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Träfflista för sökning "WFRF:(Björnsson H.) srt2:(1995-1999)"

Sökning: WFRF:(Björnsson H.) > (1995-1999)

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1.
  • Eliasson, Björn, 1959, et al. (författare)
  • Hyperinsulinaemia impairs gastrointestinal motility and slows carbohydrate absorption
  • 1995
  • Ingår i: Diabetologia. - 0012-186X. ; 38:1, s. 79-85
  • Tidskriftsartikel (refereegranskat)abstract
    • Experimental euglycaemic hyperinsulinaemia (insulin levels 46 +/- 4 mU/l) impaired the post-absorptive gastrointestinal motility in healthy individuals; the effect being particularly pronounced in the upper gastrointestinal tract (stomach and proximal duodenum). The postprandial gastric emptying, measured with a standardized 99mTc labelled meal, was also significantly delayed (t50 increased by 38% or 32 min). This was combined with a slower carbohydrate absorption (delay in peak blood glucose level about 40 min). Furthermore, during experimental hyperinsulinaemia higher blood glucose levels were seen at 120 min than at 60 min after food ingestion. This was not seen in any subject in the control study where only 0.9% NaCl was infused. Blood levels of the motility-stimulating hormone, motilin, were significantly lower during experimental hyperinsulinaemia. Thus, experimental hyperinsulinaemia impairs the gastrointestinal motility in both the postabsorptive and postprandial states. This effect is combined with a delayed carbohydrate absorption. Hyperinsulinaemia per se may thus lead to alterations in carbohydrate absorption and can also contribute to the gastrointestinal disturbances in diabetes.
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2.
  • Björnsson, Einar, 1958, et al. (författare)
  • Effects of insulin and beta-adrenergic blockade on the migrating motor complex in humans
  • 1995
  • Ingår i: Scand J Gastroenterol. - 0036-5521. ; 30:3, s. 219-24
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Interdigestive small-intestinal motility is suppressed by hyperglycemia and also by hyperinsulinemia per se. Since hyperinsulinemia may increase sympathetic activity, the present study was undertaken to ascertain to what extent insulin affects phase III of the migrating motor complex (MMC) and MMC-related duodenal retroperistalsis and whether beta-adrenergic receptors may mediate the effects of insulin. METHODS: Fasting motility was studied in eight healthy volunteers on three occasions with an eight-lumen perfused pressure catheter, with closely spaced recording points in the proximal duodenum. On the control day 5-h antroduodenojejunal manometry was performed. On another study day euglycemic hyperinsulinemic clamping was performed for 2 h after an initial basal recording. On a 3rd day motility was recorded during propranolol infusion, combined with a period of euglycemic hyperinsulinemia. RESULTS: During hyperinsulinemia complete absence of phase III of the MMC in the gastric antrum was observed, whereas 55% of the MMC had a gastric phase-III component on the control day. The duration of phase III in the proximal duodenum was decreased during hyperinsulinemia compared with the control period (p < 0.05). This inhibitory effect of insulin on the activity front was not prevented by beta blockade. Under control conditions the proportion of retroperistaltic pressure waves in the proximal duodenum was 13 +/- 8% in early phase III, increasing in late phase III to 79 +/- 15% (p < 0.01). Duodenal phase III during hyperinsulinemia showed a similar increase in retroperistalsis, from 4 +/- 4% in early phase III to 67 +/- 21% in late phase III (p < 0.01). The corresponding proportions during beta blockade were 16 +/- 10% and 86 +/- 14%, respectively. CONCLUSIONS: Hyperinsulinemia per se abolishes antral phase III and makes the duodenal phase III shorter but does not interrupt the distinct pattern of retroperistalsis in late phase III. Beta-adrenergic receptors seem not to be important for these effects of insulin or for the retroperistalsis in duodenal phase III.
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3.
