Anatomy of the clavicle and its medullary canal: a computed tomography study.

BACKGROUND: With recent literature indicating certain clavicle shaft fracture types are best treated surgically, there is renewed interest in the anatomy of the clavicle. Intramedullary fixation of clavicle fractures requires an adequate medullary canal to accommodate the fixation device used. This computed tomography anatomical study of the clavicle and its medullary canal describes its general anatomy and determines the suitability of its medullary canal to intramedullary fixation. DESCRIPTION OF METHODS: Four hundred and eighteen clavicles in 209 patients were examined using computed tomography imaging. The length and curvatures as well as the height and width of the clavicle and its canal at various predetermined points were measured. The start and end of the medullary canal from the sternal and acromial ends of the clavicle were determined. The data was grouped according to age, gender and lateralization. The average length of the clavicle was 151.15 mm with the average sternal and acromial curvature being 146° and 133°, respectively. The medullary canal starts on average 6.59 mm from the sternal end and ends 19.56 mm from the acromial end with the average height and width of the canal at the middle third being 5.61 and 6.63 mm, respectively. CONCLUSION: The medullary canal of the clavicle is large enough to accommodate commonly used intramedullary devices in the majority of cases. The medullary canal extends far enough medially and laterally for an intramedullary device to adequately bridge most middle third clavicle fractures. An alternative surgical option should be available in theatre when treating females as the medullary canal is too small to pass an intramedullary device past the fracture site on rare occasions.

Effect of anisotropy on the scaling of connectivity and conductivity in continuum percolation theory.

We investigate the effects of anisotropy on the finite-size scaling of connectivity and conductivity of continuum percolation in three dimensions. We consider a system of size X×Y×Z in which cubic bodies of size a×b×c are placed randomly. We define two aspect ratios to request anisotropy then we expect that the displacement of average connected fraction P (averaged over the realizations), about the isotropic universal curves will be a function of the two aspect ratios. This is accounted by considering an apparent percolation threshold in each direction which leads to 50% of realizations connecting in that direction. We find the aspect ratios' dependency of the apparent threshold and investigate the finite-size scaling transformations for the mean connected fraction and its associated fluctuations. Moreover, we apply a single phase pressure solver to determine the conductivity of various realizations of the system. Finally we apply the same idea to account for the effect of anisotropy on the conductivity scaling.

Identification of imidazoline-receptor binding sites in cortex and medulla of the bovine adrenal gland. Colocalization with MAO-A and MAO-B.

The distribution and relative densities of imidazoline-receptor binding sites (I-RBS) in bovine adrenal gland were determined using [3H]clonidine, [3H]2-(2-benzofuranyl)-2-imidazoline ([3H]2-BFI), and [3H]rilmenidine. In light of strong evidence that I-RBS and monoamine amine oxidase enzymes are linked, the selective radioligands [3H]RO41-1049 and [3H]RO19-6327 were used to label the distribution of MAO-A and -B enzymes, respectively. [3H]Clonidine (12 nM) labeled sites in two discrete regions of the bovine adrenal gland, the zona glomerulosa (39 +/- 7 fmol/mg tissue equivalent) and inner medulla (34 +/- 1 fmol/mg tissue). Binding was nonadrenergic (i.e., not inhibited by 100 nM methoxyidazoxan) and inhibited by 60-70% by 100 nM 2-BFI, the selective I2-RBS, suggesting binding predominantly to an I2-RBS. [3H]2-BFI (5 nM), the selective I2-RBS ligand, also labeled a high density of binding sites in the zona glomerulosa (57 +/- 9 fmol/mg) and chromaffin cells in the inner medulla (53 +/- 4 fmol/mg). These sites, however, were insensitive to clonidine (100 nM). By contrast, [3H]rilmenidine (40 nM) labeled I-RBS in all regions of the adrenal gland, that is, the zonae glomerulosa (59 +/- 10 fmol/mg), fasciculata (78 +/- 10 fmol/mg) and reticularis (63 +/- 7 fmol/mg), and outer and inner medullary chromaffin cells (42 +/- 1 and 55 +/- 2 fmol/mg, respectively). Binding to sites in the zona glomerulosa was partially inhibited (16%) by 100 nM 2-BFI. These results are consistent with previous studies indicating that [3H]rilmenidine labels an I2-RBS and additional I-RBS in rat brain and kidney. The distribution of [3H]RO19-6327 (5 nM) binding resembled that of [3H]2-BFI and [3H]clonidine binding with high densities of MAO-B enzyme located in the zona glomerulosa and chromaffin cells of the inner medulla (55 +/- 7 and 76 +/- 6 fmol/mg tissue, respectively), suggesting the colocalization of MAO-B enzyme with I2-RBS. [3H]RO41-1049 (20 nM) binding to MAO-A was highest in the zona reticularis (196 +/- 7 fmol/mg tissue) compared to the zonae glomerulosa and fasciculata (90 +/- 12 and 116 +/- 14 fmol/mg tissue) and inner medulla (149 +/- 38 fmol/mg tissue). Although the existence of I-RBS in bovine adrenal chromaffin cells is well established, this is the first description of I-RBS in the adrenal cortex. Further investigations are now required to determine whether imidazolines can affect adrenal function via actions at these sites.

