled crossover trial with two consecutive periods of 8 weeks was conducted. 30 patients with heterozygous familial hypercholesterolaemia treated concurrently with an HMG-CoA reductase inhibitor (statin) and 32 patients with type IIa primary hypercholesterolaemia with a total cholesterol concentration >6.5 mmol/l not taking lipid-lowering drug therapy were recruited from a hospital lipid clinic. The active treatment was a fortified fat spread (25 g/day) providing 2.5 g of plant sterols. The control spread was indistinguishable in taste and appearance. Comparison at the end of the two 8-week trial periods showed a statistically significant reduction in total and LDL-cholesterol with use of the fortified spread but the results were confounded by a carry-over effect, which was partly explained by changes in the background diet. Because a carry-over effect was present, further analyses were restricted to the parallel arms of the first treatment period and were conducted on an intention to treat basis. After 4 weeks, LDL-cholesterol had decreased by 0.04 mmol/l ([0.8%] 95% confidence interval -0.44-0.37 NS) in the placebo group and decreased by -0.76 mmol/l ([15.0%] 95% CI -1.03--0.48, P<0.0001) in the active treatment group. After 8 weeks, the corresponding results were 0.0 mmol/l ([0.0%] 95% CI -0.26-0.24 NS) and -0.51 mmol/l ([10.0%] 95% CI -0.73--0.29 P<0.0001). There were no significant changes in apolipoprotein AI or B concentrations in the placebo group, but there was a small but statistically significant increase in apolipoprotein AI and a decrease in apolipoprotein B in the active treatment group. HDL cholesterol and triglyceride concentrations were unchanged. There was no difference in response between patients with statin-treated familial hypercholesterolaemia and patients with type IIa hyperlipoproteinaemia. We conclude that a fortified fat spread enriched with vegetable oil sterols reduces LDL-cholesterol by 10-15% with no difference in response between hypercholesterolaemic patients prescribed statins and those not taking lipid-lowering drug therapy.

Adult↗
PubMed2003

Characterisation of some cytotoxic endpoints using rat liver and HepG2 spheroids as in vitro models and their application in hepatotoxicity studies. II. Spheroid cell spreading inhibition as a new cytotoxic marker.

Cells in liver spheroids and Hep G2 spheroids transferred from gyrotatory culture conditions and maintained in normal static culture conditions will spread out at the edges. Based on this observation, we developed a new test called the Spheroid Cell Spreading Inhibition Test (SCSIT) to screen hepatic cytotoxicity of xenobiotics and determine the spheroid cell spreading inhibition concentration (SCSIC) of test chemicals. Four model hepatoxicants, D-galactosamine, propranolol, diclofenac, and paracetamol, were studied with SCSIT in both rat liver and HepG2 spheroids. Both liver and HepG2 spheroids were prepared under gyrotatory culture conditions and used at 6 days in vitro. The results showed that all four hepatotoxicants tested inhibited cell spreading in liver spheroids (D-galactosamine at 20 mM, propranolol at 125 microM, diclofenac at 500 microM, and paracetamol at 25 mM) and HepG2 spheroids (D-galactosamine at 16 mM, propranolol at 125 microM, diclofenac at 500 microM, and paracetamol at 25 mM). The SCSIT results agreed with the conventional cytotoxic indicators, release of LDH and/or gamma-GT and the inhibition of glucose secretion from rat liver spheroids. In conclusion, this study, for the first time, described the biological characteristics of liver and HepG2 spheroid cell spreading and demonstrates its application in hepatic cytotoxicity studies. This method may be used in testing in vitro "acute" toxicity, comparing relative cytotoxicity and generating reference concentrations for subsequent studies. Therefore, SCSIT could be a useful tool for screening hepatotoxicity relevant to preclinical lead optimization and compound library screening.

Acetaminophen↗
PubMed2001

Two competing mechanisms underlying neon color spreading, visual phantoms and grating induction.

