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W Schlegel

Publications and source records attributed to W Schlegel.

At least 19 recordsLinked to original sources

The guanine-nucleotide-binding protein subunit G alpha i2 is involved in calcium activation of phospholipase A2. Effects of the dominant negative G alpha i2 mutant, [G203T]G alpha i2, on activation of phospholipase A2 in Chinese hamster ovary cells.

The mechanisms of activation of cytoplasmic phospholipase A2 (cPLA2) are complex and incompletely defined. In Chinese hamster ovary (CHO) cells, receptor stimulation of cPLA2 is due to the interaction of pathways involving the alpha subunits of at least two guanine-nucleotide-binding (G) proteins, G alpha i2 and G alpha q. Activation of cPLA2 is inhibited by pertussis toxin and G alpha i2 mutants. In addition, activation of phospholipase C via G alpha q results in increased intracellular calcium ([Ca2+]i) and activation of protein kinase C, both of which interact with and activate cPLA2. The present study was undertaken to analyze the mechanism of interaction of G alpha i2 with the phospholipase-C-stimulated pathway in the activation of cPLA2. We addressed this question using a dominant negative G alpha i2 mutant, [G203T]G alpha i2, in which Gly203 is mutated to Thr. [G203T]G alpha i2 inhibits ATP receptor activation of cPLA2. The effect of [G203T]G alpha i2 was specific to G alpha i2-activated pathways, as shown by its lack of effect on other purinergic receptor stimulated pathways: ATP stimulation of [Ca2+]i or mitogen-activated protein kinase phosphorylation is unaltered by [G203T]G alpha i2. We addressed the possibility that the activation of cPLA2 by Ca2+ and/or protein kinase C is dependent on G alpha i2. Activation of cPLA2 by the Ca2+ ionophore, ionomycin, was inhibited by 61 +/- 9% (n = 5) in [G203T]G alpha i2-expressing cells; however the ionomycin-induced [Ca2+]i rise was unaffected by [G203T]G alpha i2. Thus, [G203T]G alpha i2. specifically inhibits Ca2+ activation of cPLA2. In contrast, activation of cPLA2 via protein kinase C by phorbol 12-myristate 13-acetate was unaffected by [G203T]G alpha i2. Our results demonstrate that Ca2+ but not phorbol ester activation of cPLA2 in CHO cells is G alpha i2-dependent. The possibility is discussed that G alpha i2 is downstream of Ca2+ but upstream of protein kinase C activation of cPLA2.

Animals

Stereotactic convergent beam radiosurgery versus stereotactic conformation beam radiotherapy.

By means of preliminary results in the treatment of patients with acoustic neurinoma the achievable accuracies, dose distributions and time consumption of stereotactic LINAC-based convergent beam radiosurgery are compared to those achieved with fractionated stereotactic conformation beam radiotherapy. Characteristics of both techniques are described. With the Tübingen radiosurgery system a good adaptation of the dose distribution to spherical or oval target volumes with a steep dose gradient was achieved, whereas homogeneity and adaptation of the dose distribution to irregularly shaped targets were better with the Heidelberg conformation technique. The mechanical accuracy of the Tübingen floorstand system was 0.3 mm +/- 0.2 mm, and that of the Heidelberg mask fixation system < 1 mm. Both methods require similar total treatment times. Nine patients were treated by the Tübingen radiosurgery system. The results are compared with 12 patients treated by conformation radiotherapy in Heidelberg. In both patient groups no further tumour growth occurred. Four of 9 single dose treated patients developed side-effects, such as temporary trigeminal and facial paraesthesia hearing deterioration and oedema. In contrast, patients treated by fractionated radiotherapy showed no side-effects. Relating to the short follow-up the results indicate that single dose application has certain drawbacks for special indications. Further studies have to work out which method gives the best treatment results.

Adolescent

Highly co-operative Ca2+ activation of intermediate-conductance K+ channels in granulocytes from a human cell line.

