First MTP joint injuries: MR imaging findings in surgically managed patients.

OBJECTIVES: Determine whether MR imaging findings or demographics predict surgical management in patients with first MTP joint injuries. MATERIALS AND METHODS: Retrospective study of 161 forefoot MRs for traumatic first MTP injury (M:F 92:69, mean age 33 ± 13 yrs.). Two radiologists reviewed imaging for ligamentous, osseous, and tendinous injuries. Ligaments and tendons were graded as 0:normal, 1:sprain or strain, 2:partial tear, 3:complete tear. Osseous injuries were classified as edema, fracture, or cartilage injury. Clinical data obtained included sex, age, injury acuity, sport participation, level of sport, and treatment. Imaging findings and demographic data were assessed to determine predictive factors for surgical management. Statistics included kappa, chi-squared, Fisher's exact, and logistic regression. RESULTS: Logistic regression (odds ratio [95% CI], p-value) showed that grade 2 or 3 injuries of the plantar ligamentous complex (2.87, [1.10, 7.48], p = 0.031), grade 2 or 3 injuries of the medial collateral ligament (3.24, [1.16, 9.08], p = 0.025), and participation in collegiate or professional sports (4.34 [1.64, 11.52], p = 0.003) were associated with an increased rate of surgical intervention. k = ligamentous injury (0.71-0.83), osseous trauma (0.88-0.95), and tendon injury (0.78). All other imaging findings and demographic factors were not significant predictors of surgery (p > 0.05). CONCLUSION: Participation in collegiate or professional sports and tears of the plantar ligamentous complex or medial collateral ligament predicted surgical management in patients with first MTP trauma.

Characteristics of in vivo radiotherapy dosimetry.

The recent discussion and debate about the use of in vivo dosimetry as a routine component of the radiotherapy treatment process has not included the limitations introduced by the physical characteristics of the detectors. Although a robust calibration procedure will ensure acceptable uncertainties in the measurements of tumour dose, further work is required to confirm the accuracy of critical organ measurements with a diode or a thermoluminescent dosemeter outside the main field owing to limitations caused by a non-uniform X-ray energy response of the detector, differences between the X-ray energy spectrum inside and outside the main field, and contaminating electrons.

An update survey of UK in vivo radiotherapy dosimetry practice.

A questionnaire was distributed in 2004 to 59 radiotherapy physics departments in the UK to determine whether in vivo dosimetry practice had changed since a similar survey conducted 10 years earlier. The number of centres carrying out central axis dosimetry had increased slightly from 17 centres in 1994 to 22 centres in 2004, with a diode alone being the most commonly used detector. Twice as many centres (43) carried out critical organ dosimetry compared with those carrying out central axis measurements, and this number had also increased slightly above the 1994 value (38). A diode was used by most centres carrying out central axis dosimetry and by about 50% of centres carrying out critical organ dosimetry. The action level adopted by each centre for central axis measurements varied from >+/-3% to >+/-10% difference between the measured and the prescribed dose, with >+/-5% being the most frequent value. It was concluded that there had been little change in in vivo dosimetry practice during the time between the two surveys, and that guidance on the method and applications for in vivo dosimetry is required before recent recommendations for its widespread adoption for routine use can be satisfied.

Effect of electron contamination of a 6 MV x-ray beam on near surface diode dosimetry.

In critical organ in vivo x-ray dosimetry, the relative contaminating electron contribution to the total dose and total detector response outside the field will be different to the corresponding contributions at the central axis detector calibration position, mainly due to the effects of shielding in the linear accelerator head on the electron and x-ray energy spectrum. To investigate these contributions, the electron energy response of a Scanditronix PFD diode was measured using electrons with mean energies from 0.45 to 14.6 MeV, and the Monte Carlo code MCNP-4C was used to calculate the electron energy spectra on the central axis, and at 1 and 10 cm outside the edge of a 4 x 4, 10 x 10 and a 15 x 15 cm(2) 6 MV x-ray field. The electron contribution to the total dose varied from about 8% on the central axis of the smallest field to about 76% at 10 cm outside the edge of the largest field. The electron contribution to the total diode response varied from about 7-8% on the central axis of all three fields to about 58% at 10 cm outside the edge of the smallest field. The results indicated that a near surface x-ray dose measurement with a diode outside the treatment field has to be interpreted with caution and requires knowledge of the relative electron contribution specific to the measurement position and field size.

