Biomedical subjects
Publications and source records attributed to T Lyberg.
Highly purified colony-stimulating factor-1 induced thromboplastin activity in murine macrophages and human monocytes in vitro. The activity increase was inhibited by cycloheximide and prevented by antibodies to CSF-1.
The estimated need for surgical correction of mandibular prognathism in Norway is 500 patients each year. A questionnaire sent to the maxillofacial surgical units performing orthognathic surgery in Norway showed that in the decade from 1975 to 1985 altogether 1169 patients underwent surgical correction of mandibular prognathism; that is, only 117 patients were treated yearly [corrected]. Extraoral vertical subcondylar osteotomy of the mandibular ramus was the preferred surgical technique, performed on 57% of the patients. Intraoral vertical subcondylar osteotomy of the ramus increased in use and thus seems to be taking over for the extraoral technique. Sagittal split osteotomy was used on 25% of the patients. The different units showed great variation in their preference for the different surgical techniques. Preoperative orthodontics was widely used, on a mean of 77% of the patients. The average hospital stay was 8.5 days, somewhat longer than reported from other countries; however, geographical conditions should be taken into consideration.
The geographical distribution of 1169 Norwegian patients operated on for mandibular prognathism during the years 1975-1984 showed an accumulation of cases in the western and northern parts of the country. This skew distribution was probably due to genetic factors. No association was found between the number of operated patients and the number of orthodontists or oral and maxillofacial surgeons in the different counties. Most of the patients (69%) had less than 2 years and 10% had more than 4 years of preoperative orthodontic treatment. The use of presurgical orthodontics seemed to increase during the observation period, and the mean treatment time was shorter in the last half of the decade. The morbidity, defined as the duration of the hospital stay and the intermaxillary fixation period, was on an average 56 days, mostly dependent on the surgical unit.
The use of preformed vitallium TMJ-prosthesis in combination with a microvascular iliac bone graft is an alternative method for hemimandibular reconstruction. It has several advantages compared with earlier described methods, and we have used it successfully in two cases.
The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic lung inflammatory diseases. Human lung alveolar macrophages (LAM) obtained by lavage of healthy donors can initiate the coagulation sequence by expressing procoagulant factors. The procoagulants of LAM were in this study identified to be either thromboplastin (tissue factor) or a direct factor X activator, probably a thromboplastin/factor VII complex. LAM did not show inducible thromboplastin synthesis as did monocytes when stimulated in vitro. LAM were separated into four subpopulations by density gradient centrifugation. The specific thromboplastin activity of subpopulation cells varied inversely with their density. Low-density subpopulations of LAM released microvesicles from their surface which could be recovered in the culture medium, and which expressed procoagulant activities with the same characteristics as the LAM procoagulants. These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface contribute to local fibrin deposition in the lungs by expressing procoagulant factors.
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In a double-blind study the efficacy and tolerability of tizanidine was compared with those of carbamazepine in the management of trigeminal neuralgia. Six patients were allocated to treatment with tizanidine and six to carbamazepine. After individual titration the maximum daily doses were 18 mg and 900 mg, respectively. Among the efficacy factors used, the visual analog scale (VAS) and the overall efficacy as assessed by patients and investigator turned out to be the most appropriate. The results indicate that tizanidine was well tolerated, but the effects, if any, were inferior to those of carbamazepine.
In 52 patients with oral lichen planus topographically related to amalgam restorations, the fillings were replaced by other materials in 18, 16 of whom experienced complete remission of the lesions within 1-12 months. These results are discussed in relation to the results of epicutaneous patch tests for possible allergy to a number of mercury compounds. The term "oral lichenoid reaction", is suggested to describe these lesions.
Cultured human umbilical vein endothelial cells responded to thrombin (10(-2) - 10 NIH u/ml) with a 2-5 fold increase in thromboplastin activity. The maximum response was reached after 4 hr in serum-free medium. The effect of thrombin was fully inhibited by the presence of 50% (v/v) fetal calf serum or more in the medium, by preincubation of thrombin with hirudin or by treatment of thrombin with N-bromosuccinimide or phenylmethylsulfonyl fluoride. The thrombin-induced thromboplastin activity was inhibited by incubation of the cells with cycloheximide (2 micrograms/ml) or actinomycin D (2 micrograms/ml) showing that the response depended on de novo protein and RNA synthesis. It was also suppressed by exposure of the cells to two different phosphodiesterase inhibitors, 3-butyl-1-methyl-xanthine (5 X 10(-4) M) and rac-4 (3-butoxy-4-methoxybenzyl)-2-imidazole (5 X 10(-4) M), to the transmethylation inhibitors 3-deazaadenosine (10(-5) M) and 1-homocysteine thiolactone (2 X 10(-5) M) in combination and to the intracellular calcium antagonist 8-(N,N-diethylamino)-octyl 3,4,5,-tri-methoxybenzoate hydrochloride (8 X 10(-5) M). Our results suggest that small amounts of thrombin can induce thromboplastin synthesis in endothelial cells in vitro and that this synthesis probably is regulated by the intracellular level of cAMP, by cytoplasmic Ca2+ and possibly also by transmethylation reactions.
