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Biomedical subjects

J Blum

Publications and source records attributed to J Blum.

At least 127 records · Page 7Linked to original sources
PubMed1981

Pattern of breathing and carbon dioxide retention in chronic obstructive lung disease.

Carbon dioxide (CO2) retention occurs in some but not all patients with obstructive pulmonary disease. In order to assess if the pattern of ventilation modulates CO2 retention, 15 normocapnic (group 1) and 15 hypercapnic (group 2) patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 second (FEV1) less than or equal to 1.0 liter) were studied retrospectively. Utilizing clinical information, anion gap and acid-base nomogram, subjects with superimposed acid-base disturbances were eliminated. Therefore, only patients who exhibited steady state ventilatory patterns were studied. In group 1, mean arterial carbon dioxide tension (PaCO2) was 40 ł 2 torr and mean arterial pH (pHa) was 7.410 ł0.004. In group 2, mean PaCO2 was 52.5 ł1.2 torr and pHa was 7.390 ł0.007. No statistically significant differences between groups were present with respect to age. height, sex, lung volumes and flow rates, diffusing capacity and CO2 production. Minute ventilation was similar in both groups (7.631 liters and 7.81 liters). In group 2, the patients had a significantly higher respiratory rate per minute (22 versus 16.5) and smaller tidal volume (355 versus 463 cc) than the patients in group 1. This pattern of ventilation resulted in a larger dead space ventilation (3.98 liters versus 2.95 liters) and a lower alveolar ventilation (3.82 liters versus 4.61 liters) with consequent CO2 retention. The higher respiratory frequency in the patients in group 2 may be due to vagal stimulation from the lungs since this group had a fivefold greater incidence of chronic bronchitis and a seven-fold greater incidence of cor pulmonale than the patients in group 1.

Carbon Dioxide↗
PubMed1979

Mutagenicity of phenanthrene and phenanthrene K-region derivatives.

Phenanthrene and 9 K-region derivatives, most of them potential metabolites of phenanthrene, were tested for mutagenicity by the reversion of histidine-dependent Salmonella typhimurium TA1535, TA1537, TA1538, TA98 and TA100 and the rec assay with Bacillus subtilis H17 and M45. The strongest mutagenic effects in the reversion assay were observed with phenanthrene 9,10-oxide, 9-hydroxyphenanthrene and N-benzyl-phenanthrene-9,10-imine. Interestingly, the mutagenic potency of the arene imine was similar to that of the corresponding arene oxide. This is the first report on the mutagenicity of arene imine. The mutagenic effects of all these phenanthrene derivatives were much weaker than that of the positive control benzo[a]pyrene 4,5-oxide. Even weaker mutagenicty was found with cis-9,10-dihydroxy-9,10-dihydrophenanthrene and with trans-9,10-dihydroxy-9-10-dihydrophenanthrene. The other derivatives were inactive in this test. However, 9-10-dihydroxyphenanthrene and 9,10-phenanthrenequinone were more toxic to the rec- B. subtilis M45 strain than to the rec+ H17 strain. This was also true for phenanthrene 9,10-oxide and 9-hydroxyphenanthrene, but not with the other test compounds that reverted (9,10-dihydroxy-9,10-dihydrophenanthrenes; N-benzyl-phenanthrene 9,10-imine; benzo[a]pyrene 4,5-oxide) or did not revert (phenanthrene, 9,10-bis-(p-chlorophenyl)-phenanthrene 9,10-oxide, 9-10-diacetoxyphenanthrene) the Salmonella tester strains. Although the K region is a main site of metabolism and although all potential K-region metabolites were mutagenic, phenanthrene did not show a mutagenic effect in the presence of mouse-liver microsomes and an NADPH-generating system under standard conditions. However, uhen epoxide hydratase was inhibited, phenanthrene was activated to a mutagen that reverted his- S. typhimurium. This shows that demonstration of the mutagenic activity of metabolites together with the knowledge that a major metabolic route proceeds via these metabolites dose not automatically imply a mutagenic hazard of the mother compound, because the metabolites in question may not accumulate in sufficient quantities and therefore the presence and relative activities of enzymes that control the mutagenically active metabolites are crucial. N-Benzyl-phenanthrene 9.10-imine was mutagenic for the episome-containing S. typhimurium TA98 and TA100 but not for the precursor strains TA1538 and TA1535. This arene imine would therefore be useful as a positive control during routine testing to monitor in the former strains the presence of the episome which is rather easily lost.

Drug Evaluation, Preclinical↗
PubMed1979

[Determination of thyroxine in serum by a heterogeneous enzyme immunoassay: results of a joint trial].

