Confined and extended optical phonons in an ultrathin-layer YBa2Cu3O7/PrBa2Cu3O7 superlattice.
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Journal Article↗
Biomedical subjects
T Hahn
Publications and source records attributed to T Hahn.
Skeletal response to recombinant human growth hormone (rhGH) in children treated with long-term corticosteroids.
Corticosteroid therapy causes osteopenia and growth retardation in children; such changes are associated with diminished rates of bone formation and turnover. Since growth hormone activates bone remodeling, the biochemical and skeletal responses to rhGH were evaluated in four pediatric patients, aged 12.8 +/- 3 years, with long-term corticosteroid use (5 +/- 2 years). Recombinant human growth hormone (rhGH), 0.125 mg/kg, was given 3 times/week by subcutaneous injection for 12 months. Iliac crest bone biopsies were obtained after double tetracycline labeling before and at the end of rhGH therapy; serum levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone (intact), 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D3, osteocalcin (BGP), and insulin-like growth factor-1 (IGF-1) were measured every 3 months during the treatment period. The average dose of prednisone was 0.24 +/- 0.05 mg/kg/day initially, and this did not change during the study. Serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D3, and BGP were unchanged during the rhGH therapy, but the serum IGF-1 level increased by 71%, p < 0.01. Eroded bone perimeter and cancellous bone area did not change significantly during rhGH therapy. Bone formation rates rose from 423 +/- 475 to 781 +/- 407 microns2/mm2/day, p < 0.05, and the length of double tetracycline-labeled bone perimeter increased by 85%, p < 0.05. The bone formation rate in the growth hormone group exceeded the values of an age-matched reference group (14.3 +/- 3 years), 780 +/- 407 microns2/mm2/day versus 411 +/- 479 microns2/mm2/day, p < 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)
25-Hydroxyvitamin D 2↗
Localisation of the high affinity facilitative glucose transporter protein GLUT 1 in the placenta of human, marmoset monkey (Callithrix jacchus) and rat at different developmental stages.
In the present study, the facilitative D-glucose transporter protein GLUT 1 was localised by immunohistochemistry in the placenta of human, marmoset (Callithrix jacchus) and rat at different developmental stages. A polyclonal antiserum against a 13-amino-acid peptide of the GLUT 1 carboxy terminus was used. It identified a protein of around 50 kDa molecular weight in immunoblotting of the placental tissues. GLUT 1 was located in the syncytiotrophoblast, in cytotrophoblast cells and in fetal endothelium. Similar staining patterns, except in human extravillous cytotrophoblast cells, were observed at all differentiation stages, despite differences in the internal placental architecture of the species. In the marmoset placenta, GLUT 1 was undetectable in endothelial cells of maternal vessels. In rat placentae, trophoblastic giant cells, epithelial cells of both visceral and parietal yolk sac, yolk sac vessels and the stratum spongiosum were stained. Reichert's membrane did not immunoreact. Preadsorption of the antiserum with a 13-amino-acid peptide resulted in the loss of immunoreactivity. The results suggest that GLUT 1 is a prominent isoform of glucose transporters in mammalian placentae. It is generally abundant in placental cell populations bordering on the maternal and fetal circulations and may therefore facilitate an effective glucose supply to the fetus and placenta.
Animals↗
Advanced ovulation in gilts by the intrauterine application of a low molecular mass pronase-sensitive fraction of boar seminal plasma.
The shortening of the time interval between the onset of oestrus and ovulation in sows by the transcervical administration of seminal plasma was investigated in 23 German Landrace gilts, using the technique of single horn infusions (Mariensee model) in combination with the transcutaneous sonographic monitoring of ovaries. Preparative surgery comprised the detachment of the left uterine horn from the corpus, leaving the caudal end open to the peritoneal cavity but sealing the corpus wound. The left ovary was loosely tied to the ventral abdominal wall for better sonographic distinction. The animals were used in two to four consecutive cycles. After detection of oestrus by the teaser boar, the patent (right) horns were filled by transcervical infusion of 100 ml of a variety of test solutions. Ovulation was probed by transcutaneous sonography at intervals of 4 h thereafter. Native seminal plasma provoked ovulation in the ipsilateral ovary of the treated horn 10.7 h earlier than in the contralateral ovary. This effect was reduced to 7.3 h after charcoal treatment of seminal plasma; addition of 10 micrograms oestradiol restored the effect in full, while 10 micrograms of oestradiol in PBS shortened the time interval to only 3.3 h versus the control ovary. Little effect was seen with oestrone sulfate, none with prostaglandins in PBS or with PBS alone. The preliminary characterization of the nonsteroidal component of seminal plasma advancing ipsilateral ovulation after transcervical infusion suggests a proteinaceous nature. The activity resides in the 1-10 kDa fraction separated by ultrafiltration and is lost after treatment with pronase.
