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Biomedical subjects

H Engler

Publications and source records attributed to H Engler.

At least 55 records · Page 3Linked to original sources
PubMed1988

[Study of the long-term effects of amiodarone on thyroid function using ultrasensitive TSH measurements. Preliminary report].

The results of a prospective study of basal ultrasensitive TSH concentrations in patients during long-term treatment over 12 months with amiodarone are reported. 2 patients (3%) developed hypothyroidism, whereas no case of hyperthyroidism was observed. A significant increase in FT4 with a simultaneous decrease in T3 was demonstrated at every periodic investigation during amiodarone therapy. In most patients ultrasensitive TSH values stayed within the normal range and showed no significant alteration during treatment. A slow decline in TSH during therapy was observed in a subgroup of patients with completely euthyroid initial TSH concentrations. This TSH decrease reached statistical significance after 12 months' therapy. FT4 showed pathological results in 35% of all determinations at any time during the study, T3 in 27%, and TSH in only 17%. In conclusion, a new steady-state of thyroid tests is attained during treatment with amiodarone and most patients maintain a euthyroid function state. Assessment of ultrasensitive TSH can be recommended as a primary screening test for evaluation of thyroid function in patients under amiodarone therapy.

Amiodarone↗
PubMed1988

Coronary thrombolysis in man with pro-urokinase: improved efficacy with low dose urokinase.

Single-chain urokinase-type plasminogen activator (scu-PA), was given to 20 patients with acute myocardial infarction first alone (group I; n = 9) and then in combination with an initial bolus injection of 200,000 units of urokinase (group II; n = 11). In group I, scu-PA was administered in a dose of 15 mg up to 60 mg as an infusion over one hour. Complete reperfusion was achieved in 3/9 patients after 50 to 60 min and partial reperfusion in an additional 2 patients. In group II, a bolus injection of urokinase and 48 mg of scu-PA over one hour were given. Reperfusion was achieved in 9/11 patients after a mean of 30 +/- 22 min. Fibrinogen, alpha 2-anti-plasmin and plasminogen levels did not change from baseline in group I. In group II, fibrinogen levels decreased slightly from 272 +/- 84 mg% to 178 +/- 82 mg% (p less than 0.05) after two hours. No bleeding complications were encountered. Reocclusion at 24 hours was evaluated in 18 patients and was not seen. It was concluded that an initial bolus of urokinase improves the efficacy and the rate of thrombolysis by scu-PA.

Adult↗
PubMed1987

2-[(3-Pyridinylmethyl)thio]pyrimidine derivatives: new bronchosecretolytic agents.

2-[(3-Pyridinylmethyl)thio]pyrimidine derivatives (1a-n) promote the excretion of phenol red into the mouse trachea, indicating an increased tracheobronchial secretion. Furthermore, 2-[(3-pyridinylmethyl)thio]pyrimidine (1a) (tasuldine) produces greater excretion of phenol red into the mouse trachea after systemic administration than the known bronchosecretolytic ambroxol. Compound 1a also reduces the viscosity of canine bronchial mucus. Compound 1a has been selected for clinical investigations.

Animals↗
PubMed1986

Successful therapy of sarcoidosis-associated thrombocytopenia refractory to corticosteroids by a single course of human gammaglobulins.

Thrombocytopenia developed in a 21-year-old patient with sarcoidosis when corticosteroid therapy was discontinued. Platelet-associated IgGs were elevated. High-dose cortisone did not affect the thrombocytopenia. However, platelet counts remained normal for more than 1.5 years following intravenous treatment with a single course of human gammaglobulins.

Adult↗
PubMed1986

Aluminium hydroxide inhibits acetylsalicylic acid-induced gastric erosions in cats with Heidenhain-pouch.

The effect of Al(OH)3 was investigated on the gastric bleeding induced by acetylsalicylic acid + HCl. Cats provided with Heidenhain pouches were used. The pouch had vascular connections to the main stomach. Instillation of acidified acetylsalicylic acid into the pouch caused a marked increase in its blood content indicating the development of hemorrhagic mucosal damages. The blood loss was totally abolished by administration of Al(OH)3 into the main stomach. We, therefore, conclude that Al(OH)3 induced an enhanced release of PGE2 into the submucosa. PGE2 reached the pouch via connecting vessels originated from the main stomach. The results indicate that certain antacids induce the release of prostaglandins not only into the gastric lumen but also in the submucosa.

