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Biomedical subjects

T Wikström

Publications and source records attributed to T Wikström.

27 records · Page 2Linked to original sources
PubMed1995

Histochemical studies of hyaluronan and the hyaluronan receptor ICAM-1 in psoriasis.

Histochemical stainings of frozen sections of human normal and psoriatic skin were used to study the localization of hyaluronan (HA) and intercellular adhesion molecule 1 (ICAM-1). HA staining was found in all areas of the skin, with the exception of the stratum corneum, in both normal and psoriatic cases without any apparent quantitative differences between the conditions. The staining for ICAM-1 was detected in vessels in normal skin and at lower levels in normal areas of the skin in patients with psoriasis. However, in these patients the staining increased to about the same level as in normal skin after hyaluronidase treatment of the sections prior to staining. In psoriatic lesions, distinct staining for ICAM-1 was localized mainly to vessels and infiltrating leukocytes. Treatment of the sections with hyaluronidase increased the staining of vessels only slightly, but more strongly around leukocytes. These findings show that ICAM-1 is predominantly free from bound HA on vessel endothelium in psoriasis lesions but not on vessels in normal areas of the skin, and suggests that systematically administered HA, previously shown to reduce chronic inflammation in animal models, might have a beneficial effect in psoriasis via blocking of endothelial ICAM-1 and thereby causing a reduced invasion of leukocytes into the skin.

Histocytochemistry↗
PubMed1993

Time course of ethanol-induced changes in serotonin metabolism.

The effect of acute ethanol consumption on serotonin metabolism was examined in healthy volunteers in the fasted and fed state by determination of plasma and urinary levels of the serotonin metabolites 5-hydroxyindole-3-acetic acid (5-HIAA) and 5-hydroxytryptophol (5-HTOL). The plasma and urinary levels of 5-HIAA were reduced by about 40% and 25%, while the 5-HTOL levels were increased on an average 7-fold and 50-fold, respectively, after oral intake of ethanol (0.8 g/kg) over 30 min in a fasted state. The maximal effect on both 5-HIAA and 5-HTOL levels was found 4-6 h after starting drinking. Urinary 5-HTOL and the 5-HTOL/5-HIAA ratio did not return to baseline until 19 h after the start of the administration (i.e., about 10 h after ethanol reached zero level). The mean 24-h excretion of 5-HTOL was increased 15-fold by the ethanol intake, while the 5-HIAA excretion was not significantly different. A clear dose dependent effect was observed in one individual who also ingested a lower amount of ethanol (0.5 g/kg). When ethanol (0.8 g/kg) was ingested over 3 h together with food, the urinary level of 5-HTOL and the 5-HTOL/5-HIAA ratio did not return to baseline until after 20-22 h. In other subjects who had unlimited access to ethanol and ingested between 1.3-2.3 g/kg together with food, the time to reach baseline 5-HTOL/5-HIAA ratio in urine ranged from 20 h to over 26 h.

Adult↗
PubMed1993

Erythrocyte-leukocyte interactions in the vascular bed of isolated perfused rat lungs.

An earlier study of perfused rat lungs showed that leukocytes, given as bolus injections, seemed to become more or less permanently trapped in the pulmonary microvascular bed under erythrocyte-free perfusion. The aim of the present study was, therefore, to investigate the rheologic effects of erythrocytes on the leukocyte microcirculation of perfused rat lungs. Leukocyte and erythrocyte suspensions were given as bolus injections during cell-free, constant pressure perfusion of ventilated rat lungs. Leukocyte numbers were counted in samples of the venous effluent and flow resistance changes were computed from registrations of flow rate, arterial and venous pressures. The preparations showed a continuous efflux of leukocytes which had been trapped in the pulmonary microcirculation before the perfusion was started. A bolus infusion of erythrocytes (3 ml, hematocrit: 30%) caused a transient flow resistance increase during the passage of the erythrocyte bolus through the vascular bed. This initial peak was accompanied by an increased venous efflux of leukocytes and followed by a lower second peak, attributed to a redistribution of trapped leukocytes in the capillary bed. Infusions of mixed cell suspensions (20-30 x 10(6) leukocytes in 30% hematocrit) caused a transient resistance increase similar to that caused by erythrocytes and a sustained resistance increase, less persistent than that caused by leukocytes. The present data suggest that the infusion of erythrocytes caused a re-distribution and an increased efflux of leukocytes, pooled in the pulmonary microcirculation. The rheological effects of erythrocytes could, hypothetically, result from mechanical interactions with the leukocytes in the pulmonary microvessels.

