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Biomedical subjects

G Martin

Publications and source records attributed to G Martin.

At least 433 records · Page 24Linked to original sources
PubMed1977

Effects of chronic ethanol consumption on the catabolism of chylomicron triacylglycerol and cholesteryl ester in the rat.

Rats were fed for 24 days a liquid diet with ethanol as 36% of calories to produce hyperlipemia and hepatic steatosis. The catabolism of chylomicrons doubly-labeled in the triacylglycerol and cholesteryl ester moieties was studied in conscious rats after ingestion of their usual liquid diets with or without ethanol. A constant intravenous infusion of chylomicrons revealed a defect in chylomicron catabolism after chronic treatment with ethanol. The plasma clearance of chylomicron cholesteryl ester was impaired to a greater extent than clearance of chylomicron triacylglycerol. These findings are consistent with defective catabolism of chylomicron remnants, and suggest that the accumulation of chylomicron remnants in the plasma contributes to the development of increased post-prandial hyperlipemia and chronic hyperlipemia in association with excessive ethanol consumption.

Animals↗
PubMed1977

The palm tree cervical spine--a normal anatomical variant.

A case of "palm tree" cervical spine with cervical spondylitic myelopathy is described. It is shown that this upward course of the nerve roots over the pedicle is a variant of normal anatomy, not described in standard textbooks and that this variation may be seen on myelograms. The futility of attempting to correct the variation is described.

Female↗
PubMed1977

[The treatment of acute acoustic trauma (blast injury) with dextran 40 (author's transl)].

In a prospective study the results of treatment of 72 patients with deafness due to blast injury were assessed. All patients received infusions of Dextran 40. When treatment started within 3 days of the injury 74% showed complete recovery of hearing and the remaining 26% showed some improvement. When treatment started within 3 weeks of the injury 26.5% showed complete recovery, 61.8% had some improvement and 11.8% had no improvement. In 87.5% of those patients who attended after a longer interval no change in the audiograms occurred and only 12.5% had any significant improvement. The disappearance of tinnitus was effectively more common with early treatment. On account of these results the use of Dextran 40 is strongly advised.

Blast Injuries↗
PubMed1976

Role of gamma-carboxyglutamic acid. Cation specificity of prothrombin and factor X-phospholipid binding.

Divalent cations are required for two roles in prothrombin-phospholipid interaction. The first role, catalysis of a prothrombin protein transition has a reaction half-life of 100 min at 0 degrees and is a prerequisite to phospholipid binding. The binding sites required for the transition have a very low cation specificity. All di- and trivalent cations tested were effective in this role with the exception of beryllium. Barium catalyzed the transition but only at high concentrations (6.6 mM was required for half-reaction). Blood-clotting Factor X, another gamma-carboxyglutamic acid-containing protein, also undergoes a cation-catalyzed protein transition which is a prerequisite to Factor X-phospholipid binding. In both proteins, the transition can be monitored by a decrease in the protein's intrinsic fluorescence. Compared to prothrombin, the Factor X transition occurs much more rapidly, has a somewhat greater specificity for cations, and requires higher concentrations of cations. This indicates that the cation binding sites provided by gamma-carboxyglutamic acid are not completely uniform in all proteins. The second role of divalent cations in prothrombin-phospholipid interaction is in the actual protein-phospholipid binding. This interaction was studied by protein fluorescence quenching resulting from excitation energy transfer to a chromophore attached to the phospholipid membrane. Only strontium and barium satisfactorily replaced calcium in this role. A number of other cations form protein-phospholipid complexes but of the wrong structure. These cations inhibit the prothrombinase complex (Factor Xa, calcium, phospholipid, Factor V). The cation specificity for Factor X-phospholipid binding is the same as for prothrombin except that higher concentrations of cations are required. Factor Xa (generated by action of Russell's viper venom on Factor X) displayed the same calcium requirements for the protein transition and phospholipid interaction as Factor X. The cation requirements of the prothrombinase complex correlate with the cation requirements of prothrombin and Factor X-phospholipid binding. Strontium is the only cation that will singly replace calcium. Barium is ineffective alone because the concentrations required to catalyze the protein transitions cause precipitation of the phospholipid. Combination of certain other cations with barium will, however, substitute for calcium. The other cations (specifically magnesium or manganous ion) catalyze the protein transitions and barium forms the correct protein-phospholipid complexes.

Animals↗
PubMed1976

[Effect of angiotensin II depot administration on bioelectric functional processes of the central nervous system].

Using the average evoked potential technique, angiotensin-II depot effects (1 mg implantate = 3--4 mg/kg body weight angiotensin-II) were studied neuroelectrophysiologically in reticular, hippocampal and neocrotical structures of albino rats. A multivariate variance and discriminance analysis program revealed differentiated changes of the bioelectrical processing data of the CNS. Evidence was obtained for a varying structural sensitivity of central-nervous substructures under depot administration of angiotensin-II. In later phases of angiotensin-II action, the hippocampus was characterized by an electrographic synchronization phenomenon with high-amplitude average evoked potentials. The reticular formation, and to a lesser extent the visual cortex, showed an angiotensin-induced diminution of bioelectrical excitation. However, the intensity of the change in functional CNS patterns did not always correlate with maximal blood pressure rises. The described changes of afference processing to standardized sensory stimuli, especially in hippocampal and reticular structures of the CNS foll owing angiotensin depot action, point to a central-nervous action mechanism of angiotensin-II.

Afferent Pathways↗