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H K Lau

Publications and source records attributed to H K Lau.

52 records · Page 3Linked to original sources
PubMed1983

Restricted entry of an anti-rat epididymal protein IgG into the rat epididymis.

A rat epididymal protein (MW 32000) was isolated and purified from the rat caudal epididymal fluid. Mono-specific antiserum against this protein was raised in rabbits, purified and labelled with 125I. The labelled IgG was infused intravenously into anaesthetized male rats, and the transfer of the labelled IgG across the luminally perfused cauda epididymidis was studied. It was found that during the 2 h infusion period, radioactivity in blood rose, but no radioactivity could be detected in the perfusates, irrespective of whether the epididymis was perfused with Krebs bicarbonate solution or a solution which resembled the rat caudal fluid in ionic composition. In some experiments, rats were given a single intravenous injection of labelled IgG and radioactivity in the epididymal content was measured 10 days later. It was found that despite a high IgG level in blood and liver, no radioactivity could be detected in epididymal fluid and sperm. It is concluded that the blood-epididymis barrier restricts the passage from blood to lumen, an immunoglobulin directed against an epididymal protein.

Animals↗
PubMed1982

Studies of the prothrombin activation pathway utilizing radioimmunoassays for the F2/F1 + 2 fragment and thrombin--antithrombin complex.

We have evaluated the efficacy of utilizing radioimmunoassays (RIAs) for prothrombin activation fragments (F2/F1 + 2) and for thrombin--antithrombin complex (TAT) in purified systems and in whole blood. During venipuncture, appropriate anticoagulants were employed in order to prevent the generation of thrombin and factor Xa. The RIAs were shown to be specific for F2/F1 + 2 as well as TAT and did not interact with other plasma components. Initially, thrombin generation was studied in a purified human system of prothrombin, antithrombin, factor Xa, and factor V as well as phospholipid and Ca++. Under these conditions, the kinetics of F2/F1 + 2 and TAT generation were virtually superimposable. However, when factor V was omitted from the reaction mixture, a significantly greater amount of F2/F1 + 2 as compared to TAT was observable. Subsequently, prothrombin activation was monitored during the spontaneous coagulation of freshly drawn blood. Throughout the entire course of thrombin generation, the observable rate of formation of F2/F1 + 2 was considerably greater than that of TAT. We have examined the levels of F2/F1 + 2 and TAT in normal individuals. Our studies indicate that the concentrations of F1 + 2 and TAT average 1.97 nM and 2.32 nM, respectively. We have also quantitated the concentrations of F2/F1 + 2 and TAT in patients with disseminated intravascular coagulation. In these individuals, the levels of both components are elevated. However, the ratio of F1 + 2 to TAT ranges from 2.37 to 5.55. Thus, we conclude that under in vivo conditions, prothrombin activation is characterized by the accumulation of a stable precursor, such as prethrombin-2, and that this phenomenon may be related to an alteration of factor V function.

Antithrombins↗
PubMed1981

The influence of cimetidine, a histamine H2-receptor antagonist, on the gastric effects of reserpine in rats.

The effects of graded doses of cimetidine on both resting and reserpine-evoked gastric acid secretion were examined in relation to their influence on reserpine-induced ulceration, mast cell degranulation and mucosal microcirculatory changes in rat stomachs. Cimetidine 10 mg/kg or above reduced resting or reserpine-provoked gastric acid secretion as well as rumenal and glandular ulceration. However, non-acid-inhibiting doses, 5 mg/kg or below, continued to prevent glandular ulceration. Reserpine-evoked gastric glandular mucosal mast cell degranulation was unaffected by both acid-inhibiting and non-acid-inhibiting doses of cimetidine which dose-dependently blocked the superficial glandular mucosal microcirculatory volume changes. These results suggest that cimetidine prevents reserpine-induced glandular ulceration largely by blocking the ulcerogenic effect of histamine H2-receptor-mediated mucosal microcirculatory congestion, in contrast to antagonising rumenal lesions through acid inhibition; they also support the idea tha reserpine may release histamine mainly from the glandular mucosal mast cells. The possibility of another antiulcer mechanism, due to cytoprotection, is discussed.

Animals↗
PubMed1981

The treatment of unstable intertrochanteric fractures of the hip: a prospective trial of 150 cases.

We report a prospective clinical trial of 150 cases for the treatment of unstable intertrochanteric fracture of the neck of the femur. Three methods were tested in our series--skeletal traction with a tibial pin, medial displacement osteotomy and valgus osteotomy--with 50 patients in each group. Our results showed no significant difference between those treated with the Dimon and Hughston osteotomy and those treated by the Sarmiento osteotomy. Conservative treatment of skeletal traction for unstable fracture was found to be well tolerated by the Chinese patient. A low mortality and morbidity rate was found in this series with an overall infection rate of 4 per cent.

Aged↗
PubMed1981

Relationship between platelet secretion and prothrombin cleavage in native whole blood.

