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This study examines the interrelationships between childhood abuse, exposure to maternal domestic violence, and posttraumatic stress disorder (PTSD) symptomatology in a multiethnic sample of 111 adult female residents of a domestic violence (DV) shelter. Participants completed structured interviews about the DV and their prior violence exposure, as well as the Impact of Event Scale-Revised. As hypothesized, there was high co-occurrence between exposure to maternal DV and childhood physical and sexual abuse, and the frequency of lifetime violence exposure predicted PTSD symptomatology. A series of multiple regressions indicated a more complex pattern of relationships, in which specific forms of prior violence exposure predicted different PTSD symptom dimensions. A history of witnessing maternal DV predicted intrusion symptoms, and a history of childhood sexual abuse predicted hyperarousal symptoms. Ethnicity was not related to levels of violence exposure or to PTSD symptoms. Clinical implications of the findings are discussed.

This study examines the differential effects of adult and childhood physical and psychological abuse, abuse-specific coping, and psychological adjustment in battered women seeking emergency shelter. Multivariate regression analyses confirmed the devastating impact of psychological abuse (childhood and concurrent) on battered women's adjustment. The results corroborated prior research suggesting a cumulative vulnerability to psychological victimization in a substantial proportion of residents. Unexpectedly, frequency of physical violence was unrelated to women's distress. The study argues that modes of coping traditionally considered adaptive (e.g., engaged, proactive) may be unsafe for battered women and children. The multifaceted nature of survivors' coping choices is discussed.

Matrix metalloproteases (MMPs) are a group of zinc-dependent endopeptidases that can degrade every component of the extracellular matrix. Under normal circumstances, the levels of MMPs are tightly regulated at both transcriptional and posttranscriptional levels. However, they are up-regulated in pathological states such as inflammation. Previous investigations have suggested that MMP-12 (metalloelastase) may be an important mediator in the pathogenesis of chronic lung injury. In this study we investigated the role of metalloelastase in the pathogenesis of acute lung injury using mice containing a targeted disruption of the metalloelastase gene. Neutrophil influx into the alveolar space in metalloelastase-deficient animals was reduced to approximately 50% of that observed in parent strain mice following the induction of injury by immune complexes. In addition, lung permeability in metalloelastase-deficient mice was approximately 50% of that of injured parent strain animals with normal levels of metalloelastase and this was correlated with histological evidence of less lung injury in the metalloelastase-deficient animals. Collectively, the data suggest that metalloelastase is necessary for the full development of acute alveolitis in this model of lung injury. Further, the data suggest that reduced injury in metalloelastase-deficient mice is due in part to decreased neutrophil influx into the alveolar space.

Matrix metalloproteinases (MMPs) are upregulated locally in sites of inflammation, including the lung. Several MMP activities are upregulated in acute lung injury models but the exact role that these MMPs play in the development of the lung injury is unclear due to the absence of specific inhibitors. To determine the involvement of individual MMPs in the development of lung injury, mice genetically deficient in gelatinase B (MMP-9) and stromelysin 1 (MMP-3) were acutely injured with immunoglobulin G immune complexes and the intensity of the lung injury was compared with genetically identical wild-type (WT) mice with normal MMP activities. In the WT mice there was upregulation of gelatinase B and stromelysin 1 in the injured lungs which, as expected, was absent in the genetically deficient gelatinase B- and stromelysin 1-deficient mice, respectively. In the deficient mice there was little in the way of compensatory upregulation of other MMPs. The gelatinase B- and the stromelysin 1-deficient mice had less severe lung injury than did the WT controls, suggesting that both MMPs are involved in the pathogenesis of the lung injury. Further, the mechanism of their involvement in the lung injury appears to be different, with the stromelysin 1-deficient mice having a reduction in the numbers of neutrophils recruited into the lung whereas the gelatinase B-deficient mice had the same numbers of lung neutrophils as did the injured WT controls. These studies indicate, first, that both gelatinase B and stromelysin 1 are involved in the development of experimental acute lung injury, and second, that the mechanisms by which these individual MMPs function appear to differ.

