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Biomedical subjects

R Ferlinz

Publications and source records attributed to R Ferlinz.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Does medical education change behavior, attitude and knowledge in relation to smoking? A survey of medical students in the 1st and next to last year of study].

Among the 831 students in the first and last-but-one year of medical studies, 21% were smokers, 4% occasional smokers, 63% non-smokers and 5% former smokers. There were no statistically significant difference in smoking habits between the first and fifth years of study. The different semesters did, however, reveal significant differences with respect to their evaluation of smoking as a health hazard, their knowledgability as to the causal effects of smoking in diverse diseases, the readiness of the doctors-to-be to counsel their patients to avoid smoking, self assessment of their knowledge about smoker counselling methods, their support for the ban on cigarette advertising, and further education in the field of smoker counselling. Significant difference were to be seen between smokers, former smokers and non-smokers with respect to their personal evaluation of their smoking habits over the next five years, the assessment of smoking as a hazard to health, and the subjective burdening of smoking, the question as to the example-setting and instructive role of the physician with respect to smoking, and the question of statutory measures affecting smoking.

Adult↗
PubMed1989

[Oxygen radical production of alveolar inflammatory cells in sarcoidosis and idiopathic lung fibrosis].

Interstitial lung diseases are characterised by chronic inflammatory processes in the lower respiratory tract, parenchymal cell injury and progressive fibrosis of the alveolar structure. Oxygen radicals are claimed to be a major cause of the tissue damage in the lung. We evaluated the spontaneous and stimulated oxygen radical release of bronchoalveolar lavage (BAL) cells in 35 patients with sarcoidosis and 17 patients with IPF. In comparison with the control in both diseases the spontaneous as well as the stimulated oxygen radical release of the BAL cells is markedly increased. In IPF alveolar macrophages produce the buk part of radicals (84%). Due to their low percentage and in spite of a higher activity on a per cell basis the contribution of neutrophils to the total radical burden is only marginal. In sarcoidosis there is a positive correlation between the oxygen radical release of AM and the CD4/CD8 ratio of BAL lymphocytes. Our results demonstrate that the clinical activity of sarcoidosis and IPF is reflected by the oxygen radical release of BAL cells.

Adult↗
PubMed1988

Replacement therapy for alpha-1-protease inhibitor deficiency in PiZ subjects with chronic obstructive lung disease.

In a six-month multicenter feasibility and safety study, 20 patients, who all had a congenital deficiency of alpha-1-protease inhibitor (A1PI) of the PiZ phenotype accompanied by a chronic obstructive lung disease, were treated with human-plasma-derived A1PI. A weekly dose of 60 mg/kg, administered intravenously, was shown to be sufficient to maintain patient serum levels above the threshold limit of 35 percent, the serum level of healthy persons of the MZ phenotype. This is supposed to be the minimal effective level for protection against the elastolytic attack of the lung and, therefore, satisfies one of the most important criteria of feasibility of long-term replacement therapy. The global concentration in serum or bronchiolar lavage fluid A1PI including active and inactivated A1PI was measured immunologically by rate nephelometry and radial immunodiffusion. The functional activity of A1PI, expressed as free inhibitor activity against trypsin and leukocyte elastase, confirmed that the infused A1PI remained mostly in its active form in the circulation. Reported adverse reactions were moderate and did not require alteration to the schedule of the infusions and/or the dose and rate of administration. Antibodies to A1PI as measured by the Ouchterlony method did not develop. Laboratory and physical signs of possible hepatitis virus contamination were not observed. The long-term replacement therapy, therefore, appears to be safe.

Adult↗
PubMed1988

[Substitution therapy with alpha-1-Pi in patients with alpha-1-Pi deficiency and progressive pulmonary edema].

In a multi-centre study 20 patients with severe congenital alpha-1-Pi deficiency and progressive pulmonary emphysema received infusions of alpha-1-Pi concentrate from human plasma once weekly for six months, at an initial dosage of 60 mg/kg body-weight, in some instances slightly increased to achieve a minimum serum level above 70 mg/100 ml. The immunologically measured serum level of alpha-1-Pi rose 30 min after start of the infusion by a mean of 130% of normal, at an initial level of 13%. An exponential fall followed this rise. The lowest level occurred at the end of the first week, immediately before the next infusion, to 35% of normal, a serum level which is assumed still to provide an effective protection against elastases in the lung. There was also a definite increase of free inhibitors against both trypsin and leucocyte-elastase in serum of all patients, with a minimal level which for both was many times that of the initial value. There were no side-effects in more than 500 infusions and no dose reduction was necessary. During the entire course there were no significant changes in haematological, coagulation and biochemical test results, and lung function means remained constant. No antibodies against alpha-1-Pi were demonstrated, nor transmission of hepatitis B.