Aluminum Hydroxide↗
PubMed1986

Cytoprotective role of gastric surfactant in the ethanol-produced gastric mucosal injury of the rat.

The role of the gastric nonwettable hydrophobic layer (surfactant) was investigated in the mucosal protection against the damage induced by ethanol in the rat. Although aluminium hydroxide inhibited the development of ethanol-produced gastric hemorrhagic lesions, it did not increase the mucosal phospholipid content. Ambroxol, a known stimulant of pulmonary surfactant production, protected the gastric mucosa against ethanol by increasing the phospholipid content. Surface-active compounds such as dimethyl polysiloxane also inhibited the development of gastric injuries caused by ethanol in a dose-dependent manner. The essential phospholipid-containing drug (Essentiale) also showed a strong and dose-dependent cytoprotective effect. Among the possible constituents of the gastric surfactant, sphingomyelin was totally ineffective. Phosphatidylcholine, phosphatidylinositol and phosphatidylglycerol were able to reduce the extent of mucosal damage in a dose-dependent manner. Gastric mucosal injuries were significantly aggravated by pretreatment with phospholipase C. In conclusion, these results suggest that either the maintenance or the strengthening or even the replacement of the gastric nonwettable hydrophobic lining between the damaging agent and the gastric mucosa may contribute to the cytoprotective mechanism of certain compounds.

Aluminum Hydroxide↗
PubMed1985

Iodine content and density of thyroglobulin investigated by isopycnic centrifugation.

The density of in vitro iodinated thyroglobulin (Tgb) molecules, measured by isopycnic centrifugation, increases linearly with their iodine content. In contrast, the iodine to density (I:D) regression for differently iodinated native rat Tgbs is not constant but varies, depending on experimental conditions: For LID-fed rats the slope of the individual I:D regression line of each Tgb decreases linearly with the decreasing mean degree of iodination of the sample (r = 0.9104, P less than 0.01). On the other hand, in Tgb samples synthesized by propylthiouracil-blocked glands, the I:D regression is no longer linear. Rather, a bimodal pattern is obtained revealing a preexisting highly iodinated Tgb pool together with newly synthesized, non-iodinated protein. The results indicate: (a) the mean degree of iodination of a native Tgb cannot be estimated accurately if only its mean density is known, and (b) the degree of heterogeneity of iodination is identical for any in vivo produced Tgb sample with the same iodine content.

Animals↗
PubMed1985

Injection of anti-thy-1.2 serum breaks genetic resistance of mice against herpes simplex virus.

Nude mice have been shown to be as resistant to intraperitoneal infection with herpes simplex virus type 1 (HSV) as their heterozygous littermates. Here we document that both activation of natural killer (NK) cells and interferon induction were normal in nu/nu mice after injection of HSV. Injection of silica caused increased mortality by HSV in C57BL/6 mice. Silica, in addition, led to a significant reduction of NK cell activity but had no effect on the interferon response. Treatment of C57BL/6 mice with anti-asialo GM1 (an antiserum with a predominant effect on NK cells) caused complete abolition of the NK cell response, but had no effect on interferon induction or virus-induced mortality. In further studies a monoclonal anti-thy-1.2 antibody was utilized which possessed high activity in vivo in depleting T cell responses in mice. Injection of anti-thy-1.2 decreased NK cell activation but was without effect on the interferon response. Unexpectedly, in view of the data in nu/nu mice, this antibody increased HSV-induced mortality in C57BL/6 mice. Similar data were obtained when anti-thy-1.2 was injected into nu/nu mice. Our results are compatible with the hypothesis that T cell precursors sensitive to anti-thy-1.2 present in homozygous nude mice play a role in resistance against HSV. Furthermore, the data in the euthymic mice may indicate a role of T cells in the primary resistance of mice against HSV.

Animals↗
PubMed1985

Effects of anti-inflammatory drugs on rat paw oedema and leukocyte migration.

High doses of cyclooxygenase inhibitors (e.g. indomethacin) reduce the leukocyte accumulation in the carrageenin soaked sponges. They are, however, inactive in bradykinin-induced oedema and in the reversed passive Arthus reaction (RPA). A potent cyclooxygenase and lipoxygenase inhibitor, BW 755C, was equally active in the bradykinin-induced oedema, leukocyte migration and in the RPA. Consequently these methods may help to differentiate anti-inflammatory drugs which act via cyclooxygenase or lipoxygenase pathways in vivo.

