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PubMed1975

Platelet kinetics in canine ehrlichiosis: evidence for increased platelet destruction as the cause of thrombocytopenia.

A significant (P < 0.025) increase in the mean platelet diameter occurred in five Ehrlichia canis-infected dogs when platelet numbers decreased to 100,000/mul or less. Maximal incorporation of [(75)Se]selenomethionine into platelets of six uninfected dogs was 0.080 +/- 0.019% (mean +/- standard error) and occurred 5 to 6 days after dosage, whereas maximal incorporation was 0.036 +/- 0.004% within 2 to 3 days after dosage in seven chronically infected dogs that had thrombocytopenia. Analysis of the [(75)Se]selenomethionine curves yielded a platelet lifespan of 9 days in uninfected dogs versus 4 days in chronically infected dogs. Thus, megakaryocyte maturation and/or platelet release occurred at an accelerated rate in infected dogs, whereas increased destruction of newly produced labeled platelets diminished their number of peripheral blood. [(51)Cr]sodium chromate-labeled platelet survival was exponential, with a half-life of approximately 1 day in two dogs at 2 to 4 days postinfection and three chronically infected dogs. Platelet survival time was 8 days and rectilinear in four uninfected dogs. Platelet recovery was 39.43 +/- 2.86% in infected dogs as compared with 68.2 +/- 10.72% in uninfected dogs. Whole-body scans of one dog prior to and 7 days after infection showed that labeled platelets were destroyed primarily in the spleen. It is concluded that the thrombocytopenia in E. canis-infected dogs is the result of increased platelet destruction which begins within a few days after infection.

Animals↗
PubMed2005

Retroviral infection and selection of culture-derived platelets allows study of the effect of transgenes on platelet physiology ex vivo and on thrombus formation in vivo.

UNLABELLED: Background- We recently reported the development of culture-derived (CD) platelets with the aim to express any protein of interest in these platelets. We now report a specific protocol of retroviral infection into the progenitor cells and subsequent selection, which allows to generate large amounts of highly homogenous transgene-expressing CD platelets and to study transgene function rapidly and reliably at large-scale ex vivo and in vivo settings. METHODS AND RESULTS: After retroviral infection and selection, the activation-dependent expression profile of surface markers, aggregation, and granule release were investigated. The function of transgene-expressing CD platelets, the precursor cells of which had been retrovirally infected, compared well to noninfected CD platelets or freshly isolated platelets. Hence, the retroviral infection protocol did not alter platelet physiology. In contrast, adenoviral infection of precursors to CD platelets resulted in marked functional alterations that obviated their use in analytic experiments. Additionally, sufficient amounts of selected CD platelets were generated to warrant intravenous injections into living mice. This approach permitted study of their adhesive profile at endothelial lesions and their effect on thrombus formation in vivo by intravital videofluorescence microscopy. CONCLUSIONS: The novel selection method allowed us to produce recombinant transgene-expressing platelets in sufficient amounts to study genetically modified platelets in vitro and in vivo.

Adenoviridae↗
PubMed2003

CD40 is constitutively expressed on platelets and provides a novel mechanism for platelet activation.

CD40 is a 48-kDa phosphorylated transmembrane glycoprotein belonging to the TNF receptor superfamily. CD40 has been demonstrated on a range of cell types, and it has an important role in adaptive immunity and inflammation. CD40 has recently been described on platelets but platelet activation by CD40 has not been described. In the present study, we use flow cytometry and immunoblotting to confirm that platelets constitutively express surface CD40. CD40 mRNA was undetectable, suggesting that the protein is synthesized early in platelet differentiation by megakaryocytes. Ligation of platelet CD40 with recombinant soluble CD40L trimer (sCD40LT) caused increased platelet CD62P expression, alpha-granule and dense granule release, and the classical morphological changes associated with platelet activation. CD40 ligation also caused beta3 integrin activation, although this was not accompanied by platelet aggregation. These actions were abrogated by the CD40L blocking antibody TRAP-1 and the CD40 blocking antibodies M2 and M3, showing that activation was mediated by CD40L binding to platelet CD40. beta3 integrin blockade with eptifibatide had no effect, indicating that outside-in signaling via alphaIIbbeta3 was not contributing to these CD40-mediated effects. CD40 ligation led to enhanced platelet-leukocyte adhesion, which is important in the recruitment of leukocytes to sites of thrombosis or inflammation. Our results support a role for CD40-mediated platelet activation in thrombosis, inflammation, and atherosclerosis.

