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Träfflista för sökning "WFRF:(Wängberg I.) "

Sökning: WFRF:(Wängberg I.)

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1.
  • Ahlman, Håkan, 1947, et al. (författare)
  • Adrenocortical carcinoma--diagnostic and therapeutical implications.
  • 1993
  • Ingår i: The European journal of surgery = Acta chirurgica. - 1102-4151. ; 159:3, s. 149-58
  • Tidskriftsartikel (refereegranskat)abstract
    • To evaluate the results of treatment of a consecutive series of patients with adrenocortical carcinoma who presented during the six year period 1985 to 1991.
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2.
  • Ahlman, Håkan, 1947, et al. (författare)
  • Aspects on diagnosis and treatment of the foregut carcinoid syndrome.
  • 1992
  • Ingår i: Scandinavian journal of gastroenterology. - 0036-5521. ; 27:6, s. 459-71
  • Tidskriftsartikel (refereegranskat)abstract
    • Eight patients with the foregut carcinoid syndrome (two gastric and six bronchial primary tumors) are reported. The patients presented with complex clinical symptoms including ectopic production of adrenocorticotrophic hormone and growth hormone-releasing factors. The most alarming symptoms were facial flush and edema, accompanied by severe bronchoconstriction, which easily was misinterpreted as asthmatic attacks. Conventional bronchodilatory drugs may be potentially dangerous in these patients, in whom combined blockade of histamine receptors and treatment with cortisone and octreotide are recommended. Owing to the patients' age and general condition individualized long-term therapy was instituted. Surgical therapy under optimal protection by drugs can be of substantial value also in patients with advanced disease. One patient with life-threatening hormonal symptoms underwent hyperthermic perfusion of the liver with cytotoxic drugs, resulting in good palliation.
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3.
  • Andreasson, Kristin I. M., 1963, et al. (författare)
  • Biological weighting functions as a tool for evaluating two ways to measure UVB radiation inhibition on photosynthesis
  • 2006
  • Ingår i: Journal of Photochemistry and Photobiology B-Biology. - : Elsevier BV. - 1011-1344. ; 84:2, s. 111-118
  • Tidskriftsartikel (refereegranskat)abstract
    • To estimate the inhibitory effect of the changing UVB radiation (UVBR, 280-315 nm) on earth's ecosystems, an understanding of its wavelength dependency is needed. The tool used for these estimations is the biological weighting function (BWF), whereby the inhibition of different wavelengths is calculated. B\WFs were determined for three algae species from different classes, Phaeodactylum tricornutum (Bacillariophyceae), Dunaliella tertiolecta (Chlorophyceae) and Rhodomonas sp. (Cryptophyceae), using polychromatic irradiation, where the UVBR spectra were varied with cut-off filters. For each alga, BWFs were determined for two photosynthetic parameters; the quantum yield measured as fluorescence from Photo System II in a pulse-amplitude-modulation (PAM) fluorometer, and the fixation of C-14-labelled carbon dioxide. The BWFs were calculated with the Rundel method, using the radiation data between 270 and 360 nm with 1 nm resolution. The results show that the UVBR damages were generally higher when using the carbon fixation measurements than when measuring with the PAM technique. When using PAM, P. tricornutum in particular had a sensitivity intermediate between the sensitive Rhodomonas sp. and the more tolerant D. tertiolecta, but was as sensitive as, or even more sensitive, than Rhodomonas sp. when using carbon fixation. D. tertiolecta was shown to be less sensitive when using both techniques and the inhibition of its photosynthesis was almost as high when using PAM as when using carbon fixation. We concluded that, although the PAM technique has advantages such as being cleaner and easier to use, it is unable to Substitute the carbon fixation measurements. Not only are the algae less sensitive when measured with PAM than they are when measured as carbon fixation, the relationship between the effects on the algae measured with the two techniques also differs. As fixation of carbon dioxide integrates a larger part of the photosynthetic machinery, it should be favoured as a measure of photosynthesis. (c) 2006 Elsevier B.V. All rights reserved.
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4.