Animals↗
PubMed1984

[Immune complexes in the serum of patients with acute myeloblastic leukemia].

This study was performed to determine whether the nature of the hemolytic factor present in 54% of sera collected from patients during the active stage of acute myeloid leukemia (AML) [1] is immune complex (IC)-like. The fluid phase C1q-binding test (C1q-BT) served to analyze 92 sera from 24 patients with AML. In a first study the C1q-BT as modified by Carpentier [2] was compared to the universally accepted C1q-BT as described by Zubler [3]. Binding of C1q to heat aggregated human IgG, to tetanus toxoid (Te)/anti-Te complexes, and to serum containing heparin or fibrinogen was to a similar extent concentration-dependent; however, the binding values obtained with the method of Carpentier were always higher than with the method of Zubler. The same was found for the binding of C1q to sera from patients suffering from various diseases: using Carpentier's method approximately a 20% higher C1q-binding activity was found for all samples compared to binding activities found with Zubler's original method. The higher C1q binding did not depend on higher sensitivity of Carpentier's assay system, as the binding to sera from 60 healthy individuals was also elevated (8.1 +/- 6.0% vs 1.2 +/- 1.0% with the method of ZUBLER). In a second study AML sera were analyzed by the "extended" C1q-BT [4]. The "extended" C1q-BT uses two different C1q preparations and the assay follows the procedure described by ZUBLER. This test is able to detect immune-aggregate-mediated and non-immune-aggregate-mediated C1q binding.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigen-Antibody Complex↗
PubMed1984

Tracheal phenol red secretion, a new method for screening mucosecretolytic compounds.

A simple method for screening drugs that influence tracheobronchial secretion has been described. After i.p. application of a phenol red solution, part of the dye is secreted into the tracheal lumen. This basal secretion is increased by both parasympathomimetics and sympathomimetics. In addition, expectorants are also capable of increasing tracheal phenol red output. Therefore this method is suitable for the study of drugs that may be capable of influencing tracheobronchial secretion.

2-Hydroxyphenethylamine↗
PubMed1984

[Ulcer-protective effect of cimetidine and an antacid. Animal experiment study on an ulcer model with protracted histamine liberation].

The ulcer-protective effect of cimetidine has been compared with that of an antacid (Solugastril) containing aluminium hydroxide and calcium carbonate. Ulcers have been produced by using dialysis sacks containing histamine. This model corresponds to stress ulcers observed in risk patients. Both cimetidine and the antacid were capable of inhibiting the ulcer development in corresponding doses and applications: The present results show that an antacid might be qualified for the treatment of stress ulcers in the human therapy.

Animals↗
PubMed1983

Evidence for a functional cytoprotective effect produced by antacids in the rat stomach.

The fall in potential difference evoked by taurocholate was diminished after exposure of the gastric mucosa of rats to aluminium-containing antacids. Other parameters of barrier disruption (H+ back diffusion, Na+ influx) exhibited the same pattern and correlated with the change in potential difference. This cytoprotective-like effect was abolished in animals pretreated with indomethacin. Taurocholate significantly diminished the PGE2 content in the gastric mucosa and its release into the instillate. The PGE2 content of gastric mucosa and instillate of animals pretreated with an aluminium-containing antacid was not decreased after exposure to taurocholate.

Animals↗
PubMed1983

Prostaglandin content in the rat gastric mucosa during healing of chronic ulcers induced by acetic acid.

Non-steroidal anti-inflammatory compounds delayed the regeneration of chronic gastric ulcers induced by acetic acid in the rat. The delayed regeneration was connected with a decreased PGE2 content in the proliferating tissue. Glucocorticoid influenced neither the regeneration of mucosal damages nor the gastric PGE2 content. The carboanhydrase inhibitor, acetazolamide, also did not alter the restoration of gastric mucosa after being damaged. From the clinical point of view, the safe use of NOSAC will be emphasized in patients with ulcer anamnese. The findings with prednisolone did not confirm a similar safe use of this drug in patients.