Traveling time and traveling length in critical percolation clusters.

We study traveling time and traveling length for tracer dispersion in two-dimensional bond percolation, modeling flow by tracer particles driven by a pressure difference between two points separated by Euclidean distance r. We find that the minimal traveling time t(min) scales as t(min) approximately r(1.33), which is different from the scaling of the most probable traveling time, t* approximately r(1.64). We also calculate the length of the path corresponding to the minimal traveling time and find l(min) approximately r(1.13) and that the most probable traveling length scales as l* approximately r(1.21). We present the relevant distribution functions and scaling relations.

Pharmacology and subcellular distribution of [3H]rilmenidine binding sites in rat brain.

We have previously reported that in rat brain membranes, [3H]rilmenidine, in addition to labelling alpha2-adrenoceptors and the I2B-subtype of imidazoline receptor binding site (I2B-RBS), may label an additional I-RBS population, distinct from previously classified I1-RBS and I2-RBS. In this study, using crude or fractionated rat brain membranes we examined the possible association of [3H]rilmenidine-labelled I-RBS with the A- and B-isoforms of monoamine oxidase (MAO) by studying the inhibition of [3H]rilmenidine binding by a number of MAO inhibitors; and comparing the maximal binding density (Bmax) and subcellular distribution of [3H]rilmenidine binding sites with that of MAO-A and MAO-B catalytic sites labelled by [3H]RO41-1049 and [3H]RO19-6327 and 12-RBS labelled by [3H]2-BFI. Inhibition of [3H]rilmenidine binding by all MAO inhibitors tested produced very shallow curves (slope 0.29-0.56). Clorgyline and moclobemide (selective MAO-A inhibitors) displayed moderate affinities (60-140 nM), while pargyline (non-selective MAO-inhibitor), RO41-1049 (selective MAO-A inhibitor) and RO19-6327 (selective MAO-B inhibitor) exhibited very low affinities (> 2 microM) for 50-75% of [3H]rilmenidine-labelled I-RBS in crude brain membranes and even lower affinity for the remaining binding. Under identical buffer conditions, the Bmax of [3H]rilmenidine-labelled I-RBS (1.45+/-0.14 pmol/mg protein) was considerably lower than those of MAO-A (13.10+/-0.15 pmol/mg) and MAO-B (10.35+/-0.50 pmol/mg) sites. These results suggest that [3H]rilmenidine does not interact directly with the active catalytic site of either MAO enzyme and could at best only associate with a subpopulation of MAO molecules. Binding studies on five fractions of rat cortex homogenates-nuclear (N), heavy (M) and light (L) mitochondrial, microsomal non-mitochondrial (P), and soluble cytosolic (S) fractions-revealed that 45% of total [3H]rilmenidine binding was present in the P fraction cf. 20 and 23% in the M and L fractions, in contrast to [3H]RO19-6327 and [3H]2-BFI which bound 11-13% in the P fraction and 36-38% and 35-44% in the M and L fractions, respectively. Binding of all ligands in the N fraction was 6-15% of total. These studies reveal that [3H]rilmenidine-labelled I-RBS, unlike the I2-RBS, are not predominantly associated with mitochondrial fractions containing the MAO enzymes (and cytochrome oxidase activity), but appear to be distributed in both the mitochondrial and plasma membrane fractions in rat cerebral cortex.

[3H]Rilmenidine-labelled imidazoline-receptor binding sites co-localize with [3H]2-(benzofuranyl)-2-imidazoline-labelled imidazoline-receptor binding sites and monoamine oxidase-B in rabbit, but not rat, kidney.

