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Biomedical subjects

T Lehto

Publications and source records attributed to T Lehto.

At least 19 recordsLinked to original sources
PubMed2005

Effects of soil temperature on shoot and root growth and nutrient uptake of 5-year-old Norway spruce seedlings.

Soil temperature is a main factor limiting root growth in the boreal forest. To simulate the possible soil-warming effect of future climate change, 5-year-old Norway spruce (Picea abies (L.) Karst.) seedlings were subjected to three simulated growing seasons in controlled environment rooms. The seedlings were acclimated to a soil temperature of 16 degrees C during the first (GS I) and third growing seasons (GS III), but were assigned to random soil-temperature treatments of 9, 13, 18 and 21 degrees C during the second growing season (GS II). In GS II, shoot diameter growth was lowest in the 21 degrees C treatment and root growth was lowest in the 9 degrees C treatment. In GS III, shoot height and root length growth improved in seedlings that had been kept at 9 degrees C during GS II, indicating compensatory growth in response to increased soil temperature. The temporary decrease in soil temperature had no long-lasting significant effect on seedling biomass or total nutrient uptake. At the end of GS III, fine roots of seedlings exposed to a soil temperature of 21 degrees C in GS II were distributed more evenly between the organic and mineral soil layers than roots of seedlings in the other treatments. During GS II and GS III, root growth started earlier than shoot growth, decreased during the rapid shoot elongation phase and increased again as shoot growth decreased.

Picea↗
PubMed2004

Boron uptake by ectomycorrhizas of silver birch.

Boron (B) is an essential micronutrient for plants but it is thought not to be essential for fungi. We studied whether the extraradical mycelia of Paxillus involutus in symbiosis with silver birch (Betula pendula) take up B and transport it to the host plant. We grew mycorrhizal plants in flat microcosms with a partitioning wall, below which there was only extraradical mycelium. A boric acid solution enriched in 10B was applied to these mycelia. Increased 10B/11B isotope ratios were subsequently measured in birch leaves, stems, and roots plus mycorrhizas in the upper compartment. Boron was therefore taken up by the mycorrhizal mycelia and transported to the host plant in this species combination.

Basidiomycota↗
PubMed2002

Soil temperature, gas exchange and nitrogen status of 5-year-old Norway spruce seedlings.

Five-year-old Norway spruce (Picea abies (L.) Karst.) seedlings were subjected to three simulated growing seasons in controlled environment chambers. Plants were acclimated to a soil temperature of 16 degrees C during the first and third growing seasons, but were allocated at random to soil temperature treatments of 9, 13, 18 and 21 degrees C during the second growing season. Low soil temperature during the second growing season depressed stomatal conductance and photosynthetic rate (A) per unit of projected leaf area, although intercellular CO2 concentrations did not differ significantly between treatments. At all soil temperatures, total chlorophyll concentration first decreased and then increased, although the rate of increase and the final concentration increased with soil temperature, which may explain the effect of soil temperature on A. Neither chlorophyll a/b ratio nor leaf nitrogen concentration was significantly affected by soil temperature. Treatment differences disappeared during the third simulated growing season when plants were again acclimated to a soil temperature of 16 degrees C.

Chlorophyll↗
PubMed2001

Role of boron in drought resistance in Norway spruce (Picea abies) seedlings.

Norway spruce (Picea abies (L.) Karst.) seedlings fertilized with boron (B) at three rates were grown in a 3:7 mix of forest humus and quartz sand for 18 weeks. Half of the seedlings were not watered during the last 9 days of the experiment (drought treatment). The role of B in drought resistance was assessed by comparing the effects of seedling internal B concentration on the water relations, photosynthesis, growth and nutrition of well-watered and drought-treated seedlings. At the end of the drought treatment, needle B concentrations were 7.0 mg x kg(-1) at the lowest B supply rate and 17.5 and 23.5 mg x kg(-1), respectively, at the higher supply rates. Seedlings at the lowest B supply rate had fewer root tips and mycorrhizas than seedlings at the higher B supply rates. Drought treatment had a more pronounced effect on the water relations and net photosynthetic rate of seedlings than B treatment. Although seedlings at the higher B supply rates lost water more rapidly than seedlings at the low B supply rate-leading to faster stomatal closure and decreased photosynthesis-drought did not affect their final height, whereas drought reduced height growth of seedlings at the low B supply rate.