  • Andreasson, Kristin I. M., 1963, et al. (författare)
  • Reduction in growth rate in Phaeodactylum tricornutum (Bacillarlophyceae) and Dunaliella tertiolecta (Chlorophyceae) induced by UV-B radiation
  • 2007
  • Ingår i: Journal of Photochemistry and Photobiology B-Biology. - : Elsevier BV. - 1011-1344. ; 86:3, s. 227-233
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of UV-B radiation (UVBR, 280-315 nm) on growth rate during 72 h of incubation, was measured for two marine microalgae - Dunaliella tertiolecta (Chlorophyceae) and Phaeodactyhan tricornutum (Bacillariophyceae). The resulting inhibition of growth rate was analysed by calculating biological weighting functions (BWFs). The growth rate of D. tertiolecta was slightly more inhibited by UVBR (over the whole range of the spectrum) than was the growth rate of P. tricornutum, but the wavelength dependencies were the same. Our results were compared with results from photosynthesis experiments of Andreasson and Wangberg [1], where two methods, pulse amplitude modulation (PAM) fluorescence and carbon fixation, were measured for these same algae. The BWF for the growth rate, here, showed more wavelength dependency than the BWF for the previous two photosynthesis measurements - except for the carbon fixation BWF in P. tricornutum, which was closer to the BWF for growth rate. The wavelength dependency of the growth rate inhibition showed less variation between the species than the inhibition of the photosynthesis. (c) 2006 Elsevier B.V. All rights reserved.
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5.
  • Basson, M D, et al. (författare)
  • Biology and management of the midgut carcinoid.
  • 1993
  • Ingår i: American journal of surgery. - 0002-9610. ; 165:2, s. 288-97
  • Forskningsöversikt (refereegranskat)abstract
    • Midgut carcinoid tumors derive from gut entoderm. These tumors may cause a complex of symptoms comprising the carcinoid syndrome by secreting a wide variety of bioactive agents in addition to serotonin. Such symptoms generally follow metastases to the liver but may also occur in primary ovarian or retroperitoneal tumors. After localization and biochemical characterization, the bioactivity of these tumors should be blocked by octreotide, sometimes in combination with other pharmacologic antagonists, so that primary resection may be performed safely. If curative resection is impossible, then a cytoreductive management scheme should be employed that includes surgical debulking and hepatic arterial embolization, followed by palliation with octreotide.
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6.
  • Gårdfeldt, Katarina, 1959, et al. (författare)
  • Evasion of Mercury from coastal and open waters of the Atlantic ocean and the Mediterranean sea
  • 2003
  • Ingår i: Atmospheric Environment. - 1352-2310 .- 1873-2844. ; 37:Suppl 1
  • Tidskriftsartikel (refereegranskat)abstract
    • Dissolved gaseous mercury (DGM) was measured in coastal Atlantic seawater and in the Mediterranean Sea. The Atlantic measurements were performed during September 1999 at the Mace Head Atmospheric Research Station, situated on the Irish west coast. The measurements in the Mediterranean Sea were made along a 6000 km cruise path from 14 July to 9 August 2000 in the framework of the Med-Oceanor project. Total gaseous mercury (TGM) concentrations in air were continuously measured with a 5 min time resolution using an automated mercury analyser (Tekran 2537A) during both expeditions. Paired TGM and DGM samples from all campaigns showed that the surface water was supersaturated with elemental mercury. The mercury evasion was estimated using a gas exchange model (J. Geophys. Res. 97 (1992) 7373), which uses salinity, wind speed and water temperature as independent parameters. The predicted average mercury evasion from the coastal Atlantic water was 2.7 ng m−2 h−1 implying that the concentration of TGM in the Atlantic air is enhanced by mercury evasion from the sea. Measurements in different regions of the Mediterranean Sea showed spatial variations in DGM concentrations. The highest DGM concentration (90 pg l−1) was observed at a location in the Strait of Sicily (37°16N 11°52E). The mercury evasion in the eastern sector of the Mediterranean Sea (area: 32–36°N, 17–28°E) was generally higher (7.9 ng m−2 h−1) than that observed in the Tyrrhenian Sea (4.2 ng m−2 h−1) or in the western sector (2.5 ng m−2 h−1) (areas: 38–42°N, 8–13°E and 38–41°N, 7–8°E, respectively). Estimations of mercury evasion were also made at Mediterranean coastal sites using a dynamic chamber technique. In addition, a newly developed method making continuous in situ DGM measurements possible was tested.
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7.
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8.
  • Kölby, Lars, 1963, et al. (författare)
  • Altered influence of CCK-B/gastrin receptors on HDC expression in ECL cells after neoplastic transformation.
  • 1999
  • Ingår i: Regulatory peptides. - 0167-0115. ; 85:2-3, s. 115-23
  • Tidskriftsartikel (refereegranskat)abstract
    • Gastrin is one of the main factors controlling enterochromaffin-like (ECL) cell endocrine function and growth. Long-standing hypergastrinemia may give rise to ECL cell carcinoids in the gastric corpus in man and in experimental models. We have analysed the expression and function of CCK-B/gastrin receptors in normal ECL cells and in ECL cell tumours (gastric carcinoids) of the African rodent Mastomys natalensis. Hypergastrinemia induced by short-term (5 days) histamine2-receptor blockade (loxtidine) resulted in increased histidine decarboxylase (HDC) mRNA expression in the gastric oxyntic mucosa. This increase was significantly and dose-dependently reversed by selective CCK-B/gastrin receptor blockade (YM022). Long-term (12 months) hypergastrinemia, induced by histamine2-receptor blockade, gave rise to ECL cell carcinoids in the gastric oxyntic mucosa. CCK-B/gastrin receptor mRNA was only slightly elevated while HDC mRNA expression was eight-fold elevated in ECL cell carcinoids and was not influenced by CCK-B/gastrin receptor blockade. Thus CCK-B/gastrin receptor blockade of hypergastrinemic animals reduces the HDC mRNA expression in normal mucosa but not in ECL cell carcinoids. These results demonstrate that HDC mRNA expression in neoplastic ECL cells is not controlled by CCK-B/gastrin receptors.