1. To study Ca(2+)-activated K+ currents in dimethyl sulphoxide (DMSO)-differentiated HL-60 cells (HL-60 granulocytes), we have combined the patch clamp technique with microfluorimetric measurements of the cytosolic free Ca2+ concentration ([Ca2+]i). 2. Elevations of [Ca2+]i induced by the receptor agonist N-formyl-L-methionyl-L-phenylalanine (f-MLP), by cellular spreading or by the Ca2+ ionophore ionomycin, activated whole-cell currents. The kinetics of the current elevations closely paralleled the kinetics of the elevations in [Ca2+]i. Cellular spreading induced oscillations in [Ca2+]i and parallel oscillatory changes in the amplitude of the recorded currents. 3. The reversal potential of the Ca(2+)-activated current was a function of the extracellular K+ concentration (56.1 mV per log [K+]), demonstrating that the underlying conductance was selective for K+. 4. The current was blocked by charybdotoxin, but insensitive to apamin. 5. The whole-cell current was inwardly rectifying. No time-dependent activation or inactivation of the current could be observed within the range of voltages tested (-100 to +100 mV). 6. The dependence of the current amplitude on the measured [Ca2+]i revealed a half-maximal activation at approximately 350 nM [Ca2+]i, and a highly co-operative activation by [Ca2+]i with an apparent Hill coefficient of approximately 8. Neither the half-maximal activation by [Ca2+]i nor the apparent Hill coefficient depended on the voltage, and they were identical for Ca2+ elevations caused by the ionophore and the receptor agonist. 7. Analysis of Ca(2+)-activated single-channel events in cell-attached recordings revealed an inwardly rectifying K+ channel with a slope conductance of 35 pS. Fluctuation analysis of the Ca(2+)-activated whole-cell current suggested an underlying single-channel conductance of a similar size (28 pS). 8. In summary, we describe a charybdotoxin-sensitive, intermediate-conductance Ca(2+)-activated K+ channel in HL-60 granulocytes. The characteristics of the Ca2+ activation of this current (i.e. sensitivity to submicromolar [Ca2+]i, high co-operativity and voltage independence) are similar to the Ca2+ activation of the apamin-sensitive small-conductance K+ channel. Our results also suggest that [Ca2+]i elevations are the predominant, if not the only, activators of this channel during physiological stimulation of HL-60 granulocytes.

Apamin

Modulation of Ca2+ influx by protein phosphorylation in single intact clonal pituitary cells.

In pituitary cells, electrical activity generates characteristic oscillations of the cytosolic free Ca2+ concentration, [Ca2+]i. These oscillations are controlled by activators as well as by inhibitors of secretion. We studied, in single fura-2-loaded cells, the role of protein phosphorylation in modulating [Ca2+]i oscillations, using either okadaic acid, an inhibitor of protein phosphatases, or activators of protein kinases A and C. Okadaic acid always increased rapidly both the frequency and amplitude of [Ca2+]i oscillations. In contrast, activation of protein kinases A or C generated more complex kinetic [Ca2+]i patterns: phosphorylation due to both kinases resulted in a sustained activation of [Ca2+]i oscillations in about one-third of the cells, whereas two-thirds of the cells responded by an arrest of [Ca2+]i oscillations. This transient phase of arrest was followed, after a few minutes, by a recovery of [Ca2+]i oscillations, often with enhanced frequency. During the arrest, depolarizing the cells with an external microelectrode could not trigger an increase in [Ca2+]i. We conclude that: (i) the fine regulation between phosphorylation/dephosphorylation events is crucial for the modulation of [Ca2+]i oscillations, and (ii) protein kinases A and C can control Ca2+ influx bidirectionally.

Action Potentials

Video imaging of cytosolic Ca2+ in pancreatic beta-cells stimulated by glucose, carbachol, and ATP.

In order to define the differences in the distribution of cytosolic free Ca2+ ([Ca2+]i) in pancreatic beta-cells stimulated with the fuel secretagogue glucose or the Ca(2+)-mobilizing agents carbachol and ATP, we applied digital video imaging to beta-cells loaded with fura-2.83% of the cells responded to glucose with an increase in [Ca2+]i after a latency of 117 +/- 24 s (mean +/- S.E., 85 cells). Of these cells, 16% showed slow wave oscillations (frequency 0.35/min). In order to assess the relationship between membrane potential and the distribution of the [Ca2+]i rise, digital image analysis and perforated patch-clamp methods were applied simultaneously. The system used allowed sufficient temporal resolution to visualize a subplasmalemmal Ca2+ transient due to a single glucose-induced action potential. Glucose could also elicit a slow depolarization which did not cause Ca2+ influx until the appearance of the first of a train of action potentials. [Ca2+]i rose progressively during spike firing. Inhibition of Ca2+ influx by EGTA abolished the glucose-induced rise in [Ca2+]i. In contrast, the peak amplitude of the [Ca2+]i response to carbachol was not significantly different in normal or in Ca(2+)-deprived medium. Occasionally, the increase of the [Ca2+]i rise was polarized to one area of the cell different from the subplasmalemmal rise caused by glucose. The amplitude of the response and the number of responding cells were significantly increased when carbachol was applied after the addition of high glucose (11.2 mM). ATP also raised [Ca2+]i and promoted both Ca2+ mobilization and Ca2+ influx. The intracellular distribution of [Ca2+]i was homogeneous during the onset of the response. A polarity in the [Ca2+]i distribution could be detected either in the descending phase of the peak or in subsequent peaks during [Ca2+]i oscillations caused by ATP. In the absence of extracellular Ca2+, the sequential application of ATP and carbachol revealed that carbachol was still able to raise [Ca2+]i after exhaustion of the ATP response. This may be due to desensitization to the former agonist, since the response occurred in the same area of the cell. These results reveal subtle differences in [Ca2+]i distribution following membrane depolarization with glucose or the application of Ca(2+)-mobilizing agonists.

