| 171. |
- Ahmad, F, et al.
(author)
-
IL-3 and IL-4 activate cyclic nucleotide phosphodiesterases 3 (PDE3) and 4 (PDE4) by different mechanisms in FDCP2 myeloid cells
- 1999
-
In: Journal of Immunology. - 1550-6606. ; 162:8, s. 4864-4875
-
Journal article (peer-reviewed)abstract
- In FDCP2 myeloid cells, IL-4 activated cyclic nucleotide phosphodiesterases PDE3 and PDE4, whereas IL-3, granulocyte-macrophage CSF (GM-CSF), and phorbol ester (PMA) selectively activated PDE4. IL-4 (not IL-3 or GM-CSF) induced tyrosine phosphorylation of insulin-receptor substrate-2 (IRS-2) and its association with phosphatidylinositol 3-kinase (PI3-K). TNF-alpha, AG-490 (Janus kinase inhibitor), and wortmannin (PI3-K inhibitor) inhibited activation of PDE3 and PDE4 by IL-4. TNF-alpha also blocked IL-4-induced tyrosine phosphorylation of IRS-2, but not of STAT6. AG-490 and wortmannin, not TNF-alpha, inhibited activation of PDE4 by IL-3. These results suggested that IL-4-induced activation of PDE3 and PDE4 was downstream of IRS-2/PI3-K, not STAT6, and that inhibition of tyrosine phosphorylation of IRS molecules might be one mechnism whereby TNF-alpha could selectively regulate activities of cytokines that utilized IRS proteins as signal transducers. RO31-7549 (protein kinase C (PKC) inhibitor) inhibited activation of PDE4 by PMA. IL-4, IL-3, and GM-CSF activated mitogen-activated protein (MAP) kinase and protein kinase B via PI3-K signals; PMA activated only MAP kinase via PKC signals. The MAP kinase kinase (MEK-1) inhibitor PD98059 inhibited IL-4-, IL-3-, and PMA-induced activation of MAP kinase and PDE4, but not IL-4-induced activation of PDE3. In FDCP2 cells transfected with constitutively activated MEK, MAP kinase and PDE4, not PDE3, were activated. Thus, in FDCP2 cells, PDE4 can be activated by overlapping MAP kinase-dependent pathways involving PI3-K (IL-4, IL-3, GM-CSF) or PKC (PMA), but selective activation of PDE3 by IL-4 is MAP kinase independent (but perhaps IRS-2/PI3-K dependent).
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| 172. |
- Ahnesjö, Anders, et al.
(author)
-
Application of the convolution method for calculation of output factors for therapy photon beams
- 1992
-
In: Medical Physics. - : Wiley. - 0094-2405. ; 19:2, s. 295-301
-
Journal article (peer-reviewed)abstract
- The output factor for a therapy photon beam is defined as the dose per monitor unit relative to the dose per monitor unit in a reference field. Convolution models for photon dose calculations yield the dose in units normalized to the incident energy fluence with phantom scatter intrinsically modeled. Output factors calculated with the convolution method as the dose per unit energy fluence relative to the calculated dose per unit energy fluence in a reference field could deviate as much as 5% if corrections are not made for perturbations due to treatment head scatter. Significant perturbations are particles backscattered from the collimators to the monitor and photons forward scattered from the filter and collimators in the treatment head. The forward scatter adds an "unmonitored" contribution to the total energy fluence of the beam. A model is developed that describes the field size dependence of these perturbations for conversion of output factors, calculated with the convolution method, to machine output factors as an integrated part in treatment planning. The necessary machine characteristics are derived from measurements of the output in air for a limited set of field sizes. The method has been tested using five different multileaf collimated irregular fields at 6 MV and for a large set of rectangular fields at 5, 6, and 18 MV and found to predict output factors with an accuracy better than 1%.
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| 173. |
- Ahnesjö, Anders, et al.
(author)
-
Modeling transmission and scatter for photon beam attenuators
- 1995
-
In: Medical Physics. - : Wiley. - 0094-2405. ; 22:11, s. 1711-1720
-
Journal article (peer-reviewed)abstract
- The development of treatment planning methods in radiation therapy requires dose calculation methods that are both accurate and general enough to provide a dose per unit monitor setting for a broad variety of fields and beam modifiers. The purpose of this work was to develop models for calculation of scatter and transmission for photon beam attenuators such as compensating filters, wedges, and block trays. The attenuation of the beam is calculated using a spectrum of the beam, and a correction factor based on attenuation measurements. Small angle coherent scatter and electron binding effects on scattering cross sections are considered by use of a correction factor. Quality changes in beam penetrability and energy fluence to dose conversion are modeled by use of the calculated primary beam spectrum after passage through the attenuator. The beam spectra are derived by the depth dose effective method, i.e., by minimizing the difference between measured and calculated depth dose distributions, where the calculated distributions are derived by superposing data from a database for monoenergetic photons. The attenuator scatter is integrated over the area viewed from the calculation point of view using first scatter theory. Calculations are simplified by replacing the energy and angular-dependent cross-section formulas with the forward scatter constant r2(0) and a set of parametrized correction functions. The set of corrections include functions for the Compton energy loss, scatter attenuation, and secondary bremsstrahlung production. The effect of charged particle contamination is bypassed by avoiding use of dmax for absolute dose calibrations. The results of the model are compared with scatter measurements in air for copper and lead filters and with dose to a water phantom for lead filters for 4 and 18 MV. For attenuated beams, downstream of the buildup region, the calculated results agree with measurements on the 1.5% level. The accuracy was slightly less in situations where the scatter component is very large, as for very large fields with very short filter to detector distances. The implementation of the model into treatment planning systems is discussed.
