Which measures are to be taken in the prevention of prematurity in working women?

The aim of this study was to determine the best preventive measures for employed pregnant women. Assuming that certain working conditions constitute a risk factor for preterm birth, should we give time off to women whose jobs are strenuous, reduce their weekly hours of work, or lengthen their antenatal maternity leave in an attempt to reduce risk of preterm birth? To answer this question, a survey carried out in 50 factories showed that a reduction of weekly working hours (routinely granted in many factories at present) appears helpful in reducing the preterm birth rate : this is also true for sick leaves granted for fatigue without pathological reason : on the other hand, the lengthening of antenatal maternity leave for fatigue, without medical reason, seems without effect. In the absence of experimental evaluation of preventive measures proposed at the end of this study, we provide a model for evaluating, theoretically, the relationship efficiency/cost/acceptability of such measures. Consequently, instead of lengthening antenatal maternity leave, we suggest prescribing 1 rest week (as sick leave) per month, beginning with the 4th month of pregnancy, for women working in strenuous conditions.     

Mapping of distinct von Willebrand factor domains interacting with platelet GPIb and GPIIb/IIIa and with collagen using monoclonal antibodies

We have used monoclonal antibodies (M Abs) and proteolytic fragmentation to localize structurally the functional sites of human von Willebrand factor (vWF) responsible for interaction with membrane glycoproteins GPIb, GPIIb/IIIa, and with collagen. SpII (215 kd) and SpIII (320 kd), the S aureus V-8 protease homodimeric fragments representing the carboxy-terminal and amino-terminal segments of the vWF subunit, competitively inhibited the binding of multimeric vWF to thrombin-stimulated or ristocetin-stimulated platelets, respectively. Specific saturable binding of each fragment was observed to stimulate platelets appropriately and was inhibited only by selected M Abs that both bound to the specific fragment and inhibited the corresponding function. M Ab 9, which blocks thrombin-induced binding of vWF to platelets, inhibited binding of SpII to platelets and bound to SpII as well as to a dimeric, 86-kd thermolysin fragment composed of 42-kd and 23-kd subunits, each possessing the epitope. Binding of SpII was also inhibited by a M Ab to GPIIb/IIIa. Thus, it appears that a portion of the carboxy-terminal end of vWF contains the ligand site for the GPIIb/IIIa receptor. In contrast, M Ab H9, which blocks ristocetin- induced binding of vWF to platelets, inhibited binding of SpIII to platelets and bound to SpIII as well as to monomeric 33-kd and 28-kd subtilisin fragments. Binding of SpIII to platelets was also inhibited by a M Ab to GPIb. Thus, it appears that a small segment of the amino- terminal part of vWF contains the ligand for the platelet GPIb receptor. The collagen binding site of vWF was localized with M Ab B203, which inhibits vWF interaction with collagen. This M Ab also bound to SpIII as well as to monomeric 26-kd and 23-kd subtilisin fragments. Thus, the third functional site responsible for collagen binding appears to be localized on the amino-terminal portion of vWF, in a linear sequence different from those responsible for interaction with either of the platelet receptors. These assignments of functional sites should facilitate the localization of structural defects of vWF in the various forms of vWD and support the role of vWF as an adhesive protein with multiple interactive sites.