Adenosine Triphosphate

Determination of prostaglandin metabolites in biological samples by competitive time-resolved fluoroimmunoassay.

We describe a time-resolved fluoroimmunoassay method for the determination of 13,14-dihydro-15-ketoprostaglandin E2 (PGEM) and 13,14-dihydro-15-ketoprostaglandin F2 alpha (PGFM) in femtomolar ranges. Polyclonal antibodies were raised in rabbits and the antigen was labelled with europium by the avidin-biotin technique. A second antibody, directed to rabbit IgG, was coated onto the solid phase. The IgG-PG-europium complex was bound by the second antibody, giving a rapid and complete separation of antibody-bound and free antigen. The detection limit was 0.2 pg/assay for PGFM and 1.2 pg/assay for PGEM. The intra-assay CV ranged from 4.6% to 9.3% and the interassay CV from 6.7% to 11.4%. A good correlation was obtained between the results from TR-FIA and RIA when the method was applied to the investigation of tissues from breast cancer. We conclude that the TR-FIA is more sensitive and much faster than the RIA and avoids the use of radioactive material.

Bacterial Proteins

Inositol tetrakisphosphate isomers and elevation of cytosolic Ca2+ in vasopressin-stimulated insulin-secreting RINm5F cells.

Signal generation during the stimulation of insulin secretion by arginine vasopressin (AVP) was investigated in RINm5F cells. AVP (0.1 microM) caused a biphasic cytosolic Ca2+ ([Ca2+]i) rise, namely a rapid transient marked elevation after stimulation followed by a series of oscillations. In the absence of extracellular Ca2+, the sustained oscillations were abolished, while the initial [Ca2+]i transient was only partly decreased, indicating that the former are due to Ca2+ influx and the latter due mainly to mobilization from internal Ca2+ stores. AVP also evoked a transient depolarization of the average membrane potential. AVP-induced Ca2+ influx during the sustained phase, which was strictly dependent on receptor occupancy, was attenuated by membrane hyperpolarization with diazoxide. However, blockade of Ca2+ channels of the L- or T-type was ineffective. AVP stimulated production of diacylglycerol and inositol phosphates; for the latter both [3H] inositol labeling and mass determinations were performed. A transient increase in Ins(1,4,5)P3 was followed by a marked enhancement of Ins(1,3,4,5)P4 (8-fold) peaking at 15 s and gradually returning to basal values. Ins(1,3,4,6)P4 and Ins(3,4,5,6)P4 exhibited the most long-lasting augmentation (4- and 1.7-fold, respectively), and therefore correlated best with the period of sustained [Ca2+]i oscillations. InsP5 and InsP6 were not elevated. The effects of AVP, including the stimulation of insulin secretion from perifused cells, were obliterated by a V1 receptor antagonist. In conclusion, AVP induces protracted [Ca2+]i elevation in RINm5F cells which is associated with long-lasting increases in InsP4 isomers. The accumulation of InsP4 isomers reflects receptor occupancy and accelerated metabolism of the inositol phosphates. Activation of second messenger-operated Ca2+ channels is not necessarily implicated because of the attenuating effect of membrane hyperpolarization.

Arginine Vasopressin

Brain somatostatin receptor-G protein interaction. G alpha C-terminal antibodies demonstrate coupling of the soluble receptor with Gi(1-3) but not with Go.