Animals↗
Insulin receptors in syncytiotrophoblast and fetal endothelium of human placenta. Immunohistochemical evidence for developmental changes in distribution pattern.
The localisation of insulin receptors (IR) was investigated on cryosections of human non-pathologic first trimester and full term placentae by indirect immunohistochemistry with three different monoclonal antibodies (MABS). In placentae from 6 to 10 weeks postmenstruation (p-m.), only syncytiotrophoblast was stained, predominantly that of mesenchymal villi and syncytial sprouts, which are areas of high proliferative activity. In placentae from 11 to 14 weeks p-m., endothelial cells commenced to react with the IR MABS and the syncytiotrophoblast was less intensely labelled than at weeks 6 to 10 p-m. In term placentae, the microvillous membrane of the syncytiotrophoblast showed only patches of weak immunoreactivity. In contrast, the endothelial cells in the placenta but not in the umbilical cord were strongly stained. The amniotic epithelium in the chorionic plate and fibroblasts in the stroma were conspicuously labelled. The data indicate: (1) the receptor density on villous syncytiotrophoblast decreases and that of fetal endothelium increases' throughout gestation; (2) syncytiotrophoblast of human term placentae expresses a low level per unit area of surface IR; and (3) the majority of IR in human term placentae is located in fetal endothelium. Apart from yet unknown functional effects of maternal and fetal insulin at the placental barrier, the results suggest a growth promoting effect on the trophoblast of maternal insulin in first trimester as well as developmental effects of fetal insulin on the feto-placental vessels at term.
Antibodies, Monoclonal↗
Heterogeneous histochemical reaction pattern of the lectin Bandeiraea (Griffonia) simplicifolia with blood vessels of human full-term placenta.
Bandeiraea simplicifolia lectin (BS-I) stains vascular endothelium in various species. In humans, less than 10% of the specimens studied exhibit a reaction with BS-I. In the present histochemical study, the reactivity of BS-I with placental blood vessels and its correlation with the blood group from mother and newborn child was investigated. Acetone-fixed cryosections of representative tissue segments of human full-term placenta and umbilical cord were stained with BS-I. The staining pattern of tissues from patients with different blood groups was identical, although the reaction of BS-I in the placenta was heterogeneous. BS-I did not react with the umbilical cord. Vascular smooth muscle cells at the insertion site of the umbilical cord into the chorionic plate, and endothelium deeper in the chorionic plate, became progressively stained. The endothelial cells and tunica muscularis of smaller arteries and veins in stem villi lost their reactivity in parallel with decreasing vessel size. Arterioles and venules reacted heterogeneously. Capillaries, trophoblastic basement membranes, especially epithelial plates, and sometimes the syncytiotrophoblast were labelled in several terminal villi. The data indicate that 1) the placenta binds BS-I to fetal endothelium independent of the blood group, 2) cell-surface antigens on placental endothelial cells are expressed heterogeneously and 3) cell-surface glycans are constituted in an organ-specific manner on human endothelial cells.
Endothelium, Vascular↗
Increased neutrophil chemiluminescence production in patients with cystic fibrosis.
