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PubMed2001

Two distinct domains of Bicoid mediate its transcriptional downregulation by the Torso pathway.

The transcriptional activity of the Bicoid morphogen is directly downregulated by the Torso signal transduction cascade at the anterior pole of the Drosophila embryo. This regulation does not involve the homeodomain or direct phosphorylation of Bicoid. We analyse the transcriptional regulation of Bicoid in response to the Torso pathway, using Bicoid variants and fusion proteins between the Bicoid domains and the Gal4 DNA-binding domain. We show that Bicoid possesses three autonomous activation domains. Two of these domains, the serine/threonine-rich and the acidic domains, are downregulated by Torso, whereas the third activation domain, which is rich in glutamine, is not. The alanine-rich domain, previously described as an activation domain in vitro, has a repressive activity that is independent of Torso. Thus, Bicoid downregulation by Torso results from a competition between the glutamine-rich domain that is insensitive to Torso and the serine/threonine-rich and acidic activation domains downregulated by Torso. The alanine-rich domain contributes to this process indirectly by reducing the global activity of the protein and in particular the activity of the glutamine-rich domain that might otherwise prevent downregulation by Torso.

Animals↗

PubMed1988

Measurement of torso skin temperature under clothing.

The influence of clothing on skin temperature distributions of the torso was investigated during and after cold exposure. Volunteers were cooled for one hour at 5 degrees C while wearing clothing designed to have insulation which was intended to be relatively uniformly distributed. Three different thicknesses of clothing were used. Following thermistor measurements of skin temperatures during the cold exposures, clothing was quickly removed from the upper parts of the body to enable thermographic investigations of the temperature distributions of the front of the bare torso. The evolution of temperature distributions were then studied at different ambient temperatures (5 degrees C and 20 degrees C) as a function of the thickness of the insulation which had previously been worn. The patterns of the temperature distributions, and the range and standard deviation of torso temperatures were all found to be relatively constant in spite of the different thicknesses of clothing worn or in the time-variant mean torso temperatures which resulted. The front torso sites normally used for the determination of mean skin temperatures were found to be on portions of the torso which were cooler than the surrounding regions. It was concluded that a site midway between the umbilicus and a nipple yields a more accurate estimate of mean torso temperature in the conditions of the present study.

Body Temperature Regulation↗

PubMed1999

Horizontal vestibulo-ocular reflex and head stability in response to torso perturbations during visual search.

Eye, head, and torso movements were recorded using magnetic search coils while six normal human subjects made unconstrained eye and head movements as they searched for targets in a panoramic visual environment. Torso movements were imposed by pseudorandom rotations of a servomotor-driver chair in which subjects were seated; body motion was partially transmitted to the head as a perturbation. Horizontal vestibulo-ocular reflex (VOR) gain (eye velocity divided by head velocity) and head gain (head velocity divided by torso velocity) were determined. Measurements were performed with unaided vision and while subjects wore x4 binocular telescopic spectacles. Since the head was free to move during the experiment, much of the perturbation delivered to the torso was compensated by head rotation on the neck. During the 50 ms immediately following chair rotation, the head corrected 98% of the torso motion. For the interval 50-80 ms after the perturbation 81-85% of the perturbation was corrected by head movement. The degree of head compensation did not significantly depend on magnification or type of visual target. The density distribution for VOR gain was calculated over the entire course of each trial and was found to be sharply centered between 0.9 and 1.0 for trials with unmagnified vision. The gain density distribution with x4 telescopes was broader and centered around 1.5, reflecting visual enhancement. Gain of the VOR was also determined during four discrete epochs covering the period from 50 ms before to 130 ms after the onset of each imposed torso rotation. The first, second, and fourth epochs were 50 ms each, while the third epoch was 30 ms. The torso began to rotate in the second epoch (0-50 ms), and the onset of head rotation was in the third epoch (50-80 ms). Gains of the VOR determined during the first three epochs were in response to self-generated head rotation and were not significantly different from each other, averaging 1.0+/-0.4 (n=1604, mean+/-SD) with unaided vision and increased significantly (P<0.05) to 1.4+/-0.6 (n=2464) with telescopic spectacles. Gain of the VOR during the fourth (80-130 ms) epoch was in response to the imposed perturbation; this averaged 0.9+/-0.3 (n=1380) with unaided vision and increased significantly to 1.1+/-0.4 (n=2185) with telescopic spectacles. The wearing of telescopic spectacles thus induced an enhancement of VOR gain, which was dependent on the context of the associated head movement. The greater enhancement of VOR gain during self-generated head movement suggests that the large enhancement may be at least partially mediated by the motor program itself. However, the smaller, but still significant gain enhancement with telescopic spectacles observed during unpredictable, externally imposed head motion had a latency too short to be mediated by visual pursuit. We propose that the smaller gain enhancement during passive rotation is due to a small, context-dependent, parametric increase in the gain of canal or proprioceptive mediated eye movements.

