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Biomedical subjects

J Martinez

Publications and source records attributed to J Martinez.

At least 505 records · Page 28Linked to original sources
PubMed1978

The effects of ancrod, the coagulating enzyme from the venom of Malayan pit viper (A. rhodostoma) on prothrombin and fibrinogen metabolism and fibrinopeptide A release in man.

The action of ancrod on fibrinogen and prothrombin metabolism was studied in six healthy individuals by the use of 131I-fibrinogen and 125I-prothrombin and by measurement of blood levels of fibrinopeptide A. Two untreated healthy controls were studied at the same time. Rapid defibrinogenation occurred during the initial 3 hr ancrod infusion, and fibrinogen levels were maintained near zero throughout the study. Large quantities of non-thrombin-clottable TCA-precipitable 131I material could be demonstrated in the circulation, reaching a maximum 3 to 6 hr after ancrod infusion and clearing with a half-life of 6 hr. Gel filtration of 6 hr plasmas demonstrated the presence of complexes larger than fibrinogen, as well as degradation products of fibrinogen-fibrin. Prothrombin concentration and metabolism were unchanged by ancrod treatment. Fibrinopeptide A levels in the ancrod group were greather than 4,000 ng/ml during the initial defibrinogenation, declined to greater than 80 ng/ml, and then increased to high levels after 3 days. These studies provide explanations of previous observations concerning the specificity of ancrod and demonstrate that rapid clotting of fibrinogen and dissolution of fibrin can occur in vivo without recruitment of the classic coagulation mechanism.

Adult↗
PubMed1978

Side reactions in peptide synthesis. IX. Suppression of the formation of aminosuccinyl peptides with additives.

The base-catalyzed ring closure of beta-benzylaspartyl peptides was efficiently suppressed by the addition of phenols (with electron-withdrawing substituents) to the reaction mixtures. From a series of compounds tested, 2,4-dinitrophenol and pentachlorophenol were the most effective. No direct relationship was found between the acidity of the additives and their ability to suppress the formation of aminosuccinyl peptides. The applicability of 2,4-dinitrophenol and pentachlorophenol in practical syntheses was also examined.

Acylation↗
PubMed1977

Immobilised monomers of human liver arginase.

Human liver arginase (L-arginine amidinohydrolase, EC 3.5.3.1) was immobilised by attachment to nylon with glutaraldehyde as a crosslinking agent. Incubation of the immobilised tetrameric enzyme with EDTA followed by dialysis resulted in the dissociation of the enzyme into inactive matrix-bound and solubilised subunits. Both species recovered enzymatic activity after incubation with Mn2+, and the activity of the reactivated matrix-bound subunits was nearly 25% of that shown by the enzyme initially attached to the support in the tetrameric form. When the reactivated bound subunits were incubated with soluble subunits in the presence of Mn2+, they 'picked-up' from the solution an amount of protein and enzymatic activity almost identical to that initially lost by the immobilised tetramer after the dissociating treatment with EDTA. This occurred only in the presence of Mn2+. It is suggested that the reactivation of the subunits of arginase involves the initial formation of an active monomer, which then acquires a conformation that favours a reassociation to the tetrameric state.

Arginase↗
PubMed1977

Reversibility of cerebral atrophy in anorexia nervosa and Cushing's syndrome.

Two patients, one with malnutrition due to anorexia nervosa and one with Cushing's syndrome, showed evidence of cerebral atrophy by computed tomography (CT) of the brain. Several months after the original diagnosis of cerebral atrophy, follow-up CT studies demonstrated essentially total return to normality. It is postulated that the mechanism responsible for the described atrophic changes may be related to protein loss or fluid retention, or both. Correction of these metabolic abnormalities may be followed, as in the two cases reported here, by reversion of the CT findings to normality.

Adolescent↗
PubMed1977

Dysfibrinogenemia associated with liver disease.