Blood Platelets↗
PubMed1985

Participation of platelets in the physiologic alterations of the AGEPC response and of IgE anaphylaxis in the rabbit. Effects of PGI2 inhibition of platelet function.

To further clarify the platelet dependence of acetyl glyceryl ether phosphorylcholine (AGEPC) physiologic activity and of IgE anaphylaxis in the rabbit, PGI2 was employed as an inhibitor of in vivo platelet function. Intravenous infusion of PGI2 (1 to 2 micrograms/kg/min) inhibited the AGEPC-induced decrease in dynamic compliance, increase in total pulmonary resistance, and transient decrease in tidal volume, but the right ventricular hypertension, bradycardia, and apnea were unaffected. Although PGI2 itself produced a marked systemic hypotension, AGEPC still induced a bimodal hypotensive response. Documentation that platelet function was inhibited by PGI2 included partial inhibition of AGEPC-induced thrombocytopenia, abrogation of platelet secretion (as assessed by plasma platelet factor 4 levels), and inhibition of ex vivo platelet aggregation. The AGEPC-induced leukopenia was not affected. In another group of rabbits, chlorpheniramine pretreatment inhibited the lung mechanical changes induced by AGEPC but did not affect the ventilatory or circulatory alterations, indicating that the lung mechanical alterations (but not any of the other alterations) are mediated by platelet-secreted histamine acting via H1 receptors. In IgE-producing rabbits intravenously challenged with antigen, PGI2 had no effect on any of the physiologic alterations, despite substantial inhibition of platelet secretion. From these results, together with previous platelet depletion studies, we conclude that AGEPC may be a significant mediator of the circulatory alterations and apnea of rabbit IgE anaphylaxis by platelet-independent mechanisms, but neither AGEPC nor platelets appear to be important in mediating the anaphylactic lung mechanical alterations.

Anaphylaxis↗
PubMed1998

Fast rotating atherectomy catheter tip inhibits platelet aggregation and ATP release: a study using platelet-rich plasma.

The interaction of atherectomy devices with the arterial wall is the focus of many studies, but their effect on the surrounding blood is largely unknown. This is a detailed investigation on the effects of a rotational atherectomy device with a fast rotating tip on platelet structure and function. Platelet-rich plasma (PRP) was obtained from six volunteers, divided into 5 mL samples, and subjected to the atherectomy tip rotating at 20, 40, or 80 thousand rpm for 30 or 60 seconds. Platelet aggregation to collagen or adenosine diphosphate (ADP) was obtained in all samples by means of a dual-chamber optical aggregometer. The fast rotating catheter tip caused marked inhibition of platelet aggregation to both collagen and ADP. The maximum extent of aggregation was reduced from 85% +/-2.8 in control to 46% +/-4.8 with collagen (p<0.01) and from 86.1% +/-6.9 to 25.1% +/-4.3 with ADP (p<0.01). The rate of aggregation (measured at 4 minutes) dropped from 81.3% +/-2.7 to 40% +/-4.5 and from 73.9% +/-8.5 to 12.5% +/-2.6 (p<0.005) with collagen and ADP, respectively. These effects were related to rotating speed and duration of exposure. ATP release in response to collagen fell from 2.63 +/-0.13 nMol in control to 0.7 +/-0.1 nMol, p<0.001 after exposure to the rotating tip. There was no significant change in platelet count, nor was there formation of platelet aggregates (platelet aggregate ratio remained unchanged) to account for these phenomena. Furthermore, transmission electron microscopy showed no significant platelet disruption or release of granules, and little signs of activation were seen even after addition of collagen. This is the first study to demonstrate that exposure to a fast rotating catheter tip inhibits in vitro platelet aggregation and ATP release. There were no apparent loss of integrity of platelet structure, release of granules, or formation of platelet aggregates. This phenomenon and its clinical implication justify further investigation.

Adenosine Triphosphate↗
PubMed2004

Anti-GPVI-associated ITP: an acquired platelet disorder caused by autoantibody-mediated clearance of the GPVI/FcRgamma-chain complex from the human platelet surface.

