Dietary Diversity and Vegetable and Fruit Consumption of Households in a Resource-Poor Peri-Urban South Africa Community Differ by Food Security Status.

Sociodemographic, living standard measure, consumption of vegetables and fruit, and dietary diversity in relation to household food security were assessed. Using a hunger score, households were categorized as food secure (n = 125) or food insecure (n = 273). Food secure respondents had a higher mean dietary diversity score (3.98; 95%CI [3.79, 4.18] versus 3.65; 95% [CI 3.53, 3.77]), were more likely to eat vitamin A-rich foods (OR 1.15; 95% CI [1.05, 1.26]), a more varied diet (DDS ≥ 4, OR 1.90; 95% CI [1.19, 3.13]), and vegetables daily (OR 3.37; 95% CI [2.00, 5.76]). Cost limited daily vegetable/fruit consumption in food insecure households. Respondents with ≥ 8 years of schooling were more likely (OR 2.07; 95% CI [1.22, 3.53]) and households receiving social grants were less likely (OR 0.37; 95% CI [0.19, 0.72]) to be food secure. Results highlight the association between dietary diversity and household food security.

Role of the gamma chain Ala-Gly-Asp-Val and Aalpha chain Arg-Gly-Asp-Ser sites of fibrinogen in coaggregation of platelets and fibrinogen-coated beads.

Fibrinogen (Fg) mediates platelet aggregation and adhesion to artificial surfaces. The carboxyl terminus of the gamma chain of Fg (residues AGDV at gamma408-411) is known to play an exclusive role in platelet aggregation, while there is no known role for the consensus RGD sites in the Aalpha chain. In this study, we used flow cytometry to measure the coaggregation (CA) of platelets with Fg-coated beads, and investigated which domains in surface-immobilized Fg support platelet adhesion. CA of platelets with Fg-beads was nearly abolished in the presence of 4A5, a monoclonal antibody (mAb) whose epitope includes AGDV, while Z69/8, a mAb that also binds to the gamma chain carboxyl terminus but does not cover AGDV, had little effect. When beads were coated with recombinant Fg (rFg) lacking AGDV, CA was similarly abolished. In contrast, beads coated with Fg that lacked the RGDS site, supported platelet CA as did intact Fg. These results were confirmed in experiments that measured the binding of activated soluble glycoprotein IIb and IIIa (GPIIbIIIa), the platelet membrane glycoprotein complex known to be the Fg receptor, to immobilized Fg. This binding was inhibited by mAb 4A5, but not by mAb Z69/8. Binding was totally retained when beads were coated with Fg lacking RGDS, but was completely lost when beads were coated with Fg lacking AGDV. These results demonstrated that the AGDV sequence on the carboxyl terminus of the gamma chain of Fg plays an exclusive role in platelet adhesion to surface-immobilized Fg, while the carboxyl terminus of the Aalpha chain, including a consensus RGD site, is not required.

Glycoprotein Ib-IX-mediated activation of integrin alpha(IIb)beta(3): effects of receptor clustering and von Willebrand factor adhesion.

The interaction between the platelet glycoprotein (GP) Ib-IX complex and von Willebrand factor (VWF) initiates both hemostasis and pathological thrombosis. This interaction is not only the first adhesive event of platelets at sites of vessel injury, but also facilitates fibrinogen binding to alpha(IIb)beta(3), which subsequently results in platelet aggregation. Since it has been suggested that GP Ib-IX clustering may promote platelet activation, we investigated the effect of such clustering on both VWF-GP Ib-IX and fibrinogen-alpha(IIb)beta(3) bonds using optical tweezers. In our system, fusion of tandem repeats of FK506-binding protein (FKBP) to the cytoplasmic tail of the GP IX subunit of the GP Ib-IX complex allowed subsequent receptor clustering within the plasma membrane by the bivalent, cell-permeant small molecule ligand AP20187. We measured binding forces between polystyrene beads coated with either plasma-derived VWF or the VWF A1 domain and GP Ib-IX(FKBP)2, and those between fibrinogen-coated beads and alpha(IIb)beta(3) expressed on Chinese hamster ovary cells. The minimal detachment force between GP Ib-IX(FKBP)(2) and A1 or plasma-derived VWF doubled after AP20187 was added. The binding force between immobilized fibrinogen and alpha(IIb)beta(3) was not changed by the clustering agent; however, the strength of single fibrinogen-alpha(IIb)beta(3) bonds increased significantly after ligation of GP Ib-IX(FKBP)(2) by A1. These results demonstrate that GP Ib-IX clustering increases the overall strength of its interaction with VWF. Furthermore, signals from GP Ib-IX can activate alpha(IIb)beta(3), thereby increasing the strength of its interaction with fibrinogen.

