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The intercostal flap has many uses for torso reconstruction, whether employed as an island flap or a free flap. With modifications, it can be used as a sensory skin flap, or as a compound osteocutaneous flap to restore stability in a chest wall construction, or as a skin flap with a permanent blood supply to provide stable cover after excision of radiation ulcers.
A 60 percent degloving injury involving the torso and lower extremities of an 8-year-old boy is described. Successful management employed the use of a new trilaminar skin coverage technique. With the avulsed flap still attached to its bed, a 0.14-inch split-thickness graft of epithelium and superficial dermis is raised with a power-driven dermatome. From the same harvest site, one level deeper, a second layer consisting of split-thickness dermis (0.14 inch) is taken. Both the first and second layers are meshed and expanded. The remaining degloved flap is excised and, on a sterile bench, defatted to produce a third layer of deep dermis. In our case, this third layer was ultimately lost, but it functioned well as a temporary biologic dressing. Depending on donor-site morbidity, other potential applications of this method (i.e., major burn injuries) may be feasible.
Sudden and unexpected loading to the torso has been reported in the literature as a potential cause of low-back disorders. When such loadings occur, it is hypothesized that the body's response is designed to minimize the destabilizing postural disturbance, and to minimize the mechanical loading of the musculoskeletal system. This study tested hypotheses regarding the role of task experience in the development of preparatory strategies that potentially minimize the postural disturbance to the body and minimize the mechanical loading of the spine. These strategies were hypothesized to consist of muscle pretensioning, postural changes, and intra-abdominal pressure (IAP). Four subjects participated in five to six experimental sessions in which a sudden load was applied by dropping a weight once a minute for 30 minutes. Electromyographic (EMG) data from 10 trunk muscles, IAP data, and postural data were collected during the initial session and final sessions for each subject. The results indicate where each subject developed a unique preparatory strategy. The preparation always involved the pretensioning of the erector spinae muscles, although the coactivation of the other trunk muscles was quite variable across subjects. During the sudden loading the overall postural disturbance was not consistently reduced; however, the trunk flexion was significantly reduced in most subjects. Furthermore, the estimated spinal compression due to muscle loading was significantly reduced in all subjects.
Specification of cell fates in the nonsegmented terminal regions of developing Drosophila embryos is under the control of a signal transduction pathway mediated by the receptor tyrosine kinase Torso (Tor). Here, we identify tyrosines (Y) 630 and 918 as the major sites of Tor autophosphorylation. We demonstrate that mutation of Y630, a site required for association with and tyrosine phosphorylation of the tyrosine phosphatase Corkscrew, decreases the efficiency of Tor signaling. In contrast, mutation of Y918, a site capable of binding mammalian rasGAP and PLC-gammal, increases Tor signaling. Interestingly, when receptors contain mutations in both the Y630 and Y918 sites, Tor signaling is restored to wild-type levels. These results identify a novel mechanism whereby Tor function is regulated using compensatory signals generated from distinct autophosphorylation sites and reveal an underlying signaling pathway for terminal development.
The subdivision of the Drosophila body into distinct terminal and central domains depends on the torso (tor) protein, a putative receptor tyrosine kinase that is active at both ends of the early embryo. We show that the tor protein is uniformly expressed along the surface membrane of early embryos despite its localized activity at both poles. Further, we present evidence that polarized activity of this protein depends on other terminal gene functions, one of which may be a localized extracellular ligand generated during oogenesis. Finally, using the temperature-sensitive gain-of-function mutation torRL3, we show that different levels of active tor protein can specify distinct portions of the terminal pattern. Thus, we argue (1) that for functions as a ubiquitous surface receptor that is activated by a spatially restricted ligand, and (2) that localized activity of the tor kinase may generate one or more gradients of intracellular signals that control body pattern.