Boron↗
PubMed2001

Effects of soil temperature on biomass and carbohydrate allocation in Scots pine (Pinus sylvestris) seedlings at the beginning of the growing season.

We studied effects of soil temperature on shoot and root extension growth and biomass and carbohydrate allocation in Scots pine (Pinus sylvestris L.) seedlings at the beginning of the growing season. One-year-old Scots pine seedlings were grown for 9 weeks at soil temperatures of 5, 9, 13 and 17 degrees C and an air temperature of 17 degrees C. Date of bud burst, and the elongation of shoots and roots were monitored. Biomass of current and previous season roots, stem and needles was determined at 3-week intervals. Starch, sucrose, glucose, fructose, sorbitol and inositol concentrations were determined in all plant parts except new roots. The timing of both bud burst and the onset of root elongation were unaffected by soil temperature. At Week 9, height growth was reduced and root extension growth was much less at a soil temperature of 5 degrees C than at higher soil temperatures. Total seedling biomass was lowest in the 5 degrees C soil temperature treatment and highest in the 13 degrees C treatment, but there was no statistically significant difference in total biomass between seedlings grown at 13 and 17 degrees C. In response to increasing soil temperature, below-ground biomass increased markedly, resulting in a slightly higher allocation of biomass to below-ground parts. Among treatments, root length was greatest at a soil temperature of 17 degrees C. The sugar content of old roots was unaffected by soil temperature, but the sugar content of new needles increased with increasing soil temperature. The starch content of all seedling parts was lowest in seedlings grown at 17 degrees C. Otherwise, soil temperature had no effect on seedling starch content.

Biomass↗
PubMed2000

Detection of a soluble form of the complement membrane attack complex inhibitor CD59 in plasma after acute myocardial infarction.

Activation of the complement system has been documented in both experimental and clinical studies of acute myocardial infarction (AMI). Our earlier immunohistochemical studies have shown that the deposition of the membrane attack complex (MAC) of complement is associated with the loss of protectin (CD59), a glycosyl-phosphatidylinositol (GPI)-anchored sarcolemmal regulator of MAC, from the human and rat infarcted myocardium. In this study we detected, using an enzyme immunoassay (EIA), CD59 in the plasma of AMI patients at a concentration of 23.0+/-8.4 ng/ml (mean +/- SD; n = 17) at 4 h and 27.3+/-11.8 ng/ml (n = 24) at 24 h after AMI. Both values were significantly higher than in healthy controls (7.8+/-6.4 ng/ml; n = 20; P<0.001). The amount of CD59 correlated with the level of soluble terminal complement complexes (SC5b-9; r = 0.84; P<0.01) in the plasmas of AMI patients. Our results suggest that myocardial damage leads to release of CD59 from the sarcolemmal cell membranes during AMI.

Adult↗
PubMed1997

Binding of human and rat CD59 to the terminal complement complexes.

CD59-antigen (protectin) is a widely distributed glycolipid-anchored inhibitor of complement lysis. CD59 interacts with complement components C8 and C9 during assembly of the membrane attack complex (MAC). To evaluate species specificity of these interactions we have in the present study examined cross-species binding of isolated human and rat CD59 to the terminal complement components C8 and C9. By using primarily soluble CD59 isolated from urine (CD59U) potentially non-specific binding interactions of the phospholipid portion of the membrane forms of CD59 could be avoided. Sucrose density gradient ultracentrifugation analysis showed that human CD59U bound to both human and rat C8 in the SC5b-8 complexes. Similar binding occurred when rat CD59U was used. The degree of binding did not significantly differ between the heterologous and homologous CD59-C8 combinations. C9 from both species inhibited the binding of CD59 to soluble SC5b-8. In ligand blotting analysis human and rat CD59U bound to human and rat C8 alpha gamma-subunit and C9. Binding of human and rat CD59U was stronger to human than rat C9. In plate binding assays the erythrocyte form of CD59 (CD59E) bound to both human and rat C8. Binding of CD59E to heterologous C9 was considerably weaker than to homologous C9. Our results imply that the reciprocal binding sites between C8 and CD59 and to a lesser degree between CD59 and C9 are conserved between human and rat. Interactions of CD59 with the terminal C components are thus species selective but not 'homologously restricted'.