Acceleration↗

PubMed1998

Improved estimation of pericardial potentials from body-surface maps using individualized torso models.

Clinical applicability of inferred pericardial potentials is limited because accuracy is significantly affected by noise in surface electrocardiograms (ECGs), errors in electrode location on the torso model, and errors in the geometry and inhomogeneities of the torso model itself. To quantify effects of electrode location and geometric errors in torso-surface models, we measured locations of 190 electrodes used in body-surface mapping of 11 adults, along with over 2,000 sites on each torso surface. Measurements were made to within 2 mm with an Immersion Personal Digitizer. To quantify effects of errors in pericardial-surface models we also estimated heart position, size, and orientation in each subject from ultrasonic images registered to the body-surface coordinates. Known pericardial potentials were taken from epicardial measurements made during QRS with a 90-electrode sock in an adult male undergoing cardiac surgery. Body-surface ECGs were calculated for each individual from the pericardial maps, using standard boundary-element methods. Accuracy of zero-order-Tikhonov inverse solutions was tested in 91-node pericardial and 1,026-node torso models, individualized for each subject. With 10 microv rms noise added to surface potentials, the optimal regularization constant at each instant in QRS gave a relative error of 0.44 +/- 0.03; it was 0.47 +/- 0.03 using the composite residual and smoothing operator (CRESO) technique. When calculated body-surface potentials from the first 10 subjects were placed at corresponding electrode positions on the torso of the eleventh subject, whose heart size and orientation was the mean of the other 10 subjects, relative error increased to 0.87 +/- 0.06 for optimal regularization. CRESO failed in the fixed torso model. Results demonstrate that a fixed model does not provide useful estimates of pericardial potentials, and that individualized models enhance the performance of techniques for the estimation of regularization parameters.

Adult↗

PubMed1998

Opposing actions of CSW and RasGAP modulate the strength of Torso RTK signaling in the Drosophila terminal pathway.

In Drosophila, specification of embryonic terminal cells is controlled by the Torso receptor tyrosine kinase. Here, we analyze the molecular basis of positive (Y630) and negative (Y918) phosphotyrosine (pY) signaling sites on Torso. We find that the Drosophila homolog of RasGAP associates with pY918 and is a negative effector of Torso signaling. Further, we show that the tyrosine phosphatase Corkscrew (CSW), which associates with pY630, specifically dephosphorylates the negative pY918 Torso signaling site, thus identifying Torso to be a substrate of CSW in the terminal pathway. CSW also serves as an adaptor protein for DRK binding, physically linking Torso to Ras activation. The opposing actions of CSW and RasGAP modulate the strength of the Torso signal, contributing to the establishment of precise boundaries for terminal structure development.

Animals↗

PubMed2001

Electrocardiographic imaging: I. Effect of torso inhomogeneities on body surface electrocardiographic potentials.

