Invisible metallic microfiber in clothing presents unrecognized MRI risk for cutaneous burn.

SUMMARY: We report a case of a thermal burn that occurred during MR imaging likely caused by invisible silver-embedded microfibers in the fabric of an undershirt. As the prevalence of fabric containing nondetectable metallic microfiber increases in athletic and "tech" clothing, the importance of having patients change into safe facility-provided garments before MR imaging is emphasized.

Effective half-life of 131I in thyroid cancer patients.

The oral administration of radioactive 131I is a standard treatment for thyroid carcinoma. One consideration for this therapy is assuring that other people do not receive significant radiation exposure. In particular, federal and state regulatory authorities stipulate that no individual should receive more than 5 mSv (500 mrem) effective dose-equivalent from the released patient. Patients receiving more than 1.11 GBq (30 mCi) of 131I were traditionally confined as in-patients by regulation until their burdens of radioactivity fell below that level or until the external dose rates were less than 50 microSv (5 mrem) per hour at 1 m. Recent regulatory guidance recommends the use of biological elimination as well as physical decay in calculating the confinement time to keep the effective dose-equivalent to members of the public less than 5 mSv. Analysis of a database of more than 250 administrations of 131I for thyroid cancer shows a median effective half-life of at least 14 h, with substantial variation. Thus, discharge criteria for radiation safety purposes should be calculated on the basis of individual measurements. The release of these patients should not always be as prompt as the guidance indicates. The results also challenge some long-used assumptions regarding iodine excretion in this patient population.

MEF-2 and Oct-1 bind to two homologous promoter sequence elements and participate in the expression of a skeletal muscle-specific gene.

The murine adult IIB myosin heavy chain (IIB MyHC) gene is expressed only in certain skeletal muscle fibers. Within the proximal promoter are two A + T-rich motifs, mAT1 and mAT2, which greatly enhance muscle-specific transcription; myogenic cells contain proteins that bind to these sequences. MEF-2 binds to both mAT1 and mAT2; a mutation abolishing its binding to mAT1 greatly diminishes the activity of the promoter. Both mAT motifs also form complexes with a protein requiring a target sequence typical of POU domain proteins, which migrate in electrophoretic mobility shift assays to the same position as a complex containing purified Oct-1 and which are supershifted by an antibody specific to Oct-1; this protein is therefore probably Oct-1. Footprinting experiments demonstrate that mAT1 is preferentially occupied by MEF-2 and mAT2 by Oct-1 and that these two proteins appear to bind cooperatively to their respective sites. Although the two mAT motifs have sequences that are very similar, they nonetheless exhibit distinct behaviors and perform differently in the activation of the promoter. The contribution of the IIB MyHC gene to specification of the myogenic phenotype is thus at least in part regulated by MEF-2 and Oct-1.

The transcriptional activity of a muscle-specific promoter depends critically on the structure of the TATA element and its binding protein.

We have previously characterized the proximal promoter of the mouse IIB myosin heavy chain (MyHC) gene, which is expressed only in fast-contracting glycolytic skeletal muscle fibers. We show here that the substitution into this promoter of a non-canonical TATA sequence from the IgH gene results in inactivity in muscle cells, even though TATA-binding protein (TBP) can bind strongly to this mutated promoter. Chemical foot-printing data show, however, that TBP makes different DNA contacts on this heterologous TATA sequence. The inactivity of such a non-canonical TATA motif in the IIB promoter context appears to be caused by a non-functional conformation of the bound TBP-DNA complex that is incapable of sustaining transcription. The conclusions imply that the precise sequence of the promoter TATA motif needs to be matched with the specific functional class of upstream activator proteins present in a given cell type in order for the gene to be transcriptionally active.

Myogenic regulatory factors can activate TATA-containing promoter elements via an E-box independent mechanism.

We have studied the effect of several myogenic regulatory factors on the activity of the promoter for a mouse gene encoding a skeletal myosin heavy chain (MyHC) expressed in adult (type IIB) muscle fibers. Co-transfection of myogenic factors is necessary for activity of the IIB promoter in mouse C2 myotubes in culture but not in quail myotubes in culture. Although this promoter contains one E-box within the first 192 base pairs upstream of the transcriptional start site, mutations in this motif demonstrate that it is not required for the transactivation effect of the myogenic factors. Analysis of other mutants suggests that the MEF2 and MHox DNA-binding factor binds to an evolutionarily conserved AT-rich motif. In addition, the IIB promoter appears to require the conserved TATA motif (CTATAAAAG) in order to be activated by the AT-rich sequences. The IIB promoter constructs produce RNA transcripts which begin at the natural site of transcriptional initiation in quail myotubes and in mouse C2 myotubes after co-transfection with myogenic factors; a second, minor, start site is also used in the co-transfected C2 myotubes. Results obtained after transfection of the mouse IIB promoter constructs in quail myotube cultures suggest that the overexpression of myogenic factors in C2 cultures does not result in an environment in which the control of IIB MyHC promoter activity is aberrant. Therefore, either the myogenic factors themselves, or other proteins induced by them, seem to interact directly with the basal transcription seem to interact directly with the basal transcription machinery to allow muscle-specific gene expression.