Ristocetin- and thrombin-induced platelet aggregation at physiological shear rates: differential roles for GPIb and GPIIb-IIIa receptor.

We recently reported that washed platelets (WP) activated with ADP and expressing surface-bound vWF aggregated in flow through small tubes or in a cylindrical couette device at physiological shear rates of G = 300 s(-1)-1000 s(-1) in the absence of exogenous ligands, with GPIb-vWF partially, and activated GPIIb-IIIa totally required for the aggregation. We have now extended these studies to aggregation of platelets "activated" with ristocetin or thrombin. Washed platelet suspensions with added soluble vWF and ristocetin (0.3-0.75 mg/ml), or activated with thrombin (0.01-0.5 U/ml) but no added ligand, were sheared in a coaxial cylinder device at uniform shear rate, G = 1000 s(-1). The collision capture efficiency (alphaG) with which small aggregates form (= experimental/calculated initial rates of aggregation) was correlated with vWF platelet binding assessed by flow cytometry. The vWF-GPIb interaction was exclusively able to support ristocetin-mediated shear aggregation of metabolically active platelets, with very few vWF monomer equivalents bound per platelet (representing < or = 10 molecules of 10 million Da) required to yield high capture efficiencies (alphaG = 0.38+/-.02; n = 11), suggesting rapid and stable bond formations between vWF and GPIb. However, platelet surface-expressed vWF, generated by addition of thrombin to washed platelets, was found to mediate platelet aggregation with alphaG = 0.08+/-.01 (n = 6), surprisingly comparable to that previously reported for WP and ADP activation. Blocking the GPIIb-Illa receptor decreased alphaG by 95+/-3% (n =3), while a monoclonal antibody to the vWF site on GPIb caused a 49+/-7% (n = 8) decrease in alphaG. The partial role for GPIb thus appears to reflect a facilitative function for increasing contact time between flowing platelets, and allowing engagement of the GPIIb-IIa receptor to yield stable attachment.

Thrombin receptor occupancy modulates aggregation efficiency and platelet surface expression of vWF and thrombospondin at low thrombin concentrations.

Previous studies evaluating requirements for occupancy of thrombin receptors in normal platelet secretion and aggregation, using the thrombin antagonists hirudin and PPACK (D-Phe-Pro-Arg-chloromethylketone), have suggested that at low thrombin activating concentrations (0.025-0.13 U/ml), occupancy was required only in the first 45-60 s following activation. In our study, we differentiate between thrombin receptor occupancy requirements for surface expression of secreted adhesive proteins, for activation of GPIIb-IIIa receptors, and for aggregation of washed platelets (WP) in laminar shear flow. Platelets activated with 0.05 U/ml thrombin for 10 min to allow maximal secretion (hereafter referred to as "pre-activated platelets"), then sheared, showed a 50-70% decrease in platelet counts after 60 s of shear. Treatment of pre-activated platelets with hirudin or PPACK produced a 65% reduction of capture efficiencies, alphaG (reflecting experimental/theoretical initial rates of aggregation), as well as a 30-40% decrease in the surface expression of von Willebrand factor (vWF) and thrombospondin (TSP). However, alpha-granule membrane P-selectin expression and numbers of activated GPIIb-IIIa receptors were comparable for treated and non-treated platelets. No significant difference in any of the parameters tested was observed when platelets were similarly pre-activated with 0.2 U/ml thrombin, due to treatment with thrombin antagonists. Binding of soluble FITC-vWF (GRGDSP-sensitive) to pre-activated, thrombin antagonist treated platelets, was greatly reduced (> or =80%). Soluble Fg was shown to bind to antagonist-treated pre-activated platelets, but could not significantly enhance platelet aggregation. Although occupancy of thrombin receptors by catalytically active thrombin is required transiently for secretion and activation of platelets, there is a further requirement for thrombin occupancy at low thrombin concentrations, for optimizing initial rates of platelet aggregation, surface expression of vWF and TSP, and activated GPIIb-IIIa ligand recognition.