Platelet glycoprotein (GP) VI is a 62-kDa membrane glycoprotein that exists on both human and murine platelets in a noncovalent complex with the Fc receptor (FcR) gamma chain. The GPVI/FcRgamma-chain complex serves as the major activating receptor for collagen, as evidenced by observations that platelets genetically deficient in GPVI or the FcRgamma chain are highly refractory to collagen-induced platelet activation. Recently, several different rat anti-murine GPVI monoclonal antibodies, termed JAQs 1, 2, and 3, were produced that had the unique property of "immunodepleting" GPVI from the murine platelet surface and rendering it unresponsive to collagen or GPVI-specific agonists like convulxin or collagen-related peptide (CRP). Herein, we describe a patient with a mild bleeding disorder and a moderately reduced platelet count whose platelets fail to become activated in response to collagen or CRP and inefficiently adhere to and form thrombi on immobilized collagen under conditions of arterial shear. Although the amount of GPVI platelet mRNA and the nucleotide sequence of the GPVI gene were found to be normal, both GPVI and the FcRgamma chain were nearly absent from the platelet surface and were markedly reduced in wholeplatelet detergent lysates. Patient plasma contained an autoantibody that bound specifically to GPVI-positive, normal platelets, and cleared soluble GPVI from the plasma, suggesting that the patient suffers from a rare form of idiopathic thrombocytopenic purpura caused by a GPVI-specific autoantibody that mediates clearance of the GPVI/FcRgamma-chain complex from the platelet surface. Since antibody-induced GPVI shedding now has been demonstrated in both humans and mice, these studies may provide a rationale for developing therapeutic reagents that induce temporary depletion of GPVI for the treatment of clinical thrombosis.

Adult↗
PubMed2001

Reduction of the platelet review rate using the two-dimensional platelet method.

Accurate platelet enumeration is critical for optimal treatment of patients with platelet and bleeding disorders, leukemias, and other neoplasias. The majority of automated hematology analyzers count platelets by size differentiation alone, which may result in falsely elevated platelet counts for samples containing interfering particles such as RBC fragments, microcytes, and cell debris. Most analyzers flag questionable platelet counts, necessitating review of results with confirmation by an alternative method, thus increasing the cost of performing platelet counts and delaying results. We studied the effect of a new platelet analysis method, based on measurement of size and refractive index, on the laboratory review rate for platelet counting. We demonstrated that this method yields higher accuracy for platelet counts in samples with interferences, especially for platelet counts less than 50 x 10(3)/microL (< 50 x 10(9)/L). As a result of the 2-dimensional analysis, the review rate for platelet counts was reduced by 65% in our institution, resulting in substantial savings.

Blood Platelets↗
PubMed1995

Platelet count and platelet indices at various stages of normal pregnancy in smoking and non-smoking women.

UNLABELLED: Our objective was to compare the platelet count and platelet indices of smoking and non-smoking women at different stages of normal pregnancy. STUDY DESIGN: In 247 non-smoking and 123 smoking healthy pregnant women the platelet count, the mean platelet volume, the platelet distribution width and the plateletcrit were compared at 0-10, 11-20, 21-30 and 31-40 weeks of pregnancy. Exclusion criteria were a diastolic pressure > or = 90 mmHg, an endocrine disease, a coagulation disorder, acetylsalicylic acid or phenprocoumon use. A women was considered a smoker if she smoked more than 4 cigarettes a day. Non-smokers were defined as women reporting no smoking at all. Blood samples were run on the Sysmex NE-8000. RESULTS: There was no significant difference between the platelet count in the two groups. In the non-smoking group, the platelet count showed a significant decrease with gestational age (287 x 10(9)/l to 258 x 10(9)/l). This was not the case in the smokers group. The mean platelet volume of the smokers was significantly lower than that of the non-smokers in the last ten weeks of pregnancy (10.4 fl versus 10.7 fl). The platelet distribution width and the plateletcrit did not change under the influence of cigarette smoking. CONCLUSION: Smoking during pregnancy does not significantly affect platelet count or platelet indices.

Adult↗
PubMed2000

Platelet substitutes and novel platelet products.