INTRODUCTION: Body surface potential maps (BSPMs) and conventional ECG reflect electrical sources generated by cardiac excitation and repolarization and noninvasively provide important diagnostic information about the electrical state of the heart. Because the heart is located within the torso volume conductor, body surface potentials also reflect the effects of torso inhomogeneities, which include blood, lungs, bone, muscle, fat, and fluid. It is necessary to characterize and understand these effects in order to interpret BSPM and ECG in terms of cardiac activity without "contamination" from the inhomogeneous volume conductor. METHODS AND RESULTS: Actual measured epicardial and body surface potentials were obtained during normal sinus rhythm and for different pacing protocols from a Langendorff-perfused dog heart suspended in a human-shaped torso tank. Accurate geometry of the torso inhomogeneities was digitized from the Visual Human Project and appropriately introduced into a computer model of the tank setup. The geometry and electrical properties of the volume conductor could be varied. Both homogeneous and inhomogeneous torsos have major smoothing effects on BSPM, which is of very low resolution compared with its corresponding epicardial potential pattern. Relative to a homogeneous torso, the inhomogeneities have only a minor effect on BSPM patterns. They augment potential magnitudes depending on the pattern of epicardial activation. Variations of geometry and electrical properties within the normal physiologic range have minimal effects. CONCLUSION: Effects of torso inhomogeneities on 12-lead ECGs are minimal, and the associated ECG changes fall within the range of normal interindividual variations.

Algorithms↗

PubMed2004

Emergency department spirometric volume and base deficit delineate risk for torso injury in stable patients.

BACKGROUND: We sought to determine torso injury rates and sensitivities associated with fluid-positive abdominal ultrasound, metabolic acidosis (increased base deficit and lactate), and impaired pulmonary physiology (decreased spirometric volume and PaO2/FiO2). METHODS: Level I trauma center prospective pilot and post-pilot study (2000-2001) of stable patients. Increased base deficit was < 0.0 in ethanol-negative and < or = -3.0 in ethanol-positive patients. Increased lactate was > 2.5 mmol/L in ethanol-negative and > or = 3.0 mmol/L in ethanol-positive patients. Decreased PaO2/FiO2 was < 350 and decreased spirometric volume was < 1.8 L. RESULTS: Of 215 patients, 66 (30.7%) had a torso injury (abdominal/pelvic injury n = 35 and/or thoracic injury n = 43). Glasgow Coma Scale score was 14.8 +/- 0.5 (13-15). Torso injury rates and sensitivities were: abdominal ultrasound negative and normal base deficit, lactate, PaO2/FiO2, and spirometric volume--0.0% & 0.0%; normal base deficit and normal spirometric volume--4.2% & 4.5%; chest/abdominal soft tissue injury--37.8% & 47.0%; increased lactate--39.7% & 47.0%; increased base deficit--41.3% & 75.8%; increased base deficit and/or decreased spirometric volume--43.8% & 95.5%; decreased PaO2/FiO2--48.9% & 33.3%; positive abdominal ultrasound--62.5% & 7.6%; decreased spirometric volume--73.4% & 71.2%; increased base deficit and decreased spirometric volume--82.9% & 51.5%. CONCLUSIONS: Trauma patients with normal base deficit and spirometric volume are unlikely to have a torso injury. Patients with increased base deficit or lactate, decreased spirometric volume, decreased PaO2/FiO2, or positive FAST have substantial risk for torso injury. Increased base deficit and/or decreased spirometric volume are highly sensitive for torso injury. Base deficit and spirometric volume values are readily available and increase or decrease the suspicion for torso injury.

Abdominal Injuries↗

PubMed1995

Dissection of the Torso signal transduction pathway in Drosophila.

Cell fate choice at the anterior and posterior embryonic termini of the Drosophila embryo requires the activation of a signal transduction pathway regulated by the receptor tyrosine kinase Torso. When Torso, which is uniformly distributed in the egg cell membrane, becomes activated locally at the termini, it triggers a phosphorylation cascade that culminates with localized expression of the transcription factors, tailless and huckebein. Expression of tailless and huckebein in turn determines terminal cell fates. Several genes have been characterized which encode proteins that are involved in Torso signaling: the adaptor protein Drk, the GTP-binding protein Ras1, the guanine nucleotide exchange factor Son of sevenless, and the kinases D-Raf and D-Mek. Genetic and molecular evidence supports a model in which these proteins lie in the same biochemical pathway. When activated by its ligand the membrane-bound receptor tyrosine kinase Torso initiates a signal transduction pathway mediated by Drk, Sos, and Ras1, which in turn activates a phosphorylation cascade mediated by the kinases D-Raf and D-Mek, which ultimately control the localized expression of the transcription factors tailless and huckebein. Recently, we found that D-Raf can be partially activated by Torso in the absence of Ras1, a finding supported by the phenotype of embryos lacking either Drk or Sos activity, as well as by the phenotype of a D-raf mutation that abolishes binding of Ras1 to D-Raf. These findings indicate that full D-Raf activation requires input not only from Ras1 but also from an as yet uncharacterized Ras1-independent pathway. In addition to these molecules we have characterized the putative protein tyrosine phosphatase Corkscrew as a positive transducer downstream of Torso.