Complementary roles for fibrin(ogen), thrombospondin and vWF in mediating shear-dependent aggregation of platelets stimulated at threshold thrombin concentrations.

We have evaluated the relative contribution of the adhesive ligands, von Willebrand factor (vWF), fibrinogen (Fg) and thrombospondin (TSP), all surface-expressed on washed platelets (WP) activated with a threshold thrombin concentration (approximately 0.04 U/ml), to platelet microaggregation (PA) at shear rates (G) from 300-2000 s(-1). In suspensions of thrombin-activated WP sheared immediately (tau0), all three ligands were required for optimal aggregation at all G, as shown by a 50-70% inhibition of capture efficiencies of PA (measured from initial rates of PA), by antibodies (Abs) directed against each protein. This aggregation involved both GPIb and GPIIbIIIa, as indicated by approximately 80% and 100% inhibition by Ab 6D1 and Ab 10E5, respectively. For WP preexposed to thrombin for 10 min to ensure maximal surface expression of secreted ligands and activated GPIIbIIIa (tau0), vWF was predominantly required at all G (63-75% inhibition by anti-vWF Ab), together with TSP (35-50% inhibition by anti-TSP Ab). Under these conditions, Fg was extensively converted to fibrin, so that fibrin, rather than Fg, could participate in microaggregation, with GPIb less required than GPIIbIIIa as indicated by a 30-60% inhibition by Ab 6D1 as compared to 100% inhibition by Ab 10E5. Our results show that interactions between multiple ligands and receptors favour microaggregation depending on shear and thrombin activation conditions.

Surface-secreted von Willebrand factor mediates aggregation of ADP-activated platelets at moderate shear stress: facilitated by GPIb but controlled by GPIIb-IIIa.

We previously showed that ADP activation of washed human platelets in plasma-free suspensions supports aggregation at moderate shear stress (0.4-1.6 Nm-2) in Poiseuille flow. Although most activated platelets expressed maximal fibrinogen-occupied GPIIb-IIIa receptors, aggregation appeared to be independent of bound fibrinogen, but blocked by the hexapeptide GRGDSP. Here, we tested the hypothesis that von Willebrand factor (vWF) secreted and expressed on activated platelets mediates aggregation at moderate shear rates from 300 to 1000 s-1 corresponding to shear stresses from 0.3 to 1.1 Nm-2. Relatively unactivated platelets (< 15% expressing prebound fibrinogen) were prepared from acidified citrated platelet rich plasma (cPRP) by single centrifugation with 50 nM stable prostacyclin derivative ZK 36374 and resuspended in Tyrodes-albumin at 5 x 10(4) cells microliter-1. Flow cytometric measurements with monoclonal antibody (mAb) 2.2.9 reporting on surface-bound vWF, and with mAb S12 reporting on alpha-granule secreted P-selectin, showed that 65% and 80%, respectively, of all platelets were maximally activated with respect to maximal secretion and surface expression of these proteins. "Resting" washed platelets exhibited both surface-bound vWF and significant P-selectin secretion. We showed that mAbs 6D1 and NMC4, respectively blocking the adhesive domains on the GPIb receptor recognizing vWF, and on the vWF molecule recognizing the GPIb receptor, partially inhibited ADP-induced aggregation under shear in Couette flow, the degree of inhibition increasing with increasing shear stress. In contrast, mAb 10E5, blocking the vWF binding domain on GPIIb-IIIa, essentially blocked all aggregation at the shear rates tested. We conclude that vWF, expressed on ADP-activated platelets, is at least the predominant cross-bridging molecule mediating aggregation at moderate shear stress. There is an absolute requirement for free activated GPIIb-IIIa receptors, postulated to interact with platelet-secreted, surface bound vWF. The GPIb-vWF cross-bridging reaction plays a facilitative role becoming increasingly important with increasing shear stress. Since aurin tricarboxylic acid, which blocks the GPIb binding domain on vWF, was also found to completely block aggregation in Poiseuille flow, we conclude that it too affects the GPIIb-IIIa interaction.

Half-life of polybrominated biphenyl in human sera.