The distribution and relative densities of imidazoline-receptor binding sites (I-RBS) and monoamine oxidase (MAO)-A and -B enzyme(s) in rat and rabbit kidney were compared autoradiographically using fixed nanomolar concentrations of [3H]rilmenidine and [3H]2-(benzofuranyl)-2-imidazoline ([3H]2-BFI) to label I-RBS, and [3H]RO41-1049 and [3H]RO19-6327 to label MAO-A and -B isoenzymes, respectively. In rat kidney, high densities of I-RBS labelled by [3H]rilmenidine were observed in the cortex and outer stripe (120-280 fmol/mg tissue), in contrast to low I-RBS densities labelled by [3H]2-BFI (<4 fmol/mg). A relatively high density of [3H]RO41-1049 binding to MAO-A enzyme was present in all regions of the rat kidney (160-210 fmol/mg) compared with a low density of [3H]RO19-6327 binding to MAO-B (< 25 fmol/mg). Comparison of MAO-A and -B distributions with that of [3H]rilmenidine-labelled I-RBS strongly suggests a lack of association in rat kidney. Similarly, the extremely low densities of [3H]2-BFI-labelled I2-RBS in rat kidney contrasts with the density of MAO-A, but is consistent with the low density of MAO-B. Rabbit kidney cortex and outer stripe contained high relative densities of [3H]rilmenidine-labelled I-RBS (200-215 fmol/mg) and [3H]2-BFI-labelled I2-RBS (45-60 fmol/mg) with lower densities in the inner stripe and inner medulla (< or = 100 and 30 fmol/mg respectively). A high density of MAO-A binding was observed in the inner stripe (515 fmol/mg) with lower levels in the cortex and outer stripe (100-240 fmol/mg), while high densities of MAO-B binding were observed in the cortex and outer stripe (290-450 fmol/mg) with lower levels in the inner stripe (65 fmol/mg). The correlation between the localization of [3H]rilmenidine-labelled I-RBS and [3H]RO19-6327-labelled MAO-B in rabbit kidney (r = 0.87, P = 0.057) suggest that [3H]rilmenidine may label a binding site co-existent with MAO-B, but not MAO-A (n.s.), in this tissue, but rilmenidine did not inhibit [3H]RO41-1049 or [3H]RO19-6327 binding. The distribution of [3H]2-BFI-labelled I2-RBS overlapped the combined distributions of both MAO-A and -B isoenzymes, suggesting that [3H]2-BFI may label sites on both enzymes in the rabbit, but [3H]2-BFI binding only correlated with [3H]RO19-6327 (r = 0.84, P = 0.07), not [3H]RO41-1049 binding (n.s.). Moreover, 2-BFI only inhibited [3H]RO19-6327, not [3H]RO41-1049 binding. These data are consistent with reports that I2-RBS are located on MAO-B and allosterically influence the catalytic site. The relationship of [3H]rilmenidine- and [3H]2-BFI-labelled I-RBS and the identity of non-MAO-associated [3H]rilmenidine-labelled I-RBS requires further investigation.

The effect of treatment with a slow-releasing oxytocin preparation at the onset of oestrus on the ovulation rate of Merino ewes.

The effect of a slow-releasing oxytocin preparation on the ovulation rate of Merino ewes was investigated. Synchronised Merino ewes were subcutaneously injected with a slow-releasing preparation containing 10 IU oxytocin, 48 hours after sponge withdrawal. Laparoscopic examination of the ovaries of all ewes was performed 10 d after the oxytocin treatment in order to determine the number of corpora lutea per ewe. The ovulation rate of the adult ewes of the treated and control groups was 179.1% and 159.1% respectively (p < 0.05) while that of the 2-tooth ewes was 108.3% and 112.8% respectively (p > 0.05). It would appear that a higher ovulation rate can be obtained by a single injection of a slow-releasing oxytocin preparation at the onset of oestrus. The lack of response in the 2-tooth ewes was probably due to their relatively low body weight.

[3H]2-(2-Benzofuranyl)-2-imidazoline, a highly selective radioligand for I2-imidazoline receptor binding sites. Studies in rabbit kidney membranes.