Somatostatin (SST) receptors activate potassium channels, stimulate protein phosphatases, inhibit adenylate cyclase and close calcium channels. These multiple effects are controlled by guanine nucleotide binding (G) proteins of the pertussis toxin-sensitive Gi and Go types. In the present study we have identified the G proteins coupling with brain SST receptors. To this end, brain SST receptors were solubilized in G-protein coupled form. Binding of the SST analogue MK 678 to the solubilized receptor was completely inhibited by guanosine 5'-O-thiotriphosphate (IC50 = 100 nM), reflecting decreased receptor affinity for agonist following uncoupling of the receptor and G protein(s). Antibodies raised against specific COOH-terminal peptides of the G proteins Gi(1-3), Go, and Gz were used to probe for SST receptor-G protein coupling in this system. Antibodies binding to the COOH-terminal regions of Gi1 and Gi2 (antibody AS) and Gi3 (antibody EC) inhibited binding of 125I-MK 678 (75 pM) by 57 +/- 4% and 48 +/- 5%, respectively. The effects of these antibodies were concentration-dependent and additive, such that in combination AS and EC completely inhibited binding. Antibodies binding to the COOH-terminal region of Go (GO) and Gz (QN) did not affect binding of 125I-MK 678, indicating that neither Go nor Gz are associated with the brain SST receptor. Prelabeling of the receptor with 125I-MK 678 prior to addition of antibody induced the formation of a "locked conformation" of the agonist-bound receptor-G protein complex which was insensitive to antibody. In conclusion, Gi1 and/or Gi2 and Gi3 are coupled in approximately equal proportions to the brain 125I-MK 678-binding SST receptor, accounting for all of the G protein coupling of this receptor.

Adenylate Cyclase Toxin

Radiotherapy treatment planning of basal meningiomas: improved tumor localization by correlation of CT and MR imaging data.

A localization technique, based on three-dimensional CT and MR imaging data for precision radiotherapy of basal meningiomas, is presented. Indications for radiotherapy included unresected tumors, gross disease remaining despite surgery, and recurrences. The patient's head was fixed in a stereotactic localization system which is usable at the CT, MR and the linear accelerator installations. The geometrical distortion of MR imaging data was evaluated in three dimensions by phantom measurements. The geometrical distortion was "corrected" (reducing displacements to the size of a pixel) by calculations based on modelling the distortion as a fourth order two-dimensional polynomial. The target volume was defined in three-dimensional MR imaging data after application of 0.1 mmol/kg b.w. Gd-DTPA solution and transferred precisely from MR onto CT data to provide a map of the radiation attenuation coefficient for dose calculation. The superior soft tissue contrast of MR showed an excellent tumor delineation especially when the bony base of the skull obscured the target in CT images. Target volume, calculated dose distribution, and critical structures could be transferred between CT and MR imaging data and displayed as three-dimensional shaded structures for better assessment for matching of target volume and dose distribution. With the described planning system a more precise target definition of basal meningiomas was possible by integration of the superior tumor delineation in MR compared with CT.

Computer Graphics

Computer systems and mechanical tools for stereotactically guided conformation therapy with linear accelerators.

An integrated system for fractionated, stereotactically guided conformation radiotherapy has been developed. The system components are a stereotactic fixation system that can be used each treatment day, a localization, and positioning unit that can be used during x-ray computer tomography, magnetic resonance imaging, positron emission tomography, and radiographical examinations as well as for treatment. Conformal precision radiotherapy is planned with a new three-dimensional treatment planning system (Voxel-Plan-Heidelberg) which comprises, among others options, a three-dimensional image correlation procedure as well as routines for the calculation of coplanar and non-coplanar irradiations with irregularly shaped fields. Two different multi-leaf collimators have been designed for precision radiotherapy in the head and neck region. A manual multi-leaf collimator is used for irradiations with stationary beams or for moving beam treatments with invariable irregularly shaped fields. This collimator system is now being used for patient treatments. The design of a computer controlled multi-leaf collimator unit for multiple fixed field irradiation techniques is discussed. All system components are aimed at conforming dose distributions for fractionated radiotherapy treatments to the target to improve sparing of adjacent normal tissues, and at achieving a sufficient geometrical accuracy in the dose application.

Computer Systems

Regulation of Ca2+ influx in myeloid cells. Role of plasma membrane potential, inositol phosphates, cytosolic free [Ca2+], and filling state of intracellular Ca2+ stores.