Polybrominated biphenyl (PBB), a flame-retardant material, was introduced into the food chain in Michigan in 1973 due to a manufacturing and distribution mistake. Following public concern about the long-term health effects of PBB in humans, a cohort of PBB-exposed Michigan residents was assembled in 1975. We initiated this study to determine the half-life of PBB in human sera and to understand how continued body burden relates to the possible adverse health consequences of PBB exposure. To determine the half-life, eligible persons were selected from the cohort if they had at least two PBB measurements 1 year apart and had an initial level > or = 20 pbb. There were 163 persons who met the criteria with a median PBB level of 45.5 ppb. The estimated half-life is 10.8 years (95% CI, 9.2-14.7 years). The body burden of PBB in exposed persons will decrease only gradually over time. For persons with an initial level of 45.5 ppb of PBB, it will take more than 60 years for their PBB levels to fall below the current level of detection of 1 ppb.

An epidemiological assessment of immunization programme participation in the Philippines.

Because a large proportion of preschool children failed to present for free diphtheria-pertussis-tetanus (DPT) immunizations in a poor, rural area of the Philippines, we undertook an epidemiological analysis of their characteristics. The parents of 159 children were interviewed to determine the demographic, attitudinal, knowledge, and administrative correlates of immunization status. Logistic regression was used to model immunization status. Children were less likely to be immunized if they had a high score on an Adversity Index (composed of measures of the weather, the number of visits the team made, the distance, the appropriateness of the time of day, and miscellaneous problems), if they received health care from a native mother and child health specialist, if a parent was not on the town council, and if pain was an important deterrent. By contrast, many demographic and attitudinal measures that have traditionally been thought to predict health behaviour were not useful discriminators. Recommendations are made for immunization programme management. The general use of this method for programme planning is elaborated.

PIP: Because a large proportion of preschool children failed to present for free diphteria-pertussis-tetanus (DPT) immunization in a poor, rural area of the Philippines, the authors undertook an epidemiological analysis of their characteristics. The parents of 159 children were interviewed to determine the demographic, attitudinal, knowledge, and administrative correlates of immunization status. Logistic regression was used to model immunization status. Children were less likely to be immunized if they had a high score on an Adversity Index (composed of measures of the weather, the number of visits the team made, the distance, the appropriateness of the time of day, and miscellaneous problems), if they received health care from a native mother and child health specialist, if a parent was not on the town council, and if pain was an important deterrent. By contrast, many demographic and attitudinal measures that have traditionally been thought to predict health behavior were not useful discriminators. Recommendations are made for immunization program management. The general use of this method for program planning is elaborated.

CDC and ATSDR electronic information resources for health officers.

This article catalogs some of the Centers for Disease Control and Prevention's (CDC) more important information resource offerings, which make public health information accessible via computer and automated telephone systems and on electronic media (diskette and CD-ROM). We review mechanisms for (1) finding and retrieving CDC reports, (2) querying CDC's numeric data files, (3) transmitting surveillance and other data files to CDC, (4) exchanging electronic mail with CDC staff, and (5) disseminating state and local public health information and data by using CDC tools. Each resource is followed with a section on how to obtain access to these resources.

CDC WONDER: a cooperative processing architecture for public health.

CDC WONDER is an information management architecture designed for public health. It provides access to information and communications without the user's needing to know the location of data or communication pathways and mechanisms. CDC WONDER users have access to extractions from some 40 databases; electronic mail (e-mail); and surveillance data processing. System components include the Remote Client, the Communications Server, the Queue Managers, and Data Servers and Process Servers. The Remote Client software resides in the user's machine; other components are at the Centers for Disease Control and Prevention (CDC). The Remote Client, the Communications Server, and the Applications Server provide access to the information and functions in the Data Servers and Process Servers. The system architecture is based on cooperative processing, and components are coupled via pure message passing, using several protocols. This architecture allows flexibility in the choice of hardware and software. One system limitation is that final results from some subsystems are obtained slowly. Although designed for public health, CDC WONDER could be useful for other disciplines that need flexible, integrated information exchange.

Abdominal pregnancy in the United States: frequency and maternal mortality.

