Risk factors for recurrence of hemorrhagic endovasculitis of the placenta.

OBJECTIVE: To assess the potential for recurrence of placental hemorrhagic endovasculitis and to identify clinical or pathologic cofactors that might influence recurrence of this lesion or subsequent pregnancy outcome. METHODS: Ninety-seven women with a placenta affected by hemorrhagic endovasculitis, who also had at least one placenta referred to the Michigan Placental Tissue Registry from a subsequent pregnancy, were identified from 10,531 referrals between 1978 and 1988. Histologic slides from 209 placentas and clinical data from 211 infants (two sets of twins) from initial (first) and subsequent referrals were analyzed. Placentas were graded for the presence, extent, and severity of hemorrhagic endovasculitis and chronic villitis of unknown etiology; for placental lesions indicative of hypertensive maternal vessel disease; and for intravascular nucleated erythrocytes and chorionic thrombi. Maternal data included age, gravidity, number of previous losses, and history of toxemia or hypertension. All data were analyzed for significance using chi2 and t tests. Outcome assessment was based on recurrence of hemorrhagic endovasculitis and infant viability with the second referral. RESULTS: With first referrals, 80 of 98 infants (81.6%) were stillborn. Among second referrals, 26 of 98 infants (26.5%) were stillborn. Hemorrhagic endovasculitis recurred in 28 second placentas (28.9%); of these, 18 infants (64.3%) were stillborn. Higher rates of recurrence were found with progressively higher first-referral chronic villitis severity scores (P < .02), higher hypertensive placental lesion scores (P < .001), and first referrals with a history of toxemia or hypertension (P < .02). Recurrence of hemorrhagic endovasculitis was higher in patients with two or more of these factors in first referrals (P < .001). Subsequent stillbirth was more frequent with progressively higher first-referral hypertensive placental lesion scores (P < .01) and in first placentas with two or more risk factors (P = .064). Hemorrhagic endovasculitis severity scores, intravascular nucleated erythrocytes, and chorionic thrombi were associated with stillbirth in index pregnancies only. Maternal age, gravidity, or history of prior losses were not predictive. CONCLUSIONS: Placental hemorrhagic endovasculitis is associated with pregnancy loss and can recur in some patients. Interrelations among placental hemorrhagic endovasculitis, chronic villitis, maternal hypertension, and adverse outcomes in subsequent pregnancies are apparent. This information may be useful in patient counseling.

Telling the story: narrative in newspaper accounts of a men's collegiate basketball tournament.

The concept of narrative or story is increasingly being used as s theoretical model for informing research dealing with a wide array of sociocultural phenomena, especially those concerned with communication. Narrative is prevalent in mass media accounts of many different kinds of events. The inherent serialized structure of sport is conducive to media coverage in narrative form. This article uses a narrative perspective to examine journalistic accounts of the 1982 Atlantic Coast Conference (ACC) men's basketball tournament. We found that the accounts contain three major components of narrative: theme, plot, and characters. Winning is the central theme, and it contributes to shaping the plot and characters. The plot is simple and straightforward and centers on the question, "Who will win?" The characters are relatively flat and lack robustness--players offer exceptional athletic skills to coaches who strategically blend their talents. A breakdown occurs between the goal of winning and the goal of entertaining spectators, and this highlights the short-term importance of winning and the longer term importance of performing to entertain spectators. The narrative supports capitalistic economic relations, stemming from the central theme of winning and its ties to competitive individualism, teamwork, and consumerism.

The possible role of isoantigens in protective immunity to malaria.

The possibility that autoimmune responses to modified red cell antigens might be involved in protective immunity to malaria was investigated in Plasmodium berghei infection of August rats. Animals rendered anaemic by phenylhydrazine treatment at the time of immunization showed significantly greater protection than rats given antigen alone, or phenylhydrazine alone. Adoptive transfer experiments indicated that this enhanced response could be transferred with spleen cells.

Erythrocyte destruction and protective immunity to Malaria: enhancement of the immune response by phenylhydrazine treatment.

Malaria infection is characterized by extensive destruction of erythrocytes. In addition, the surface membrane of parasitized erythrocytes becomes biochemically and antigenically modified. Thus during infection the host immune system is exposed to massive amounts of modified erythrocytes on a scale not normally considered in conventional immunological experiments. The haemocytoxic drug phenylhydrazine hydrochloride has been used to mimic, in otherwise normal animals, the effect of the modification and destruction of erythrocytes which occurs in malaria. The experiments demonstrated that protective immunity to Plasmodium berghei KSP11 infection in rats and mice is significantly enhanced by this treatment, that this effect generates memory, can be transferred with spleen cells, and can have both enhancing and suppressive action on the protective immune response.

