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Biomedical subjects

T Eller

Publications and source records attributed to T Eller.

17 recordsLinked to original sources
PubMed1993

Tumor necrosis factor alpha (TNF alpha) and transforming growth factor beta 1 (TGF beta 1) stimulate fibronectin synthesis and the transdifferentiation of fat-storing cells in the rat liver into myofibroblasts.

Transforming growth factor-beta (TGF beta 1) and tumor necrosis factor alpha (TNF alpha) stimulate the transdifferentiation of fat-storing cells (FSC) in the rat liver into highly active and "synthetic" myofibroblast-like cells (MFBIC). This activation has been documented by differential-interference contrast and light microscopy using morphologic criteria (a reduction in the number and size of fat droplets, cell flattening and the development of long cytoplasmic extensions), by the loss of retinyl-palmitate (measured by HPLC) and by the enhanced expression of iso-alpha smooth muscle actin (demonstrated by immunofluorescence microscopy). Furthermore, while cell growth measured by the cell count and DNA content is slightly inhibited by TGF beta 1 (0.81 of the control), the combination of TGF beta 1 with TNF alpha stimulates cell proliferation to 1.44 times of the control. In addition the combination of TGF beta and TNF alpha potentiated the stimulatory effect on fibronectin synthesis (TGF beta alone: 1.4 times control; TNF alpha alone: 2.2 times control; TGF beta plus TNF alpha: 4.7 times control). The total protein synthesis was not altered by TGF beta or TNF alpha. In summary the results obtained identify TGF beta and TNF alpha as mediators stimulating key events in liver fibrogenesis (i.e. FSC proliferation, FSC transdifferentiation into MFBIC, and fibronectin synthesis).

Adipose Tissue↗
PubMed1992

Significance and quantitative analysis of von Willebrand factor in human platelets.

The von Willebrand factor (vWF) is found in plasma and in platelets. The concentration and multimeric composition of the vWF in platelets of 160 patients with bleeding tendency were examined since very little is known about the platelet vWF. For quantitative analysis of the platelet vWF, a modified ELISA was established. A reference range from 70%-130% of platelet vWF concentration considered normal was established by examining 80 healthy blood donors. 16.9% of the 160 patients showed a decreased vWF concentration in platelets only, while all the other coagulation parameters were normal. 3 of our patients belong to the same family and suggesting an autosomal dominant genetic transmission for the von Willebrand disease type 1-3. The data also suggests, that a quantitative and qualitative analysis of the vWF in plasma and platelets is required for an exact diagnosis of the von Willebrand disease.

Blood Donors↗
PubMed1992

Effects of long-term treatment with lovastatin on the clotting system and blood platelets.

In a study of 20 patients with hypercholesterolemia (type IIa) the effects of lovastatin (20-80 mg/day) on various clotting and thrombosis parameters were monitored for 12 months. On 11 occasions various cholesterol fractions and clotting parameters were determined in each patient. In addition, the clotting inhibitors AT III, protein C, protein S, and C1-esterase inhibitor and the fibrinolysis parameters plasminogen and alpha 2-antiplasmin were examined. Platelet function was monitored on the basis of spontaneous and induced (collagen, ADP, epinephrine, ristocetin) aggregation. Lovastatin in the above dosage brought about a 66 mg/dl (from 320 +/- 12.6 to 254 +/- 12.0 mg/dl) reduction in the total cholesterol level and a 56 mg/dl (from 244 +/- 11.4 to 188 +/- 12.1 mg/dl) reduction in LDL cholesterol at the end of the study. Fibrinogen showed a significance decrease during the study period, whereas PT and aPTT remained unaffected. The initial slopes of the ADP-induced platelet aggregation revealed a significant decrease. C-reactive protein and platelet count remained within the normal range, indicating no significant change. Thrombin clotting time, AT III, C1-esterase inhibitor, plasminogen, and alpha 2-antiplasmin were not modified. Protein C and S behaved in a contradictory way, but remained within the normal range. Long-term treatment with lovastatin was associated with a significant reduction of fibrinogen levels and platelet aggregation induced by ADP in type-IIa hypercholesterolemic patients. These alterations, as well as their role in cardiovascular disease, should be the subject of further investigations.

Adolescent↗
PubMed1992

[Diagnostic strategies for detection of the von Willebrand syndrome].

The von Willebrand disease (vWD) is the most severe coagulopathy. Because of the complex biochemical structure of the von Willebrand factor (vWF), a great number of types and subtypes of the vWD were found. A screening of vWD can only be done by examining the bleeding time, the ristocetin cofactor activity (risto) and by an immunological determination of the vWF concentration. Examinations of 200 patients with a bleeding tendency showed that the ratio vWF/risto < 0.7 indicates a high probability for an abnormal multimeric structure of vWF. The exact determination of the vWD subtype then has to be done by a SDS-agarose gel electrophoresis. In 16.8% of our patients we found a decreased vWF concentration in the platelets. These patients showed normal plasmatic coagulation factors, but a bleeding tendency and a prolonged bleeding time. For diagnosis of vWD the bleeding time, immunological determination of the vWF and the risto should be done first. If a ratio vWF/risto < 0.7 or a prolonged bleeding time with a bleeding tendency is found, the separation of the vWF multimers into plasma and platelets and the determination of the vWF concentration in platelets should be carried out for an exact diagnosis of vWD.