Animals↗

PubMed1992

Torso injury patterns and mechanisms in car crashes: an additional diagnostic tool.

Torso injuries among car occupants involved in sever collisions are often life threatening. This study considers whether knowledge of the type of impact and associated trends of torso injuries would assist the rapid diagnosis of injuries by emergency personnel. For the purpose of this analysis the pelvis was included in the torso. The data source was the Cooperative Crash Injury Study which holds detailed injury information on over 6200 car crash occupants. Restrained front seat occupants with an ISS of 16+ who were involved in frontal or side collisions were selected. A total of 286 occupants fell into these selection criteria. The frequency of injury to each torso part was determined to give an approximate likelihood of injury in each impact configuration. The injury data were further analysed to look for patterns of injury in frontal or side impacts. The likelihood of all torso injuries, except sternal and lumbar spinal injuries, increased in side impacts, particular examples being the spleen and pelvis. There were statistically significant associations between injuries to different torso parts. In frontal impacts rib fracture indicates the distinct possibility of underlying organ injury. Vehicle damage data coupled with readily diagnosed injuries can suggest the possibility of less easily detectable injuries.

Abdominal Injuries↗

PubMed2001

Modelling the line of action for the oblique abdominal muscles using an elliptical torso model.

When modelling the line of action of a muscle, anatomical considerations must be included if the model is to realistically mimic the muscle behaviour. The internal and external oblique muscles are examples of muscles that do not follow a straight line between origin and insertion, instead having to wrap around the torso. A model is presented which describes the shape of the torso using a right elliptical cylinder of varying dimensions. The muscle lines of action are then calculated based on this underlying torso shape. The model has been successfully fitted to the data reported by Stokes and Gardner-Morse (Journal of Biomechanics 32(3) (1999) 311). When compared to a linear model, the use of the torso model results in a 15% increase in the axial twist moment, and decreases in the lateral bend and extension moments (5% and 2%, respectively), able to be generated by the internal and external oblique muscles combined in upright stance. These differences become larger (up to 37%) when the torso is flexed, extended or twisted. The structure of the torso model allows it to be used to model any posture without significant increases in the overall model complexity.

Abdominal Muscles↗

PubMed2005

The effect of pallet distance on torso kinematics and low back disorder risk.

Intervention research for prevention of occupational low back injuries has focused on the effects of reducing extreme torso flexion and the external moment. Little is known about prevention strategies for torso twisting and lateral bending. The objective of this study was to assess the effect of pallet distance with regard to a constant lift origin on the torso kinematics and a measure of low back disorder risk. Fifteen male participants transferred 11.3 kg boxes from a constant origin to six different regions on a pallet. Two pallet distances with regard to the lift origin were investigated. ANOVA indicated that increasing the pallet distance resulted in increases in torso kinematics (velocities and accelerations) as well as a measure of risk of low back disorder. The increases in torso kinematics (e.g. twisting and lateral awkward postures and bending velocities) occurred mostly at the lower height regions on the pallet. It is concluded that increasing the pallet distance with regard to the lifting origin, with the intention to influence the participant to take a step during a palletizing task does not appear to be an effective intervention strategy to reduce the risk of low back disorder associated with torso kinematics.

Adult↗

PubMed2000

Effect of myocardial anisotropy on the torso current flow patterns, potentials and magnetic fields.