T cells and protective immunity to Plasmodium berghei in rats.

Experiments were carried out in which unfractionated spleen cells, and T lymphocyte subpopulations characterized by certain experimental criteria, were isolated at various times from rats infected with Plasmodium berghei. By adoptive transfer it was shown that unfractionated spleen cells, and T cells alone, could transfer protection to syngenic recipients as early as 11 days after infection of the cell donors. The protection conferred by T cells increased with the duration of the infection in the donors, at least up to 100 days. The additional presence of B cells in transferred lymphocyte populations enhanced their protective capacity over that shown by T cells alone. The role of T cells in protective immunity to malaria is discussed.

Preliminary studies of artificial immunization of rats against Plasmodium berghei and adoptive transfer of this immunity by splenic T and T + B cells.

Protective T lymphocyte and T+B lymphocyte responses in rats artificially immunized against P. berghei have been demonstrated by adoptive transfer. The techniques used could be developed for detailed analysis of protective lymphocyte responses generated by various methods of immunization, and their relationship to immunity.

Cold isohaemagglutinins in Plasmodium berghei-infected rats reacting with parasitized reticulocytes.

Significant levels of cold IgM and IgG isohaemagglutinins were detected in the serum of rats infected with Plasmodium berghei KSP 11. Peak titres occurred 15 days after initial infection at the time when the parasitaemia was dropping rapidly, or 7 days after a second challenge infection. Infected reticulocytes were much more sensitive to agglutination than uninfected cells, but absorption experiments demonstrated isoantigenicity in the determinants involved. This result indicated that the presence of the parasite resulted in exposure of membrane isoantigens normally masked. Agglutination could be inhibited with fractions with pIs 7.7-7.8 obtained from parasitized reticulocytes. Formaldehyde and glutaraldehyde-fixed infected cells each gave distinct agglutination reactions, different from unfixed cells.

Protective immunity to malaria. Studies with cloned lines of Plasmodium chabaudi chabaudi and P. berghei in CBA/Ca mice. II. The effectiveness and inter- or intra-species specificity of the passive transfer of immunity with serum.

Serum was obtained from CBA/Ca mice infected, reinfected or superinfected with parasites taken one or two syringe passages from cryopreserved reference stabilates derived from cloned lines of the AS or CB isolates of P.c. chabaudi. Serum was also collected from mice superinfected with parasites derived from a cloned line of P. berghei KSP-11. When injected into normal syngeneic recipients subsequently challenged with homologous or heterologous parasites, these sera mediated some or all of the following modifications to the breakthrough parasitaemias which invariably occurred (i) an extension of the pre-patent period (ii) an extension of the time taken for the parasitaemia to reach 2% (iii) a reduction of peak parasitaemia (iv) protraction of the initial peak of parasitaemia. These modifications were particularly evident with serum from superinfected mice and to a lesser extent with serum from animals reinfected once after recovery from a primary infection. Serum taken during the course of such a primary infection produced extended pre-2% periods, other effects being only marginal. Serum mediated modifications produced by reinfection and superinfection serum appeared largely species-specific with a limited degree of cross-reactivity. Intraspecific specificity was also apparent with serum from P.c. chabaudi AS or CB reinfected or superinfected mice, although marginal cross-immunity was again observed. When analysed by the fluorescent antibody technique on smears of methanol fixed parasitized erythrocytes, reinfection and superinfection sera were almost totally cross-reactive both within and across species. Preliminary evidence that parasites breaking through the effects of these sera may constitute a phenotypic antigenic variant is presented and possible mechanisms for the parasitaemia modifying effects of the various sera discussed.

The binding of antibodies from Plasmodium berghei-infected rats to isoantigenic and parasite-specific antigenic sites on the surfaces of infected reticulocytes.

Ferritin-labelling techniques at the ultrastructural level have shown that antiserum from August rats immune to P. berghei infection contains antibodies which bind to the surfaces of parasitized reticulocytes but not to uninfected cells. Two antibody specificities have been demonstrated by comparing antisera i absorbed with infected reticulocytes, ii absorbed with uninfected reticulocytes, and iii unabsorbed. Ferritin labeling was much increased with antiserum preabsorbed with uninfected reticulocytes, and also with heat-inactivated serum, indicating a blocking effect on parasite-specific antibody binding by cold-reacting anti-erythrocyte isoantibodies known to be present. Energy-dependent aggregation, shedding and endocytosis of labelled material was observed at the surfaces of unfixed infected reticulocytes.