Increased free radical production has been suggested as a possible mechanism involved in lung deterioration of patients with cystic fibrosis (CF). Vitamins A and E are known to be involved in the defense mechanism preventing damage caused by free radicals. Both vitamins are fat-soluble and are therefore malabsorbed in patients with CF. We hypothesized that low concentrations of vitamins A and E may be involved in the increased free radical production of these patients. Neutrophils' chemiluminescence and superoxide and hydrogen peroxide production were examined in 11 patients with CF aged 4 to 14 years, and 10 age-matched healthy controls. All our patients were on prolonged supplementation with vitamins A and E, but the control group was not supplemented. Serum vitamins A and E levels and neutrophil vitamin E concentrations were examined concomitantly. Chemiluminescence production was increased 10 minutes after neutrophil stimulation by phorbol myristate acetate (PMA) as compared with that in normals (20,400 +/- 9,463 v 11,990 +/- 3,778 cpm, P < .03). No difference was found in superoxide or hydrogen peroxide production between CF patients and controls. Serum vitamin A levels were significantly higher in CF patients compared with healthy controls (0.641 +/- 0.049 v 0.398 +/- 0.038 mg/L, P < .04) and so were vitamin E levels (13.94 +/- 2.25 v 5.64 +/- 1.15 mg/L, P < .05). Neutrophil vitamin E concentrations were higher in CF patients compared with healthy controls (70.8 +/- 26.0 v 23.6 +/- 9.0 micrograms/10(6) cells). We conclude that neutrophils from CF patients exhibit increased chemiluminescence activity not related to increased free radical production or fat-soluble vitamin deficiency.
Adolescent↗
Effects of the synthetic glucocorticoid triamcinolone acetonide on vasoactive hydrolases of the human placenta in vitro.
Therapy with glucocorticoids during pregnancy is still debated. Previously reported effects of glucocorticoid application in rats resemble certain symptoms of preeclampsia. Therefore, we studied in vitro the effects of the synthetic glucocorticoid triamcinolone acetonide soluble (0.1-10 mM) on placental alpha-glutamyl amino-peptidase, microsomal alanyl aminopeptidase, dipeptidyl peptidase IV, acetylcholinesterase and butyrylcholinesterase in purified trophoblast monolayers and villous explants from first trimester (n = 5) and term placentae (n = 9) using bio- and histochemical methods. In term placentae quantitative histochemistry (microdensitometry) of trophoblast monolayers revealed an increase of alpha-glutamyl aminopeptidase and microsomal alanyl aminopeptidase activity up to 149% and 126% respectively, after treatment with supraphysiological doses. In trophoblast monolayers from first trimester alpha-glutamyl aminopeptidase activity was not affected, whereas microsomal alanyl aminopeptidase activity increased by 25%. Dipeptidyl peptidase IV staining was reduced to 26%. Biochemical measurements of alpha-glutamyl aminopeptidase and microsomal alanyl aminopeptidase activity in homogenates of cultured villi revealed effects similar to those found by microdensitometry in trophoblast monolayers. In contrast, dipeptidyl peptidase IV activity increased in explants of term placentae by 47%. Acetyl- and butyrylcholinesterase activities were reduced in term placental villi by 38% and 40%, respectively. The data indicate that glucocorticoids may affect the activity of hydrolases which are thought to be involved in local placental blood pressure modulation.
Acetylcholinesterase↗
Investigation of the low-energy component of primary cosmic radiation on the outside of spacecrafts.
We have developed a method to investigate the low-energy radiation environment on the outside of spacecrafts. Thereby, ultra-thin thermoluminescent (TL) detectors on the base of CaF2:Mn-PTFE are arranged in stacks and exposed to the unshielded cosmic radiation. The dose distribution within a stack is determined by successive evaluation of the thin TL sheets. The analysis of LiF thermoluminescent detector glow curves permits conclusions on the dose contribution caused by either low-energy electrons or by protons. The method was applied aboard Russian COSMOS spacecrafts as well as the MIR station. It was shown that along low-earth orbits dose rates up to 10 Gy/day within the first few mg/cm2 are typical, mainly as a result of the electron impact.
Cosmic Radiation↗
Differential lectin binding to the fibrinoid of human full-term placenta: correlation with a fibrin antibody and the PAF-Halmi method.
