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Biomedical subjects

E Fink

Publications and source records attributed to E Fink.

At least 109 records · Page 6Linked to original sources
PubMed1982

[Antimalarial 6-aminoquinolines. XIV. 6-(4-Diethylamino-1-methylbutylamino)-4-methoxy-2-methyl- and -2,4-dimethylquinolines with variations of substituents in positions 5 and 8].

3 derivatives 2g--i of 6-(4-diethylamino-1-methylbutylamino)-4-methoxy-2-methylquinoline and 6 derivatives 2k--p of 6-(4-diethylamino-1-methylbutylamino)-2,4-dimethylquinoline were synthesized with variations of substituents in positions 5 and 8 (--H, --OH, --OCH3, --CH3, --Cl) with the aim of studying the influence of these substituents, which facilitate, complicate or prevent oxidation to o- and (or) p-quinones, on antimalarial activity and toxicity. One methoxy group is necessary for activity against Plasmodium vinckei in position 5 or 8, no substituent that prevents oxidation is allowed in para position to this methoxy group.

Aminoquinolines↗
PubMed1982

[Antimalarial 6-aminoquinolines XV. 6- and 4-aminoquinolines with a tertiary basic alkylated amino group].

Antimalarial 6-aminoquinolines (1a-c) were acylated (3a-c, 5a) and alkylated (4a-c, 6a) at the secondary aromatic 6-amino group with the aim of studying the influence of a tertiary aromatic 6-amino group on antimalarial activity and toxicity. 4 derivatives (9e-g) of 4-amino-7-chloroquinoline with a tertiary aromatic 4-amino group were synthesized to study the influence of such a variation on the biological activity of the 4-aminoquinolines. The N-alkylated derivatives 4a-c, 6a, 9f-g were active against malaria (P. vinckei/mice).

Aminoquinolines↗
PubMed1981

The effects of lead, d-amphetamine, and time of day on activity levels in the mouse.

Mice were exposed to lead acetate (0.5%) pre- and postnatally, and activity levels were assessed at 21 days of age. Two measures of open field activity were employed at two different times of day across three doses of d-amphetamine. These factors influence the results observed in lead exposed mice and demonstrate that lead's effects on activity are not invariant. Implications for future research as well as the suggestion of an animal model for childhood hyperactivity are discussed.

Animals↗
PubMed1981

[Antimalarial 6-aminoquinolines. XIII. 5,8-Dialkoxyderivatives of 6-(4-diethylamino-1-methylbutylamino)-2-methyl- and 6-(4-diethylamino-1-methylbutylamino)-2,4-dimethylquinoline (author's transl)].

13 analogues 3c-p of 6-(4-diethylamino-1-methylbutylamino)-5,8-dimethoxy-2-methylquinoline (2a) and 6-(4-diethylamino-1-methylbutylamino)-5,8-dimethoxy-2,4-dimethylquinoline (2b) were synthesized with variations of alkoxysubstituents (-O-n-C4H9, -O-n-C8H17, -O CH(CH3)2, -O(CH2)2OCH3, -O(CH2-CH2O)2CH3, -O(CH2)2N(C2H5)2) in positions 5 and(or) 8 with the aim of studying the influence on antimalarial activity and toxicity. All derivatives were active against P, vinckei (mouse).

Aminoquinolines↗
PubMed1981

Suppressive and causal prophylactic activity of floxacrine in various avian malaria models.

Floxacrine, a 7-chloro-10-hydroxy-3(4-trifluoromethylphenyl)-3, 4-dihydroacridine-1,9-(2H, 10H)-dione and various standard malarials were found to be distinctly less active against avian malaria parasites than against rodent or nonhuman primate malaria parasites. Especially the suppressive action against asexual stages of P. gallinaceum, P. praecox and P. cathemerium was markedly reduced in comparison with that ascertained in mice infected with P. berghei. Similar results were observed in sporozoite-induced infections of P. gallinaceum and P. cathemerium respectively. Expressed as quotient of calculated causal prophylactic activity (CPD50) floxacrine was 42 and pyrimethamine 54 times more active against P. berghei yoelii than P. gallinaceum. The blood schizontocidal effect of floxacrine proved superior to that of mefloquine, chloroquine and mepacrine, whereas the causal prophylactic activity was slightly inferior to that of pyrimethamine but superior to that of primaquine. In vitro floxacrine revealed no effect against sporozoites of P. gallinaceum even at concentrations of 100 mcg/ml.

Acridines↗
PubMed1980

Tumor host relations. VI. Is alpha-ketoglutarate a tumor marker? Association with tumor extent in humans--correlation with tumor size in rats.