To test the possibility that a functionally abnormal fibrinogen may exist in some patients with liver disease, we studied the plasma and purified fibrinogens of five patients whose plasma thrombin times were prolonged at least 40% over normal controls. In no patient was there evidence of disseminated intravascular coagulation and/or fibrinolysis. No abnormalities were detected by immunoelectrophoresis of plasmas or purified fibrinogens. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of reduced patient fibrinogens showed normal mobility and amount of Aalpha, Bbeta, and gamma chains. Alkaline polyacrylamide gel electrophoresis and gradient elution, DEAE-cellulose chromatography of admixtures of radio-iodinated patient (125)I-fibrinogen and normal (131)I-fibrinogen showed identical mobility in the gel and simultaneous elution from the column, respectively. Thrombin and Reptilase (Abbott Scientific Products Div., Abbott Laboratories, South Pasadena, Calif.) times of purified patient fibrinogens were prolonged, and calcium ions improved but did not completely correct these defects. Increasing amounts of thrombin progressively shortened the clotting times of patient fibrinogens but not to the level of normal. Addition of equal amounts of patient fibrinogen to normal fibrinogen resulted in a prolongation of the thrombin time of the normal protein. Thrombin-induced fibrinopeptide release was normal. Fibrin monomers prepared from patient plasmas and purified fibrinogens demonstrated impaired aggregation at low (0.12) and high (0.24) ionic strength. These studies demonstrate that some patients with liver disease and prolonged plasma thrombin times have a dysfibrinogenemia functionally characterized by an abnormality of fibrin monomer polymerization.

Alcoholism↗
PubMed1977

Functional and metabolic properties of human asialofibrinogen.

The role of sialic acid in the functional and metabolic properties of purified human fibrinogen was investigated. Fibrinogen treated with Vibrio cholerae neuraminidase released 90 percent of its sialic acid without evidence of proteolysis, as indicated by the presence of intace A alpha, B beta, and gamma chains on sodium dodecylsulfate (SDS)-polyacrylamide gels of the reduced asialoprotein. The thrombin and Reptilase clotting times of human asialofibrinogen were shortened compared to those of normal fibrinogen. Fibrinopeptide release was normal in rate and amount, but asialofibrin monomer aggregation was increased at both low and high ionic strength. Similarly, the asialo-derivative of fibrinogen Philadelphia (functionally characterized by impairment of fibrin monomer aggregation) demonstrated shortening of its thrombin and Reptilase times and improvement in its monomer aggregation especially at high ionic strength. Asialofibrin showed a normal capacity to form cross-linked fibrin as demonstrated by normal gamma-chain dimerization and alpha-chain polymerization. Simultaneous metabolic studies of human normal fibrinogen and asialofibrinogen in rabbits revealed only a modest decrease in the half-life of the asialoprotein compared to the intact protein, with no preferential uptake of the asialo-derivative by the liver. Control studies with rabbit normal fibrinogen and asialofibrinogen in rabbits revealed the same modest difference in half-life. Thus, asialofibrinogen clots faster due to enhancement of its monomer aggregation, has a normal capacity to form cross-linked fibrin, and does not differ significantly in its metabolic properties from normal fibrinogen. The possible influence of sialic acid in the functional abnormality of some congenital dysfibrinogenemias is discussed.

Blood Coagulation Tests↗
PubMed1976

[Lengthening of the peptide chain at the C-terminal end of a glycosylamino acid].

An O-glycodipeptide was synthesized by lengthening the peptide chain on the C-terminal side of a glycosylamino acid unit. N-(Benzyloxycarbonyl)-3-O-(2,3,4,6-tetra-O-acetyl-beta-D-glucopyranosyl)-L-threonine o-nitrophenyl ester and pentachlorophenyl ester were condensed with glycine benzyl ester to give both the same glycodipeptide, [N-(benzyloxycarbonyl)-3-O-(2,3,4,6-tetra-O-acetyl-beta-D-glucopyranosyl)-L-threonyl]glycine benzyl ester (9). The two anomers, N-(benzyloxycarbonyl)-3-O-(2,3,4,6-tetra-O-acetyl-alpha- and beta-D-glucopyranosyl)-L-threonine pentachlorophenyl ester were also prepared. 1H-N.m.r. studies ascertained the structure and anomeric configuration expected.

Dipeptides↗
PubMed1976

[Interpretation of the right bundle-branch block appearing after repair of ventricular septal defect].

Based on a study of 43 cases the authors attempt to assess the exact aetiology of the appearance of right bundle branch block, which is seen very frequently after repair of a ventricular septal defect. A comparison of the electrocardiograms with the anatomical type of VSD, the surgical approach, and the size of the septal defect would seem to indicate that a monofascicular block by a lesion of the right branch of the bundle of His is responsible. The correlations are not, however, absolute, and in a certain number of cases a simple peripheral lesion was to blame. The importance of precise knowledge of the case of the branch is that it is possible that first a bi- and then a tri-fasicular block will develop; this means that complete atrioventricular block is one of the long-term sequelae of surgery. In the authors' experience of 43 cases, only one tri-fascicular block developed.

Adolescent↗
PubMed1976

Immunosuppressive therapy of Factor VIII inhibitors.

Immunosuppressive therapy was used in seven hemophiliac and three nonhemophiliac patients with factor VIII inhibiors. Permanent disappearance of the inhibitor occurred in three hemophiliac and two nonhemophiliac patients following treatment with cyclophosphamide and factor VIII. Critical factors influencing the response to therapy may include both the titer and duration of the inhibitor and the degree of intervening factor VIII exposure prior to immunosuppressive therapy. Two severe hemophiliacs with low titer inhibitors that disappeared without specific therapy are also reported.

Adolescent↗
PubMed1976

Fluid-percussion model of mechanical brain injury in the cat.

Mechanical brain injury was produced in 36 cats with a fluid-percussion model in which brain damage or dysfunction is produced by a single, brief, hydraulically-induced pressure transient that is conducted through the brain. Fluid-percussion injury induce elastic deformation of the brain resembling the brain deformation known to occur following head impact. Physiological responses and pahtological changes following injury were expressed as a function of peak pressure. Macroscopic central nervous system lesions concentrated at the pontomesencephalic junction, cervicomedullary junction, and in the cerebellar tonsils were consistently observed at and above 2.6 atmospheres (atm). At higher levels of injury (greater than or equal to 3.2 atm) there was extensive basal subarachnoid hemorrhage. At very high levels of injury (greater than 4.0 atm) hemorrhagic contusions were noted at the cerebral hemisphere impact site. A spectrum of neuronal alterations was identified in the damaged areas. Computer analysis showed correlation of electroencephalographic (EEG) changes with the neuropathological changes, since EEG recovery became severely impaired above 2.6 atm. No EEG changes were noted below 1.5 atm. From 1.5 to 2.2 atm there was a physiological response to injury but no significant changes were seen on neuropathological examination. This range of injury should permit further studies of the more subtle changes following mechanical brain injury without intraparenchymal hemorrhage or subarachnoid hemorrhage. The fluid-percussion model relates brain deformation following mechanical loading to a single pressure transient that is easily measured and controlled. Further quantitative investigation into the pathobiology of mechanical brain injury following graded brain deformation is thus made possible.

Animals↗
PubMed1975

[Abnormal origin of 1 of 2 pulmonary arteries from the ascending aorta].

In relation with 4 cases of anomalous branching of one pulmonary artery from the ascending aorta, the main clinical, angiographic, physiopathologic, therapeutic and embryologic features of this malformation were reviewed. It appeared that the natural history of this malformation is a severe one, and only a corrective surgical treatment is liable to secure survival and cure. This anomaly was also encountered, very rarely, in Fallot's tetralogy, and two cases of this combination were reported.

Aorta↗