The low energy X-ray response of the LiF:Mg:Cu:P thermoluminescent dosemeter: a comparison with LiF:Mg:Ti.

LiF:Mg:Cu:P thermoluminescent dosemeters (TLD) can be used for the same X-ray dosimetry applications as LiF:Mg:Ti, with each type having the disadvantage of a response dependent on energy, particularly at low energies. Measurements were made of the response per unit air kerma of LiF:Mg:Cu:P and LiF:Mg:Ti to nine quasi-monoenergetic X-ray beams with mean energies from 12 keV to 208 keV. Each measurement was normalized to the value produced by 6 MV X-rays. LiF:Mg:Cu:P was found to under-respond to a majority of these radiations whereas LiF:Mg:Ti over-responded to a majority. Their smallest relative measured response was produced by the lowest energy beam, and the maximum measured relative response of 1.15+/-0.07 and 1.21+/-0.07 for LiF:Mg:Cu:P and LiF:Mg:Ti, respectively, occurred at 33 keV. Energy response coefficients were derived from these measurements to estimate the error introduced by using either type of TLD to measure the dose from an X-ray spectrum different to that used for its absolute response calibration. It was calculated that if the response of either type of TLD was calibrated at 100 kVp, then an error of no more than +/-2% would be introduced into measurements of tube output at potentials of 50-130 kVp. LiF:Mg:Cu:P was found to introduce a larger error (up to 30%) into the measurement of body exit dose than LiF:Mg:Ti at tube potentials of 40-150 kVp, if its absolute response was calibrated using the corresponding body entrance beam. The method should allow this type of error to be estimated in other dosimetry applications for either type of TLD.

Near surface photon energy spectra outside a 6 MV field edge.

The purpose of this study was to investigate the difference between a 6 MV linear accelerator x-ray energy spectrum outside the field edge near a phantom surface, and the corresponding spectrum on the central axis. The Monte Carlo code MCNP-4A was used to calculate the spectra on the central axis and at 1, 2, 5 and 10 cm from the edge of a 4 x 4 cm2, 10 x 10 cm2 and 15 x 15 cm2 field. Compared to the spectrum on the central axis, the spectra outside the field edge showed two distinct regions: a broad peak below about 0.5 MeV, and a lower amplitude, less rapidly changing region at higher energies from 0.5 to 6 MeV. The lower energy peak was due to scattered photons, and the higher energy component was due mainly to primary photons transmitted through the jaws of the secondary collimator. The potential impact of these spectral differences on critical organ photon dosimetry was determined by calculating the ratio of the sensitivity of a Scanditronix EDD-5 diode and of a LiF:Mg:Ti thermoluminescent dosimeter (TLD) outside the field edge to their respective sensitivity at the calibration position on the central axis. The lower energy peak combined with the non-uniform energy sensitivity of each detector produced up to a two-thirds overestimate of x-ray dose outside the field by the diode, whereas the response ratio of the TLD was about unity. These results indicated that a similar evaluation was required for profile measurements of a dynamic wedged field and measurements in an intensity modulated beam with either type of detector.

Functional localization of single active ion channels on the surface of a living cell.

The spatial distribution of ion channels in the cell plasma membrane has an important role in governing regional specialization, providing a precise and localized control over cell function. We report here a novel technique based on scanning ion conductance microscopy that allows, for the first time, mapping of single active ion channels in intact cell plasma membranes. We have mapped the distribution of ATP-regulated K+ channels (KATP channels) in cardiac myocytes. The channels are organized in small groups and anchored in the Z-grooves of the sarcolemma. The distinct pattern of distribution of these channels may have important functional implications.

Hybrid scanning ion conductance and scanning near-field optical microscopy for the study of living cells.

We have developed a hybrid scanning ion conductance and scanning near-field optical microscope for the study of living cells. The technique allows quantitative, high-resolution characterization of the cell surface and the simultaneous recording of topographic and optical images. A particular feature of the method is a reliable mechanism to control the distance between the probe and the sample in physiological buffer. We demonstrate this new method by recording near-field images of living cells (cardiac myocytes).

Cell volume measurement using scanning ion conductance microscopy.

