Biomedical subjects

A Sturk

Publications and source records attributed to A Sturk.

131 records · Page 8Linked to original sources

PubMed1981

Quantitative endotoxin determination in blood with a chromogenic substrate.

A method is described for the quantitative determination of endotoxins in blood. The method is based upon the endotoxin-dependent activation of a proenzyme present in Limulus amebocyte lysate. This activated enzyme is measured by using the chromogenic substrate S 2422. Inhibitors and activated coagulation factors possibly interfering in the assay are removed by dilution and boiling. The method has been proven to be fast (2.5 h), sensitive and reproducible with a detection limit of 10 ng/l. Preliminary results comparing the results of blood cultures with the endotoxin assay indicate a good correlation.

Bacteria↗

PubMed1980

Human blood platelet membrane glycoproteins. Resolution in different polyacrylamide gel electrophoretic systems.

The separation of the major platelet membrane glycoproteins of normal subjects and subjects with well defined platelet membrane glycoprotein abnormalities have been examined using four different polyacrylamide gel electrophoretic techniques (continuous and discontinuous). The mobilities of the resolved glycoprotein bands have been correlated with the glycoprotein nomenclature proposed for the conventional sodium dodecyl sulphate-phosphate buffer system. Since the glycoprotein distribution varies depending on the system used, the merits of each method should be considered before application to a specific problem.

Acetates↗

PubMed1979

Studies on the mechanism of ristocetin-induced platelet aggregation: binding of factor VIII to platelets.

The effect of ristocetin on the binding of [125I]factor VIII to platelets was studied. High and low affinity F.VIII binding sites exist on platelets. The high affinity sites bind 13 times more F.VIII than the low affinity sites. Ristocetin increased the binding of F.VIII to both types of binding sites by increasing the affinity of F.VIII for the platelet and increasing the total number of platelet binding sites. Chymotrypsin-treated platelets were not aggregated by ristocetin and F.VIII: these platelets have less of the major platelet membrane glycoproteins and bind much less [125I]F.VIII than do buffer-treated platelets with and without ristocetin.

Antigens↗

PubMedDate not supplied

Acetylsalicylic acid inhibits platelet PAI-1 antigen release without affecting circulating PAI-1 antigen in plasma.

An important plasminogen activator-inhibitor (PAI-1) is present in plasma and concentrated in alpha-granules of platelets. PAI-1 is released during platelet stimulation in vitro. It is presently unknown to what extent the treatment with acetylsalicylic acid (ASA) inhibits platelet PAI-1 release and if release inhibition has an effect on plasma PAI-1 levels. We therefore investigated by a double-blind placebo-controlled crossover study the effects of oral ASA (500 mg/day for 3 days) on platelet PAI-1 release and on plasma PAI-1 levels of healthy male volunteers. The PAI-1 release from platelets stimulated by arachidonic acid and collagen was significantly reduced by ASA: from average values of 88 and 80% to 14 and 17%, respectively (p less than 0.01). However, plasma PAI-1 levels were not modified by this treatment. We can conclude that platelet PAI-1 release does not play a role in modulating the plasma PAI-1 levels in healthy volunteers.

Adult↗

PubMedDate not supplied

The effect of storage on platelet morphology.

Platelet concentrates were stored for one, two or three days at 4 degrees C (unagitated) or at room temperature (unagitated and linearly agitated). After washing the concentrates twice at room temperature and then incubating them for 60 minutes at 37 degrees C, the platelet morphology was investigated by scanning and transmission electron microscopy. Platelets in freshly prepared concentrates were slightly activated, indicated by some pseudopod formation. Platelets stored at 4 degrees C rapidly lost the normal discoid shape. After three days of storage their surface membranes showed extensive folding, they were slightly vacuolated, and had lost most of their granules. Incubation of cold-stored platelets at 37 degrees C did not induce return to the discoid shape. Room temperature storage resulted in reversal of the slight initial platelet activation. After three days of unagitated room temperature storage the platelets were slightly more vacuolated than those stored with agitation. Room temperature storage usually resulted in well-preserved discoid platelets; however, some agitated platelet concentrates stored at room temperature contained a high proportion of odd shaped cells. This finding could not be correlated with pH change. The failure of platelets stored at 4 degrees C to return to the discoid shape after incubation at 37 degrees C could explain their short survival following transfusion. These results also provide a morphologic correlation with the reported slightly better recovery and survival of platelets stored at room temperature with agitation compared with those stored without agitation.

Blood Platelets↗