Animals↗
PubMed1997

Suppression of alternative complement pathway activity by radiographic contrast media.

The authors examined the effect of four different kinds of contrast media (ionic/non-ionic, monomer/dimer) on the activation of the complement (C) system (haemolytic activity and anaphylatoxin generation) in vitro. In addition, the authors compared the effect of contrast media on inulin-mediated generation of the anaphylatoxin derivative C3a des Arg in sera from urticarial reactors and their non-reacting controls. It was observed that the incubation of commercial iohexol, ioxaglate, iodixanol and meglumin amidotriz solutions in normal human serum (NHS) resulted in a dose-dependent decrease in the haemolytic activity of the alternative C pathway. Contrary to expectations the contrast media did not activate C in NHS. Instead, inulin-induced generation of C3a des Arg was inhibited by all the four contrast media. The strongest inhibitor was ioxaglate, an ionic dimer. No significant difference between the urticarial reactors and non-reactors in the inhibition of C3a des Arg generation was observed. In analyzing the mechanism of C inhibition we found that the contrast media solutions, particularly the ionic ones, prevented formation of the alternative pathway C3 convertase, C3bBb, by inhibiting the binding of factor B to surface-associated C3b molecules. The results suggest that the previously observed decrease in haemolytic C titres by contrast media is due to direct suppression of C activity rather than activation-induced consumption.

Complement C3-C5 Convertases↗
PubMed1997

Effects of light quality on growth and N accumulation in birch seedlings.

We studied the effects of light quality and nutrient supply on growth and nitrogen accumulation in silver birch (Betula pendula Roth) seedlings to test three hypotheses: (1) growth of birch seedlings is sensitive to changes in light quality; (2) the response of birch seedling growth to light quality depends on nutrient supply; and (3) assimilation and allocation of nitrogen by birch seedlings are affected by light quality. The two light regimes simulated the spectral quality of sunlight and shadelight, but did not differ in photosynthetic photon flux density, and the two nutrient supply regimes differed in the rate of supply, but not in the composition, of mineral nutrients. Accumulation and allocation of dry weight and nitrogen were strongly affected by nutrient supply regime, but light quality had little effect. During the first 15 days of the experiment, the largest effect of light quality was on height growth, which was greater in seedlings in simulated shadelight than in seedlings in simulated sunlight. Light quality had little effect on dry weight and nitrogen allocation to the stem during this period. However, at the end of the experiment (Day 29), there was an increase in N concentration per unit dry weight in leaves and stems of seedlings in the simulated shadelight plus high nutrient supply treatment.

Journal Article↗
PubMed1996

Structural composition and functional characterization of soluble CD59: heterogeneity of the oligosaccharide and glycophosphoinositol (GPI) anchor revealed by laser-desorption mass spectrometric analysis.