Induction of the R7 photoreceptor cell fate in the developing eye of Drosophila depends on the activation of the sevenless receptor tyrosine kinase in the R7 precursor cell. The sevenless protein is expressed transiently in 8 of the 20 precursors of an ommatidium. Activation of the sevenless kinase in these eight cells indicates that six of them are competent to become R7 cells. To test the competence of all 20 ommatidial precursors in a temporally unrestricted manner we have used a constitutively activated sevenless kinase created by fusing the extracellular domain of a mutant torso protein, another Drosophila receptor tyrosine kinase, to the sevenless kinase. Our results show that competence to develop as neuronal cells in response to sevenless activity is spatially and temporally limited to the cells expressing sevenless. Therefore, the expression of sevenless marks a preexisting pattern of developmental potential in the disc epithelium.
Determination of cell fate at the posterior termini of the Drosophila embryo is specified by the activation of the torso (tor) receptor tyrosine kinase. This signaling pathway is mediated by the serine/threonine kinase D-raf and a protein tyrosine phosphatase corkscrew (csw). We found that expression of an activated form of Ras1 during oogenesis resulted in embryos with tor gain-of-function phenotypes. To demonstrate that p21ras/Ras1 mediates tor signaling, we injected mammalian p21ras variants into early Drosophila embryos. We found that the injection of activated p21v-ras rescued the maternal-effect phenotypes of both tor and csw null mutations. These rescuing effects of p21v-ras are dependent on the presence of maternally derived D-raf activity. In addition, wild-type embryos show a terminal-class phenotype resembling csw when injected with p21rasN17, a dominant-negative form of p21ras. Furthermore, we have analyzed the maternal-effect phenotype of Son of sevenless (Sos), a positive regulator of Ras1, and showed that embryos derived from germ cells lacking Sos+ activity exhibit a terminal-class phenotype. Our study demonstrates that the Drosophila p21ras, encoded by Ras1, is an intrinsic component of the tor signaling pathway, where it is both necessary and sufficient in specifying posterior terminal cell fates. p21ras/Ras1 operates upstream of the D-raf kinase in this signaling pathway.
The maternally expressed Drosophila gene torso (tor) is a receptor tyrosine kinase that, when activated, initiates a signal transduction cascade that is responsible for the proper differentiation of the terminal, nonsegmented regions of the embryo. l(1)pole hole, the Drosophila raf-1 serine-threonine kinase homolog, and corkscrew, a tyrosine phosphatase, have been shown previously to function in this signal transduction pathway. We have identified other products in this pathway by carrying out a mutagenesis screen for dominant suppressors of a tor gain-of-function allele. More than 40 mutations, some of which fall into seven complementation groups, have been characterized genetically. Two of these correspond to mutations in ras-1 and Son of sevenless (Sos), which also function in the sevenless and EGF receptor (Der) tyrosine kinase pathways. The phenotypes of several other Su(tor) mutations suggest that they also function in other receptor tyrosine kinase-activated pathways at different times during Drosophila development.
The dorsal (dl) nuclear gradient initiates the differentiation of the mesoderm, neuroectoderm, and dorsal ectoderm by activating and repressing gene expression in the early Drosophila embryo. This gradient is organized by a Toll signaling pathway that shares many common features with the mammalian IL-1 cytokine pathway. Here we present evidence that a second signaling pathway, controlled by the torso (tor) receptor tyrosine kinase, also modulates dl activity. Evidence is presented that the tor pathway selectively masks the ability of dl to repress gene expression but has only a slight effect on activation. Intracellular kinases that are thought to function downstream of tor, such as D-raf and the rolled MAP kinase, mediate this selective block in repression. Normally, the Toll and tor pathways are both active only at the embryonic poles, and consequently, target genes (zen and dpp) that are repressed in middle body regions are expressed at these sites. Constitutive activation of the tor pathway causes severe embryonic defects, including disruptions in gastrulation and mesoderm differentiation, as a result of misregulation of dl target genes. These results suggest that RTK signaling pathways can control gene expression by antirepression, and that multiple pathways can fine-tune the activities of a single transcription factor.