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| 174. |
- Ahrén, B, et al.
(author)
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Effects of minor increase in serum calcium on the immunoheterogeneity of parathyroid hormone in healthy subjects and in patients with primary hyperparathyroidism
- 1995
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In: Hormone Research. - 0301-0163. ; 43:6, s. 9-294
-
Journal article (peer-reviewed)abstract
- To study possible influences of a mild increase in serum-ionized calcium concentration that is seen during daily life on circulating parathyroid hormone (PTH) immunoheterogeneity, we used sequence-specific PTH assays to determine serum intact PTH, C-terminal PTH and N-terminal PTH following oral calcium (1.5 g) in healthy subjects (n = 7). This was also performed in patients with primary hyperparathyroidism (pHPT; n = 10) to see if their regulation of circulating PTH molecular forms is normal. Compared to healthy subjects, the patients were hypercalcemic (p < 0.05) and had higher levels of PTH in all three assays (p < 0.001). Following the oral calcium load, serum-ionized calcium increased by 0.08 +/- 0.03 mmol/l in the patients and by 0.07 +/- 0.03 mmol/l in the healthy subjects after 90 min, whereas serum intact PTH, C-terminal PTH and N-terminal PTH were reduced, both in the healthy subjects and in the patients. Suppression by calcium of both intact PTH and C-terminal PTH were impaired in the patients (p < 0.05 and p < 0.001), whereas suppression of N-terminal PTH was normal. Furthermore, the C/i and N/i ratios were higher at the highest calcium concentration achieved after calcium intake in the healthy subjects than in the basal state in the patients (p < 0.05), in spite of the larger degree of hypercalcemia in the latter (1.40 +/- 0.06 vs. 1.31 +/- 0.02 mmol/l; p < 0.05). Thus, (1) a minor increase in serum-ionized calcium that is seen during daily life alters the relative circulating concentrations of PTH versus its fragments; (2) the impaired sensitivity to calcium in pHPT is not evident for the suppression of N-terminal PTH, and (3) pHPT is accompanied by altered immunoheterogeneity of circulating PTH.
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| 175. |
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| 176. |
- Ahrén, B, et al.
(author)
-
Potential clinical use of the EDTA-infusion test
- 1993
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In: European Journal of Clinical Chemistry and Clinical Biochemistry. - 0939-4974. ; 31:6, s. 8-353
-
Journal article (peer-reviewed)abstract
- The introduction of assays for the intact parathyrin (parathyroid hormone) has dramatically improved the diagnosis and follow-up of patients with primary hyperparathyroidism. However, in some patients with mild or intermittent hypercalcaemia, when plasma concentrations of intact parathyrin may be within the normal reference concentrations, the diagnosis of primary hyperparathyroidism may still be problematic. In these patients, the EDTA-infusion test is of potential value, as it also might be in patients with equivocal operative findings.
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| 177. |
- Ahrén, Dag, et al.
(author)
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Phylogeny of nematode-trapping fungi based on 18S rDNA sequences
- 1998
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In: FEMS Microbiology Letters. - : Oxford University Press (OUP). - 0378-1097 .- 1574-6968. ; 158:2, s. 179-184
-
Journal article (peer-reviewed)abstract
- The small subunit (SSU) ribosomal DNA (18S rDNA) from 15 species of nematode-trapping fungi and closely related non-parasitic species were sequenced. Phylogenetic analysis indicated that species within the genera of Arthrobotrys, Dactylaria, Dactylella, Monacrosporium and Duddingtonia formed a monophyletic and isolated clade among an unresolved cluster of apothecial ascomycetes. The phylogenetic patterns within this clade were not concordant with the morphology of the conidia nor the conidiophores, but rather with that of the infection structures. The results from the different methods of tree reconstruction supported three lineages; the species having constricting rings, the non-parasitic species and the species having various adhesive structures (nets, hyphae, knobs and non-constricting rings) to infect nematodes.
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| 178. |
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| 179. |
- Aigner, Mats
(author)
-
Singular Ginzburg-Landau Vortices
- 1998
-
Doctoral thesis (other academic/artistic)abstract
- In this thesis we study the critical Ginzburg-Landau action, defined on fields in the plane which are allowed to have a finite number of singularities. We show that a topological invariant, the degree, can be defined under the assumption of finite action only. The action is bounded below by a constant times the degree, and the fields which realize this lower bound satisfy a first order differential equation. The critical points of the action satisfy a second order differential equation. Using methods of C. Taubes, we give a classification of all finite action solutions to the first order equation, and we show that if there is at most one singularity, then the first and second order equations are equivalent. By different methods we then construct solutions to the second order equation with more than one singularity which does not solve the first order equation.
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| 180. |
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