A 4-year survey is presented on the alpha-ketoglutarate (KG) values in whole blood of 200 patients with malignant neoplasms mainly of the gastrointestinal tract and the female breast. A group of patients with benign surgical diseases served as control. KG showed an association with the extent of the primary tumor classified according to the TNM-scheme. The percentages of single values above the 2s-range of the control were as follows: T2: 18%,T3: 41%, and T4: 64%. The mean value of KG had highly significantly increased already in stage T2 as compared to the control group. Rats bearing the Yoshida sarcoma showed a significant correlation between the tumor size and the daily excretion of KG into urine during the early stage of tumor growth. The results suggested that KG cannot be regarded as an early tumor marker in humans, but may be of some value as an aid for the differential diagnosis in advanced tumor stages.

Animals↗
PubMed1980

Biochemistry and functional aspects of human glandular kallikreins.

Human urinary kallikrein was purified by gel filtration on Sephacryl S-200 and affinity chromatography on aprotinin-Sepharose, followed by ion exchange chromatography on DEAE-Sepharose. In dodecylsulfate gel electrophoresis two protein bands with molecular weights of 41,000 and 34,000 were separated. The amino acid composition and the carbohydrate content of the kallikrein preparation were determined; isoleucine was identified as the only aminoterminal amino acid. The bimolecular velocity constant for the inhibition by diisopropyl fluorophosphate was determined as 9 +/- 2 1 mol-1 min-1. The hydrolysis of a number of substrates was investigated and AcPheArgOEt was found to be the most sensitive substrate for human urinary kallikrein. Using this substrate an assay method for kallikrein in human urine was developed. It was shown by radioimmunoassay that pig pancreatic kallikrein can be absorbed in the rat intestinal tract. Furthermore, in dogs the renal excretion of glandular kallikrein from blood was demonstrated by radioimmunological methods.

Amino Acids↗
PubMed1980

Isolation of an enzymatically active glandular kallikrein from human plasma by immunoaffinity chromatography.

A glandular kallikrein from human plasma was isolated by immunoaffinity chromatography and characterized. The molecular weight was determined to 40,000 by gel filtration. The enzyme preparation liberates kinins from human HMW kininogen (specific activity: 0.328 HMW kininogen-U/A280 unit), lowers the blood pressure of dogs after intravenous injection (specific activity: 1090 KE/A280 unit), is inhibited by diisopropyl fluorophosphate and aprotinin, but not by SBTI. In the radioimmunoassay for human urinary kallikrein parallel binding curves were obtained. AcPheArgOEt, DVal-LeuArgOEt and ZTyrONp are cleaved with identical rates by the kallikrein preparation and human urinary kallikrein.

Chromatography, Affinity↗
PubMed1980

Radioimmunoassay of human urinary kallikrein: determination of human urinary kallikrein, II.

A radioimmunoassay for the determination of human urinary kallikrein was developed. The sensitivity of the assay was 0.5 microgram/l. Dose-response curves of human submandibular and parotid saliva, sweat, pancreatic juice and bile paralleled the standard curve obtained with purified human urinary kallikrein. Substances with similar antigenic determinants were also found in human serum, ascites, seminal plasma, amniotic fluid, cervical mucus, tears, liquor and faeces, but not in human breast milk and gastric juice. Moreover, immunoreactive material was detected in the urine of guinea pigs, orangoutangs and chimpanzees, but not in the urine of rats, cats and rabbits. Porcine acrosin and kallikrein, as well as bovine trypsin and chymotrypsin, showed no cross reactivity.

Cross Reactions↗
PubMed1980

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

Basal 24 hour urinary kallikrein excretion of 20 patients with uncomplicated essential hypertension did not differ significantly from that of 18 normotensive age-matched control subjects. 4 of the 20 hypertensive patients, however, had low kallikrein excretion. Furosemide (40 mg i.v.) caused an increase of urinary kallikrein excretion in the normotensive subjects and in most of the patients with essential hypertension. The stimulating effect of furosemide was less pronounced or even absent in 7 hypertensives. No circadian rhythm of urinary kallikrein excretion was observed. There were weak correlations between 24 hour kallikrein excretion and urinary volume (r=0.59; p < 0.05), and potassium excretion (r=0.51; p < 0.05) in the normotensives. In the hypertensives correlations were found between 24 hour kallikrein excretion and potassium excretion (r=0.51; p < 0.05), aldosterone excretion (r=0.57; p < 0.01), and creatinine clearance (r=0.59; p < 0.01). Our findings do not support the concept that the renal kallikrein-kinin system might play a primary role in the pathogenesis of essential hypertension.