Despite many advances in the safety, processing and storage of conventional 22 degrees C liquid-stored allogeneic platelet concentrates, there are still significant drawbacks to standard platelet concentrates used in transfusions for patients with thrombocytopenia. Efforts to overcome these shortcomings have been undertaken in both academic and commercial settings, resulting in an array of novel platelet products and substitutes that are currently at various stages of development. This review summarises the recent developments in lyophilised platelets, infusible platelet membranes (IPM), red cells bearing arginine-glycine-aspartic acid (RGD) ligands, fibrinogen-coated albumin microcapsules and liposome-based agents as putative alternatives to conventional transfusions involving allogeneic platelet concentrates. These various products are designed to replace the use of allogeneic donor platelets with modified or artificial platelets, to augment the function of existing platelets and/or provide a procoagulant material capable of achieving primary haemostasis in patients with thrombocytopenia. Preclinical studies have been encouraging for several of these platelet substitutes and novel platelet products, however, to date, only a few of these products have entered human trials. With the ongoing development of these diverse products, properties necessary for haemostatic effectiveness will become apparent. Safety and efficacy, however, must be demonstrated in preclinical and Phase I - III clinical trials, before these novel agents can be used clinically for patients with thrombocytopenia.

Animals↗
PubMed1987

Inhibition of human tumor cell induced platelet aggregation by antibodies to platelet glycoproteins Ib and IIb/IIIa.

Tumor cell induced platelet aggregation was shown to be inhibited in a dose dependent manner by preincubation of human platelets with antibodies to platelet glycoprotein Ib and the IIb/IIIa complex. Combination of antibody to Ib and antibody to the IIb/IIIa complex at concentrations which produced half maximal inhibition of platelet aggregation alone caused complete inhibition of tumor cell induced platelet aggregation. Antibodies to platelet glycoproteins Ib and the IIb/IIIa complex also inhibited platelet synthesis of thromboxane A2, but not synthesis of 12-hydroxyeicosatrienoic acid. Inhibition of tumor cell induced platelet aggregation with antibodies against platelet glycoproteins suggests a role for these glycoproteins in tumor cell-platelet interactions and possibly platelet facilitated tumor cell metastasis.

Antibodies↗
PubMed1976

Effect of platelet age on adhesiveness to collagen and platelet surface charge.

Adhesion to collagen was investigated as a function of platelet age in rat platelets. Platelet adherence was measured using EDTA-containing platelet- rich plasma which was added to preparations of collagen fibers clamped between magnetic stirrers by recording changes in light transmission. The plot of light transmission versus logarithm of time was linear and allowed calculation of a slope factor which related to the rate of adherence. Neither the amount of collagen nor the platelet count were limiting in the test. Young platelet populations (less than or equal to 1 day old) were obtained during the recovery phase from immune induced thrombocytopenia. Old platelet populations were prepared by blocking thrombopoiesis with cyclophosphamide. Young platelets showed a moderate but statistically significant increase in adhesivity to collagen but old platelets did not differ significantly from randomly aged platelets in this function. The electrophoretic mobility of platelets was not affected by their age.

Animals↗
PubMed2000

Heparin-induced thrombocytopenia: new evidence for the dynamic binding of purified anti-PF4-heparin antibodies to platelets and the resultant platelet activation.

Immune heparin-induced thrombocytopenia (HIT) is associated with antibodies directed against a complex of platelet factor 4 (PF4) and heparin. We were able to affinity purify anti-PF4-heparin IgG (HIT IgG) from the plasma of 2 patients with HIT. Under conditions that were more physiological and sensitive than those in previous studies, we observed that this HIT IgG caused platelet aggregation on the addition of heparin. Platelets activated with HIT IgG increased their release and surface expression of PF4. We quantitated, for the first time, the binding of affinity-purified HIT iodine 125-IgG to platelets as they activated in a plasma milieu. Binding of the HIT IgG was dependent on heparin and required some degree of platelet activation. Blocking the platelet FcgammaRII with the monoclonal antibody IV.3 did not prevent HIT IgG binding to activated platelets. We concluded that anti-PF4-heparin IgG is the component in these HIT plasmas that induces platelet aggregation. The Fab region of HIT IgG binds to PF4-heparin on the surface of activated platelets. We propose that only then does the Fc portion of the bound IgG further activate the same or adjacent platelets through the Fc receptor. Our data support a dynamic model of platelet activation in which released PF4 enhances further antibody binding and more release.

Anticoagulants↗
PubMed2000

Platelet surface P-selectin molecules increased after exposing platelet to a high shear flow.