2-(2-Benzofuranyl)-2-imidazoline (2-BFI) has recently been characterised as a selective ligand for the I2-type of imidazoline-receptor binding site(s) (I2-RBS). The present studies determined the relative levels of specific [3H]2-BFI binding to membrane homogenates of brain and kidney from rat, guinea pig and rabbit and identified the pharmacological characteristics of [3H]2-BFI binding sites in rabbit kidney membranes. Rabbit kidney membranes had the highest relative density of specific [3H]2-BFI binding of all tissues studied (2000 fmol/mg protein). Rabbit brain and guinea pig kidney had moderate levels of specific [3H]2-BFI binding (350-500 fmol/mg protein), while rat kidney and guinea pig and rat brain displayed much lower densities of binding (40-65 fmol/mg protein). Studies of [3H]2-BFI binding kinetics in rabbit kidney homogenates revealed binding to two distinct sites with Kd values of 0.10 +/- 0.01 nmol/l and 1.00 +/- 0.36 nmol/l respectively. Equilibrium saturation studies were also consistent with the presence of two binding sites-[3H]2-BFI (0.01-20 nmol/l) bound to sites with affinities of 0.10 +/- 0.01 nmol/l and 0.92 +/- 0.13 nmol/l and binding densities of 470 +/- 80 and 840 +/- 60 fmol/mg protein (n = 3), representing 36 and 64% respectively. Drug inhibition studies revealed that L-adrenaline; alpha 1-adrenoceptor drugs (prazosin, L-phenylephrine) and alpha 2-adrenoceptor drugs (rauwolscine, methoxyidazoxan, 2-(2,4-(O-methoxyphenyl)-piperazin-1-yl)-ethyl-4, 4-dimethyl-1,3-(2H,4H)-isoquinolindione (ARC-239) had extremely low affinities for [3H]2-BFI binding sites (IC50 > or = 10 mumol/l). Putative I1-RBS compounds, p-aminoclonidine, moxonidine, imidazole-4-acetic acid and cimetidine, inhibited [3H]2-BFI binding to rabbit renal membranes with low to very low affinities (Ki values 3 to > or = 100 mumol/l), suggesting [3H]2-BFI does not label I1-RBS in rabbit kidney membranes. I2-RBS compounds-2- (4,5-dihydroimidaz-2-yl)-quinoline (BU224), 2-(4,5-dihydroimidaz-2-yl)-quinoxaline (BU239), idazoxan and cirazoline-potently inhibited [3H]2-BFI binding (Ki values 0.37-1.6 nmol/l), confirming the labelling of I2-RBS. Inhibition of [3H]2-BFI binding by certain compounds was consistent with their interaction with two binding site populations-for example (drug, Ki values) guanabenz, 0.65 nmol/l and 0.17 mumol/l; naphazoline, 0.94 nmol/l and 2.8 mumol/l; amiloride, 76 nmol/l and 26 mumol/l rilmenidine, 150 nmol/l and 50 mumol/l; and clonidine, 230 nmol/l and 70 mumol/l. The high affinity of amiloride for a high proportion (85%) of the binding is consistent with the presence of the I2A-subtype of I-RBS in rabbit kidney. These results demonstrate that [3H]2-BFI is a highly selective and high affinity radioligand for I2-RBS which should be useful for the further characterisation of these sites in mammalian tissues.

Effect of oxytocin treatment during oestrus on the ovulation rate of Merino ewes.

The effect of oxytocin treatment on the ovulation rate of Merino ewes was investigated. Intravenous doses (0.1 IU) of oxytocin were administered to synchronised ewes (n = 54) every 30 min for a 24 h period beginning at the onset of oestrus. Laparoscopic examination of the ovaries of all ewes that had displayed overt oestrus following sponge withdrawal was performed 10 d after the beginning of oxytocin treatment to determine the number of corpora lutea per ewe. The ovulation rates of the treated and control groups were 174.5% and 144%, respectively (p < 0.01). It would appear that a higher ovulation rate can be obtained by repeated low-dose intravenous injection of oxytocin during oestrus.

Differential characteristics and localisation of [3H]oxazoline and [3H]imidazoline binding sites in rat kidney.

Comparative autoradiography revealed that the imidazolines [3H]p-aminoclonidine and [3H]idazoxan labelled high densities of alpha 2A-adrenoceptor sites in the inner medulla and inner stripe of the outer medulla of rat kidney. In contrast, the oxazoline [3H]rilmenidine labelled a high density of non-adrenergic sites in the cortex and outer stripe of the outer medulla, a lower density in the inner stripe and inner medulla and a low density of alpha 2A-adrenoceptor sites in inner medulla. The existence of novel, non-adrenergic oxazoline sites of potential functional importance in rat kidney has important implications for the classification of imidazoline receptors.