CD59 (protectin) is a glycophosphoinositol (GPI)-anchored inhibitor of the membrane attack complex of complement found on blood cells, endothelia and epithelial cells. In addition to the lipid-tailed CD59, soluble lipid-free forms of CD59 are present in human body fluids. We have investigated the detailed structural composition of the naturally occurring soluble urinary CD59 (CD59u) using peptide mapping, anion-exchange chromatography, sequential exoglycosidase digestion and matrix-assisted laser-desorption mass spectrometry (MALDI-MS). CD59u exhibited an average M(r) of 12444 in MALDI-MS. Mass analysis of the isolated C-terminal peptide (T9) indicated that a GPI-anchor (at Asn-77) without an inositol-associated phospholipid was present in soluble CD59u. By using residue-specific exoglycosidases, chemical modification and MALDI-MS structures of seven different GPI-anchor variants were determined. Variant forms of the anchor had deletions and/or extensions of one or more monosaccharide units. Sialic acid linked to an N-acetylhexosamine-galactose arm was found in two GPI-anchor variants. The N-linked carbohydrate side chain of CD59u (at Asn-18) also displayed considerable heterogeneity. The predominant oligosaccharide chains were fucosylated biantennary and triantennary complexes with variable sialylation. Mono Q anion-exchange chromatography resolved urinary CD59 into nine different fractions that bound equally well to the terminal complement SC5b-8 complexes. Despite binding to C5b-8, soluble CD59u inhibited complement lysis at an approx. 200-fold lower efficiency than erythrocyte CD59. These results document the structural heterogeneity of both the GPI anchor and N-linked oligosaccharide of CD59 and demonstrate that the phospholipid tail is needed for the full functional activity of CD59. The site of cleavage between the diradylglycerol phosphate and inositol suggests that a mammalian phospholipase D could be involved in the solubilization of GPI-anchored proteins.

Amino Acid Sequence↗
PubMed1996

Complement activation in the central nervous system following blood-brain barrier damage in man.

The central nervous system (CNS) is virtually isolated from circulating immunological factors such as complement (C), an important mediator of humoral immunity and inflammation. In circulation, C is constantly inhibited to prevent attack on host cells. Since a host of diseases produce an abnormal blood-brain/cerebrospinal fluid (blood-brain/CSF) permeability allowing C protein extravasation, we investigated if C activation occurs in CSF in vitro and in CNS in vivo during subarachnoid hemorrhage (SAH) or brain infarction. After SAH (n = 15), the terminal complement complex (TCC) concentration on days 0 to 2 was higher in the CSF, 210 +/- 61 ng/ml, than in the plasma, 63 +/- 17 ng/ml, but null in the CSF of controls (n = 8) or patients with an ischemic stroke (n = 7). TCC was eliminated from the CSF after SAH (24 +/- 10 ng/ml on days 7 to 10). Incubation of normal human CSF with serum in vitro also activated the terminal C pathway. In 10 fatal ischemic brain infarctions, immunohistochemical techniques demonstrated neuronal fragment-associated deposition of C9 accompanied by neutrophil infiltration. We conclude that the C system becomes activated intrathecally in SAH and focally in the brain parenchyma in ischemic stroke. By promoting chemotaxis and vascular perturbation, C activation may instigate nonimmune inflammation and aggravate CNS damage in diseases associated with plasma extravasation.

Adult↗
PubMed1995

Activation of the terminal complement cascade in renal infarction.

Ischemic injury is an important cause of functional derangement in the kidney. The complement (C) system has previously been shown to be an important mediator of ischemic tissue injury in myocardial infarction. In the present study we therefore investigated the possible role of C in renal ischemic lesions. The deposition and distribution of various C components (C1q, C3c, C3d, C4, C5, C6, C9) and regulators [vitronectin, clusterin and protectin (CD59)] in human renal infarction lesions were studied by indirect immunofluorescence microscopy. Deposition of components of the terminal C complex (TCC), as well as vitronectin and clusterin, were observed throughout the infarcted areas. The strongest deposits were seen on the membranes of tubular epithelial cells and in the tubular lumina of the infarction areas, especially in the border zone between normal and infarcted tissue. Using markers for different segments of tubuli (Tamm-Horsfall glycoprotein and brush border antigens) it was possible to localize deposits of TCC predominantly to the proximal tubuli. In the glomeruli of the infarcted areas deposits of TCC were seen as a crescent-like pattern at and immediately beneath the Bowman's capsule. The expression of cell membrane-associated protectin was diminished in tubular epithelial cells of the infarction lesions. A clue for the possible mechanism of C activation in renal infarction was obtained from in vitro experiments, in which the contact of normal human serum with urine was observed to lead to the generation of TCC.(ABSTRACT TRUNCATED AT 250 WORDS)

Complement Activation↗
PubMed1995

Urinary excretion of protectin (CD59), complement SC5b-9 and cytokines in membranous glomerulonephritis.

