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Biomedical subjects

P A Castaldi

Publications and source records attributed to P A Castaldi.

At least 55 records · Page 3Linked to original sources
PubMed1981

Anti platelet agents for strokes and myocardial infarction: a critical appraisal of recent clinical trials.

Attempts at prevention of arterial thrombosis with platelet inhibitors have been the subject of a number of major trials in recent years. These trials were prompted by earlier observations that aspirin takers seemed to fare better after acute myocardial infarction and were further stimulated by the recent growth of knowledge about the role of vascular and platelet prostaglandins. The trials have sought to establish that aspirin (ASA), sulphinpyrazone and dipyridamole may prevent thrombosis in the form of recurrence of transient ischaemic attack (TIA) and stroke or reduce the recurrence rate and mortality after acute myocardial infarction. No single trial has provided conclusive evidence although there is a strong suggestion of some benefit from ASA. With further understanding of PG metabolism and the effects of inhibitors new approaches are likely to emerge in the near future.

Aspirin↗
PubMed1980

Essential thrombocythaemia.

The results of detailed studies of 3 patients with essential thrombocythaemia (ET) are presented. Qualitative tests of platelet function were abnormal, and autologous platelet survivals were diminished. Megakaryocyte ploidy distribution analysis showed an increased proporttion of cells with high ploidy, and buoyant density distribution analysis showed increased proportions of less dense platelets. Ultrastructural studies of the platelets showed proliferation of the dense tubular system with deficiency of the surface-connected canalicular system. Megakaryocyte electron microscopy showed abnormal distribution of demarcation membrane complex and granules. The precise functional abnormality of the platelets in ET has not yet been defined, but a release defect of variable severity with corresponding morphological abnormalities of dense tubular and surface-connected canalicular systems, seems the most likely explanation.

Adult↗
PubMed1980

The effect of platelets on the in vitro response to prothrombin complex concentrates in F.VIII inhibitor plasma.

Incubation of prothrombin complex concentrates, both non-activated and activated, in plasma enhances coagulation. The effect is reduced with time and is augmented when platelets are present. Such concentrates correct the coagulation abnormality in vitro in haemophilic plasmas with factor VIII inhibitors and the correction is greater in platelet rich than platelet poor plasma. Platelets appear to protect incubated concentrates from inhibitors present in plasma. Platelets may play a role in mediating the in vivo clot-promoting activity of some components of these concentrates. This effect may contribute to unwanted thrombosis or, conversely, may facilitate the sometimes-observed haemostatic effect of concentrates in patients with inhibitors of factor VIII.

Blood Coagulation↗
PubMed1979

Coagulation in the sand crab (Ovalipes bipustulatus).

The coagulation mechanism of the sand crab (O. bipustulatus) has been investigated. From the coagulocytes (amoebocytes) present in the crab haemolymph (blood), fibrinogen (coagulogen) was isolated. It was shown to be homogeneous by electrophoresis on S.D.S. polyacrylamide gel and had a molecular weight similar to the A alpha-chain of human fibrinogen. Unlike human fibrinogen. Unlike human fibrinogen it cannot be dissociated by reduction. In fibrin polymerization, a crosslinking process takes place and this process was inhibited by glycine ethyl ester. A fibrin stabilizing factor is present in the crab haemolymph and this protein was able to cross-link human fibrin in the same manner as human factor XIII.

Animals↗
PubMed1979

A case of paroxysmal nocturnal haemoglobinuria terminating in a myeloproliferative syndrome.

This report discusses the case of a 60-year-old man who presented in 1969 with thrombocytopenia and mild marrow hypoplasia. A diagnosis of paroxysmal nocturnal haemoglobinuria (PNH), was established. The subsequent course included episodes of overt intravascular haemolysis. Thrombocytopenia reverted on several occasions during Oxymetholone therapy. The terminal phase of the illness was marked by the development of a leukocytosis and densely hypercellular bone marrow with splenomegaly. The features were those of a myeloproliferative disorder, although frank leukaemia did not develop.

Alkaline Phosphatase↗
PubMed1978

Hereditary C2 deficiency associated with immune complex disease.

A patient presenting with a syndrome probably due to immune complex deposition was investigated and found to possess an inherited C2 complement deficiency. Family studies indicated that the deficiency was transmitted as an autosomal recessive trait. HLA typing for the HLA-A and HLA-B specificities and HLA-D specificities indicated a close linkage between the HLA and C2 genes, as has been described elsewhere. The HLA-A and B locus specificities HLA-AW25 and HLA-B18 were coded for by each of the two chromosomes carrying the C2(0) gene. However, the two chromosomes differed at the HLA-D locus, as one coded for HLA-DW2 whilst the other did not. This case, therefore, provides a unique haplotype and may be of importance in mapping the C2(0) locus, as it suggests that the gene order on chromosome 6 is HLA-D, C2(0), HLA-B, HLA-A. Extensive complement component assays indicated that utilization of complement in the patient was occurring via the alternate complement pathway. It is suggested that, as a result of the C2 deficiency, infections with viruses and other agents could lead to an immune complex disease due to an impaired capacity to effectively eliminate circulating complexes.

Adult↗
PubMed1978

Isolation and insolubilisation of human F VIII by affinity chromatography.

A simple procedure has been developed for the isolation of coagulation factor VIII (F VIII) from plasma in a form which induces a monospecific antibody in rabbits. Amino acid precipitation from plasma was followed by gel filtration on Sepharose 4B and further purification was achieved by affinity chromatography on heparin-Sepharose. The material so isolated was identified by immunoelectrophoresis and lacked coagulant activity. The antiserum produced in rabbits inhibited F VIII coagulant activity and von Willebrand factor activity as measured by ristocetin platelet agglutination. The isolated IgG fraction insolubilised with CNBr-Sepharose 4B retained the ability to complex with F VIII. This complex possessed F VIII coagulant activity which could be removed in 0.6 M NaCl and dissociated in 8 M urea.

Amino Acids↗
PubMed1977

The role of factor XI in the coagulant activity of platelets.

Washed platelets were ruptured by freezing and thawing; a coagulant activity was released which would correct the clotting time of factor XI (FXI)-deficient plasma only in the presence of kaolin. Platelets from a FXI-deficient patient treated in a similar fashion also released a coagulant activity which could be absorbed onto Sepharose-heparin and eluted similarly to plasma FXI. Collagen was employed to induce a coagulant activity in platelet-poor plasma (PPP) and platelet-rich plasma (PRP) in the presence and absence of antibodies developed to purified FXI and FXII. The presence of FXII antibody had little effect on the activity induced in PRP. However, the presence of FXI antibody eliminated the difference between PPP and PRP. An activity was induced when FXI-deficient PRP was incubated with collagen and none with PPP. One type of collagen failed to induce a coagulant activity.

Blood Coagulation↗
PubMed1976

The structure of human thrombin in relation to autolytic degradation.

Human thrombin was obtained by activation of human prothrombin with venom of the Australian Taipan (Oxyuranus scutellatus scutellatus). This thrombin was precipitated with ammonium sulphate (75% saturation) and subsequently purified by gel-filtration (Sephadex G-75), ion-exchange (CM-Sephadex C-50) and affinity (aminobenzamidine-CH-Sepharose) chromatography. The final preparation (affinity thrombin) had a specific activity of 2340 Iowa units per absorbance unit (A1cm280). Thrombin proteins focused between 5 and 7, while prothrombin proteins focused to pH values less than 5. SDS-acrylamide gel electrophoresis indicated molecular weights of greater than 70 000 for prothrombin and 39 000, 28 000, 25 000-23 000 and 15 000-13 000 for affinity thrombin proteins. The 39 000-dalton species predominated (greater than 90%) when the enzyme was inhibited with phenylmethanesulphonyl fluoride prior to dialysis for SDS electrophoresis. Lack of such inhibition reduced the amount of the 39 000-dalton species to less than 60% with concomitant increase of the smaller species. Peptide mapping studies indicated that the smaller species were structurally related to the 39 000-dalton species. The amino acid compositions of the histidine and/or tyrosine containing peptides indicated a high degree of homology with bovine thrombin. It has been established that human thrombin can exist in at least two secondary structural forms, of different molecular weights, probably due to autolytic degradation of the largest (39 000-dalton) form.

Amino Acid Sequence↗
PubMed1975

Changes in coagulation factors and platelet function in response to progestational agents.

Levels of coagulation factors I, II, V, VII-X, VIII, IX, X, plasminogen and antithrombin III, were determined at midcycle in 17 test subjects using oral contraceptive agents, and in 10 control subjects. Immunoassay of factor II and antithrombin III was also carried out, and platelet aggregation quantitatively assessed. Significant increases were found in the activity of factors II, V, VII-X, X and plasminogen, but factor II antigen levels did not change. Platelet aggregation with collagen was significantly enhanced. No change occurred in antithrombin III activity or antigen levels.

Adolescent↗