The effects of myocardial anisotropy on the torso current flow patterns, voltage and the magnetic field were examined using an anatomically realistic torso model of an adult male subject. A finite element model of the torso was built with 19 major tissue types identified. The myocardial fibre orientation in the heart wall was included with a voxel resolution of 0.078 x 0.078 x 0.3 cm. The fibre orientations from the canine heart which are available in the literature were mapped to our adult male subject's human heart using deformable mapping techniques. The current and potential distribution in the whole torso were computed using an idealized dipolar source of +/-1.0 V in the middle of the septum of the heart wall as a boundary condition. An adaptive finite element solver was used. Two cases were studied. In one case the myocardium was isotropic and in the other it was anisotropic. It was found that the current density distribution shows a very noticeable difference between the isotropic and anisotropic myocardium. The resultant magnetic field in front of the torso was computed using the Biot-Savart law. It was found that the magnetic field profile was slightly affected by the myocardial anisotropy. The potential on the torso surface also shows noticeable changes due to the myocardial anisotropy.

Abdomen↗

PubMed1998

Effect of differential delivery of isoflurane to head and torso on lumbar dorsal horn activity.

BACKGROUND: The spinal cord appears to be the site where anesthetic agents prevent movement in response to noxious stimuli. When isoflurane is differentially delivered to the head and torso (with low torso concentrations), cranial anesthetic requirements increase compared with systemic administration. The aim of the current study was to test the hypothesis that isoflurane action in the brain has descending influences on spinal cord dorsal horn neurons. A secondary aim was to determine the association, if any, of high cranial concentrations of isoflurane (>6%) with dorsal horn activity. METHODS: Ten goats were anesthetized with isoflurane and the carotid arteries and jugular veins isolated and cannulated for cerebral bypass. A laminectomy was performed for recording from single lumbar dorsal horn neurons with hind limb mechanical receptive fields (one cell per goat). A standard noxious mechanical stimulus was applied to the dew claw or hoof bulb during a control period with end-tidal isoflurane at 1.3% and during bypass with the following head/torso isoflurane concentrations: 1.3%/1.3%, 3.2%/1.3%, 9.4%/1.3%, 1.3%/0.2%, 3.0%/0.2% and 8.8%/0.3%. RESULTS: When torso isoflurane concentration was 1.3%, increasing cranial isoflurane concentration to 3% or 9% had no significant effect on the activity of dorsal horn units. When torso isoflurane was 0.2-0.3%, spontaneous activity increased; however, at these torso concentrations, evoked responses were significantly decreased (-60%) only when cranial isoflurane concentration was increased to 9%. CONCLUSIONS: Isoflurane action in the brain had an inhibitory effect on dorsal horn activity with the combination of supraclinical cranial and low torso concentrations.

Anesthetics, Inhalation↗

PubMed1998

Extracting isovolumes from three-dimensional torso geometry using PROLOG.

Three-dimensional (3-D) finite element torso models are widely used to simulate defibrillation field quantities, such as potential, gradient, and current density. These quantities are computed at spatial nodes that comprise the torso model. These spatial nodes typically number between 10(5) and 10(6), which makes the comprehension of torso defibrillation simulation output difficult. Therefore, the objective of this study is to rapidly prototype software to extract a subset of the geometric model of the torso for visualization in which the nodal information associated with the geometry of the model meets a specified threshold value (e.g., minimum gradient). The data extraction software is implemented in PROLOG, which is used to correlate the coordinate, structural, and nodal data of the torso model. A PROLOG-based environment has been developed and is used to rapidly design and test new methods for sorting, collecting, and optimizing data extractions from defibrillation simulations in a human torso model for subsequent visualization.

Algorithms↗

PubMed1989

Reciprocal effects of hyper- and hypoactivity mutations in the Drosophila pattern gene torso.

In Drosophila, five "terminal" polarity genes must be active in females in order for them to produce embryos with normal anterior and posterior ends. Hypoactivity mutations in one such gene, torso, result in the loss of the most posterior domain of fushi tarazu expression and the terminal cuticular structures. In contrast, a torso hyperactivity mutation causes the loss of central fushi tarazu expression and central cuticular structures. Cytoplasmic leakage, transplantation, and temperature-shift experiments suggest that the latter effect is caused by abnormal persistence of the torso product in the central region of the embryo during early development. Thus, the amount and timing of torso activity is key to distinguishing the central and terminal regions of the embryo. Mutations in the tailless terminal gene act as dominant maternal suppressors of the hyperactive torso allele, indicating that the torso product acts through, or in concert with, the tailless product.