Modulation of transcription factor activity leading to changes in cell behavior (e.g., differentiation versus proliferation) is one of the critical outcomes of receptor tyrosine kinase (RTK) stimulation. In the early Drosophila embryo, activation of the torso (tor) RTK at the poles of the embryo activates a phosphorylation cascade that leads to the spatially specific transcription of the tailless (tll) gene. Our analysis of the tor response element (tor-RE) in the tll promoter indicates that the key activity modulated by the tor RTK pathway is a repressor present throughout the embryo. We have mapped the tor-RE to an 11-bp sequence; using this sequence as the basis for protein purification, we have determined that the proteins GAGA and NTF-1 (also known as Elf-1, product of the grainyhead gene) bind to the tor-RE. We demonstrate that NTF-1 can be phosphorylated by MAPK (mitogen-activated protein kinase), and that tll expression is expanded in embryos lacking maternal NTF-1 activity; these results make NTF-1 a likely target for modulation by the tor RTK pathway in vivo. The data presented here support a model in which activation of the tor RTK at the poles of the embryos leads to inactivation of the repressor and therefore, to transcriptional activation (by activators present throughout the embryo) of the tll gene at the poles of the embryo.
We describe here a high-order (cubic Hermite) coupled finite element/boundary element procedure for solving electrocardiographic potential problems to be ultimately used for solving forward and inverse problems on an anatomically accurate human torso. Details of both numerical procedures and the coupling between them are described. Test results, illustrating the accuracy and efficiency of this combination for both two-dimensional (2-D) and three-dimensional (3-D) problems, are also given.
We have previously proposed two novel solutions to the inverse problem of electrocardiography, the generalized eigensystem technique (GES) and the modified generalized eigensystem technique (tGES), and have compared these techniques with other numerical techniques using both homogeneous and inhomogeneous eccentric spheres model problems. In those studies we found our generalized eigensystem approaches generally gave superior performance over both truncated singular value decomposition (SVD) and zero-order Tikhonov regularization (TIK). In this paper we extend the comparison to the case of a realistic heart-torso geometry. With this model, the GES and tGES approaches again provide smaller relative errors between the true potentials and the numerically derived potentials than the other methods studied. In addition, the isopotential maps recovered using GES and tGES appear to be more accurate than the maps recovered using either SVD and TIK.
Data from simulations of the anterior myocardial infarction (AMI) and inferior myocardial infarction (IMI) are presented. One infarct located in the anterior section of the left ventricle and a second one in the inferior wall of the left ventricle were modeled. A high-resolution finite element model of a heart and torso was used in this study. Differences in the normal and infarcted fields were computed. Our data suggest that the infarcted region contribution to the total magnetic field can be accounted for by an equivalent current dipole. It might also be possible to detect an infarct from these difference fields constructed for different cases of myocardial infarction. More simulations are needed to determine the relations between infarct sizes and locations and magnetic fields. These relations might then be used to detect various cases of myocardial infarction.
We have previously proposed an inverse algorithm for fitting potentials due to an arbitrary bio-electrical source to a single equivalent moving dipole (SEMD) model. The algorithm achieves fast identification of the SEMD parameters by employing a SEMD model embedded in an infinite homogeneous volume conductor. However, this may lead to systematic error in the identification of the SEMD parameters. In this paper, we investigate the accuracy of the algorithm in a realistic anatomic geometry torso model (forward problem). Specifically, we investigate the effect of measurement noise, dipole position and electrode configuration in the accuracy of the algorithm. The boundary element method was used to calculate the forward potential distribution at multiple electrode positions on the body surface due to a point dipole in the heart. We have found that the position and not the number of electrodes as well as the site of the origin of the arrhythmia in the heart have a significant effect on the accuracy of the inverse algorithm, while the measurement noise does not. Finally, we have shown that the inverse algorithm preserves the topology of the source distribution in the heart, thus potentially allowing the cardiac electrophysiologist to efficiently and accurately guide the tip of the catheter to the ablation site.
Several cases with serial photographs and commentary summarize experiences with well over 200 transposition "banner" flaps on the torso. The technique allows aesthetically acceptable reconstructions on the trunk by attention to detailed planning.