From an analysis of 11 abdominal pregnancy-related deaths and an estimated 5221 abdominal pregnancies in the United States, we estimated that there were 10.9 abdominal pregnancies per 100,000 live births and 9.2 per 1000 ectopic pregnancies; the mortality rate was 5.1 per 1000 cases. Although the risk of having an ectopic pregnancy is rising, the risk of abdominal pregnancy, which is probably always a sequel of a missed ruptured ectopic pregnancy, is apparently declining; this may be due to improved prenatal care. However, only one of nine women who reached the hospital alive had an accurate preoperative diagnosis of abdominal pregnancy, which suggests that preventing abdominal pregnancy-related death may depend, at least in part, upon increasing physicians' awareness of its clinical features.

Ectopic pregnancy mortality in the United States, 1970-1983.

Ectopic pregnancy is now the second leading cause of maternal mortality in the United States. We describe changes in ectopic pregnancy mortality and characterize the risk of death from ectopic pregnancy for different groups, using ectopic pregnancy deaths identified by the national Vital Statistics System for 1970-1983, ectopic pregnancy-related deaths investigated by the Centers for Disease Control for 1979-1982, and ectopic pregnancy cases estimated from the National Hospital Discharge Survey for 1970-1983. During both 1970-1976 and 1977-1983, women of black and other races were at significantly increased risk of death from ectopic pregnancy compared with white women. This increased risk held for all ages and all geographic regions. Little variation existed in the risk of death from ectopic pregnancy by age and geographic region. From 1970-1983, the risk of death from ectopic pregnancy declined among all races and ages in all regions. These data suggest that black women, and in particular teenagers and older women, may have inadequate access to gynecologic and prenatal services. Active outreach may reduce the risk of death from ectopic pregnancy.

Older maternal age and infant mortality in the United States.

We used data from the National Infant Mortality Surveillance project to examine the effect of older maternal age on infant mortality for the 1980 United States birth cohort. The 1,579,854 births and 14,591 deaths of singletons who were black or white and whose mothers were 25-49 years of age were included. Direct standardization was used to calculate birth-weight-adjusted relative risks of neonatal and postneonatal mortality, using the birth weights of infants with maternal age 25-29 as the standard. We found that the risk of infant mortality was nearly equal for infants born to mothers 25-29 and 30-34 years of age; infants born to mothers 35-39 years of age were at a slightly elevated (18% higher) risk, and those born to mothers 40-49 years of age were at a much more elevated (69% higher) risk. Among whites, the higher neonatal mortality associated with a maternal age of 35-39 was mostly due to an increased prevalence of low birth weight; among blacks, it was due to higher birth-weight-specific risks. Neither white nor black postneonatal mortality risks were much elevated until a maternal age of 40-49, and this last elevation was mostly due to higher birth-weight-specific risks. These findings suggest that infertility and fetal mortality aside, and considering only the effect on infant mortality, it is relatively safe for women to postpone childbearing into their middle, and perhaps late, thirties.

DATA2000: CDC WONDER information system linking Healthy People 2000 objectives to data sets.

To monitor progress on the Healthy People (HP) 2000 objectives, planners and researchers will need information on relevant data sources. DATA2000 is a project designed to identify these data and link them with objectives and to develop a computerized information system providing access to this information. Sources of information on objectives and data included Healthy People 2000, catalogs and data bases of data sets, and the HP 2000 Steering Committee. We created an "assessment" of the utility of the data set for the particular objective. A Centers for Disease Control (CDC) WONDER-based information system was developed (using methods previously described). We identified 204 data sets and created 408 assessments. All but one of the objectives were paired with corresponding data. Over half the data come from CDC. The CDC WONDER-based information system crosslinks the objectives, data sets, and assessments and provides 5-10 pages of information about each. Understanding the contribution of prevention will be critical in planning reforms of the health care system. DATA2000 can be an important resource in this process.

The epidemiology of injuries to bicycle riders.

Over half a million injuries related to bicycle crashes were seen in U.S. hospital emergency rooms in 1982. The data reviewed show a strong link between bicycle/motor vehicle collisions, head injury, and serious morbidity and mortality.

Young maternal age and infant mortality: the role of low birth weight.