Blood Coagulation Tests↗
PubMed1986

Technique of experimental aneurysm formation in the rat common carotid artery using the milliwatt carbon dioxide laser and the adventitia patch model.

Aneurysms were induced in the rat common carotid artery by using the milliwatt carbon dioxide laser to weld an adventitia patch over a hole. This technique proved to be effective and reliable as demonstrated by the 100% incidence of aneurysm formation at the patch site in 28 rats killed 1 week or later after the procedure. It is suggested that this technique may be used to produce intracranial aneurysms in experimental animals due to the minimal vessel manipulation required.

Aneurysm↗
PubMed1985

A novel approach for the study of thromboxane A2 and prostaglandin H2 receptors using an 125I-labeled ligand.

Previous studies of eicosanoid receptors have utilized 3H-labeled ligands. However, 125I has a higher theoretical specific activity (approximately 2000 Ci/mmole) than 3H (29 Ci/mmole), which provides a potential advantage for 125I ligand binding studies when the receptor density is low. Since eicosanoids do not possess an easily iodinatable structure (e.g. a phenol or imidazole ring), it is not feasible to directly incorporate 125I into the molecule. The thromboxane A2/prostaglandin H2 receptor antagonist, cis-7-(2-p-hydroxyphenylethanolaminocyclopentyl)-heptanoic acid (cis-APO), was synthesized to test the concept that it could be labeled with 125I and used as a ligand for binding studies. cis-APO is a structural analog of 13-azaprostanoic acid, a TXA2/PGH2 antagonist [G. C. Le Breton, D. L. Venton, S. E. Enke and P. V. Halushka, Proc. natn. Acad. Sci. U.S.A. 76, 4097 (1979)], in which the omega aliphatic chain was substituted with 2-p-hydroxyphenylethanol, which contains a phenolic group. [127I]cis-APO was synthesized by insertion of 127I (stable isotope) into the phenolic portion of the molecule under alkaline conditions. [125I]-cis-APO was synthesized via insertion of 125I (unstable isotope) into the molecule in the presence of chloramine T. cis-APO inhibited human platelet aggregation induced by the thromboxane mimetic U46619 [C. Malmsten, Life Sci. 18, 169 (1976)]. The IC50 for cis-APO was 6.4 +/- 0.7 microM and for [127I]-cis-APO was 9.8 +/- 1.3 microM (P less than 0.001). [125I]-cis-APO binding to a human platelet membrane preparation at 4 degrees was time and protein concentration dependent, saturable, and reduced or abolished by trypsin or boiling respectively. The Kd for iodo-cis-APO determined at equilibrium using a Scatchard analysis was 1.48 microM and the maximum binding capacity was 18.7 pmoles/mg protein. The forward rate constant (k+1) was 2.3 X 10(3) M-1 s-1 and the dissociation constant (k-1) was 2.12 X 10(-3) s-1. The Kd determined from k-1/k+1 was 0.92 microM. These observations show that the omega side chain of eicosanoid analogs can be substituted with a phenolic group, iodinated, and retain biological activity. These molecules may then be utilized to study thromboxane A2 or prostaglandin H2 receptors.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1980

Ibuprofen improves survival from endotoxic shock in the rat.

During endotoxemia, there is a significant increase in arachidonic acid-derived metabolites. To test the hypothesis that one or more of these metabolites play a significant role in the pathogenesis of endotoxic shock we investigated the therapeutic efficacy of varying doses of ibuprofen, a cyclooxygenase inhibitor, on the pathophysiologic sequelae of endotoxic shock in the Long-Evans rat, induced by S. enteritidis endotoxin (20 mg/kg). Pretreatment with ibuprofen (1-3.75 mg/kg) produced an optimal survival rate of 80% compared to only 11% in the vehicle-treated group. Doses of 0.1, 0.5 and 30 mg/kg of ibuprofen also significantly (P < .05) improved survival over nontreated shocked controls. Plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha(PGF1 alpha) levels rose from < 200 pg/ml to 2207 +/- 282 (N = 16) and 840 +/- 59 (N = 8), respectively, within 30 min after injection. The rise in plasma thromboxane B2 and 6-keto-PGF1 alpha levels was reduced with ibuprofen (3.75 and 30 mg/kg) to < 200 pg/ml. Ibuprofen (3.75 and 30 mg/kg) reduced thrombin-induced in vitro platelet thromboxane B2 synthesis by 95 and 99%, respectively. The severity of coagulopathies as reflected by elevations in serum fibrogen/fibrin degradation products and lysosomal integrity were likewise significantly reduced (40%) with ibuprofen (3.75 mg/kg) pretreatment. These results are consistent with the hypothesis that arachidonic acid metabolites play a significant early role in the pathogenesis of endotoxic shock. Our observations suggest potential benefits from agents which inhibit fatty acid cyclooxygenase.