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9.
  • Kölby, Lars, 1963, et al. (författare)
  • Histamine metabolism of gastric carcinoids in Mastomys natalensis.
  • 1998
  • Ingår i: The Yale journal of biology and medicine. - 0044-0086. ; 71:3-4, s. 207-15
  • Tidskriftsartikel (refereegranskat)abstract
    • Pharmacological inhibition of gastric acid secretion and subsequent hypergastrinemia in Mastomys natalensis is an experimental model well suited for the study of gastric carcinoid formation. The genetic susceptibility of Mastomys to develop such tumors is a feature reminiscent of the situation in patients with the MEN-1 Zollinger Ellison syndrome, in whom tumor-induced hypergastrinemia, promotes the development of gastric carcinoids. Chronic hypergastrinemia, induced by the irreversible H2-receptor antagonist loxtidine will cause carcinoid formation in Mastomys already after four to six months. As in humans, gastric carcinoids in Mastomys are mainly composed of enterochromaffinlike (ECL) cells and have low malignant potential. Administration of exogenous gastrin to normal young animals increases the expression of histidine decarboxylase (HDC) mRNA in the oxyntic mucosa within 30 minutes. Endogenous hypergastrinemia, induced by short-time loxtidine treatment (three to 29 days) enhances the expression of HDC mRNA, histamine contents and ECL cell numbers in the oxyntic mucosa. Long-term loxtidine treatment (seven to 21 months) results in sustained hypergastrinemia and tumor formation. Tumor-bearing animals exhibited an increase in HDC mRNA and histamine content in the oxyntic mucosa as well as increased urinary excretion of the main histamine metabolite, tele-methylimidazole acetic acid (MeImAA). Subsequent to cessation of loxtidine treatment for two weeks, all parameters of histamine metabolism were normalized in tumor-bearing animals. These results indicate that gastric carcinoids developing during hypergastrinemia are well-differentiated neoplasms whose histamine synthesis and metabolism is regulated by plasma gastrin.
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10.
  • Kölby, Lars, 1963, et al. (författare)
  • Histidine decarboxylase expression and histamine metabolism in gastric oxyntic mucosa during hypergastrinemia and carcinoid tumor formation.
  • 1996
  • Ingår i: Endocrinology. - 0013-7227. ; 137:10, s. 4435-42
  • Tidskriftsartikel (refereegranskat)abstract
    • Histamine is an important stimulator of gastric acid secretion. In experimental animals, inhibition of acid secretion by long term histamine2 receptor blockade causes hypergastrinemia, proliferation of enterochromaffin-like (ECL) cells, and formation of histamine-producing gastric carcinoids. The aim of this study was to examine the role of gastrin in histamine synthesis and metabolism of the oxyntic mucosa of normal, hyperplastic, and carcinoid-bearing Mastomys natalensis. Administration of exogenous gastrin to normal animals increased histidine decarboxylase (HDC) messenger RNA (mRNA) expression in the oxyntic mucosa within 30 min, indicating that gastrin stimulates histamine synthesis by regulating HDC mRNA abundance. Endogenous hypergastrinemia, induced by short term histamine2 receptor blockade (loxtidine) for 3-29 days, did not induce tumors, but enhanced the expression of HDC mRNA (2- to 4-fold elevated) and histamine contents (2-fold elevated) in the oxyntic mucosa. Long term histamine2 receptor blockade (7-21 months) resulted in sustained hypergastrinemia and ECL tumor formation. Tumor-bearing animals had a 4-fold increase in HDC mRNA expression and histamine contents of the oxyntic mucosa. Urinary excretion of the histamine metabolite methyl-imidazole-acetic acid was 2-fold elevated. Tumor-bearing animals recovering from histamine2 receptor blockade were normogastrinemic and had normal levels of HDC mRNA and histamine in the oxyntic mucosa as well as normal excretion of methyl-imidazole-acetic acid. The results indicate that ECL cell carcinoids developing during hypergastrinemia are well differentiated tumors that respond to high gastrin levels with increased histamine synthesis and secretion.
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