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Biomedical subjects

J L Tullis

Publications and source records attributed to J L Tullis.

15 recordsLinked to original sources
PubMed1979

L-asparaginase effect on antithrombin-III levels.

The effect of L-asparaginase (L-asp) therapy on circulating antithrombin-III (AT-III) was monitored in three patients with acute lymphoblastic leukemia. Serial determination for AT-III by both a functional assay and an immunologic assay demonstrated a rapid decrease in serum AT-III levels, followed by a protracted recovery beyond the period of L-asp exposure. One of the three patients developed a reversible venous thrombosis of the arm. The mechanism of the L-asparaginase effect may be related to peripheral degradation of AT-III or to inhibition of production.

Adult↗
PubMed1978

Intraaterial hepatic infusion and intravenous adriamycin for treatment of hepatocellular carcinoma: a clinical and pharmacology report.

Four patients received intraarterial (ia) hepatic infusion and 10 received intravenous (iv) adriamycin for hepatocellular carcinoma. Four of each group are evaluable. The remaining 6 patients died within 14 days of intravenous therapy and are, therefore, considered nonevaluable. Patients received 2 to 9 courses of adriamycin every 3 weeks. One half of each group of evaluable patients had partial responses (pr). The group had pr for 22.5 weeks (range 8 to 37). The iv group had pr 27.2 weeks (range: 16 to 38.5). Mean survival was 21 weeks for nonresponders, and 43 weeks for responders. Intraarterial infusion did not protect patients from adriamycin toxicity. Cardiac and liver toxicity were not seen, but marrow and gastrointestinal toxicity developed at 1.2 X 10(-7)M adriamycin serum level. Adriamycin disappearance curves after ia and iv therapy were similar for similar bilirubin levels, and prolonged with hyperbilirubinemia. Ascites fluid did not accumulate detectable adriamycin. Pharmacokinetics are described in this report.

Adolescent↗
PubMed1978

Platelet antithrombin deficiency: a new clinical entity.

A kindred with a history of multiple thromboses was studied for coagulant abnormalities. A deficiency of serum antithrombin III was found in approximately half of the 13 family members by either coagulant or immunologic assay. No clear relationship between antithrombin III deficiency and a history of thrombosis was present. Platelet antithrombin assays were also studied in the same subjects. Ten of the 13 members were deficient. None of the remaining three had a history of thrombosis. On the basis of these findings, the hypothesis is proposed that in some cases familial hypercoagulability may be due to a platelet antithrombin deficiency and that the serum antithrombin III deficiency in some cases is a secondary rather than a primary effect.

Adolescent↗
PubMed1978

Ristocetin precipitation test: a new simple test for detection of fibrin monomer and fibrin degradation products.

The ristocetin precipitation test was designed as a simplified test to detect fibrin monomers and fibrinogen/fibrin degradation products (FPD/fdp). The ristocetin precipitation test is positive in plasma samples containing either fibrin monomer (greater than 5--10 microgram/ml) or early fdp (greater than 50--100 microgram/ml). The ristocetin precipitation test is negative in plasma with fibrinogen concentrations to 1,000 mg/dl or fibrinogen degradation products FDP) and late fdp to 400 microgram/ml. The ristocetin precipitation test is positive in plasmas collected from rabbits after the infusion of thrombin (2.7 u/kg) or thrombin and streptokinase (10,000 u/kg); the test is negative in plasmas from animals treated with streptokinase or saline solution alone. The ristocetin precipitation test is negative in normal human plasmas and plasmas from patients who have primary firbinogenolysis, but positive in plasmas from patients with disseminated intravascular coagulation. These results suggest that the restocetin precipitation test can be a useful test for the detection of plasma fibrin monomers and early fdp.

Animals↗
PubMed1978

Plateletpheresis by discontinuous centrifugation: effect of collecting methods on the in vitro function of platelets.