Acid Phosphatase↗
PubMed1976

Afferents to the cerebellar lateral nucleus. Evidence from retrograde transport of horseradish peroxidase after pressure injections through micropipettes.

HRP was injected by pressure from glass capillary micropipettes unilaterally into the lateral nucleus of rat so as to encompass the entire nucleus, but without spread into the interpositus nuclei. The cells of origin of the afferents to the lateral nucleus were studied after retrograde transport of the HRP. The reticulotegmental nucleus of the pons was labelled bilaterally and is the major source of crossed and uncrossed reticular imputs. The pontine nuclei also provide extensive crossed and uncrossed afferents. The inferior olive gives a large crossed olivo-lateral nucleus projection and a minor uncrossed input. The trigeminal nuclear complex--the nucleus of the spinal tract and the mesencephalic, principal sensory, and motor nuclei--all provide uncrossed afferents. The rostral portion of the lateral reticular nucleus gives a small crossed and uncrossed projection while the perihypoglossal nuclei and the dorsal parabrachial body give crossed afferents to the lateral nucleus. The norepinephrine afferent system from the locus coeruleus is represented by one or two heavily labelled cells and the serotonin raphe systems come from at least five raphe subgroups, the dorsal, superior centralis, pontis, obscurus and magnus nuclei. No evidence was found for commissural fibers between ipsilateral or contralateral cerebellar nuclei, or afferent axons from the spinocerebellar nuclei and the paramedian retricular nucleus. The significance of these sources of afferent imputs to the lateral cerebellar nucleus is discussed. The question is raised of the direct relationship between size of terminal axonal arborization and the quantity of HRP granules present in a cell retrograde transport. The limitations of the HRP method for detecting subtle local differences in the distribution of afferents within the heterogeneous groups of neurons in the lateral nucleus are discussed.

Animals↗
PubMed1976

Hemangiomas of the internal auditory canal.

Three patients who presented with symptoms and signs of acoustic tumors are described: one of them had an arteriovenous malformation and the other two had cavernous hemangiomas. The common feature in all these patients was the presence of marked facial weakness with or without fasciculations and a complete loss of hearing in the presence of a small tumor. The cerebrospinal fluid protein was normal in these patients. Polytomography and Pantopaque cisternograms were used to make the diagnosis. Since these lesions are circumscribed, they are suitable for removal using microneurosurgical techniques.

Adult↗
PubMedDate not supplied

Protective effects of trans-13-APT, a thromboxane receptor antagonist, in endotoxemia.

The effect of the thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptor antagonist trans-7[2-(p-hydroxyphenethylamino)-cyclopentyl]-heptanoic acid (trans-13-APT) on certain pathogenic sequelae of endotoxic shock and associated changes in arachidonic acid metabolism in the rat was investigated. trans-13-APT, an analog of 13-azaprostanoic acid, was synthesized and found to block human platelet aggregation induced by the thromboxane mimetic U46619. Pretreatment with trans-13-APT did not significantly alter the elevations in plasma immunoreactive (i) TxB2 or iPGE, 0.5 or 4 h after the intravenous administration of Salmonella enteritidis endotoxin. However, in the trans-13-APT-pretreated group, 4 h after administration of the endotoxin, plasma i6-keto-PGF1 alpha was significantly (p less than 0.05) reduced to 1.2 +/- 0.3 ng/ml (n = 17) compared with vehicle-treated rats (2.4 +/- 0.5 ng/ml; n = 18). The elevation in plasma i6-keto-PGF1 alpha seen 0.5 h (n = 17/group) after endotoxin infusion was not altered by trans-13-APT. trans-13-APT also significantly (p less than 0.05) attenuated the endotoxin-induced fall in platelet count (135 +/- 27 X 10(3)/mm3 vs. 350 +/- 65 X 10(3)/mm3 and hypoglycemia (73 +/- 9 vs. 97 +/- 7 mg/dl), but not the leukopenia. Since the reticuloendothelial system may be an important source of iTxB2 and i6-keto-PGF1 alpha during endotoxemia, in vitro studies were conducted with adherent peritoneal cells. High concentrations of trans-13-APT (50 and 100 microM) significantly reduced (p less than 0.05) basal but not endotoxin-induced synthesis of iTxB2 and i6-keto-PGF1 alpha by isolated adherent rat peritoneal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