Rats were subjected to acute lung injury by the intra-alveolar formation of IgG immune complexes of bovine serum albumin (BSA) and anti-BSA. In this model of injury, complement activation occurs and large numbers of neutrophils invade the interstitium and alveolar space. In the present study, animals were treated with intratracheal catalase concomitantly with anti-BSA or after a lag period of 5-120 min. Catalase treatment at time-zero or at 5 min post injury failed to prevent lung injury as indicated by permeability change, histological features, and neutrophil influx. However, treatment after a delay of 15-30 min (but not 120 min) afforded substantial protection. Consistent with past findings [19], lung injury was accompanied by an accumulation of matrix metalloproteinase 9 (MMP-9) in bronchoalveolar lavage (BAL) fluid. There was a strong correlation between inhibition of injury and reduction in MMP-9 levels. In vitro studies conducted in parallel revealed that unstimulated alveolar macrophages did not produce measurable MMP-9, while there was a large induction following exposure to the same immune complexes that initiated injury in vivo. MMP-2 was also slightly upregulated under the same conditions. Concomitant treatment with catalase greatly inhibited MMP-9 production by macrophages in response to immune complexes, but this treatment had little effect on basal production of either MMP-9 or MMP-2 by macrophage. The same concentration of catalase that suppressed MMP-9 elaboration also inhibited the production of tumor necrosis factor alpha. In contrast, when neutrophils were treated with catalase and then exposed to immune complexes, the antioxidant failed to prevent the release of either MMP-2 or MMP-9. Taken together, these findings demonstrate that antioxidant treatment interferes with elaboration of MMPs by alveolar macrophages. Protection against lung injury is correlated with reduction in MMP levels in the BAL fluid.

The virulence of Leishmania mexicana is determined by the concerted action of several parasite molecules. These cells lose their infectivity to host macrophages after prolonged cultivation in axenic growth media. Both virulent and attenuated variants of the parasite cells were cloned. The differential display reverse transcription-polymerase chain reaction technique was employed to understand whether this natural attenuation of the parasite cells is accompanied by differential expression of selected genes in those cells. Twelve different dinucleotide-anchored oligo(dT) antisense primers were used to make cDNAs from poly(A)+ mRNAs isolated from a clonal population of virulent and avirulent cells following a protocol optimized for Leishmania mRNAs. Those cDNAs were subjected to amplifications using each of the three different arbitrary decanucleotide primers and the corresponding anchored oligo(dT) primer. This procedure revealed four virulent-specific cDNA probes and one avirulent-specific cDNA probe. Differential expressions of these genes were confirmed by northern hybridization using the cloned cDNA probes. These results indicate that differential expression of genes may be the key in determining the molecular basis of leishmanial virulence.

This paper provides a data base and analysis of the effectiveness of the public medical education system in Oklahoma. It provides the facts from which future decisions for Oklahoma health manpower policies might be developed.

Vibrio fluvialis and Vibrio furnissii have been associated with diarrhea but have rarely been isolated in the United States. We received strains of V. fluvialis and V. furnissii that were isolated from the stool of a 1-month-old baby. A description of these two strains and the case history of the patient are given in this report.

Fluxes of biogenic carbonates moving out of the euphotic zone and into deeper undersaturated waters of the North Pacific were estimated with free-drifting sediment traps. Short-duration (1 to 1.5 day) sampling between 100 and 2200 meters points to a major involvement in the oceanic carbonate system by a class of organisms which had been relegated to a secondary role-aragonitic pteropods. Pteropod fluxes through the base of the euphotic zone are almost large enough to balance the alkalinity budget for the Pacific Ocean. Dissolution experiments with freshly collected materials shed considerable light on a mystery surrounding these labile organisms: although plankton collections from net tows almost always contain large numbers of pteropods, these organisms are never a major component of biogenic materials in long-duration sediment trap collections. Their low abundance in long-duration collections results from dissolution subsequent to collection. Shortduration sampling showed significant increases in the ratio of calcitic foraminifera to aragonitic pteropods in undersaturated waters, indicating the more stable mineralogic form, calcite, was preserved relative to aragonite. Approximately 90 percent of the aragonite flux is remineralized in the upper 2.2 kilometers of the water column.