Protectin (CD59) is a low molecular weight glycophosphoinositol-anchored inhibitor of the membrane attack complex of complement (MAC) that is present, for example, on the membranes of endothelial cells and on epithelial cells of glomeruli and distal tubuli. To examine for the possibility that CD59 becomes detached from cell surfaces following cell injury, this study evaluated renal excretion of CD59 in patients with idiopathic membranous glomerulonephritis (MGN; N = 21), diabetic nephropathy (DNP; N = 15) and in healthy control subjects (N = 13). CD59 in human urine was quantitated by a competitive solid-phase radioimmunoassay having approximately 13 kDa soluble urinary CD59 as a standard. Immunofluorescence microscopy demonstrated a decreased expression of CD59 in the glomeruli of MGN patients. Using a Triton X-114 phase separation method 91 to 97% of urinary CD59 was found to be in a soluble form without anchor-associated phospholipid. The mean (+/- SEM) level of urinary CD59 was 5.6 +/- 0.2 micrograms/ml in MGN patients, 3.7 +/- 0.4 micrograms/ml in healthy controls (P < 0.001) and 2.6 +/- 0.1 in DNP patients (P < 0.001). When related to urinary creatinine (UCr) the corresponding values were 11.9 +/- 5.6, 4.8 +/- 0.3 (P = 0.021) and 4.4 +/- 0.2 (P < 0.002), respectively. The amount of CD59 in urine correlated with the urinary excretion of soluble terminal complement complexes, SC5b-9 (r = 0.594, P < 0.006) in MGN patients. The excretion of CD59 also correlated with the excretion of the inflammatory mediator IL-1 beta (r = 0.671, P = 0.001) but not with TNF-alpha (r = 0.314, P = 0.178). No correlation of CD59 excretion was observed with duration of the disease level of proteinuria, serum albumin concentration or serum creatinine level. Based on these findings we speculate that the increased excretion of CD59 into urine in MGN patients is due to complement activation and inflammation induced shedding of CD59 from glomerular cells.

Adult↗
PubMed1994

High-density lipoproteins can act as carriers of glycophosphoinositol lipid-anchored CD59 in human plasma.

CD59 (protectin) is a glycophosphoinositol (GPI) lipid-anchored inhibitor of complement lysis that is expressed on the membranes of blood cells, endothelial cells, epithelial cells and cardiomyocytes. CD59 may be shed from cell surfaces, e.g. during cell injury, but when entering human plasma its fate is unknown. In this study we observed that radiolabelled lipid-anchored CD59, but not soluble urinary CD59 without anchor lipid, incorporated into high-density lipoprotein (HDL) particles when mixed with human serum and analysed by high resolution gel filtration and anti-apoA-I affinity chromatography. Only a small proportion of CD59 entered the low-density lipoprotein (LDL) fraction. HDL particles were capable of incorporating 25-42% of [125I]CD that was preinserted into the membranes of rabbit erythrocytes (RaE) and transferred 7-14% of [125I]CD59 back to RaE or to cultured human endothelial cells (EA.hy 926). Immunoaffinity purification and immunoblotting analysis demonstrated that HDL isolated from normolipidemic human serum contained small amounts of CD59. These results suggest that HDL particles could be involved in the recycling of GPI lipid-anchored molecules released from cell surfaces.

Animals↗
PubMed1994

Urinary excretion of cytokines and complement SC5b-9 in idiopathic membranous glomerulonephritis.