The in vitro function of platelets collected by two different methods during centrifugal plateletpheresis was compared. The RBC method involves collecting platelets with red cells followed by a supplementary spin to remove them, whereas the no-RBC method requires collecting platelets only from the buffy coat without red cells. Platelet response to adenosine diphosphate (ADP), epinephrine and collagen was slightly reduced in platelet-rich plasma (PRP) prepared by no-RBC technique and was markedly decreased in samples obtained by the RBC technique when compared to prepheresis controls. The decrease in platelet response to ADP, epinephrine and collagen was apparent in three testing systems: aggregation, release of serotonin and reptilase clot retraction. Both plasma and platelets appeared to be affected by the pheresis procedure. Platelet preparations obtained by both RBC and no-RBC techniques showed an increase of platelet factor 3 activity and an enhancement of aggregation, release of serotonin and clot retraction induced by thrombin as compared to prepheresis controls. Postpheresis platelet-poor plasma contains platelet membrane fragments which exhibit a high platelet factor 3 activity. The results showed that the RBC method, although providing a higher platelet yield, caused more qualitative alterations in platelets than in those obtained by no-RBC method, and that both methods of collecting platelets activated the procoagulant activity of platelets.

Blood Platelets↗
PubMed1977

Annual discourse--don't eat the quails.

Physicians were the first individuals recorded by name in history. Their attempts to define disease influenced fundamentally the cultures and religions of the world. Surgical skills, although highly developed in ancient times, appear to have been less well documented historically than medical disorders. Because of the greater threat to survival that diseases posed, they became incorporated into religious customs. Contagious diseases also influenced greatly the laws, traditions and historical events of the Bible. Leprosy provided a physical example that presumably represented an image of sin, but it probably was no more prevalent as a disease during Biblical times than at present. Many of the Biblical stories assumed to be allegorical may have been founded on medical fact. For example, it appears likely that the quails that poisoned the wandering Jews were contaminated with cyanide.

Animals↗
PubMed1977

Platelet antithrombins: role of thrombin binding and the release of platelet fibrinogen.

The nature of platelet antithrombin was elucidated by comparison of thrombin binding and antithrombin activities of intact platelets and by purification of antithrombin from platelet lysates using glycerol osmotic lysis, ethanol precipitation and Sephadex gel filtration techniques. The major portion of the antithrombin and thrombin binding activity of intact platelets is lost after brief sonication. The antithrombin activity in destroyed platelets is found to be due to platelet fibrinogen. Treatment of platelets with PGE1 (100 microng/ml) markedly inhibits (greater than 80%) the release of platelet fibrinogen induced by thrombin. However, the PGE1 treatment produced slight (less than 30%) but significant decrease of antithrombin activity of intact platelets, whereas the binding of thrombin to platelets was not affected by PGE1 treatment. The amounts of thrombin bound to and inactivated by PGE1-treated platelets at the same cell concentration are identical. The above results suggest that platelets contain at least two antithrombin activities. One, which accounts for the major portion of platelet antithrombin is mediated by thrombin binding to platelets. The other, which attributes to a lesser extent to platelet antithrombin activity, is due to the release of platelet fibrinogen. Also, antithrombin is readily demonstrated in a plasma medium indicating physiological significance of platelet antithrombin.

Antithrombins↗
PubMed1976

Aggregation of platelets and inert particles induced by thrombin.

Thrombin-induced platelet aggregation and release were investigated in washed platelet suspensions and in suspensions of inert particles in order to evaluate the role of fibrinogen-fibrin transformation in aggregometer tracings. Thrombin (0.25-2.0 U/ml) produced two waves of light transmission increase (LTI) in both platelet and inert particle suspensions containing fibrinogen, and concomittantly aggregates were observed under phase microscopy. Without fibrinogen, thrombin induced rapid release of platelet ADP but failed to cause second wave of LTI. The kinetics of LTI in platelet and inert particle systems were related to both thrombin and fibrinogen concentrations. A rapid second wave of LTI could be produced by direct interaction of thrombin-treated platelets or inert particles with polymerizing fibrin, and was inhibited by sodium sulfite and low pH of 5.1 which prevent fibrin monomer polymerization. No fibrin strands were noted in platelet aggregates fixed at the completion of the second wave of LTI. Apyrase and PGE1 inhibited the rate of first but not that of second wave LTI. The results suggest that the release of platelet ADP induced by thrombin primarily affects the first phase aggregation, and the second phase may result from interaction of thrombin-exposed platelets and polymerizing fibrin. Thus, the blood coagulation mechanism may be directly involved in platelet aggregation.