BACKGROUND: P-selectin is known to play a crucial role in leucocyte recruitment at sites of vascular injury. Although platelet surface expression of P-selectin molecules are well known to occur after platelet stimulation by chemical agonists such as alpha-thrombin, it is still uncertain whether P-selectin expression occurs in the process of the more physiological platelet activation pathway mediated by interaction between von Willebrand factor (vWF) and platelet receptor proteins, including glycoprotein (GP) Ibalpha and GP IIb/IIIa, occurring under high shear rates generated by blood flow. METHODS: We have developed a method to detect P-selectin molecules expressed on platelet surface with flow-cytometer and monoclonal antibody, which can bind exclusively to P-selectin (WGA1), directly conjugated with fluorescein isothiocynate. This method allowed us to measure platelet surface P-selectin molecules semiquantitatively. RESULTS: We demonstrated that a significant increase in platelet surface P-selectin molecules occur after exposing platelets to a relatively high shear rate of 10,800 s(-1). We have also demonstrated that shear-induced surface expression of P-selectin as well as microparticle release from platelets depended at least on the interaction between von Willebrand factor and glycoprotein Ibalpha, a platelet surface receptor for the former. CONCLUSIONS: Shear-induced von Willebrand-mediated surface expression of P-selectin may play a role in leucocyte recruitment in platelet thrombi at vascular injury sites.

Antibodies, Monoclonal↗
PubMed1979

In vivo platelet retention in human bleeding-time wounds. I. Normal subjects and patients with platelet dysfunction.

PRB was measured in standardized skin puncture wounds. Platelets in wound blood samples collected in EDTA-heparin-containing micropipettes were counted electronically following gravity separation of plasma. The relationship between the wound platelet count (expressed as percent of the venous blood platelet count) and time was found to be linear during the first 3 min of bleeding. The slope of the linear regression line for percent of venous blood platelet count vs. time was 20.8 +/- 8.9 (mean +/- S.D.) in 31 normal subjects. Nine of 10 patients with significant, nonpharmacologic platelet dysfunction were found to have markedly decreased PRB. The determination of PRB was found to be reproducible, and control studies excluded platelet clumping and sedimentation of platelets as factors which significantly influenced the results. In contrast to previous observations, the results of this study indicate that platelets are removed from circulating blood at an increasing rate during the first 3 min of bleeding in normal subjects. Furthermore, a significant degree of EDTA-reversible clumping of platelets normally occurs during bleeding. The method described permits an accurate assessment of the quantitative and dynamic aspects of platelet participation in the arrest of bleeding. The determination of PRB holds promise in the evaluation of the biological significance of in vitro evidence of platelet dysfunction, and it may be useful in the evaluation of patients with hemorrhagic and thromboembolic disorders.

Blood Coagulation↗
PubMed2002

[Change of platelet count and P-selectin in preserved platelet concentrates].

To observe the change of quantity and quality of platelets preserved in a full-sealed bag, and explore the difference of platelets preserved in oscillating and static conditions at (22 +/- 2) degrees C, the platelet concentrates were prepared with a CS-3000-plus blood cell separator, the platelet counts were performed with automatic blood cell analyzer and P-selectin in supernatant of platelet concentrates was detected by ELISA. The results showed that both of platelet count and P-selectin content in the platelet concentrates had no significant difference between oscillating and static preservation condition. With prolongation of preserved time, the platelet count decreased and P-selectin content increased gradually in both preserved conditions. There was no difference in the platelet counts during 0 - 72 hours preservation in both conditions, and significant difference was seen in 96 - 120 hours preservation. It was concluded that the expired date for platelet product preserved in CS-3000-plus blood cell separator full-sealed system should be 3 days. Under the condition of (22 +/- 2) degrees C, the quality of the platelet preserved in oscillating state is not superior to static preservation.

Blood Platelets↗
PubMed1992

Effects of splenectomy on immune thrombocytopenic purpura in (NZW x BXSB) F1 mice: analyses of platelet kinetics and anti-platelet antibody production.