Quantitative autoradiographic localization in rat brain of alpha 2-adrenergic and non-adrenergic I-receptor binding sites labelled by [3H]rilmenidine.

alpha 2A-Adrenergic receptor (AR) and non-adrenergic imidazoline receptor (I-R) binding sites have been previously characterized in rat cerebral cortex membranes using the N-substituted oxazoline, [3H]rilmenidine ([3H]Ril) [King, P.R. et al., Eur. J. Pharmacol., 218 (1992) 101-108]. In the present study, in vitro autoradiography was used to quantify the regional distribution of these receptors throughout the rat neuroaxis. The distribution and relative density (fmol/mg tissue) of I-Rs was examined in the presence of 1 microM adrenaline to block the adrenergic component of 40 nM [3H]Ril binding and non-specific binding was measured in the presence of another oxazoline, Bay a6781 (10 microM). Both alpha 2A-ARs and I-Rs were broadly, but heterogeneously, distributed. In forebrain, high levels of [3H]Ril-labelled alpha 2A-AR sites were observed in the anterior olfactory nucleus, the piriform, entorhinal and perirhinal cortices, lateral septum, bed nucleus of the stria terminalis, several thalamic nuclei, the amygdala and the arcuate, dorsomedial and posterior hypothalamic nuclei. In hindbrain, alpha 2A-AR sites were concentrated in locus coeruleus, lateral parabrachial nucleus, nucleus of the solitary tract and area postrema. I-R sites accounted for 50% or more of specific [3H]Ril binding (40 nM) in most cortical and hypothalamic nuclei, nucleus of the solitary tract, cranial motor nuclei and most spinal cord layers. The highest densities of I-Rs were found in the arcuate, dorsomedial and posterior hypothalamic nuclei, the locus coeruleus, the area postrema, the cranial motor nuclei and associated with spinal motor neurones. A very high concentration of I-Rs was also detected in the pineal gland. The distribution of alpha 2-AR sites determined resembled that reported with [3H]p-aminoclonidine which appears to specifically label alpha 2-ARs and not I1-R sites in rat brain sections, and [3H]methoxyidazoxan which is a selective alpha 2-AR antagonist. The regional and cellular distribution of I-R binding sites was unlike the distribution of putative I1-R sites labelled by [3H]clonidine in human brain, although comparable autoradiographic mapping studies in rat brain have not been done using this ligand. The regional and cellular distribution of [3H]-labelled I-R binding sites had both similarities and differences to that reported using the imidazoline ligand, [3H]idazoxan, with common labelling of areas such as area postrema, arcuate and interpeduncular nuclei and pineal gland with the two ligands, and differential relative binding levels ([3H]Ril > [3H]idazoxan) associated with hippocampal pyramidal cells and brainstem and spinal motor neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Reproducibility of bone ages when performed by radiology registrars: an audit of Tanner and Whitehouse II versus Greulich and Pyle methods.

This audit analysed the Tanner and Whitehouse II twenty bone (TW2) method of bone age assessment which was used in our department, and compared it with the Greulich and Pyle (GP) method. 50 previous bone ages were independently re-calculated by each of three registrars using both techniques, with the time taken to perform each assessment being recorded. For each method the interobserver variation was analysed in terms of the spread of results. The intraobserver variation in TW2 was determined by comparing the bone age originally reported with that subsequently calculated on the same film by the same registrar. The average spread of results was 0.74 years for TW2 method, and 0.96 years for the GP method and this difference is not statistically significant at the 5% level. The average intraobserver variation to TW2 was 0.33 years, but with 95% confidence limits of -0.87 to +1.53 years. The average time taken was 7.9 min for TW2 and 1.4 min for GP assessments. It was concluded that the GP method gave similar reproducibility and was faster than the TW2 method. Following clinical discussion the routine departmental bone age assessment method was changed from the TW2 to the GP method.

Clinical and demographic characteristics of voluntary and involuntary psychiatric inpatients.

Voluntary and involuntary psychiatric inpatients were compared on demographic, social and clinical characteristics. Chi-squared tests of independence revealed significant differences in age and financial support based on status at admission. No significant differences were found with respect to diagnostic category. It was concluded that demographic, social and clinical characteristics do not clearly discriminate between voluntary and involuntary inpatients.