Placental fibrinoid is thought to contain various glycoproteins originating from cell secretion and tissue degeneration, occasionally merged with fibrin. Information on the characteristics and derivation of the various fibrinoid components, however, is still fragmentary. Therefore, the present histochemical study on acetone-fixed placental tissue sections compared the staining pattern of FITC-conjugated lectins from Ulex europaeus (UEA-I), Bandeiraea simplicifolia (BS-I) and Lycopersicon esculentum (LEA) with the reactivity of a fibrin antibody and a modified paraldehyde-fuchsin stain. Using different color reactions, the latter histological method identified two types of fibrinoid, which correlated well with fibrin-type and matrix-type fibrinoid. Immunohistochemically, fibrin was detected at the intervillous border of the basal plate, in some inner parts and in perivillous fibrinoid. UEA-I bound to endothelial cells and partially to fibrin-type fibrinoid of villi and the basal plate, thus indicating a reaction with immured and disintegrated remnants of endothelial and blood cells. LEA stained fibrin-negative (i.e. matrix-type) fibrinoid homogeneously within the basal plate; the small reactive areas within the perivillous fibrinoid may belong to degenerating trophoblastic residues, because in villi LEA specifically reacted with the syncytiotrophoblast. BS-I heterogeneously labeled matrix-type fibrinoid deposits in the basal plate which surrounded decidual cells and subpopulations of extravillous trophoblast. In cell islands, BS-I also stained fibrinoid surrounding trophoblast cells heterogeneously. The data (1) confirm the existence of two types of placental fibrinoid, fibrin-type and matrix-type fibrinoid, (2) suggest that both types of fibrinoid contain different glycoconjugates, and (3) demonstrate the practical usefulness of the modified paraldehyde-fuchsin method for the identification of the two types of fibrinoid.
Endothelium, Vascular↗
Non-Michaelis-Menten kinetics of zero-trans glucose uptake by trophoblast cells from human term placentae and by choriocarcinoma (JEG-3/JAR) cells.
Maternal glucose is a major substrate for placental and fetal metabolism. The kinetics of its uptake into placental trophoblast cells has not been characterised yet and was therefore investigated in the present study. In addition to trophoblast cells isolated from human term placentae, JEG-3 and JAR choriocarcinoma cells were used. Measurements were carried out in 5 s intervals until 30 s with the non-metabolisable glucose analogue 3-O-[14C]methyl-D-glucose using confluent cells adhering to glass coverslips. L-[1-14C]glucose was used to correct for extracellular trapped tracer and diffusion. The uptake was rapid and saturable. It reached equilibrium after 30 s at 20 degrees C and could be inhibited by 0.4 mmol/l cytochalasin B up to 98%. The choriocarcinoma cells took up twice as much glucose as trophoblast cells. Fitting the experimental data to the Michaelis-Menten equation by non-linear regression failed to adequately describe the data, even when a contribution of diffusion to total uptake was considered. Introducing the Hill coefficient n into the Michaelis-Menten equation significantly improved the quality of the fits as was assessed by three statistical criteria. Using this equation modified for allosteric kinetics (v = k[To] [S]n)/(Km + [S]n)), parameters were calculated as Km = 12 mmol/l, Vmax = 17 fmol/l s-1 per cell, n = 1.1 for trophoblast cells; Km = 13 mmol/l, Vmax = 27 fmol/l s-1 per cell, n = 1.2 for JEG-3 cells and Km = 29 mmol/l, Vmax = fmol/l s-1 per cell, n = 1.4 for JAR cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Cell Adhesion↗
Verapamil inhibits B-cell proliferation and tumor necrosis factor release and induces a clinical response in B-cell chronic lymphocytic leukemia.
Four B-CLL patients, treated with verapamil for cardiac problems, showed substantial reduction of lymphadenopathy in one, a 3- and 5-year stabilization of B-CLL in two patients, and a dramatic decrease in lymphocyte count, lymphadenopathy and splenomegaly in one stage IV patient. We therefore studied the effects of verapamil on B-CLL cells in vitro. In 13 samples we observed that verapamil strongly inhibited in vitro proliferation of pokeweed mitogen (PWM) stimulated and unstimulated cells. Using a cytotoxic bioassay, we found that verapamil markedly inhibited the spontaneous and PMW-induced release of tumor necrosis factor (TNF) by B-CLL cells. These findings suggest that verapamil may block B-CLL cell proliferation through inhibition of TNF release and thereby may contribute to the management of B-CLL.
Aged↗
Differential responses of fetal, neonatal, and adult myelopoietic progenitors to interferon and tumor necrosis factor.