To study the mediation of Ca2+ influx by second messengers in myeloid cells, we have combined the whole-cell patch clamp technique with microfluorimetric measurements of [Ca2+]i. Me2SO-differentiated HL-60 cells were loaded with the fluorescent Ca2+ indicator Indo-1, allowed to adhere to glass slides, and patch-clamped. Receptor agonists and Ca(2+)-ATPase inhibitors were applied by superfusion and inositol phosphates by microperfusion through the patch pipette. In voltage-clamped cells, [Ca2+]i elevations with a sustained phase could be induced by (a) the chemoattractant receptor agonist FMLP, (b) the Ca(2+)-releasing second messenger myo-inositol(1,4,5)trisphosphate [Ins(1,4,5)P3], as well as its nonmetabolizable analogues, and (c) the Ca(2+)-ATPase inhibitor cyclopiazonic acid, which depletes intracellular Ca2+ stores. In the absence of extracellular Ca2+, responses to all stimuli were short-lasting, monophasic transients; however, subsequent addition of Ca2+ to the extracellular medium led to an immediate [Ca2+]i increase. In all cases, the sustained phase of the [Ca2+]i elevations could be inhibited by millimolar concentrations of extracellular Ni2+, and its amplitude could be decreased by depolarization of the plasma membrane. Thus, the sustained phase of the Ca2+ elevations was due to Ca2+ influx through a pathway sensitive to the electrical driving force and to Ni2+. No Ca2+ influx could be observed after (a) plasma membrane depolarization in resting cells, (b) an imposed [Ca2+]i transient independent of receptor activation, or (c) microperfusion of myo-inositol(1,3,4,5)tetrahisphosphate (Ins(1,3,4,5)P4). Also, Ins(1,3,4,5)P4 did not have additive effects when co-perfused with a submaximal concentration of Ins(1,4,5)P3. Our results suggest that, in myeloid cells, activation of chemoattractant receptors induces an electrogenic, Ni(2+)-sensitive Ca2+ influx via generation of Ins(1,4,5)P3. Ins(1,4,5)P3 might activate Ca2+ influx directly, or by depletion of intracellular Ca2+ stores, but not via [Ca2+]i increase or Ins(1,3,4,5)P4 generation.

Calcium

Epidermal derived growth factor stimulates the prostaglandin F2 alpha-synthesis in rabbit luteal cells.

Isolated rabbit luteal cells from day 6 and 12 of pseudopregnancy were cultured with hCG, EGF, and EGF together with arachidonic acid (AA) in serum-free culture medium for 96 hours. The hCG stimulation of the progesterone (P) synthesis was more pronounced on day 6 then on day 12. EGF alone did not change significantly the production of either P or PGF2 alpha. AA increased the production of PGF2 alpha on day 6 and 12 significantly (3.9-fold on day 6, P < 0.005; 7-fold on day 12, P < 0.001). AA together with EGF increased the level of PGF2 alpha more pronounced when compared with AA alone (7.2-fold on day 6, P < 0.025; 9.8-fold on day 12, P < 0.05). The progesterone production of the cells remained unchanged during EGF exposure. We conclude that EGF together with AA is able to stimulate the PGF2 alpha biosynthesis in cultured rabbit luteal cells. Therefore, EGF could be relevant as an additional regression factor in rabbits. This mechanism seems to be independent from the progesterone synthesis.

Animals

[Recurrences, the surgical and radiological side effects and new developments in the breast-preserving treatment of breast carcinoma].

In the Department for Gynecology and the Department for Gynecologic Radiology, University of Heidelberg, breast conserving therapy was carried out in 1,330 patients with breast cancer between 1975 and 1990. The tumor size was up to 3 cm, 28% showed positive nodes. The medium age was 47.6 years, segmental resection was the standard operation, whole breast irradiation with 50 Gy and an additional boost of 10 Gy was standard irradiation schedule. After five years (n = 307) the following results were observed: local failure 6.8%, regional lymph node recurrence 2.1%, overall survival 88.3%, disease-free survival 81.2%. Five out of 36 of the death-cases died without recurrence. Significant factors for local failure were following: 1. lymphangiosis of more than 1 cm in size around the tumor (p = 0.03); 2. intra-ductal non-invasive cancer of more than 1 cm in size around the primary (p = 0.01); 3. intra-ductal non-invasive cancer reaches the margin of resection (p less than 0.00001). With segmental resection (2 cm margin macroscopically free of tumor) showed in 19% histologically tumor beyond the margins so-called residuals. In the other three quadrants additional second primaries of (multicentric cancers) macroscopical size could be confirmed in an additional study. In case of high risk for local failure more radicality in operation as well as in irradiation is recommended.

Adult

Activation by bacterial lipopolysaccharide causes changes in the cytosolic free calcium concentration in single peritoneal macrophages.