To determine the relationship between platelet secretion and prothrombin conversion in whole blood, the release of platelet factor 4 and the generation of a X(a)-specific cleavage product of prothrombin, fragment 1 + 2, were measured during the coagulation of whole blood. There was a parallel increase in the concentration of the two proteins. Over the first 5 min of incubation, platelet factor 4 concentration increased 6 ng/ml per min, and after 6-7 min, the rate of release increased to 750 ng/ml per min. Over the initial 5-7 min of incubation, fragment 1 + 2 concentration increased 1.5 pmol/ml per min with a subsequent increase of 45 pmol/ml per min. Incubation with 10 muM prostaglandin E(1) or 15 muM prostaglandin I(2) inhibited secretion of platelet factor 4 and delayed the onset of the rapid phase of fragment 1 + 2 generation by 8 min, while stimulation of platelet secretion with 1 mug/ml collagen suspension enhanced production of fragment 1 + 2. The addition of either 10 muM epinephrine or 100 ng/ml collagen suspension to whole blood did not affect either platelet factor 4 release or fragment 1 + 2 generation, although the combination of 3 muM epinephrine and 100 ng/ml collagen suspension enhanced platelet release and prothrombin cleavage. The relationship between platelet factor 4 release and prothrombin cleavage was also studied in Factor VIII-deficient blood. When 0.001 U/ml factor VIII activity was present, <80 ng/ml platelet factor 4 were released, and no fragment 1 + 2 was generated after 30 min of incubation. The addition of 0.008-0.08 U/ml Factor VIII activity progressively increased platelet factor 4 release and prothrombin cleavage. Platelet factor 4 release was normal at 0.08 U/ml Factor VIII activity, whereas prothrombin cleavage was still delayed. Very little thrombin, the amount generated by the cleavage of 3-5 nM fragment 1 + 2, was needed to induce release of platelet factor 4.

Aspirin↗
PubMed1979

The isolation and characterization of a specific antibody population directed against the prothrombin activation fragments F2 and F1 + 2.

We have raised antisera against human prothrombin activation fragment F2 in rabbits and have chromatographed the respective immunoglobulin G fractions on prothrombin-Sepharose, Pr1-Sepharose, and F2-Sepharose immunoadsorbents. The specific antibody population obtained was utilized to construct a double antibody radioimmunoassay capable of measuring as little as 0.8 ng/ml of this component. Our studies suggest that the immunoreactive site defined by this antibody population is most probably located within the negatively charged COOH-terminal region of F2. The immunologic expression of this area is unaffected by denaturation or reduction-alkylation of F2 as well as by attachment of polypeptide to the NH2-terminal of this component. However, the presence of covalently bound polypeptide at the COOH-terminal of F2 reduces its immunologic reactivity by 300- to 400-fold. Prothrombin, Pr1, and Pr*1, which contain the F2 region as part of their covalent structure, are at least 4000 to 7000 times less immunoreactive than F2 on a molar basis. Conversion of these components to thrombin as well as activation fragments generates the theoretically predicted level of immunoreactivity. Masking of the immunoreactive site within these zymogens is due to two phenomena. Firstly, covalent attachment of polypeptides on the COOH-terminal of the F2 segment significantly depresses the reactivity of this region. Secondly, a critical S--S bridge aids in the sequenstration of the immunoreactive site. This cross-link may facilitate interactions between the COOH-terminal of the F2 segment and other regions of the zymogen.

Amino Acid Sequence↗
PubMed1979

Disodium cromoglycate: a novel gastric antiulcer agent?

The influence of oral pretreatment with disodium cromoglycate (2.5 or 5 mg/kg X 9 doses) on the 4-h gastric effects of i.p. injected reserpine (5 mg/kg) was examined in rats. Disodium cromoglycate markedly prevented reserpine-induced ulceration, mucosal mast cell degranulation and superficial mucosal microcirculatory changes in the glandular portion of the stomach wall. These interesting results points to the possibility that disodium cromoglycate may also have gastric antiulcer effects in man.

Animals↗
PubMed1975

Ligand binding properties of hemoglobin 3 of the trout, Salmo gairdneri. The occurrence of an acid Bohr effect in the absence of heme-heme interaction.

The four components of hemoglobin from the rainbow trout (Salmo gairdneri) have been isolated. The oxygen affinities of the first two components eluted from the DEAE-cellulose column have much smaller pH dependencies than the last two components. These components have very low O2 affinities at low pH. The effect of pH on the equilibrium and kinetics of ligand binding to the third fraction, the pH-dependent component present in greatest amounts, has been studied. Measurements of ligand binding equilibria demonstrate the presence of both an alkaline and an acid Bohr effect. In the region of the alkaline Bohr effect the value of n in the Hill equation is a function of ligand affinity. For CO binding n decreases as the pH is decreased until at pH 6, the minimum ligand affinity is reached. At this pH there is also a complete loss of cooperative ligand binding. Decreasing the pH further results in an increase of ligand affinity, but this acid Bohr effect is not associated with a reappearance of cooperativity. This suggests that Fraction 3 of S. gairdneri is frozen in the low affinity, deoxygenated conformation at low pH and that the quaternary structure does not change even when fully liganded. However, the properties of the low affinity conformation of this hemoglobin are pH-dependent.

Animals↗