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Biomedical subjects

G Kemp

Publications and source records attributed to G Kemp.

At least 55 records · Page 3Linked to original sources
PubMed1976

Bleeding disorder with abnormal wound healing, acid-soluble clots and normal factor XIII.

An unusual bleeding disorder clinically resembling factor XIII deficiency is presented. The only detectable coagulation abnormality was rapid clot dissolution in 1% monochloroacetic acid. This abnormality was ascribed to the sustained increase of a pepsin-like plasma protease which is activated at low pH. Asystematic search for similar phenomena revealed that massive blood transfusion may also enhance plasma-clot solubility in acid, possibly by release of a red cell protease. We conclude that the acid clot solubility test is not a specific indicator of factor XIII deficiency, but this simple assay is recommended for further studies of acid plasma protease activity. The diagnostic relevance and pathophysiologic importance of increased pepsin-like activity in plasma remain to be elucidated.

Acetates↗
PubMed1976

Hypoxanthine excretion during preservation of rabbit kidneys for transplantation. An assessment of the ischaemic damage.

The loss of 5'-adenine nucleotides from kidney tissue subjected to acute ischaemia can be indirectly estimated by washing out the end product of catabolism, hypoxanthine, from the ischaemic tissue to the perfusate. As a correlation has previously been demonstrated between the duration of the previous normothermic ischaemia and the washout of hypoxanthine during preservation, hypoxanthine has been studied as a prospective measurement of ischaemic renal damage, by transplantation of rabbit kidneys. The results were compared to the already established parameters L-lactate and lactate dehydrogenase. Different ischaemic traumata and methods of preservation have been employed in order to determine the relationship of these parameters to the ischaemic kidney damage as evaluated by the functional regeneration of the grafts after autotransplantation. The wash-out of hypoxanthine was found to be correlated to such a degree to the reversibility of the ischaemic cell degeneration that a certain in vitro exclusion of the irreversibly damaged kidney grafts was possible. It is concluded that hypoxanthine can function as a reliable and sensitive measurement for the in vitro establishment of the ischaemic kidney parenchymal damage, and that it can be employed clinically with advantage.

Animals↗
PubMed1975

Plasmic degradation of human fibrinogen. III. Molecular model of the plasmin-resistant disulfide knot in monomeric fragment D.

A mixture of fragments D, derived from fibrinogen by plasmic degradation, was S-reduced and carboxymethylated. Individual chains were separated by gel filtration on Sephadex G-100 and characterized by peptide mapping, N-terminal amino acid analysis, polyacrylamide electrophoresis in sodium dodecyl sulfate, and amino acid composition. It was demonstrated that all D species contain the same alpha- and beta-chain remnants, having mol. wts of 10 000 and 45 000, respectively. Their heterogeneity was shown to be caused by the gradual degradation of the gamma-chain at its C-terminal end. Denatured fragment D was further degraded with plasmin in the presence of 2 M urea. One beta- (mol. wt 17 000) and two gamma-fragments (mol. wts 5000 and 6000) were split from fragment D, in addition to non-characterized small peptides, leaving behind a plasmin-resistant core, designated as fragment d. Fragment d was in turn reduced and carboxymethylated, and the resulting constituent chains were isolated by chromatography on carboxymethyl-cellulose and Sephadex G-100. The reduced alpha-, beta- and gamma-chain remnants of fragment d were found to have been derived from the N-terminal portion of fragment D and have estimated mol. wts of 9000, 24 000 and 13 000, respectively. A tentative scheme for the conversion of an early fragment D into the core fragment d is proposed. Our results conclusively support the model of asymmetric degradation of fibrinogen, according to which 2 mol of monomeric fragment D are produced from 1 mol of fibrinogen.

Amino Acid Sequence↗
PubMed1975

Effect of diuretics on urinary excretion of cephalothin in humans.

Diuretics and antibiotics are frequently used concomitantly. The possibility of drug interactions led us to study the effects of several diuretics on the renal elimination of cephalothin. Five healthy volunteers received a constant infusion of 500 mg of sodium cephalothin per h for 9 h on 4 consecutive days. Each day, after the third hour of infusion, the subjects were given one of the following in varying order: (i) furosemide (1 mg/kg, intravenous), (ii) mercaptomerin (250 mg, intramuscular), (iii) mannitol (25 g, intravenous), or (iv) no diuretic (control day). Fluid losses were replaced hourly. Serum and complete urine collections were obtained each hour and assayed for creatinine and cephalothin (bioassay). Clearances (milliliter per minute) and urinary excretions (milligram per hour) of cephalothin did not differ either when the diuretic day values were compared with control day, or when pre- and postdiuretic results on the same day were compared. Creatinine clearances were not affected by diuretics except for a transient rise after furosemide.

Adult↗
PubMed1975

Surface properties of phorbol esters and their interaction with lipid monolayers and bilayers.

The potent tumor-promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA) is surface active and was found to occupy a limiting area of 62 sq A/molecule in monolayers at the air-water interface. The interfacial tension of aqueous TPA solutions is decreased by increasing the bulk-phase TPA concentrations up to 2 x 10(-6) M,beyond which no further decreases were observed. This concentration is in agreement with the apparent solubility limit previously obtained. The apparent aqueous solubility limit of the more hydrophobic phorbol-didecanoate is 5 x 10(-8) M. Interaction of TPA with egg phosphatidylcholine monolayers at the air-water interface was shown by an increase in the surface pressure of the monolayer from 22 dynes/cm, initial film pressure, to 34 dynes/cm 90 min after introduction of TPA into the aqueous subphase. It was shown by gel filtration chromatography that a similar phorbol derivative, tritiated phorbol-didecanoate, binds to phospholipid vesicles. Differential scanning calorimetry also indicated that the addition of either TPA or an inactive stereoisomer, 4-alpha-phorbol-didecanoate, to phospholipid bilayers results in a marked reduction of the enthalphy of the minor transition of dipalmitoylphosphatidylcholine liposomes. Several fluorescence polarization probes for membrane fluidity indicate that TPA does not affect this membrane parameter. Further, the presence of TPA induces no measurable change in the cation permeability of phospholipid vesicles, the conductance of planar bilayer membranes, or the electrophoretic mobility of negatively charged liposomes. The lack of a specific effect with bilayers alone, combined with the documented physiological effects at low TPA concentrations, point to the possibility of a specific membrane component as the receptor for TPA at the plasma membrane.

Binding Sites↗
PubMed1969

R factor transmission in vivo.

Experimental infections were induced in weanling pigs orally both with nalidixic acid (NA)-sensitive and -resistant strains of Salmonella choleraesuis var. kunzendorf, designated RC221 and RC221NA, respectively. Prior to the time of infection, cultures of normal bacterial flora were isolated from swine fecal matter and screened for the presence of R factors. A majority of these bacterial isolates harbored transferable resistances. Both strains RC221 and RC221NA have been shown to be competent recipients in vitro of the R factors present in the normal intestinal flora. The property of NA resistance greatly facilitated recovery of the infecting organism. After infection, salmonellae from liver, lung, spleen, lymph node, intestine, and feces were screened for the presence of R factors. Transfer of drug resistance in vivo was a rare occurrence; however, if infected specimens, particularly intestinal, were incubated in nutrient broth prior to plating, R factor transfer occurred, presumably in the test tube. Changes in recipient cultures were frequently observed after introduction of R factors from organisms of pig origin into the S. choleraesuis var. kunzendorf test organisms. Alterations include changes in typing reaction, granular growth in broth, differences in colony form, and reduction of virulence.

Animals↗