This paper describes the evaluation of a heterologous enzyme immunoassay for the determination of total thyroxine in serum by a group of seven clinical chemical laboratories. The test follows the principles of the enzyme linked immunosorbent assay (ELISA) and uses peroxidase as a marker. The evaluation of analytical reliability yielded the following results within the analytical range from 39 unto 322 nmol/l: 1. Within-batch precision ranged from 3.1 unto 10.4% (coefficient of variation) with single analyses. 2. Between-batch precision ranged from 3.7 unto 20.4% with single analyses. 3. Between-laboratories precision ranged from 5.4 unto 6.8%. 4. Pure thyroxine, added to serum or thyroxine-free serum, gave recoveries between 93 and 120%. 5. Analysis of control sera gave results essentially comparable to the assigned values based upon radioimmunoassays. 6. Analysis of 288 clinical sera gave slightly higher results by the enzyme immunoassay than by the analogous radioimmunoassay from the same manufacturer. 7. Comparison with other methods of analysis (radioimmunoassays, competitive protein ligand assays, hormonal iodine assay) yielded partly comparable, partly higher results. 8. Comparison with the homogenous enzyme immunoassay (EMIT) led to comparable results. 9. Interference due to hyperlipemia or hemolysis was not observed. 10. There might be an interference in hyperbilirubinaemic sera, due to an as yet unknown factor. With respect to practicability the ELISA-test compares favourably with the analogous solid phase radioimmunoassay. The main differences are the absence of radioactive material and a longer shelf-live of reagents. Following the manual procedure the time taken to perform the enzyme immunoassay is slightly longer than for the analogous radioimmunoassay.

Enzyme-Linked Immunosorbent Assay↗
PubMed1977

[Effect of droperidol on the creatine phosphokinase activity in acute myocardial infarct].

In 141 patients with acute myocardial infarction, creatine phosphokinase isoenzyme (CPK-MB) was determined by the activation method with dithiothreitol (RAO et al.: Clin. Chim. Acta 21, 1612 [1975]). 15 out of 16 patients with atypical negative CPK-MB values within the first 3 days after infarction had been treated with 5-10 mg droperidol, a neuroleptic drug dispensed for its antiemetic effect. In a prospective study in 7 patients, CPK-MB determined serially showed a decrease or persistently low or negative values within 1 minute after injection of 5 mg droperidol and lasting 24-36 hours after injection. In contrast, CPK-MB determined by immunoprecipitation did not change its typical pattern after use of droperidol. Hence, negative or low values of CPK-MB in acute myocardial infarction must be expected after droperidol if determination is by the activation method with dithiothreitol.

Creatine Kinase↗
PubMed1976

Haemodynamic diversity and plasma renin activity in labile arterial hypertension.

Haemodynamic studies were made on 31 patients with labile hypertension at rest and during exercise. Plasma renin activity (PRA) was measured in 8 of them. Five haemodynamic types could be recognised and they could be arranged into two groups. The first was characterised by an increase of calculated peripheral resistance, sometimes permanent, sometimes revealed by effort, sometimes in relation to an increased cardiac output; this would appear to predict the development of permanent hypertension. The second group was characterised by normal systemic resistances, adapted to the cardiac output which was either normal or increased; the significance of labile hypertension in these cases was uncertain; from the haemodynamic studies one was unable to distinguish a transient emotive hypertension from potential permanent hypertension. The PRA was raised in the supine position and greatly increased by an orthostatic posture in the 8 patients tested, suggesting therefore an underlying neuro-adrenergic mechanism. In some patients with labile hypertension the haemodynamic tests were normal at rest and during effort. Others had different responses, which may be the result of varieties of hyper-sympathetic activity, either pure or predominantly beta-adrenergic (increased cardiac output, peripheral resistance adapted to the output) or combined beta and alpha (increased cardiac output with raised peripheral resistance) or mainly alpha-adrenergic (normal cardiac output, increased peripheral resistance).

Adult↗
PubMed1976

Male pseudohermaphroditism with hypertension due to a 17alpha-hydroxylation deficiency.

A case of male pseudohermaphroditism aged 48 years with systemic hypertension and hypokalaemic alkalosis is described. Results of metabolic studies point to a 17alpha-hydroxylase deficiency demonstrated by low cortisol (0-56 mg/24 h), high corticosterone (270 mg/24 h) and 11-deoxycorticosterone (5 mg/24 h) secretion rates. Adrenocorticotrophin and gonadotrophin levels were markedly raised but plasma androstenedione (3 ng/dl), testosterone (17 ng/dl), oestrone (3 ng/dl) and oestradiol(1-8 ng/dl) were all low. Plasma aldosterone levels and secretion rates in urine were low and were surprisingly unaffected by dexamethasone therapy although low renin levels rose with a marked return of the erect posture effect. Therapeutic levels of dexamethasone were, however, followed by incipient renal failure.

Acute Kidney Injury↗
PubMed1975

[Labile arterial hypertension. Hemodynamic study with measurement of renin activity].

Plasma renin activity (PRA) was increased and highly sensitive to stimulation in eight cases of labile hypertension (HT), which were also studied haemodynamically. This increase in PRA would appear to result from neuro-adrenergic hyperactivity. The haemodynamic were characterised by a diversity which may be explained on the basis of differentiated sympathetic hyperactivity: exclusive or predominant beta-adrenergic activity causing a hyperkinetic cardiac state with moderate HT adapted to the increased cardiac output; A simultaneous alpha- and beta-adrenergic activity resulting in cardiac hyperkinesis with a relative or potential increase in peripheral resistance; isolated or predominant alpha-adrenergic hyperactivity causing a potential increase in peripheral resistance revealed or increased by effort, in the presence of a normal cardiac output. In certain cases of labile HT however, despite an increased PRA, haemodynamic findings were normal at rest and with effort, at the time of catheterisation.

Adult↗