Variations in the cytosolic free Ca2+ concentration [( Ca2+]i) upon LPS exposure were studied in single rat peritoneal macrophages loaded with fura-2 under carefully controlled conditions. Of a total of 60 cells examined, 47% responded to LPS (1 microgram/ml) with an increase in [Ca2+]i. Macrophages were heterogeneous with regard to the LPS response, with individual cells exhibiting single rapid and transient increases in [Ca2+]i, multiple transients, or slower and more sustained variations. In 62% of the responding cells, a second exposure to LPS elicited a [Ca2+]i rise, although usually to a slightly lower peak value. Thus, rapid desensitization to LPS does not occur in the majority of these macrophages. EGTA did not abolish the response of those cells that exhibited a single rapid transient in [Ca2+]i, indicating that the source of the initial [Ca2+]i rise was the intracellular stores. There was no obvious correlation between the type of response to LPS and the initial morphologic features (rounded vs polarized) of the cells. Our present work shows unequivocally that LPS induces increases in macrophage [Ca2+]i and, thereby, lends substantial support to the hypothesis that [Ca2+]i is a second messenger in LPS-mediated activation of the macrophage.

Animals

Adenosine A1 receptor-induced inhibition of Ca2+ transients linked to action potentials in clonal pituitary cells.

Adenosine is a potent paracrine/autocrine feedback inhibitor of cell activation in a variety of tissues. Adenosine action was studied in pituitary cells, in which spontaneous electrical activity causes characteristic oscillations of the cytosolic free Ca2+ concentration, [Ca2+]i. Cells of the GH3B6 rat pituitary tumor line were studied by microspectrofluorimetry using the Ca2+ probes indo-1 and fura-2, in part in combination with electrophysiological tight seal whole cell recordings, obtained with the novel approach of patch perforation. It was demonstrated that adenosine receptor activation by N6-(R-phenyl-isopropyl)-adenosine (PIA) caused a block of electrical activity and abolished the ensuing alterations in [Ca2+]i. PIA mimicked the inhibitory action of somatostatin. Adenosine effects are mediated by A1 receptors in these cells and are antagonized by IBMX, an adenosine receptor blocker. PIA also suppressed action potentials that were elicited by the activation of protein kinase C with the phorbol ester PMA, or during the second phase of TRH action. In contrast, no interference was notable on TRH-induced intracellular Ca2+ mobilization. In addition to the abolition of Ca2+ transients, PIA lowers basal [Ca2+]i in some cells. It is proposed that in addition to the inhibition of adenylate cyclase, A1 receptor action on [Ca2+]i is an important element in the control of excitable pituitary cells.

Action Potentials

Modification of a three-dimensional treatment planning system for the use of multi-leaf collimators in conformation radiotherapy.

The multi-leaf collimator of the DKFZ is designed as a low cost add-on device for conventional linear accelerators for radiotherapy. The technical specification of the computer controlled collimator is described briefly. A major limitation in the use of the wide capabilities of multi-leaf collimators in the clinic is still an appropriate treatment planning system. This paper describes treatment planning and dose calculation techniques for multi-leaf collimators and shows examples where the capabilities of the collimator are used extensively.

Dose-Response Relationship, Radiation

Three-dimensional photon radiotherapy planning for laryngeal and hypopharyngeal cancers. 1. Conventional rotational technique.

Three-dimensional dose distributions have been computed for the photon radiation therapy of laryngeal and hypopharyngeal cancers, using biaxial and eccentric rotatory techniques. Treatment plans obtained under various conditions of irradiation with a 15 MV linear accelarator (MEVATRON 77, Siemens) are analysed and compared. Dose delivery to the tumour and the degree of spinal cord protection are evaluated for both treatment techniques. The eccentric plan is somewhat superior to the biaxial one, suggesting a justifiable preference to use this method in the radiation treatment of these tumours. Simulations show that extreme care is needed in positioning the axis: an accuracy of +/- 3 mm is required in the sagittal plane.

Humans

Three-dimensional photon radiotherapy planning for laryngeal and hypopharyngeal cancers. 2. Conformation treatment planning using a multileaf collimator.

Three-dimension dose distributions have been computed for 15 MV X-ray radiation therapy (MEVATRON 77, Siemens) of laryngeal and hypopharyngeal cancers using isocentric rotational technique with multileaf collimator. Using a new concave contour tracing algorithm, satisfactory dose delivery to the target volume and efficient protection of the normal tissues can be achieved.

Humans