We report a novel scanning ion conductance microscopy (SICM) technique for assessing the volume of living cells, which allows quantitative, high-resolution characterization of dynamic changes in cell volume while retaining the cell functionality. The technique can measure a wide range of volumes from 10(-19) to 10(-9) liter. The cell volume, as well as the volume of small cellular structures such as lamelopodia, dendrites, processes, or microvilli, can be measured with the 2.5 x 10(-20) liter resolution. The sample does not require any preliminary preparation before cell volume measurement. Both cell volume and surface characteristics can be simultaneously and continuously assessed during relatively long experiments. The SICM method can also be used for rapid estimation of the changes in cell volume. These are important when monitoring the cell responses to different physiological stimuli.

The X-ray and electron benchmarking of the Monte Carlo codes MCNP-4A and 4B on different computers.

MCNP (Monte Carlo N-Particle) is a Monte Carlo transport code which has been of widespread use in modelling the dosimetry of ionizing radiations. The most recent version (4B) features improved electron transport compared with the previous version 4A. The processing time required by a number of computing systems to carry out X-ray and electron transport calculations using both versions of the code was compared. Version 4A was installed onto a Dec Alpha Server 8200, a personal computer (Pentium 90 MHz), and a Sun Sparc20, 10, 4 and 1+. MCNP-4B was also installed onto the Sun Sparc20. The benchmark tests consisted of determining the transmission of 2 MeV X-rays and 30 MeV electrons through lead. It was found that the Dec Alpha Server 8200 was the fastest computing platform, and the Sun Sparc1+ was the slowest for both tests. The difference in computational speed between different platforms was not matched by the corresponding differences in price. The time required by version 4B to complete the X-ray and electron benchmark tests was found to be 1.4 and 2.3 times greater than version 4A, respectively, without any difference in the results of the calculation for each type of radiation. This suggests that in cases where computing time is important, it may be preferable to use version 4A instead of 4B.

Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2.

Deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. However, the disorder is usually incompletely corrected by suppression of cortisol, suggesting additional and irreversible changes, perhaps in the kidney. To examine this further, we produced mice with targeted disruption of the 11beta-HSD2 gene. Homozygous mutant mice (11beta-HSD2(-/-)) appear normal at birth, but approximately 50% show motor weakness and die within 48 hours. Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone. Young adult 11beta-HSD2(-/-) mice are markedly hypertensive, with a mean arterial blood pressure of 146 +/- 2 mmHg, compared with 121 +/- 2 mmHg in wild-type controls and 114 +/- 4 mmHg in heterozygotes. The epithelium of the distal tubule of the nephron shows striking hypertrophy and hyperplasia. These histological changes do not readily reverse with mineralocorticoid receptor antagonism in adulthood. Thus, 11beta-HSD2(-/-) mice demonstrate the major features of SAME, providing a unique rodent model to study the molecular mechanisms of kidney resetting leading to hypertension.

Measuring the progression of foreign-body reaction to silicone implants using in vivo MR microscopy.

We used in vivo magnetic resonance (MR) microscopy to follow the growth of fibrous capsule as a foreign body reaction to silicone implants in rats. Anesthetized rats were imaged 1, 7, 14, and 28 days after silicone-coated MR imaging coils were sutured to their neck muscles. On the twenty-eighth day, rats were sacrificed and coils and adjacent tissues were removed en bloc and fixed in formalin, reimaged with MR, and sectioned for conventional histology. Three-dimensional (3-D) spin-echo [3DFT] acquisition gave in-plane resolution of 32 x 32 microns in vivo and 16 x 16 microns ex vivo. All MR images showed a diffuse band of elevated signal intensity between the silicone of the coil and adjacent tissue. The border of the hyperintense band was thin and not well defined at seven days post-implantation. From 7-28 days, the band showed relatively homogeneous signal intensity and its thickness increased 44% on the rectus muscle side and 78% on the subcutaneous side. The capsule thickness determined either by MR in vivo and ex vivo microscopy or conventional histology was not significantly different, and there was a significant correlation between thickness measurements among those methods. MR in vivo microscopy provides sufficient resolution and spatial information to serially evaluate the growth of the foreign body fibrous capsule over time, thus achieving greater accuracy and consistency in measurements.

11Beta-hydroxysteroid dehydrogenase 1 in adipocytes: expression is differentiation-dependent and hormonally regulated.

11Beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) catalyses the reversible metabolism of physiological glucocorticoids (cortisol, corticosterone) to inactive metabolites (cortisone, 11-dehydrocorticosterone), thus regulating glucocorticoid access to receptors. 11Beta-HSD-1 expression is regulated during development and by hormones in a tissue specific manner. The enzyme is highly expressed in liver, where it may influence glucocorticoid action on fuel metabolism, processes also important in adipose tissue. Here we show that 11beta-HSD-1 is expressed in white adipose tissue, in both the adipocyte and stromal/vascular compartments, and in the adipocyte cell lines 3T3-F442A and 3T3-L1. In these cells, 11beta-HSD-1 expression is induced upon differentiation into adipocytes and is characteristic of a 'late differentiation' gene, with maximal expression 6-8 days after confluence is reached. In intact 3T3-F442A adipocytes the enzyme direction is predominantly 11beta-reduction, activating inert glucocorticoids. The expression of 11beta-HSD-1 mRNA is altered in fully differentiated 3T3-F442A adipocytes treated with insulin, dexamethasone or a combination of the hormones, in an identical manner to glycerol-3-phosphate dehydrogenase (GPDH) mRNA (encoding a key enzyme in triglyceride synthesis and a well-characterised marker of adipocyte differentiation). The demonstration of 11beta-HSD-1 expression in adipocytes and its predominant reductase activity in intact 3T3-F442A adipocytes suggests that 11beta-HSD-1 may play an important role in potentiating glucocorticoid action in these cells. 3T3-F442A and 3T3-L1 represent useful model systems in which to examine the factors which regulate 11beta-HSD-1 gene expression and the role of 11beta-HSD-1 in modulating glucocorticoid action in adipose tissue.

Characterization of mutations in patients with multiple endocrine neoplasia type 1.

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors of the parathyroids, pancreatic islets, and anterior pituitary. The MEN1 gene, on chromosome 11q13, has recently been cloned, and mutations have been identified. We have characterized such MEN1 mutations, assessed the reliability of SSCP analysis for the detection of these mutations, and estimated the age-related penetrance for MEN1. Sixty-three unrelated MEN1 kindreds (195 affected and 396 unaffected members) were investigated for mutations in the 2,790-bp coding region and splice sites, by SSCP and DNA sequence analysis. We identified 47 mutations (12 nonsense mutations, 21 deletions, 7 insertions, 1 donor splice-site mutation, and 6 missense mutations), that were scattered throughout the coding region, together with six polymorphisms that had heterozygosity frequencies of 2%-44%. More than 10% of the mutations arose de novo, and four mutation hot spots accounted for >25% of the mutations. SSCP was found to be a sensitive and specific mutational screening method that detected >85% of the mutations. Two hundred and one MEN1 mutant-gene carriers (155 affected and 46 unaffected) were identified, and these helped to define the age-related penetrance of MEN1 as 7%, 52%, 87%, 98%, 99%, and 100% at 10, 20, 30, 40, 50, and 60 years of age, respectively. These results provide the basis for a molecular-genetic screening approach that will supplement the clinical evaluation and genetic counseling of members of MEN1 families.

The integrated concentration of cortisone is reduced in obese children.

We evaluated the possibility that there is enhanced conversion of cortisol (F) to cortisone (E) in obese children. IC-E was measured from 15 lean children aged 12.7 +/- 2.2 years, body mass index Z-score (BMI-SD) = -0.35 +/- 0.82, IC-F = 197 +/- 70 nM/l and 9 obese children aged 12.3 +/- 3.2 years, BMI-SD = + 4.7 +/- 2.1, IC-F = 149 +/- 53 nM/l. IC-E was higher in lean children 76 +/- 25 nM/l compared to obese 60 +/- 11 nM/l (p < 0.04). There was no difference in the ratio of IC-E/IC-F between lean 0.40 +/- 0.10 and obese subjects 0.42 +/- 0.09 (p < 0.06). IC-E was directly correlated with IC-F: IC-E = 0.25 x IC-F + 26 (n = 24, r2 = 0.57, p < 0.0001). In a multiple regression model (overall r2 = 0.32, p < 0.02), IC-E was related to BMI-SD inversely (p < 0.0054) and influenced as well by interaction of BMI-SD with sex (p < 0.043), IC-E being lower in boys with increasing body mass. In childhood, obesity is associated with decreased plasma IC-E and IC-F levels, the ratio of IC-E/IC-F is independent of body mass. Reduced IC-E levels in obese children are most likely due to the impact of body mass on IC-F.