Alpha 2-adrenoceptor and catecholamine-insensitive binding sites for [3H]rilmenidine in membranes from rat cerebral cortex.

The kinetic and pharmacological characteristics of the binding of the oxazoline antihypertensive drug, [3H]rilmenidine, to membranes of rat cerebral cortex have been determined. Computerised resolution of curvi-linear, equilibrium binding isotherms was consistent with the existence of two distinct binding sites for [3H]rilmenidine: Kd 17.3 +/- 7.41 nM, Bmax 0.197 +/- 0.06 pmol/mg protein and Kd 254 +/- 48 nM, Bmax 1.59 +/- 0.08 pmol/mg protein. Moreover, the resolution of two association and dissociation rates also suggested the existence of two binding site populations. Drug inhibition studies revealed that specific binding of [3H]rilmenidine (2 nM) was only inhibited by a maximum of 50% by the catecholamines, adrenaline and noradrenaline, but was completely inhibited by some oxazolines, by guanabenz (a guanidino drug) and by several imidazoline compounds including naphazoline, oxymetazoline and clonidine. Binding isotherms for these drugs were also best fit by a two-site model. The relative Ki values at the high affinity site for [3H]rilmenidine and the number of these high affinity sites are consistent with this site being an alpha 2-adrenoceptor. The high affinity of oxymetazoline and low affinity of prazosin for high affinity [3H]rilmenidine binding sites together with the rank order of potency of oxymetazoline greater than phentolamine greater than SKF 104078 greater than ARC-239 greater than prazosin suggest that [3H]rilmenidine binds to the alpha 2A sub-type of adrenoceptor. Computer-resolved Ki values for drugs at the larger number of lower affinity binding sites were very similar to Ki values determined in the presence of 10 microM adrenaline (used to block alpha 2-adrenoceptor binding).(ABSTRACT TRUNCATED AT 250 WORDS)

Nature of [3H]rilmenidine binding to membranes of rat cerebral cortex.

The binding of [3H]rilmenidine to membranes of rat cerebral cortex was studied in order to ascertain which receptor populations this novel antihypertensive interacts with in the cortex. A catecholamine-sensitive, alpha 2-adrenoceptor binding site was identified which represented up to 50% of specific, 2 nmol/L [3H]rilmenidine binding and was displaceable by the catecholamines in the rank order epinephrine----norepinephrine----dopamine----isoproterenol. Some imidazolines such as clonidine, naphazoline, and idazoxan and the guanidino compound guanabenz completely and potently inhibited [3H]rilmenidine binding from both catecholamine-sensitive and -insensitive sites. The substituted imidazole and guanidine, cimetidine, and amiloride, respectively, showed no affinity for [3H]rilmenidine binding. The pharmacologic profile of the catecholamine-insensitive [3H]rilmenidine site in rat cerebral cortex suggests it may be novel, as it has the features of an imidazoline-guanidino-oxazoline binding site. However, its identity requires further characterization.

Appraising the quality of drug-evaluation research: I. A method of meta-analysis for acute treatment medications.

The present paper focuses on drug-evaluation research, and describes a method of meta-analysis for evaluating the methodological quality of a body of research focusing on the study of an acute treatment medication. An illustrative application of this procedure to research evaluating lithium treatment for acute mania revealed general problems with diagnostic reliability and the reliability of the dependent variable, and a tendency to ignore the statistical power aspects of determining sample size. The implications of this are discussed in terms of a need to further clarify lithium's role in treating this disorder.

The trait anxiety-perception score: a composite predictor for state anxiety.

This article describes the development and initial evaluation of the A-Trait-Perception (ATP) score, a composite predictor for state anxiety. The ATP score is constructed from trait anxiety and situation perception data derived from the Endler Multidimensional Anxiety Scales (EMAS; Endler, Edwards, & Vitelli, 1989). ATP mathematically combines the individual's trait anxiety and situation perception profiles and adjusts these with a multiplier that reflects the individuals' sensitivity to particular types of situational elements in terms of state anxiety inducement. The utility of the resulting composite variable as a predictor of state anxiety was examined in the context of two field studies. Results of both studies indicated that the ATP variable offered a superior prediction of state anxiety, as compared to four individual trait anxiety facets (social evaluation, physical danger, ambiguous and daily routines). The theoretical import of these results is discussed.