The effects of autologous serum on basal and isoproterenol (IPR) or prostaglandin E1 (PGE1) stimulated adenosine 3',5' cyclic monophosphate (cAMP) levels were investigated in human lymphocytes. For all blood donors, serum (25% (v/v)) lowered the basal cAMP content. In contrast, the responsiveness of the lymphocyte cAMP accumulation to (-)-IPR was increased. This effect was most clearly demonstrable in bicarbonate buffered incubation medium (40-50% increase of maximal response), but was also seen in phosphate buffered medium (10-20% increase). Serum did not alter the sensitivity of the lymphocytes to IPR. The response to PGE1, which was a considerable more effective stimulator of cAMP accumulation than IPR, was not affected in any consistent way by serum. The results indicate that serum influences the regulation of lymphocyte cAMP and that this effect may partly be exerted at the level of the beta-adrenoceptors.
Confluent monolayers of human umbilical vein endothelial cells in culture responded with a 5-fold increase in thromboplastin (tissue factor) synthesis when exposed to 12-O-tetradecanoyl-phorbol-13-acetate (TPA) (50 ng/ml) or endotoxin (ETX) (25 micrograms/ml) for 16 hr. This induced thromboplastin synthesis was markedly inhibited by exposure of the cells to two different phosphodiesterase inhibitors, methylisobutylxanthine (MIX) and rac-4(3-butoxy-4-methoxybenzyl)-2-imidazole idinone (RO-20-1724) and to the transmethylation inhibitors 3-deazaadenosine (DZA) and 1-homocysteine thiolactone (Hcy) in combination. It was slightly (TPA) or not at all (ETX) inhibited upon exposure of the cells to the intracellular calcium antagonist 8-(N,N-diethylamino)-octyl 3,4, 5-trimethoxybenzoate hydrochloride (TMB-8). However, in the presence of MIX TMB-8 had a moderate additional inhibitory effect on TPA-induced thromboplastin response. The thromboplastin response of endothelial cells in vitro thus probably depends on transmethylation events for its full expression. It is also strongly modulated by the intracellular level of cAMP.
Thromboplastin production in human monocytes gains steadily increasing significance as a pathogenetic factor in relation to human disease. A vast variety of stimuli can cause the induction of thromboplastin synthesis in monocytes, apparently through plasma membrane perturbation. Some of the possible signal compounds conveying information from the membrane to the intracellular-responding apparatus have been studied. Available data allow the conclusion that changes in intracellular concentrations of Ca2+, cyclic nucleotides and arachidonic acid metabolites as well as transmethylation reactions are of importance and modulate the integrated response which leads to increased synthesis and insertion of apoprotein III (the protein component of thromboplastin) in the plasma membrane.
The importance of the blood coagulation sequence as an integral part in the pathogenesis of diseases inside as well as outside the blood vessels is becoming increasingly apparent. Mononuclear phagocytes have important functions in initiation of coagulation by producing several procoagulant substances, including thromboplastin, the potent trigger of the extrinsic pathway. Increasing evidence demonstrates the clinical importance of monocyte and macrophage thromboplastin synthesis in the pathogenesis of a variety of diseases. This review surveys the role of monocyte/macrophage thromboplastin in relation to inflammatory diseases, cancer, disseminated intravascular coagulation and diseases of the blood vessels, thrombosis and atherosclerosis.
Human monocytes in vitro respond to various agents (immune complexes, lectins, endotoxin, the divalent ionophore A 23187, 12-O-tetradecanoyl-phorbol 13-acetate [TPA], purified protein derivative [PPD] of Bacille Calmette-Guerin) with an increased synthesis of the protein component of thromboplastin. The effect of cyclic AMP and cyclic GMP on this response has been studied. Dibutyryl-cyclic AMP, prostaglandin E1 and the phosphodiesterase inhibitors 3-butyl-1-methyl-xanthine (MIX) and rac-4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (Ro 20-1724), separately and in combination have a pronounced inhibitory effect on the response to immune complexes and PPD, and a moderate effect on the response to endotoxin and lectins. The effect on TPA response and on the response to A 23187 was slight. Dibutyryl-cyclic GMP (1 mM) gave a slight inhibition of the TPA and IC response, but had essentially no effect on the response to other inducers. The intracellular cAMP level increased when monocytes were incubated with IC, TPA or A 23187 followed by a decrease to basal levels within 1-2 hr, whereas lectin (PHA) and PPD did not induce such changes. The cAMP response to endotoxin varied. Stimulation with IC induced an increase in monocyte cGMP levels, whereas the other stimulants did not cause such changes.
Human umbilical vein endothelial cells in culture synthesize thromboplastin upon stimulation with phytohaemagglutinin (PHA) or the tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (TPA). The thromboplastin activity is further strongly enhanced in a time dependent reaction by the presence of gel-filtered platelets or platelet aggregates. This effect was demonstrable at platelet concentrations lower than those normally found in plasma, it may thus be of pathophysiological relevance. The thromboplastin activity increased with increasing number of platelets added. Cycloheximide inhibited the increase, suggesting that de novo synthesis of the protein component of thromboplastin, apoprotein III, is necessary. When care was taken to remove monocytes no thromboplastin activity and no apoprotein III antigen could be demonstrated in suspensions of gel-filtered platelets, platelets aggregated with thrombin or homogenized platelets when studied with a coagulation assay and an antibody neutralization technique.