Adult↗
PubMed1980

Correlation of contrast angiography and histologic pattern with gallium uptake in primary liver-cell carcinoma: noncorrelation with alpha-feto protein. Concise communication.

Seventeen patients with histologically proven primary liver-cell carcinoma were evaluated by a technetium-99m sulfur colloid liver scan as well as with gallium-67 citrate. Twelve of the 17 patients (71%) showed gallium uptake in the tumor. Eleven of the 12 patients (92%) with a moderately or well-differentiated tumor showed increased gallium activity in the abnormality seen on the sulfur colloid scan. The exception in this group was a tumor with a large central area of necrosis. Four of five patients with a poorly differentiated or atypical carcinoma showed absence of gallium activity. Only six of 11 patients with a hypervascular tumor showed a marked increase in gallium uptake. Correlation of gallium with alpha-feto-protein, and with hepatitis antigen A, was poor. We conclude that gallium uptake in primary liver-cell carcinoma will be significant when the tumor shows a moderately to well-differentiated histologic pattern, unless significant necrosis is present. If the blood supply is markedly impaired, gallium uptake is reduced. However, a hypervascular blood supply does not necessarily ensure increased gallium avidity.

Angiography↗
PubMed1979

Tumor host relations. I. Increased plasma cortisol in tumor-bearing humans compared with patients with benign surgical diseases.

Plasma cortisol was measured by a protein binding technique in 81 patients with malignant tumors of different extent and various sites and in 82 patients with benign surgical diseases. The mean value of the tumor patients (x +/- s = 165 +/- 69 micrograms cortisol/l plasma) was increased significantly compared with the benign surgical disorders (100 +/- 45 micrograms/l). Within the group of patients with benign surgical disorders there was little variation by the type of disease (cortisol mean values given in brackets): benign breast tumors (95), gall stones (107), ulcer of the stomach and duodenum (96), hernia (78), appendicitis acuta (112), and struma (90). The results are in accordance with the hypothesis that glucocorticoids are involved in the increased protein catabolism of skeletal muscles and other signs of cachectic tumor patients.

Adolescent↗
PubMed1979

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

1. Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension. 2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension. 3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found. 4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.

Adult↗
PubMed1979

Isolation, characterization and radioimmunoassay of corticosteroid-binding globulin (CBG) in human serum -- clinical significance and comparison to thyroxine-binding globulin (TBG).

Isolation of the corticosteroid-binding globulin CBG was achieved by 5 chromatographical steps on cortisol Sepharose, QAE-Sephadex A-50, Con A-Sepharose and hydroxylapatite. The purity of the isolated CBG was demonstrated in polyacrylamide gel electrophoresis, SDS electrophoresis, immunodiffusion and ultracentrifugation. Microheterogeneity was shown in isoelectric focusing by 5 bands in the pH range of 3.7--4.2, which could be reduced to one major band after neuraminidase treatment. The equimolar binding of cortisol to CBG was demonstrated by binding studies. The association constant for cortisol was 2.8 x 10(8)M-1, for progesterone 1.7 x 10(6)M-1. From analytical ultracentrifugation, the molecular weight was calculated on 50 700; the sedimentation coefficient was 3.6 S, the partial specific volume 0.690 ml/g, the Stokes radius 38 A and the frictional coefficient ratio 1.5. A specific radioimmunoassay for CBG was established using the purified CBG for immunization, radioiodination and for calibration standards. The normal range of CBG levels in human serum was 2.4--4.4 mg/100 ml (mean +/- 2 SD). Studies were performed to compare the levels of CBG and thyroxine-binding globulin (TBG). No sex differences but a significant biphasic age dependence were observed for both proteins. In pregnancy and under oestrogen treatment of women and men, CBG was demonstrated to be the more distinct indicator of oestrogenic activity as compared with TBG, whereas the sensitivity of TBG was more pronounced to supposedly antioestrogenic substances like Danazol, and in severe disease. No coincidence of genetic CBG and TBG deficiencies have been found so far.

Amino Acids↗
PubMed1979

Meningoencephalitis in chronic Trypanosoma brucei rhodesiense infection of the white mouse.

A more recently isolated strain of T.b. rhodesiense (eatro 1989) induced a chronic infection in most of 180 intraperitoneally infected NMRI-mice, surviving 6 to 9 weeks on an average. A meningoencephalitis beginning with a meningitis one week after infection and being fully developed after 4 weeks was demonstrable by investigating 22 animals killed at random between 7 and 42 days after infection. The inflammatory reactions observed correspond to those known from the late stage of human trypanosomiasis in their nature and way of spreading. Hence, this infection seems to offer a suitable model for studying a human like meningoencephalitis and for screening of compounds for activity during the late stage of human sleeping sickness.

Animals↗