Acetates↗
PubMed1983

Herpes simplex virus - induced interferon production and activation of natural killer cells in SM/J mice. Relation to antiviral resistance.

We have studied the susceptibility of SM/J mice to intraperitoneal (i.p.) infection with herpes simplex virus type 1 (HSV) and have searched for correlations of susceptibility with the activation of Natural Killer (NK) cells and with local induction of interferon. SM/J were exceedingly susceptible to virus infection as they could be killed by less than 10 plaque forming units (PFU). The NK cell system of these mice, as measured by the activity of spleen cells against YAC-1 lymphoma cells, was hyperreactive, which is in agreement with previous findings of others. The peritoneal exudate cells (PEC) of uninfected mice had no activity. However, 18 h after i.p. injection of HSV NK cell activity was detected in the PEC population, which was at least as high as that in C57BL/6 mice that are resistant to HSV infection. Thus it appears as if the NK cell system does not play a major role in antiviral resistance in our experimental system. In contrast, from our previous work it would rather appear that the magnitude of the early local interferon response is important for resistance. The current data obtained in SM/J mice are in accordance with this, in that these highly susceptible mice are deficient in their early interferon response. Homozygous beige mice were found to be as resistant to infection with HSV as C57BL/6 mice. While the NK cell activity in their PEC population after injection of HSV was low, the titers of locally induced interferon were as high as those in the controls.

Animals↗
PubMed1983

Herpes simplex virus type 1-induced interferon production and activation of natural killer cells in mice.

Cultures of peritoneal exudate cells (PEC) of non-immune C57BL/6 mice reacted to infectious herpes simplex virus type 1 (HSV), but not to non-infectious virions by producing interferon. Similarly, when the virus preparations were injected intraperitoneally (i.p.) and interferon was determined in the wash-out fluid, interferon could only be detected after injection of infectious HSV. All interferons were mixtures of interferon-alpha and -beta. The cell that produced interferon was not sensitive to anti-theta serum or anti-asialo-GM1 serum, it was retained on nylon wool columns and removed by plastic adherence. Silica treatment of PEC abolished HSV-induced interferon production whereas irradiation by 2000 R was without effect. Pure cultures of mouse T cells did not produce interferon when treated with infectious HSV whereas pure cultures of mouse bone marrow macrophages did produce interferon. Thus, we suggest that in PEC the cells which produced interferon were of the macrophage lineage. In further experiments we have analysed in vivo activation of natural killer (NK) cells in the peritoneal cavity of mice. Non-infectious virions were as effective as infectious HSV and doses of HSV too low to induce measurable titres of interferon caused a marked activation of NK cells.

Animals↗
PubMed1983

Reversible and irreversible inhibition of thyroid peroxidase-catalyzed iodination by thioureylene drugs.

The mechanism of reversible and irreversible inhibition of thyroid peroxidase (TPO)-catalyzed iodination by thioureylene drugs was investigated using a model incubation system. The major observations may be summarized as follows. 1) TPO is inactivated by 1-methyl-2-mercaptoimidazole and propylthiouracil even in the presence of a relatively high concentration of iodide. The extent of this inactivation depends on the ratio of iodide to drug. 2) Spectral changes observed on oxidation of the drugs with the peroxidase-iodide system were very similar to those observed when the drugs were oxidized nonenzymatically with I3-. These findings support the view that oxidized iodine is an intermediate in TPO-catalyzed oxidation of the drugs. 3) Under conditions where TPO is largely inactivated, inhibition of iodination is complete and irreversible. Drug metabolism, on the other hand, occurs to a limited extent. 4) Under conditions where TPO is only partially inactivated, inhibition of iodination is transient (reversible). In this case, drug metabolism is extensive, and higher oxidation products (sulfate and sulfinic acid) are observed. Inhibition of iodination occurs only during the interval required to reduce the drug concentration to a low level. Thereafter, iodination may occur at a rate close to that observed in the absence of drug. Based on these and other observations, a scheme is presented to explain the mechanism of reversible and irreversible inhibition of iodination. In essence, the type of inhibition depends on the relative rates and extent of TPO inactivation and drug oxidation. These rates, in turn, depend primarily on the iodide to drug concentration ratio. A high ratio favors extensive drug oxidation and reversible inhibition. A low ratio favors TPO inactivation and irreversible inhibition.

Animals↗