A possible regulatory role for conserved promoter motifs in an adult-specific muscle myosin gene from mouse.

The mouse gene encoding a myosin heavy chain (MHC) protein expressed in type IIB fibers of adult skeletal muscle has been cloned and its promoter isolated. A number of DNA sequence motifs are found within the first 2.5 kilobases of the promoter which are similar to motifs present in the promoters of other muscle-specific genes. One sequence located at approximately -940 base pairs corresponds to the motif called MEF1 which has been shown in other muscle genes to bind the myogenic regulatory factors of which MyoD is one example. The MEF1 site of this adult IIB MHC promoter does indeed bind MyoD although this factor is normally thought to be involved in early muscle cell differentiation. The IIB MHC promoter also has several motifs located in the first 200 base pairs which are strikingly conserved between this mouse gene and several chicken skeletal MHC genes. Of these evolutionarily conserved sequences, two motifs rich in A and T residues appear to be major contributors to the muscle-specific transcriptional activity of the mouse IIB MHC promoter when transfected into quail myogenic and non-myogenic cells. These observations suggest an important functional role for these AT-rich sequence motifs in the regulation of genes of the MHC family.

Evolutionarily conserved promoter motifs and enhancer organization in the mouse gene encoding the IIB myosin heavy chain isoform expressed in adult fast skeletal muscle.

We have isolated the mouse gene for the MHC isoform expressed in adult type IIB (fast-contracting, glycolytic) skeletal muscle fibers, and determined the DNA sequence of the promoter region. This sequence represents the first example of a promoter for a gene encoding an adult-specific isoform of a mammalian skeletal MHC. The proximal 200 bp of the promoter contains several sequence motifs which are identical or very similar to homologous motifs found in the promoters of a family of chicken skeletal MHC genes. Of these, two novel AT-rich sequences may be important for regulation of the promoter. A second feature of the mouse IIB MHC promoter sequence concerns a number of sequence motifs located at ca. -1,000 bp which are organized in a similar fashion in the IIB MHC promoter and a homologous region of promoter of the mouse muscle creatine kinase gene.

The nature of the background in radionuclide ventriculography: deductions from the mathematical behaviour of the ejection fraction.

The relationship between the ejection fractions calculated from 'uncorrected' radionuclide time activity curves (UEF) and angiographic ejection fractions (AEF) in 200 catheterized patients yielded the regression equation AEF = 1.74 UEF + 0.21. It follows from this linear relationship that the left ventricular ejection fraction can be estimated by linear regression without explicit background correction: RREF = 1.74 UEF + 0.21, where RREF is the radionuclide regression ejection fraction. We first investigated the possibility that changes in photon self-attenuation within the cardiac chambers cause the observed mathematical characteristics of the cardiac background, B. Self-attenuation was calculated for cylindrical and spherical ventricular models. The results were insensitive to the particular geometry and would have only a small effect on the observed EF. Alternatively, the 'background' may result from extra-ventricular radiation scattering from the heart into the detector. If we assume that B should be proportional to the ventricular scattering volume, Bd = Kd EDC for diastole and Bs = Ks ESC for systole, the background corrected ejection fraction will be BCEF = K UEF + (1-K) where K = (1-Ks)/(1-Kd). This agrees with the form of the empirical regression equation.

Measurement of the ventricular stroke volume ratio by gated radionuclide angiography.

The ventricular stroke volume ratio or VSVR (left/right) was measured by gated radionuclide angiography in 33 normal subjects, using a 30 degree caudal slant-hole collimator and computer-generated functional images to aid in definition of the right ventricle. The mean ratio was found to be 1.06 +/- 0.05, compared to the normal value of 1.00. Comparative studies indicated that definition of the right ventricle based on the end-diastolic frame alone or standard collimation without caudal angulation commonly causes overestimation of the VSVR and considerably greater variance between measurements. Such errors are the result of inadequate atrioventricular separation and/or underestimation of the right-ventricular region.

Gated radionuclide angiographic evaluation of valve regurgitation.

Gated radionuclide angiography is a new noninvasive technique that can be used to calculate the ratio of left and right ventricular stroke volumes. This stroke volume ratio, which must be unity in normal subjects, increases in patients with aortic or mitral regurgitation in direct proportion to the degree of left ventricular volume overload, provided no shunts or regurgitant right heart lesions are present. In 22 patients with aortic or mitral regurgitation there was excellent correlation between the stroke volume ratio determined with gated radionuclide angiography and with standard quantitative catheterization methods (r = 0.79). Measurement of valve regurgitation with this radionuclide method also correlated well with data obtained from semiquantitative aortic root or left ventricular cineangiography (r = 0.72). Twenty-one of the 22 patients with valve regurgitation had an abnormally elevated stroke volume ratio, thereby suggesting that gated radionuclide angtiography may be useful in detecting or excluding hemodynamically significant valve regurgitation.