Clinical Trials as Topic↗
PubMed1987

A macrophage-suppressing 40-kD protein in a case of pulmonary alveolar proteinosis.

Pulmonary alveolar proteinosis (PAP) is a rare disease of unknown etiology. Macrophage dysfunctions are claimed to be involved in the pathogenesis. We investigated phagocytosis and oxidative metabolism of alveolar macrophages in a case of pulmonary alveolar proteinosis. These cells phagocytize normally and phagocytizable stimulants cause a normal oxidative burst. In response to the membrane signals phorbolmyristate acetate and aggregated immunoglobulin, however, no stimulated turnover of the oxidative metabolism can be observed. A 40-kD protein found in the lavage fluid mediates this macrophage-inhibiting effect. This phenomenon may contribute to the frequent opportunistic infections seen in PAP patients. It can be concluded from our data that the high frequency of infections with opportunistic species in these patients can be reduced by therapeutic bronchoalveolar lavage. By this procedure the abnormal macrophage-suppressing protein can be washed out of the lung at an early stage of the disease.

Adult↗
PubMed1984

Drug metabolism in man and its relationship to that in three rodent species: monooxygenase, epoxide hydrolase, and glutathione S-transferase activities in subcellular fractions of lung and liver.

Activities of drug metabolizing enzymes were determined in subcellular fractions of lung biopsies from 12 human subjects and in liver biopsies from 15 other human subjects. Monooxygenase (MO) activity with 7-ethoxycoumarin as a substrate and epoxide hydrolase (EH) activity with benzo[a]pyrene 4,5-oxide as a substrate were measured in the microsomal fraction, glutathione S-transferase (GST) activity toward 2,4-dinitrochlorobenzene in the cytosolic fraction. MO activity was further characterized by the use of inhibitors known to act preferentially on different MO forms. To facilitate extrapolations from test results obtained in animals to man enzyme activities were also determined in corresponding fractions from commonly used laboratory animals, Sprague-Dawley rat, NMRI mouse, and Syrian golden hamster. All investigated specific activities were lower in lung than in liver preparations by factors ranging from 2.4 to 7 in the mouse, 4 to 18 in rat and hamster, and 11 to 697 in man. The high ratio between liver and lung activity in man occurred with MO and is due to an extremely low activity in human lung. It is not clear whether this low activity is predominantly due to low amounts of enzyme or to inhibitors known to be present in human lung preparations. With this exception of human lung MO, species differences in the investigated enzyme activities were moderate. Among the three rodent species, rat was most similar to man, with none of the investigated activities differing by a factor more than 2. The mouse differed from these two species by considerably higher MO and GST activities in both organs, and by a relatively low EH activity in liver for the investigated substrates, while the hamster displayed comparatively high lung GST and EH and liver GST and MO activities. MO inhibition patterns by different in vitro inhibitors were similar in the same organs of different species, but differed in lung and liver. Standard concentrations of the diagnostic inhibitors led to preferential inhibition of lung MO by metyrapone and considerably less by tetrahydrofuran, while for liver MO the reverse was true. In both organs, the standard concentration of alpha-naphthoflavone had only very weak effects. In conclusion, man and commonly used laboratory rodents are not grossly different with respect to the investigated enzyme activities with the possible exception of lung MO. For the substrates investigated, the rat represented clearly the best model for man among the studied animal species.

Adult↗
PubMed1983

Double-blind co-operative trial to compare trimethoprim-sulfalene and co-trimoxazole in the treatment of lower respiratory tract infections.

Two fixed trimethoprim-sulfonamide combinations were compared in a clinical trial for their effectiveness and safety in the treatment of patients with acute lower respiratory tract infections (pneumonia, bronchopenumonia, purulent tracheobronchitis, ect.). 46 in-patients were randomly allocated to Kelfiprim (trimethoprim 250 mg + sulfalene (sulfamethopyrazine) 200 mg) or to co-trimoxazole (trimethoprim 320 mg + sulfamethoxazole 1600 mg) and were treated for 1-2 weeks under double-blind conditions. Assessment of effectiveness was based on daily follow-up of subjective and objective signs and symptoms, on changes in X-ray picture, and on microbiological and laboratory findings. Response to therapy was excellent or good in 86% of patients receiving Kelfiprim and in 79% of those given cotrimoxazole. Transient side-effects were observed in three patients under Kelfiprim (two allergic reactions and one G.I. complaint) and in one under co-trimoxazole (altered kidney function).

Adult↗