Engaging the experts: Popular science education and breast cancer activism

In the early 1990s, breast cancer activists in the United States challenged the scientific establishment to include lay activists in the inner circles of science policy making. Within a few years, activists' demands extended beyond policy to inclusion in the everyday practices of science, that is, in the formulation of research questions, the design of scientific studies and the review of scientific grant proposals. While some activists refer to themselves as consumers, their participation in the practices of science has taken them beyond the narrow framework of consumption and cast them as producers, rather than simply consumers, of scientific knowledge. This paper describes a science education program organized by breast cancer activists to prepare them for involvement in the scientific arena. The specific goals of this educational program are to teach basic concepts of biology and epidemiology and critical appraisal of scientific literature and research studies, as well as to examine the institutional practices of science. By simultaneously engaging with the content and the politics of science in Project LEAD, breast cancer activists acquire tools that allow them not only to influence science policy but to evaluate the truth claims of science. In the process, they take a more active and direct role in determining the nature of knowledge produced about breast cancer.     

Psychosis-induced posttraumatic stress disorder.

Conventional theories about stressors severe enough to lead to PTSD have focused on external events. Historically, however, psychosis has been considered one of the most severe stressors to which one can be subjected. The impact of psychosis, in the case of schizophrenia, may be mistaken for the psychosis itself. The possibility of a comorbid, psychosis-induced PTSD should be considered in persons who have experienced a psychotic illness. Recognition of the syndrome may lead to more effective and emphathic clinical treatment of persons with severe mental illness.     

Inhibition of a dihydropyridine, omega-conotoxin insensitive Ca2+ channel in rat synaptosomes by venom of the spider Hololena curta.

Inhibition of the N and L type Ca2+ channels with omega conotoxin GVIA (omega-CgTx) together with the dihydropyridine (-)-202-791 produces slight reduction (congruent to 25%) of K(+)-evoked Ca2+ influx in mammalian synaptosomes. These results and others suggest the existence of a third high threshold voltage sensitive calcium channel (VSCC) responsible for the majority of influx. Venom from the funnel web spider Hololena curta potently and persistently inhibited Ca2+ influx in rat cortical synaptosomes (IC50 1:10,000 or 4.21 micrograms/venom protein/ml of synaptosomes). Also Ca2+ influx in cerebellar synaptosomes was inhibited in a similar manner. K(+)-evoked tritium release from synaptosomes labeled with [3H]noradrenaline was inhibited by Hololena venom (congruent to 60% reduction at 10 micrograms/venom protein). Inhibition of Ca2+ influx by venom was unaffected by combined omega-CgTx and (-)-202-791 pretreatment (both 1 microM). Hololena venom and its active constituent should provide useful tools to investigate the role of this novel Ca2+ channel in neuronal function.     

Selective Embolization of Glomus Jugulare Tumors

Four patients with grade C or D₁ glomus jugulare tumors who underwent preoperative highly selective embolization followed by infratemporal fossa removal of their tumors were compared to three patients undergoing surgery alone with respect to intraoperative blood loss, operative time, cranial nerve palsy, length of hospitalization, and perioperative complications. Embolized patients demonstrated a marked reduction in blood loss (650 vs 1375 cc) compared with the nonembolized group. Operative time was shortened (by 51 minutes). Facial nerve function did not appear related to embolization but was directly related to intraoperative nerve manipulation. Hospital stay, perioperative complications, and lower cranial nerve palsies were not related to embolization.     

Soluble egg antigen-stimulated T helper lymphocyte apoptosis and evidence for cell death mediated by FasL(+) T and B cells during murine Schistosoma mansoni infection

Granuloma formation around schistosomal eggs is induced by soluble egg antigens (SEA) and mediated by the activity of CD4(+) Th lymphocytes and their cytokines. Regulation of the inflammatory Th cell response during infection is still insufficiently understood. The hypothesis of this study was that activation-induced cell death (AICD) of CD4(+) T cells is involved in the immune inflammatory response. This study investigated the dynamics of splenic and granuloma CD4(+) Th cell apoptosis and Fas ligand (FasL) expression during the acute and chronic stages of murine schistosomal infection. Enhanced apoptosis of freshly isolated CD4(+) Th lymphocytes commenced after egg deposition and persisted during the peak and modulated phases of granuloma formation. After oviposition, CD4(+), CD8(+), and CD19(+) splenocytes and granuloma cells expressed elevated levels of FasL but FasL expression declined during the downmodulated stage of infection. In culture, SEA induced splenic and granuloma CD4(+) T-cell apoptosis and stimulated expression of FasL on splenic but not granuloma CD4(+) T cells, CD8(+) T cells, and CD19(+) B cells. SEA-stimulated splenocytes and granuloma cells preferentially lysed a Fas-transfected target cell line. Depletion of B cells from SEA-stimulated splenic cultures decreased CD4(+) T cell apoptosis. Coculture of purified splenic B cells with CD4(+) T cells and adoptive transfer of purified B cells indicated that antigen-stimulated B cells can kill CD4(+) Th cells. However, CD4(+) T cells were the dominant mediators of apoptosis in the granuloma. This study indicates that AICD is involved in the apoptosis of CD4(+) T cells during schistosomal infection.     

Intramedullary fixation of unstable forearm fractures in children

Although most forearm fractures in children are appropriately treated with closed reduction and cast immobilization, certain unstable fractures of the radius and ulna are best treated operatively. We present our technique of using flexible intramedullary fixation to stabilize these fractures. Retrograde fixation of the radius is obtained with a 5/64th or 3/32nd Steinmann pin, and stabilization of the ulna is achieved with a 1/8th inch Rush rod. Complications from this technique are few. The rods are usually removed after fracture union to avoid painful hardware.     

Abducted, hyperextended small finger deformity of nonneurologic etiology

The abduction and hyperextension deformity of the small finger is usually associated with ulnar nerve palsy. Six patients who sustained an abduction force to their small finger presented with the finger in an abducted and hyperextended position. All patients were neurologically intact and were unable to adduct or flex the finger at the metacarpophalangeal joint. Surgical findings in these patients included rupture of the radial sagittal band, collateral ligament, and junctura tendinum. Sequential division of these structures in cadaveric hands confirmed that all these tissues had to be deficient for this deformity to occur. The traumatic abducted, hyperextended small finger deformity may respond to conservative treatment, but surgery is sometimes necessary.