Abdomen↗

PubMed1993

Biochemical analysis of torso and D-raf during Drosophila embryogenesis: implications for terminal signal transduction.

Determination of anterior and posterior terminal structures of Drosophila embryos requires activation of two genes encoding putative protein kinases, torso and D-raf. In this study, we demonstrate that Torso has intrinsic tyrosine kinase activity and show that it is transiently tyrosine phosphorylated (activated) at syncytial blastoderm stages. Torso proteins causing a gain-of-function phenotype are constitutively tyrosine phosphorylated, while Torso proteins causing a loss-of-function phenotype lack tyrosine kinase activity. The D-raf gene product, which is required for Torso function, is identified as a 90-kDa protein with intrinsic serine/threonine kinase activity. D-Raf is expressed throughout embryogenesis; however, the phosphorylation state of the protein changes during development. In wild-type embryos, D-Raf is hyperphosphorylated at 1 to 2 h after egg laying, and thereafter only the most highly phosphorylated form is detected. Embryos lacking Torso activity, however, show significant reductions in D-Raf protein expression rather than major alterations in the protein's phosphorylation state. This report provides the first biochemical analysis of the terminal signal transduction pathway in Drosophila embryos.

3T3 Cells↗

PubMed2005

Torso stabilization reduces the metabolic cost of producing cycling power.

Many researchers have used cycling exercise to evaluate muscle metabolism. Inherent in such studies is an assumption that changes in whole-body respiration are due solely to respiration at the working muscle. Some researchers, however, have speculated that the metabolic cost of torso stabilization may contribute to the metabolic cost of cycling. Therefore, our primary purpose was to determine whether a torso stabilization device would reduce the metabolic cost of producing cycling power. Our secondary purpose was to determine the validity of the ergometer used in this study. Nine male cyclists cycled on a Velotron cycle ergometer at mechanical power outputs intended to elicit 50, 75, and 100% of their ventilatory threshold at 40, 60, and 80 rpm, with and without torso stabilization. Power was controlled by the Velotron in iso-power mode and measured with an SRM powermeter. We determined metabolic cost by indirect calorimetery and recorded power output. Torso stabilization significantly reduced metabolic cost of producing submaximal power (1%), and reduction tended to be greatest at the lower pedaling rates where pedaling force was greatest (1.6% at 40 rpm, 1.2% at 60 rpm, 0.2% at 80 rpm). Power, measured with the SRM powermeter, was strongly correlated with that specified to the Velotron ergometer control unit (R(2) > 0.99). We conclude that muscular contractions associated with torso stabilization elicit significant metabolic costs, which tend to be greatest at low pedaling rates. Researchers who intend to make precise inferences regarding metabolism in the working muscles of the legs may wish to provide torso stabilization as a means of reducing variability, particularly when comparing metabolic data across a wide range of pedaling rates.

Adult↗

PubMed1996

Variation in the number of activated torso receptors correlates with differential gene expression.

Activation of receptor tyrosine kinases triggers many developmental decisions, yet we do not understand how activation of a single receptor can be transduced into different cell responses. The torso pathway in Drosophila provides a model to address this issue since it generates more than one response in the embryo. The torso receptor tyrosine kinase is activated at the embryonic poles under the control of trunk, a protein with similarities to several types of extracellular growth factors. Activation of torso is responsible for the development of a variety of structures, whose appearance can be correlated with activation of at least two different genes along the terminal region. In this study we have analyzed mutations in torso and trunk that express low levels of the respective proteins. We show that different amounts of torso or trunk molecules correlate with the expression of different zygotic genes, implicating changes in the number of activated torso molecules as one of the mechanisms defining differential gene expression. We suggest that variation in the number of activated receptors at the cell surface is a general mechanism that leads to differential gene expression and thus the generation of different cell responses.

Animals↗