Neon color spreading is closely related to the photopic visual phantom illusion, since these two completion phenomena are characterized by in-phase lightness induction, and the only difference in the stimulus configuration is the difference in the inducer height. This idea was supported by the present study. Neon color spreading showed almost the same function of critical spatial frequency as photopic visual phantoms (Experiment 1), and the critical spatial frequency was constant as the inducer height was changed (Experiment 2). We also examined the relationship between neon color spreading and grating induction (characterized by counterphase lightness induction) in critical spatial frequency (Experiment 3) and in magnitudes of lightness induction (Experiment 4) as a function of the inducer height. The inducer height at which in-phase (neon color spreading) appearance gave way to counterphase (grating) induction was approximately 0.1 deg. These results suggest that neon color spreading shares a common neural mechanism with the photopic visual phantom illusion and that this mechanism is different from, and competes with, the mechanism of grating induction.

Color Perception↗
PubMed1999

Colour at edges and colour spreading in McCollough effects.

Broerse and O'Shea [(1995) Vision Research, 35, 207-226] proposed that the subjective colours in McCollough effects (MEs) consist of two components: edge colours appearing along the edges of contours, and spread colours radiating from edge colours into adjacent uncontoured regions of test patterns. This proposal was examined in five experiments. First, we demonstrated that fine coloured lines located immediately adjacent to the edges of otherwise achromatic square-wave gratings (i.e. colour-fringed gratings) are sufficient to induce MEs comparable in strength to MEs induced with desaturated versions of traditional uniformly-coloured gratings (Experiments 1 & 2). We then quantified edge and spread colours while varying light/dark duty cycles (white-bar width) in gratings with colour-fringed edges (Experiment 3), uniformly-coloured gratings (Experiment 4), and in achromatic gratings tinged with ME colours after adaptation to colour-fringed gratings (Experiment 5). Whereas the perceived magnitude of edge colours remained constant in all cases, spread colours remained constant only for uniformly-coloured gratings. For both MEs and gratings with colour-fringed edges, spread colours decreased as a function of increasing duty cycle, confirming that conventional MEs may be simulated by gratings with colour-fringed edges. We propose that edge colours arise as a consequence of neural operations correcting for the eye's chromatic aberration, while spread colours reveal a neural filling-in process operating to achieve colour constancy. In seeking to implement these suggestions, we present a putative framework based on the receptive-field properties of single cells described in contemporary neurophysiological investigations of colour.

Adaptation, Ocular↗
PubMed2001

Artificial neural network model for the assessment of lymph node spread in patients with clinically localized prostate cancer.

OBJECTIVES: To develop an artificial neural network (ANN) model to predict lymph node (LN) spread in men with clinically localized prostate cancer and to describe a clinically useful method for interpreting the ANN's output scores. METHODS: A simple, feed-forward ANN was trained and validated using clinical and pathologic data from two institutions (n = 6135 and n = 319). The clinical stage, biopsy Gleason sum, and prostate-specific antigen level were the input parameters and the presence or absence of LN spread was the output parameter. Patients with similar ANN outputs were grouped and assumed to be part of a cohort. The prevalence of LN spread for each of these patient cohorts was plotted against the range of ANN outputs to create a risk curve. RESULTS: The area under the receiver operating characteristic curve for the first and second validation data sets was 0.81 and 0.77, respectively. At an ANN output cutoff of 0.3, the sensitivity achieved for each validation set was 63.8% and 44.4%; the specificity was 81.5% and 81.3%; the positive predictive value was 13.6% and 6.5%; and the negative predictive value was 98.0% and 98.1%, respectively. The risk curve showed a nearly linear increase (best fit R(2) = 0.972) in the prevalence of LN spread with increases in raw ANN output. CONCLUSIONS: The ANN's performance on the two validation data sets suggests a role for ANNs in the accurate clinical staging of patients with prostate cancer. The risk curve provides a clinically useful tool that can be used to give patients a realistic assessment of their risk of LN spread.

False Negative Reactions↗