  • Nettelbladt, Otto S, et al. (författare)
  • Combined fluorine-18-FDG and carbon-11-methionine PET for diagnosis of tumors in lung and mediastinum
  • 1998
  • Ingår i: Journal of Nuclear Medicine. - 0161-5505 .- 1535-5667. ; 39:4, s. 640-647
  • Tidskriftsartikel (refereegranskat)abstract
    • We evaluated the value of PET using 18F-fluorodeoxyglucose (FDG) and 11C-methionine, individually or in combination, to distinguish malignant from benign tumors and to identify or exclude mediastinal metastases.METHODS:Seventeen patients with a tumor in the lung or mediastinum were evaluated with 18F-FDG and 11C-methionine PET. For morphological comparison, we used CT, and all findings were confirmed by histology of surgical resection specimens (n = 16) or by cytology (n = 1).RESULTS:All tumors were visualized equally well with both tracers, and there were no false-positive results. In 2 patients with a malignant tumor, coexisting pneumonia was correctly diagnosed as an inflammatory lesion because of its wedge-like shape. PET correctly excluded hilar invasion and mediastinal lymph node metastases in 10 of 14 patients with primary lung tumor. PET identified mediastinal metastases in 4 of 4 patients. CT failed to detect mediastinal tumor spread in 2 patients and gave a false-positive reading in 2 others. Significantly higher uptake (SUV) and transport rate (slope) values were obtained from malignant than benign lesions with both tracers. No major differences were seen in either the levels of significance or accuracy when the two tracers were compared. Slope values did not add further information to what was obtained with SUV. Density correction of SUV and slope values, to avoid the influence of surrounding air as well as tumor heterogeneity, increased these differences somewhat. Both tracers distinguished malignant from benign lesions with a 93% sensitivity and an accuracy of 89%-95%, but sensitivity improved to 100% when values from both tracers were combined.CONCLUSION:Fluorine-18-FDG and 11C-methionine PET visualized all tumors equally well and detected mediastinal spread better than CT. For differentiation purposes, the problems of false-positive and false-negative PET findings could not be safely overcome in a limited number of cases either by the use of both tracers, by the additional use of slope values or by lesion density correction.
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4.
  • Tencer, J, et al. (författare)
  • Decreased excretion of glycosaminoglycans in patients with primary glomerular diseases
  • 1997
  • Ingår i: Clinical Nephrology. - 0301-0430. ; 48:4, s. 212-219
  • Tidskriftsartikel (refereegranskat)abstract
    • Urine glycosaminoglycans (GAG) concentrations were measured in 150 patients with primary glomerulonephritides: endocapillary glomerulonephritis, mesangial proliferative glomerulonephritis, IgA nephropathy, membranous glomerulonephritis and minimal change nephropathy, and in 63 healthy controls and 19 patients with diabetes nephropathy. The urine GAG to creatinine ratios (GCR) were significantly reduced (p < 0.01) in all the glomerulonephritides investigated (0.20 mg/mmol in endocapillary glomerulonephritis, 1.60 mg/mmol in mesangial proliferative glomerulonephritis, 1.74 mg/mmol in IgA nephropathy, 1.09 mg/mmol in membranous nephropathy, and 1.16 mg/mmol in minimal change nephropathy) compared to healthy controls (2.87 mg/mmol) but not compared to diabetes patients (1.17 mg/mmol). Also, the GCR in a group of 23 non-albuminuric glomerulonephritis patients (1.98 mg/mmol) was shown to be significantly decreased (p < 0.01) compared to healthy controls. Moreover, the GCR was significantly lower (p < 0.01) in endocapillary glomerulonephritis than in any of the other diseases studied. The GAG excretion per functioning glomerular area, calculated as fractional GAG excretion (FGE), was decreased in all the glomerulonephritides investigated compared to both healthy controls and diabetes nephropathy. The decreased GAG excretion in glomerulonephritides, obtained in the present study, might be a consequence of decreased synthesis or turnover of GAG in the functioning nephrons whereas the mechanisms for the reduced GAG excretion in diabetes nephropathy might be of a different nature. Urinary GAG excretion in this group of glomerular disorders and particularly in endocapillary glomerulonephritis, may lead to new approaches in non-invasive renal diagnostics and, particularly with regard to the differentiation of acute and chronic forms of glomerulonephritides.
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