This study was performed to evaluate the accuracy of multichannel magnetocardiographic (MCG) and body surface potential mapping (BSPM) in localizing three-dimensionally the tip of an amagnetic catheter for electrophysiology without fluoroscopy. An amagnetic catheter (AC), specially designed to produce dipolar sources of different geometry without magnetic disturbances, was placed inside a physical thorax phantom at two different depths, 38 mm and 88 mm below the frontal surface of the phantom. Sixty-seven MCG and 123 BSPM signals generated by the 10 mA current stimuli fed into the catheter were then recorded in a magnetically shielded room. Non-invasive localization of the tip of the catheter was computed from measured MCG and BSPM data using an equivalent current dipole source in a phantom-specific boundary element torso model. The mean 3-dimensional error of the MCG localization at the closer level was 2 +/- 1 mm. The corresponding error calculated from the BSPM measurements was 4 +/- 1 mm. At the deeper level, the mean localization errors of MCG and BSPM were 7 +/- 4 mm and 10 +/- 2 mm, respectively. The results showed that MCG and BSPM localization of the tip of the AC is accurate and reproducible provided that the signal-to-noise ratio is sufficiently high. In our study, the MCG method was found to be more accurate than BSPM. This suggests that both methods could be developed towards a useful clinical tool for nonfluoroscopic 3-dimensional electroanatomical imaging during electrophysiological studies, thus minimizing radiation exposure to patients and operators.
OBJECTIVE: To determine the utility of the ED physical examination and laboratory analysis in screening hospitalized pediatric blunt trauma patients for intra-abdominal injuries (IAIs). METHODS: The authors reviewed the records of all patients aged <15 years who sustained blunt traumatic injury and were admitted to a Level 1 trauma center over a four-year period. Patients were considered high-risk for IAI if they had any of the following at ED presentation: decreased level of consciousness (GCS < 15), abdominal pain, tenderness on abdominal examination, or gross hematuria. Patients without any of these findings were considered moderate risk for LAI. The authors compared moderate-risk patients with and without IAIs with regard to physical examination and laboratory findings obtained in the ED. RESULTS: Of 1,040 children with blunt trauma, 559 (54%) were high-risk and 481 (46%) were moderate-risk for IAI. 126 (23%) of the high-risk and 22 (4.6%) of the moderate-risk patients had IAIs. Among moderate-risk patients with and without IAIs, those with IAIs were more likely to have abdominal abrasions (5/22 vs 34/459, p = 0.008), an abnormal chest examination (11/22 vs 86/457, p = 0.01), higher mean serum concentrations of aspartate aminotransferase (AST) (604 U/L vs 77 U/L, p < 0.001) and alanine aminotransferase (ALT) (276 U/L vs 39 U/L, p = 0.002), higher mean white blood cell (WBC) counts (16.3 K/mm3 vs 12.8 K/mm3, p < 0.001), and a higher prevalence of >5 RBCs/hpf on urinalysis (7/22 vs 54/427, p = 0.02). There was no significant difference (p > 0.05) between moderate-risk patients with and without IAIs in initial serum concentrations of amylase, initial hematocrit, drop in hematocrit >5 percentage points in the ED, or initial serum bicarbonate concentrations. CONCLUSION: In children hospitalized for blunt torso trauma who are at moderate risk for IAI, ED findings of abdominal abrasions, an abnormal chest examination, and microscopic hematuria as well as elevated levels of AST and ALT, and elevated WBC count are associated with IAI.
Using stable materials capable of mimicking any soft tissues of the human body--quantitatively with respect to speed of sound, density, and attenuation coefficient and semiquantitatively with respect to scatter--we have constructed a torso section phantom containing simulated bowel gas, kidney, kidney fat pad, liver, tumor, cyst, bony structures, and resolution fibers. Simple geometries and precise knowledge of ultrasonic properties allow artifacts to be produced and explained with great confidence. Artifacts due to refraction and reflection are particularly dramatic. Phantoms such as this should be useful as stage one phantoms for training ultrasonographers. Such phantoms should also be of use to those who are doing research in ultrasonic image processing. This might involve, for example, recognizing image artifacts and reducing their effect in the formation of the image.