Animals↗
PubMed1992

C-CAM (Cell-CAM 105) is a calmodulin binding protein.

C-CAM (Cell-CAM 105) is a transmembrane cell adhesion molecule belonging to the immunoglobulin superfamily. It mediates intercellular adhesion of rat hepatocytes and occurs in various isoforms in several epithelia, vessel endothelia and leukocytes. We now report that purified liver C-CAM interacts specifically with calmodulin. Binding was observed both when 125I-labeled C-CAM was used in a dot-blot assay and when 125I-labeled calmodulin was used in a gel overlay assay. Experiments with protease-generated peptides indicated that calmodulin bound to the cytoplasmic domain of C-CAM. Analyses of whole liver membranes demonstrated that C-CAM is one of five major proteins that bind calmodulin in a calcium-dependent manner.

Adenosine Triphosphatases↗
PubMed1992

Urinary excretion of 5-hydroxyindole-3-acetic acid and 5-hydroxytryptophol after oral loading with serotonin.

The urinary excretion patterns of the serotonin (5-hydroxytryptamine; 5-HT) metabolites 5-hydroxyindole-3-acetic acid (5-HIAA) and 5-hydroxytryptophol (5-HTOL) were examined after ingestion of bananas, a food rich in 5-HT. The bananas contained on an average 25 micrograms 5-HT/g pulp. Both urinary 5-HIAA and 5-HTOL increased markedly (15- to 30-fold) shortly after eating 3-4 bananas, with the highest concentrations found in urine specimens collected after 2-4 h, and did not return to normal until after 8-10 h. The excretion of 5-HIAA increased from a control mean value of 3.9 mg/24 h to 12.7 mg/24 h, when conventional diets were supplemented with 3-4 bananas. The corresponding results for 5-HTOL were 16.8 micrograms/24 h and 60.7 micrograms/24 h, respectively. Of the banana-derived 5-HT ingested, 60-80% was recovered in the urine as 5-HIAA and only 0.3-0.5% as 5-HTOL. However, since both the time-course and relative increase in 5-HTOL was similar to that of 5-HIAA, there was no effect on the urinary 5-HTOL to 5-HIAA ratio. By contrast, acute alcohol consumption produced a considerable elevation of this ratio.

Administration, Oral↗
PubMed1991

Determination of urinary 5-hydroxyindole-3-acetic acid by high-performance liquid chromatography with electrochemical detection and direct sample injection.

A method for the routine quantitative determination of the major serotonin metabolite 5-hydroxyindole-3-acetic acid (5-HIAA) in urine is described. 5-HIAA was analyzed without prior sample cleanup, using an automated high-performance liquid chromatography system with isocratic elution and electrochemical detection (+0.60 V versus a Ag/AgCl reference electrode). The urine samples were mixed with a solution of the internal standard (5-hydroxyindole-3-propionic acid) and centrifuged. The supernatant was transferred to sealed glass vials, and a 2-microliters aliquot was injected directly onto a C18 reversed-phase analytical column, using an automatic sample injector. Samples of urine could be stored for several months at -80 or at +7 degrees C for 2 days without loss of 5-HIAA. However, a gradual decline with time occurred in crude samples stored at room temperature or above, as well as in urine samples diluted with the mobile phase. The detector response was linear in the range of 0-65 mumol/l 5-HIAA, and the intra- and interassay coefficients of variation were about 5 and 7%, respectively (n = 10).

Chromatography, High Pressure Liquid↗
PubMed1991

Inhibition of human blood aldehyde dehydrogenase activity by cigarette-smoke condensate.

The effect of a cigarette-smoke condensate (CSC) and three CSC subfractions on the aldehyde dehydrogenase (ALDH; EC 1.2.1.3) activity in human blood cells was examined under physiological conditions in vitro. Incubation of intact or sonicated cells with different concentrations of crude CSC resulted in a dose-dependent reduction of the ALDH activity. The inactivation was only restored in part after extensive washing of the cells, indicating that the inhibition observed was mainly irreversible. The nonvolatile (NV) subfraction of the CSC caused a reduction in ALDH activity similar to that obtained with crude CSC, while the semivolatile (SV80) and volatile (SV20) subfractions did not significantly affect ALDH. The present results, showing that the human blood cell ALDH is inactivated by constituents of cigarette smoke in vitro, suggest that the blood ALDH activity reduction found in habitual smokers is also caused by components formed during the combustion of tobacco.

Aldehyde Dehydrogenase↗