Effects of splenectomy on platelet kinetics and production of anti-platelet antibodies were studied in male (NZW x BXSB) F1 (W/B F1) mice, which are known as the animal model of immune thrombocytopenic purpura (ITP). Studies on organ localization of radiolabeled platelets revealed that splenic uptake significantly increases in W/B F1 mice in comparison with that of normal controls. W/B F1 mice showed a significant increase in platelet counts and, in contrast with sham-operated controls, high levels of platelet counts were maintained up to 6 weeks after splenectomy. Platelet lifespans (PLSs) did not reach normal levels, although prolonged PLSs were observed. In addition, platelet-associated antibody (PAA) values showed a tendency towards transient decrease, but there was no change in platelet-bindable serum antibodies (PBAs). These findings indicate that the suppression of anti-platelet antibody production is essential to the treatment of ITP; splenectomy may not be effective in treating severely affected ITP patients because, although the spleen is one of the major sites of platelet sequestration and antibody production, reticulo-endothelial systems (RESs) (liver, bone marrow, lymphnodes, etc.) other than the spleen are also responsible for the destruction of platelets. We therefore consider the W/B F1 mouse to be a useful model of human ITP, and believe that it provides valuable information for the development of new therapeutic agents in patients with ITP, especially those who do not respond to splenectomy.

Animals↗
PubMedDate not supplied

Oxidative metabolism in platelets, platelet aggregation, and hematology in patients undergoing multiple hyperbaric oxygen exposures.

Repeated hyperbaric oxygen (HBO2) treatments at 2.2 ATA for 90 minutes each are used to treat chronically ill patients with problem wounds, but there are concerns about the cytotoxicity of oxygen to blood cells and platelet function during prolonged HBO2 therapy. We recruited 31 consenting patients scheduled for multiple HBO2 treatments to evaluate oxidative metabolism in platelets, platelet aggregation, and hematology (mean age +/- standard error, 61 +/- 2.6 years, 20 males, 11 females). Venous blood was collected before and after the 1st and 20th HBO2 treatments. No effect of HBO2 was observed on red cell counts, hematocrit, hemoglobin, mean red cell volume (MCV), platelet counts, basal levels of lactate production by platelets, ferric reducing ability of plasma (FRAP), or plasma protein. The capacity for oxidative metabolism (lactate ratio) in platelets was not affected by HBO2, except in smokers where it increased by the 20th HBO2 treatment. Mean lymphocyte count was increased by 38% after the 20th treatment. There was also a 23% increase in platelet protein content, and a 24% increase in arachidonic acid-dependent platelet activation. Collagen-dependent platelet aggregation was unaffected. Blood glucose showed HBO2-dependent variability, but remained in the normal range. Plasma lactate levels decreased significantly from 3.2 to 2.5 mmol/l by the end of the study. Overall, we found no evidence that 20 HBO2 sessions caused adverse effects on platelet aggregation or oxidative metabolism in platelets, red or white cell counts, or total antioxidant status of the plasma.

Acetaminophen↗
PubMed1991

Collagen-induced exposure of anionic phospholipid in platelets and platelet-derived microparticles.

We have shown recently that the calcium-dependent phospholipid-binding protein annexin V (placental anticoagulant protein I) can be used to study the exposure of anionic phospholipid after platelet activation. In this study we have further examined the mechanism of this process. Collagen-induced exposure of annexin V binding sites correlated directly with increased ability to support activity of the reconstituted prothrombinase complex. The potency of annexin V as an inhibitor of platelet prothrombinase was the same as its Kd for platelets. Prior incubation of platelets with 5'-p-fluorosulfonylbenzoyladenosine or p-chloromercuribenzenesulfonate had no significant effect on annexin V binding. Similarly, inhibition of platelet cyclic endoperoxide synthesis by acetylsalicylic acid or indomethacin did not inhibit annexin V binding. Staurosporine inhibited collagen-induced, but not A23187-induced, annexin V binding. Agents that increase intraplatelet cyclic nucleotides partially inhibited collagen-induced annexin V binding. Thus, collagen-induced exposure of anionic phospholipid appears to depend primarily on increases in intraplatelet free calcium and may be independent of ADP- or endoperoxide-mediated pathways. Binding sites for annexin V on microparticles derived from collagen-stimulated platelets were demonstrated by flow cytometry and gel filtration. In addition, prior incubation of platelets with 100 nM annexin V inhibited factor Va binding to both platelets and platelet-derived microparticles. These results support the concept that the procoagulant effect of platelets and platelet-derived microparticles is mediated by calcium-induced exposure of anionic phospholipids.

4-Chloromercuribenzenesulfonate↗