Correlation of clinical, endocrine and molecular abnormalities with in vivo responses to high-dose testosterone in patients with partial androgen insensitivity syndrome.

OBJECTIVE: To investigate the responses of two patients previously diagnosed as Reifenstein's syndrome to graded high-dose testosterone in terms of hormone levels, nitrogen balance and sebum secretion and to attempt to correlate these parameters with the properties of their androgen receptors and mutations in the androgen receptor gene. DESIGN: Nitrogen balance was determined by comparing controlled nitrogen intake to the amount excreted. Sebum excretion was measured on the forehead. Patients were studied during control periods (no treatment) and during administration of testosterone propionate. Blood samples were used as a source of genomic DNA and to measure peripheral hormone levels; androgen receptor binding was determined using genital skin fibroblasts. PATIENTS: Two patients of XY karyotype, with ambiguous external genitalia and problems of testicular descent who had required mastectomy as teenagers. Normal male controls of proven fertility. MEASUREMENTS: Nitrogen balance, sebum excretion rate and peripheral hormone levels (testosterone, dihydrotestosterone, LH and FSH) were studied before and after testosterone therapy (1 or 5 mg/kg/day). Genomic DNA was extracted from peripheral blood leucocytes and regions of the androgen receptor gene amplified by polymerase chain reaction using pairs of specific primers. Mobility of amplified DNA from patients was analysed on denaturing gradient acrylamide gels and fragments differing in mobility from those of normal controls were sequenced. Fibroblasts were cultured from scrotal skin biopsies and androgen receptor binding parameters, subcellular localization and up-regulation were determined. RESULTS: Testosterone therapy resulted in raised plasma testosterone, dihydrotestosterone and oestradiol in both patients. In patient 1 (lesser genital abnormality), LH was suppressed by 5 mg/kg/day testosterone to the upper limit of the normal range but FSH remained low normal. Both LH and FSH were suppressed by testosterone treatment in patient 2 (greater genital abnormality). Nitrogen retention was increased in both patients (4.2 and 3.0 g/24 h respectively); sebum excretion rate increased to normal in patient 1 but showed no change in patient 2. Mutations in the androgen receptor gene were identified in both patients. In patient 1 a single nucleotide change from adenosine to guanosine resulted in the substitution of glycine for glutamic acid at position 772 within the hormone binding domain of the receptor. In patient 2 a single nucleotide mutation from guanosine to adenosine resulted in the substitution of lysine for arginine at position 608 (exon 3) situated in the second zinc finger of the DNA binding domain. Both patients had a normal number of androgen binding sites in genital skin fibroblasts but those in patient 1 showed reduced binding affinity and rapid dissociation of receptor/ligand complexes while those in patient 2 showed defective nuclear localization. CONCLUSION: In patients with partial androgen insensitivity syndrome the type of androgen receptor mutation and responses to short-term androgen treatment can be correlated with the individual's potential to virilize. If there is a mutation in the androgen receptor DNA binding domain the patient may show little ability to virilize either spontaneously at puberty or after androgen treatment. Sebum excretion appears to be more discriminating than nitrogen balance or gonadotrophin suppression as an index of tissue response to androgens.

A survey of current in vivo radiotherapy dosimetry practice.

A questionnaire was sent out to 57 radiotherapy physics departments in the United Kingdom to determine the type of dosemeters used for in vivo measurements inside and outside X-ray treatment fields, and whether any correction is made for energy dependence when the dose to critical organs outside the main beam is estimated. 44 responses were received. 11 centres used a semi-conductor for central axis dosimetry compared with only two centres which used thermoluminescent dosimetry (TLD). 37 centres carried out dosimetry measurements outside the main beam; 25 centres used TLD and 12 centres used a semi-conductor detector. Of the 16 centres measuring the dose at both sites. 11 used a semi-conductor for the central axis measurement, but only four of those 11 changed to TLD for critical organ dosimetry despite the latter's lower variation in energy response. None of the centres stated that they made a correction for the variation in detector energy response when making measurements outside the main beam, indicating a need for a more detailed evaluation of the energy response of these detectors and the energy spectra outside the main beam.