Human fetal liver (FL) and neonatal cord blood (CB) granulocyte-monocyte colony-forming progenitor cells (GM-CFC) are unique in their physiological environment and in certain proliferative and differentiative capacities. Tumor necrosis factor (TNF) and interferon (IFN) may inhibit or stimulate the growth of human bone marrow GM-CFC in vitro. The effects of recombinant human (rh) TNF-alpha, rhIFN-alpha, and rhIFN-tau on recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF)-stimulated clonogenic cultures of day 7 GM-CFC from FL and umbilical CB were compared with rhGM-CSF-stimulated GM-CFC from normal human bone marrow (BM). We demonstrate that, in comparison to BM progenitor cells, GM-CFC from both FL and CB were highly resistant to growth inhibition by all three cytokines. Furthermore, clonogenic growth of progenitors from FL and CB was markedly potentiated by IFN-tau in GM-CSF-stimulated cultures and was stimulated by IFN-tau in the absence of GM-CSF. Depletion of potential accessory cells resulted in a marked stimulatory response of CB cells to TNF-alpha, in the presence of GM-CSF, while it did not alter the responses to IFN. The stimulatory effects of IFN-tau and TNF-alpha may be indirectly mediated, at least in part, through induction of increased GM-CSF production and increased GM-CSF receptor expression by fetal cells. Divergent responses of myelopoietic cells, derived from various hematopoietic compartments, to regulatory actions of cytokines may provide a basis for further understanding the role of the environment in maturation and differentiation of granulocytes and monocytes.
Adult↗
Renormalization of phonons in a (Y/Pr)Ba2Cu3O7 superlattice investigated by Raman spectroscopy.
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Journal Article↗
Scaling of the angular dependence of the critical current density in high-Tc superconductors.
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Journal Article↗
Location and activities of acetylcholinesterase and butyrylcholinesterase in the rat and human placenta.
The location and physiological functions of acetylcholinesterase and butyrylcholinesterase in the placenta are still debated. In the present study the activities of both enzymes were studied histochemically in the rat and human placenta, using an optimized Karnovsky/Roots method. Additionally, they were measured biochemically. Acetylcholinesterase was active in the syncytiotrophoblast, cytotrophoplast cells and the visceral and parietal yolk sac epithelial cells of the rat (n = 10) and in the syncytiotrophoblast, cytotrophoblast cells, endothelial cells and the media of fetal blood vessels of the human placenta (n = 9). Butyrylcholinesterase could not be detected histochemically. Biochemically measured levels at certain developmental stages of the placenta revealed maximum acetylcholinesterase activity in the 8th week p.m. human placentae (102.9 nmol.min-1 per mg protein), 35% lower activity in the 12th week p.m., and minimum (44.1 nmol.min-1 per mg protein) in term placentae. In contrast, maximum butyrylcholinesterase activity was measured in week 12 p.m. (106.9 nmol.min-1 per mg protein). In rat placentae, butyrylcholinesterase activity on gestational day 21 reached 150% of the level on gestational day 16. Acetylcholinesterase activity remained constant. In placentae of pre-eclamptic patients, acetylcholinesterase and butyrylcholinesterase activities were found to be increased by 16% and 45%, respectively. The results suggest that placental acetylcholinesterase can no longer be considered as derived from maternal blood, but is primarily located within rat and human placental tissue.
Acetylcholinesterase↗
Enzyme histochemical evidence for the presence of potential blood pressure regulating proteases in cultured villous explants from human first trimester placentae.
The proteases dipeptidyl peptidase IV, angiotensinase A and microsomal alanyl aminopeptidase are present in the human term placenta where they may be involved in the local modulation of placental blood pressure. In order to establish an in vitro model system to study the significance of these proteases in disorders related to pregnancy-induced hypertension, the activity of the proteases was localized histochemically in cultured explants of villi from human first trimester placentae. These studies revealed a similar distribution pattern of the activity of the proteases of cryostat sections of first trimester placental villi and in cultured tissue of the same placentae. Dipeptidyl peptidase IV and angiotensinase A activity were present in cytotrophoblast cells and dipeptidyl peptidase IV activity was found in the syncytiotrophoblast, respectively. Additionally, the activity of the proteases was visualized in various populations of stromal cells. Comparing our results with former studies, the protease activity pattern in first trimester placentae was found to be the same as in term placentae. Despite morphological changes of the tissue after 14 d in culture the localization of the proteases remained unchanged up to 52 d of culture. The results suggest that placental explants may serve as a suitable in vitro model for experimental studies on the role of proteases in pregnancy-induced hypertension.
Aminopeptidases↗
Interferon alpha-2a and ciprofloxacin synergistically inhibit leukemic cell growth.
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Bone Marrow Cells↗