Adenosine Diphosphate↗
PubMed1975

Colchicine uptake and binding by human platelets.

The uptake and binding of antimitotic alkaloid colchicine has been demonstrated in washed preparations of human pletelets. A silicone oil technique was adapted so that both uptake and binding of 14C-colchicine were examined in the same platelet preparations. The time dependence and amount of colchicine taken up and bound by different pletelet preparations during a 90 to 120 min incubation period were highly reproducible. Both colchicine uptake and binding by intact platelets, and colchicine binding by preparations of lysed platelets were specific and temperature dependent. Colchicine uptake was slowly reversible. Magnesium and GTP enhanced colchicine binding by lysed platelet preparations but calcium decreased binding. exposure of platelets to either cold (4 degrees C) or to thrombin, which disrupt platelet microtubules, produced significant increases in colchicine uptake and binding. The thrombin effect was maximal at 37 degrees C and resulted in a greater increase in uptake and binding than that produced by either cold treatment alone or, by cold treatment followed by incubation with thrombin at 37 degrees C. The amount of increase in uptake and binding produced by thrombin was independent of both thrombin (1--5 Units/10(9) platelets) and colchicine concentrations (1--50 X 10(-6) M). It is postulated that thrombin may initiate the formation, or make available, colchicine binding sites (microtubule subunits) within platelets.

Blood Platelets↗
PubMed1975

Antithrombin activity of intact human platelets.

Antithrombin activity has been identified in intact washed human platelets. An apparent activity was demonstrated at platelet concentrations above 0.31 X 10(9)/ml, when platelet suspensions were incubated with 2.0 NIH units/ml of thrombin. Neither red cells nor white cells revealed antithrombin activity. No significant loss of the platelet antithrombin activity was observed after ten successive washings or after treatment of platelets with antibodies to antithrombin III or alpha2-macroglobulin. Almost the same amount of antithrombin activity as normal platelets was demonstrated in the platelets from an afibrinogenemic patient. Pre-treatment of platelets with trypsin, papain, and neuroaminidase reduced the activity significantly, whereas lipase was without effect. The platelet antithrombin reacted with thrombin in less than 3 seconds, and this rapid reaction of platelet antithrombin was different from that of plasma antithrombin III or fibrinogen. The thrombin-like clotting activity of ancrod was inhibited by fibrinogen but not platelets. Also, unlike plasma antithrombin III or fibrinogen, brief exposure to heat (56 degrees C or 60 degrees C) reduced considerable amounts of platelet antithrombin activity. These results suggest that platelets possess a specific antithrombin with different characteristics from other known antithrombins.

Afibrinogenemia↗
PubMedDate not supplied

Precipitation of fibrin monomers and fibrin degradation products by ristocetin.

Ristocetin, at relatively low concentrations (1.0 mg/ml-1.5 mg/ml), can selectively precipitate fibrin monomers and fibrin degradation products (fdp) from plasma without effect on fibrinogen or fibrinogen degradation products (FDP). 125I-labeled fibrin monomers and fibrin degradation products were precipitated by ristocetin when their plasma concentrations were greater than 0.25 microgram/ml and 50 microgram/ml, respectively. In order to obtain a visible precipitated, 2 microgram/ml of fibrin monomers of 50 to 100 microgram/ml of fibrin degradation products were necessary. These effects were optimally observed under the following conditions: (1) temperature, 20 C to 37 C; (2) pH, 7.0 to 7.5; and (3) incubation time, 15 to 60 minutes. Late-fibrin degradation products are approximately eight times less sensitive to ristocetin-induced precipitation than early-fibrin degradation products. Plasma medium is essential for the differentiation of fibrin monomers and fibrin degradation products from fibrinogen and fibrinogen degradation products by ristocetin. These results suggest that the specific detection of fibrin monomers and fibrin degradation products in plasma may be easily performed by ristocetin.

Anticoagulants↗