Placental 11 beta-hydroxysteroid dehydrogenase: a key regulator of fetal glucocorticoid exposure.

OBJECTIVE: Placental 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which converts active cortisol to inactive cortisone, has been proposed to be the mechanism guarding the fetus from the growth retarding effects of maternal glucocorticoids; however, other placental enzymes have also been implicated. Placental 11 beta-HSD is unstable in vitro, and enzyme activity thus detected may not be relevant to the proposed barrier role. We have therefore examined placental glucocorticoid metabolism in dually perfused freshly isolated intact human placentas. DESIGN: Placentas were obtained from randomly selected normal term deliveries. The maternal circuit was perfused with physiological concentration of cortisol, the fetal effluent collected and steroid metabolites separated and quantified using silica columns (Sep-pak Plus) and HPLC. RESULTS: Most of the maternally administered cortisol was metabolized to cortisone, and no conversion of cortisone to cortisol was detected. Cortisone was the only product of cortisol metabolism. Inhibition of 11 beta-HSD with glycyrrhetinic acid allowed cortisol to gain direct access to the fetal circulation. CONCLUSION: We conclude that human placental 11 beta-HSD plays a crucial role in controlling glucocorticoid access to the fetus. Other enzymes are not significant contributors at physiologically relevant cortisol concentrations.

11beta-hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress.

Glucocorticoid hormones, acting via nuclear receptors, regulate many metabolic processes, including hepatic gluconeogenesis. It recently has been recognized that intracellular glucocorticoid concentrations are determined not only by plasma hormone levels, but also by intracellular 11beta-hydroxysteroid dehydrogenases (11beta-HSDs), which interconvert active corticosterone (cortisol in humans) and inert 11-dehydrocorticosterone (cortisone in humans). 11beta-HSD type 2, a dehydrogenase, thus excludes glucocorticoids from otherwise nonselective mineralocorticoid receptors in the kidney. Recent data suggest the type 1 isozyme (11beta-HSD-1) may function as an 11beta-reductase, regenerating active glucocorticoids from circulating inert 11-keto forms in specific tissues, notably the liver. To examine the importance of this enzyme isoform in vivo, mice were produced with targeted disruption of the 11beta-HSD-1 gene. These mice were unable to convert inert 11-dehydrocorticosterone to corticosterone in vivo. Despite compensatory adrenal hyperplasia and increased adrenal secretion of corticosterone, on starvation homozygous mutants had attenuated activation of the key hepatic gluconeogenic enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, presumably, because of relative intrahepatic glucocorticoid deficiency. The 11beta-HSD-1 -/- mice were found to resist hyperglycamia provoked by obesity or stress. Attenuation of hepatic 11beta-HSD-1 may provide a novel approach to the regulation of gluconeogenesis.

The response of a MOSFET, p-type semiconductor and LiF TLD to quasi-monoenergetic x-rays.

A metal oxide semiconductor field effect transistor (MOSFET), p-type semiconductor and a TLD can all be used for x-ray dosimetry, with each system having the common disadvantage of a response which is dependent upon the incident photon energy, particularly for energies < 1 MeV. A Pantak HF-320 quasi-monoenergetic x-ray unit was used to determine the response of two Thomson and Nielson TN-502RD MOSFETs, a Scanditronix EDP-10 semiconductor (build-up cap 10 mm: tissue equivalence), an EDD-5 semiconductor (build-up cap 4.5 mm: tissue equivalence) and an Lif:Mg:Ti TLD over the energy range 12-208 keV. The sensitivity of each detector was normalized to the value produced by exposure to 6 MV x-rays. The maximum relative sensitivities of the two MOSFET detectors were 4.19 +/- 0.25 and 4.44 +/- 0.26 respectively, occurring at an incident x-ray energy of 33 keV. The maximum relative sensitivity of the Scanditronix EDP-10 of 2.24 +/- 0.13 occurred at 65 keV, and for the EDD-5, it was 7.72 +/- 0.45 at 48 keV. The TLD produced a maximum relative sensitivity of 1.31 +/- 0.09 at 33 keV. Compared with available data based on heteroenergetic x-ray sources, these measurements have identified a more representative response for each detector to low-energy x-rays.