In 1980, there were 562,330 babies born in the United States to teenage mothers (19 years of age or younger). The offspring of teenage mothers have long been known to be at increased risk of infant mortality, largely because of their high prevalence of low birth weight (less than 2,500 grams). We used data from the National Infant Mortality Surveillance (NIMS) project to examine the effect of young maternal age and low birth weight on infant mortality among infants born in 1980 to U.S. residents. This analysis was restricted to single-delivery babies who were either black or white, who were born to mothers ages 10-29 years, and who were born in one of 48 States or the District of Columbia. Included were 2,527,813 births and 28,499 deaths (data from Maine and Texas were excluded for technical reasons). Direct standardization was used to calculate the relative risks, adjusted for birth weight, of neonatal mortality (less than 28 days of life) and postneonatal mortality (28 days to less than 1 year of life) by race and maternal age. There was a strong association between young maternal age and high infant mortality and between young maternal age and a high prevalence of low birth weight. Neonatal mortality declined steadily with increasing maternal age. After adjusting for birth weight, the race-specific relative risks for babies born to mothers less than 16 years of age were still elevated from 11 to 40 percent, compared with babies born to mothers 25-29 years of age. Otherwise, all the relative risks were nearly equal to 1. By contrast, most of the association between young maternal age and postneonatal mortality persisted after birth weight adjustment in all maternal age groups.These results suggest that the prevention of neonatal mortality and, to a lesser extent, postneonatal mortality among babies born to teenagers depends on preventing low birth weight. The prevention of postneonatal mortality may depend more on other factors, such as assisting teenagers with better parenting. Finally, although there maybe few biological reasons to postpone childbearing,teenage childbearing continues to place the mother and her baby at a social disadvantage.

Presentation and interpretation of food intake data: factors affecting comparability across studies.

Non-uniform, unclear, or incomplete presentation of food intake data limits interpretation, usefulness, and comparisons across studies. In this contribution, we discuss factors affecting uniform reporting of food intake across studies. The amount of food eaten can be reported as mean portion size, number of servings or total amount of food consumed per day; the absolute intake value for the specific study depends on the denominator used because food intake data can be presented as per capita intake or for consumers only. To identify the foods mostly consumed, foods are reported and ranked according to total number of times consumed, number of consumers, total intake, or nutrient contribution by individual foods or food groups. Presentation of food intake data primarily depends on a study's aim; reported data thus often are not comparable across studies. Food intake data further depend on the dietary assessment methodology used and foods in the database consulted; and are influenced by the inherent limitations of all dietary assessments. Intake data can be presented as either single foods or as clearly defined food groups. Mixed dishes, reported as such or in terms of ingredients and items added during food preparation remain challenging. Comparable presentation of food consumption data is not always possible; presenting sufficient information will assist valid interpretation and optimal use of the presented data. A checklist was developed to strengthen the reporting of food intake data in science communication.

What is vinculin needed for in platelets?

UNLABELLED: Summary. BACKGROUND: Vinculin links integrins to the cell cytoskeleton by virtue of its binding to proteins such as talin and F-actin. It has been implicated in the transmission of mechanical forces from the extracellular matrix to the cytoskeleton of migrating cells. Vinculin's function in platelets is unknown. OBJECTIVE: To determine whether vinculin is required for the functions of platelets and their major integrin, α(IIb) ß(3) . METHODS: The murine vinculin gene (Vcl) was deleted in the megakaryocyte/platelet lineage by breeding Vcl fl/fl mice with Pf4-Cre mice. Platelet and integrin functions were studied in vivo and ex vivo. RESULTS: Vinculin was undetectable in platelets from Vcl fl/fl Cre(+) mice, as determined by immunoblotting and fluorescence microscopy. Vinculin-deficient megakaryocytes exhibited increased membrane tethers in response to mechanical pulling on α(IIb) ß(3) with laser tweezers, suggesting that vinculin helps to maintain membrane cytoskeleton integrity. Surprisingly, vinculin-deficient platelets displayed normal agonist-induced fibrinogen binding to α(IIb) ß(3) , aggregation, spreading, actin polymerization/organization, clot retraction and the ability to form a procoagulant surface. Furthermore, vinculin-deficient platelets adhered to immobilized fibrinogen or collagen normally, under both static and flow conditions. Tail bleeding times were prolonged in 59% of vinculin-deficient mice. However, these mice exhibited no spontaneous bleeding and they formed occlusive platelet thrombi comparable to those in wild-type littermates in response to carotid artery injury with FeCl(3) . CONCLUSION: Despite promoting membrane cytoskeleton integrity when mechanical force is applied to α(IIb) ß(3) , vinculin is not required for the traditional functions of α(IIb) ß(3) or the platelet actin cytoskeleton.