Factors associated with acceptance and full publication of GI endoscopic research originally published in abstract form.

BACKGROUND: Many abstracts submitted to annual scientific meetings never come to full publication in peer-reviewed journals. The objective of this study was to determine factors associated with the fate of endoscopic research abstracts submitted to the annual scientific meeting of the American Society for Gastrointestinal Endoscopy (ASGE). METHODS: All abstracts (n = 461) submitted to the annual meeting of the ASGE in May of 1994 were retrospectively reviewed. The following databases were searched for evidence of publication of abstracts in full-manuscript form: Medline, HealthSTAR, Current Contents, CINHAL, and Cancerlit. All abstracts were reviewed between May 4, 1998 and June 30, 1998. Univariate and multivariate analysis were performed to determine the association between abstract characteristics and acceptance for presentation at the meeting and for publication. RESULTS: Fifty-five percent (247/451) of submitted abstracts were accepted for presentation. In univariate analysis, pediatric studies, prospective studies, randomized studies, and studies from university-affiliated medical centers (UAMC), were more likely to be accepted for presentation (p < 0.05). In multivariate analysis, the variables: pediatric studies (p = 0.01), prospective studies (p = 0.005), randomized studies (p = 0.06), and studies from UAMC (p = 0.01) predicted acceptance of abstracts for presentation at the meeting. The overall publication rate was 25.1%. The publication rates 1, 2, 3, and 4 years after the meeting were 6.7%, 16.2%, 22.8%, and 25.1%, respectively. Multivariate Cox proportional hazards analysis showed that accepted abstracts (p = 0.0003) studies reporting positive results (p = 0.0015), and studies from outside the United States (p = 0.036) were more likely to be published in manuscript form. CONCLUSIONS: The overall publication rate of abstracts reporting endoscopic research is 25%, lower than that in any published report from other medical societies. Abstracts from the United States were less likely to be published in full-manuscript form. Although there was no positive outcome bias for acceptance of abstracts for presentation at the meeting, there was bias toward publication of statistically significant results. Further investigations are warranted to determine the variation in the publication of research results according to country of origin and to determine factors that hinder publication of GI endoscopic research in manuscript form.

Overlapping and divergent actions of estrogen and the neurotrophins on cell fate and p53-dependent signal transduction in conditionally immortalized cerebral cortical neuroblasts.

The developing cerebral cortex undergoes overlapping periods of neurogenesis, suicide, and differentiation to generate the mature cortical plate. The following experiments examined the role of the gonadal hormone estrogen in comparison to the neurotrophins, in the regulation of p53-dependent cortical cell fate. To synchronize choices between neurogenesis, apoptosis, and neural differentiation, embryonic rat cerebral cortical neuroblasts were conditionally immortalized with the SV40 large T antigen containing the tsA58/U19 temperature-sensitive mutations. At the nonpermissive temperature, cessation of large T antigen expression was accompanied by induction of p53, as well as the p53-dependent proteins, wild-type p53-activated fragment-1/Cdk (cyclin-dependent kinase)-interacting protein-1 (p21/Waf1), Bcl (B-cell lymphoma)-associated protein (Bax), and murine double minute 2 (MDM2), that lead to cell cycle-arrest, suicide, and p53 inhibition, respectively. Simultaneously, neuroblasts exit cell cycle and die apoptotically or differentiate primarily into astrocytes and immature postmitotic neuroblasts. At the nonpermissive temperature, estrogen specifically induced an antagonist-independent increase in phosphorylated p53 expression, while increasing p21/Waf1 and decreasing Bax. Coincidentally, estrogen rapidly increased and then decreased MDM2 relative to controls, suggesting temporal modulation of p53 function. Both estrogen and neurotrophins prevented DNA fragmentation, a marker for apoptosis. However, estrogen also induced a transient increase in released lactate dehydrogenase, suggesting that estrogen simultaneously induced rapid cell death in a subpopulation of cells. In contrast to the neurotrophins, estrogen also increased cell proliferation. Both estrogen and the neurotrophins supported neuronal differentiation. However, in contrast to the neurotrophins, estrogen only supported the expression of a subset of oligodendrocytic markers. These results suggest that estrogen and the neurotrophins support overlapping and distinct aspects of differentiation in the developing cerebral cortex.

Fas/Apo [apoptosis]-1 and associated proteins in the differentiating cerebral cortex: induction of caspase-dependent cell death and activation of NF-kappaB.

The developing cerebral cortex undergoes a period of substantial cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas mRNA and protein are transiently expressed in subsets of cells within the developing rat cerebral cortex during the peak period of apoptosis. Fas-immunoreactive cells were localized in close proximity to Fas ligand (FasL)-expressing cells. The Fas-associated signaling protein receptor interacting protein (RIP) was expressed by some Fas-expressing cells, whereas Fas-associated death domain (FADD) was undetectable in the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP), an inhibitor of Fas activation, was also expressed in the postnatal cerebral cortex. Fas expression was more ubiquitous in embryonic cortical neuroblasts in dissociated culture compared to in situ within the developing brain, suggesting that the environmental milieu partly suppresses Fas expression at this developmental stage. Furthermore, FADD, RIP, and FLIP were also expressed by subsets of dissociated cortical neuroblasts in culture. Fas activation by ligand (FasL) or anti-Fas antibody induced caspase-dependent cell death in primary embryonic cortical neuroblast cultures. The activation of Fas was also accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorporation of nucleic acids and nuclear translocation of the RelA/p65 subunit of the transcription factor NF-kappaB. Together, these data suggest that adult cortical cell number may be established, in part, by an active process of receptor-mediated cell suicide, initiated in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain.