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Biomedical subjects

H Z Movat

Publications and source records attributed to H Z Movat.

At least 19 recordsLinked to original sources
PubMed1979

Molecular heterogeneity of Hageman trait (factor XII deficiency): evidence that two of 49 subjects are cross-reacting material positive (CRM+).

We have studied plasmas of 49 individuals with homozygous Hageman trait from 42 kindreds, all of which contained less than 1% of the Hageman factor (factor XII) clotting activity of pooled normal plasmas. Forty-seven plasmas contained less than 1% of Hageman factor antigen. In two other, unrelated individuals with Hageman trait, nonfunctional material immunologically indistinguishable from normal Hageman factor was detected in plasma by radioimmunoassay at concentrations of 39% and 80%, respectively. These plasmas did not contain circulating anticoagulants against Hageman factor and, as in ordinary Hageman trait, displayed impaired surface-mediated plasma reactions such as fibrinolysis and kinin generation. Upon immunodiffusion against anti-Hageman factor serum, these plasmas formed a single precipitin line of complete identity with normal plasma or purified Hageman factor. Upon immunoelectrophoresis, the precipitin line had the same mobility as normal Hageman factor. Nonfunctional Hageman factor and normal Hageman factor behaved identically on a Sephadex G-150 column (apparent MW = 100,000) and on sucrose density-gradient centrifugation (4.5S). Nonfunctional Hageman factor was adsorbed to kaolin as readily as normal Hageman factor, suggesting that the binding site to negatively charged surfaces is different from functional sites. Antiserum raised against Hageman factor-like material in a CRM+ Hageman trait plasma specifically inactivated Hageman factor activity in normal plasma. The plasmas of three heterozygotes in these families contained approximately twice as much Hageman factor antigen as Hageman factor activity, whereas those of 16 heterozygotes in ordinary (CRM-) Hageman trait families contained approximately equal amounts of activity and antigen. The present study indicates that rarely homozygous Hageman trait may be CRM+ and that this defect is genetically determined.

Cross Reactions↗
PubMed1979

Kinetics of prostaglandin production in various inflammatory lesions, measured in draining lymph.

Efferent lymph was collected over long periods via catheters surgically placed in popliteal and prefemoral lymph nodes of sheep. Prostaglandin (PG) E and F equivalents were measured with a radioimmunoassay. After stimulation with heat-killed Escherichia coli, PG levels rose dramatically in the efferent lymph but were undetectable in the contralateral control lymphatics or in the systemic circulation. When E coli were infused directly into a lymph node, the PG levels in the effluent lymph were inhibited with indomethacin. Carrageenan, delayed hypersensitivity, and lymphocyte transfer reactions were also studied. In the classic acute inflammations (caused by E coli and carrageenan) the PG levels rose early in the response (first 4 to 6 hours) compared with delayed production in the immune reactions. With PPD, PG levels peaked between 10 and 20 hours after injections, while PG rose 127 hours after allogeneic lymphocytes were injected. These results are discussed in relation to the role of PG in inflammation, and the use of the sheep lymphatic model in PG research is emphasized.

Animals↗
PubMed1978

Surface activation of factor XII (Hageman factor)--critical role of high molecular weight kininogen and another potentiator).

When factor XII was adsorbed to kaolin it slowly became activated and converted prekallikrein to kallikrein. In the presence of HMW-kininogen the rate of activation of factor XII and consequently that of prekallikrein was markedly enhanced. The enhancing effect of HMW-kininogen was a dose-dependent phenomenon. In order to enhance the activation of factor XII on a surface the HMW-kininogen molecule had to be intact. Cleavage of HMW-kininogen by kallikrein decreased the enhancing effect of HMW-kininogen, there being an inverse relation between the bradykinin-generated and the capacity to enhance factor XII activation. Another 'potentiator' of factor XII activation was isolated from proteins adsorbed to aluminum hydroxide. This potentiator further increased the activation of factor XII, also in a dose-dependent fashion. It was postulated that factor XII is slowly converted into its active form by exposure to negatively charged surfaces; that this process is enhanced by kallikrein and further accelerated by HMW-kininogen and the 'potentiator'; and that these enhancing substances probably act by opening active sites on the factor XII molecule.

Factor XII↗
PubMed1978

An aminopeptidase of human neutrophil leucocytes--its possible role in enhanced vascular permeability.

An aminopeptidase of human leukocyte lysosomes was partially purified by chromatography on SP-Sephadex, Sephadex G-200 and QAE-Sephadex. By QAE-Sephadex and isolelectric focusing it showed microheterogeneity, focusing at pH 3.7 and 4.1. By gel filtration its molecular weight was estimated to be approx. 200,000. The enzyme had leucine amino peptidase activity and pharmacological assays indicated that it converted lysyl- or methionyl-lysyl-bradykinin to bradykinin. Conversion of lysyl-bradykinin to bradykinin could be confirmed also by chromatography on CM-cellulose. When the neutrophil-derived enzyme acted on methionyl-lysyl-bradykinin it increased its effect of enhancing vascular permeability, when injected intradermally into guinea pits. Thus the enzyme may play a role in neutrophil leukocyte-mediated vascular phenomena of the inflammatory reaction.

Aminopeptidases↗
PubMed1977

The role of hyperemia in cellular hypersensitivity reactions.

The three physiological processes vascular permeability, blood flow and lymphocyte migration were all enhanced in tuberculin reactions induced in guinea pigs and sheep and also in normal lymphocyte transfer reactions in sheep. Microspheres labelled with 85Sr were used to measure blood flow to dermal sites and it was found that cellular hypersensitivity reactions had blood flows 7-25 times that of normal skin at the reaction peak. Vascular permeability was measured as an increase in the flow rate of afferent lymph or, in guinea pigs, as the enhanced leakage of intravascular 125I-albumin. When the permeability-inducing peptide bradykinin was injected directly into tuberculin reaction, the resulting permeability was greater than the sum of the tuberculin and bradykinin permeability taken individually and it was concluded that the hyperemia enhanced the permeability-inducing capacity of bradykinin. When the traffic of lymphocytes through hypersensitivity lesions was measured in sheep by cannulating the regional afferent lymph vessels and continuously collecting the lymph, the increase in lymphocyte traffic was of the same order of magnitude as the increase in blood flow. It is suggested than the antigen-induced enhancement of blood flow caused the increase in lymphocyte traffic and that the mechanism was similar to that occurring within lymph nodes during the immune response to all antigens.

Animals↗