Idiopathic membranous glomerulonephritis (iMGN) has previously been shown to be associated with urinary excretion of terminal complement complexes while increased urinary levels of cytokines have been reported in mesangial proliferative glomerulonephritis. In the present cross-sectional study urinary excretion of IL-1 beta, TNF-alpha, IL-6, and soluble C5b-9 (SC5b-9) was examined for 23 patients with iMGN, 16 patients with diabetic nephropathy (DNP), and 17 healthy subjects. IL-1 beta excretion (pg/mg crea) was significantly higher in iMGN patients (375, range 162-11,000) than in DNP patients (39, range 22-59, P < 0.001) or healthy controls (151, range 23-481, P < 0.001). TNF-alpha excretion rate (pg/mg crea) was clearly higher (38, range 21-700) in iMGN patients than in DNP patients (14, range 8-52, P < 0.001) or healthy subjects (11, range 7-26, P < 0.001). Median IL-6 excretion (pg/mg crea) was only marginally higher in iMGN patients (73, range 0-850) than in healthy subjects (64, range 3-158, P = 0.02) but significantly higher than in DNP patients (29, range 17-47, P < 0.001). No significant correlation with corresponding serum values was observed for urinary IL-6 or TNF-alpha excretion. Urinary IL-1 beta and TNF-alpha correlated with decreased renal function. Five of 23 patients showed progression of iMGN over a follow-up of 6 months. The excretion of all cytokines, TNF-alpha in particular, was significantly higher in patients with a progressive disease than in the other patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Interactions of soluble CD59 with the terminal complement complexes. CD59 and C9 compete for a nascent epitope on C8.

Human CD59-Ag is a glycophosphoinositol lipid-anchored inhibitor of the membrane attack complex of complement (MAC). We have examined the interactions of CD59 with the terminal complement complexes using soluble CD59 purified from human urine (CD59U). CD59U bound to SC5b-8, SC5b-9, and MAC complexes when present during their formation. When SC5b-8, SC5b-9, and MAC were allowed to perform, progressively less 125I-CD59U bound to the complexes. Terminal SC5b-9 complexes isolated from activated sera no longer bound CD59U, indicating that the binding sites had become inaccessible in the fully assembled SC5b-9 complex. Unlike acylated myocardial CD59 (CD59H) neither CD59U nor PIPLC-treated CD59H became incorporated into poly-C9 complexes, suggesting that the interaction of CD59 with C9 requires the lipid anchor. Human C9 and heterologous C9 from guinea pig serum, as well as the YTH53.1 anti-CD59 mAb, inhibited the binding of CD59U to SC5b-8. On the other hand, soluble CD59U did not inhibit binding of C9 to SC5b-8, although CD59E has been shown to limit the number of C9 molecules entering into MAC. This suggests that two interaction sites between C5b-8 and C9 exist: one conferring the initial binding of C9 into the C5b-8 complex, and a second directing the insertion of C9 into the lipid bilayer. The latter interaction is the prerequisite for C9 polymerization and the target for interference by CD59.

Animals↗
PubMed1990

Dentists' hearing and exposure to high speed turbine dental drill noise.

Effect of high speed turbine dental drill noise (DDN) on dentists' hearing at present and during the era of noisier drills was investigated. Hearing of two generations of dentists, power spectral density (PSD) functions of DDN from various drills and the equivalent level (LAeq) of a modern dental operatory were studied. The LAeq was 65 dB with 1 and 50% probability distribution levels of 74 and 57 dB, respectively. DDN was tonal with the spectrum peak always above 6 kHz, containing within 128 Hz frequency band 28-85% of the total noise energy in the PSD function. A cartridge type ball bearing drill from early 1960's was found noisier than an air bearing drill or a modern sealed head ball bearing drill by 8.5 and 5 dB, respectively. Sound pressure levels of DDN ranged from 68 to 79 dBA, being within safe limits. The high values earlier reported for cartridge type or worn drills could not be verified. Hearing of dentists free from clear ear pathology was found good and very similar to the reference, representing a population with no exposure to noise. There was no difference in hearing of 46 dentists 33-42 years of age, examined in 1973 and among whom there had been exposure to early and noisier drill, as compared to hearing of 56 dentists of similar age and years in dentistry, examined in 1988 and who had only been exposed to quieter drills of the 1970's. Noise dose and audiometric measurements were in agreement and indicated that DDN is not and has never been a risk to dentists' hearing.

Adult↗