Data Withholding in Academic Genetics: Evidence From a National Survey

Context  The free and open sharing of information, data, and materials regarding published research is vital to the replication of published results, the efficient advancement of science, and the education of students. Yet in daily practice, the ideal of free sharing is often breached. Objective  To understand the nature, extent, and consequences of data withholding in academic genetics. Design, Setting, and Participants  Mailed survey (March-July 2000) of geneticists and other life scientists in the 100 US universities that received the most funding from the National Institutes of Health in 1998. Of a potential 3000 respondents, 2893 were eligible and 1849 responded, yielding an overall response rate of 64%. We analyzed a subsample of 1240 self-identified geneticists and made a limited number of comparisons with 600 self-identified nongeneticists. Main Outcome Measures  Percentage of faculty who made requests for data that were denied; percentage of respondents who denied requests; influences on and consequences of withholding data; and changes over time in perceived willingness to share data. Results  Forty-seven percent of geneticists who asked other faculty for additional information, data, or materials regarding published research reported that at least 1 of their requests had been denied in the preceding 3 years. Ten percent of all postpublication requests for additional information were denied. Because they were denied access to data, 28% of geneticists reported that they had been unable to confirm published research. Twelve percent said that in the previous 3 years, they had denied another academician's request for data concerning published results. Among geneticists who said they had intentionally withheld data regarding their published work, 80% reported that it required too much effort to produce the materials or information; 64%, that they were protecting the ability of a graduate student, postdoctoral fellow, or junior faculty member to publish; and 53%, that they were protecting their own ability to publish. Thirty-five percent of geneticists said that sharing had decreased during the last decade; 14%, that sharing had increased. Geneticists were as likely as other life scientists to deny others' requests (odds ratio [OR], 1.39; 95% confidence interval [CI], 0.81-2.40) and to have their own requests denied (OR, 0.97; 95% CI, 0.69-1.40). However, other life scientists were less likely to report that withholding had a negative impact on their own research as well as their field of research. Conclusions  Data withholding occurs in academic genetics and it affects essential scientific activities such as the ability to confirm published results. Lack of resources and issues of scientific priority may play an important role in scientists' decisions to withhold data, materials, and information from other academic geneticists.      

Differentiation of memory T cells to virus plaque-forming cells and cytotoxic T lymphocytes

The aims of this study were to define the T-cell subpopulation(s) detected by the virus plaque assay, and particularly to determine whether the virus plaque assay could be used to enumerate cytotoxic T lymphocytes. In addition, studies were undertaken to ascertain whether cell proliferation was required for development of cytotoxic effector function and virus plaque formation by these subpopulations. The results of experiments with a secondary mouse mixed lymphocyte culture (MLC) model indicated that 70 percent of virus plaque-forming cells bore the Ly 1 phenotype and 30 percent the Ly 2,3 phenotype. Three lines of evidence suggested that cytotoxic T lymphocytes (CTL) can be detected by this assay: the fact that some virus plaque-forming cells (V-PFC) bear the same Ly phenotype as CTL; the use of an inhibitor of DNA synthesis indicated that proliferating cells could be eliminated with no effect on V-PFC production and cytotoxic activity of the Ly 2,3 cell population; and that infection of primed lymphocyteswith vesicular stomatitis virus before (MLC) stimulation eliminated cytotoxic activity. In primary MLC, development of V-PFC and CTL was completely abolished by cytosine arabinoside. In contrast, in secondary MLC, some CTL and V- PFC were generated by antigenic stimulation in the absence of proliferation. However, the development of both functions became progressively more susceptible to cytosine arabinoside as the time between primary immunization and in vitro boosting is increased. It is suggested that there may be a considerable disparity between the number of existing effector cells at any given time and the cytotoxic potential, i.e. the number of cells capable of being generated by antigenic stimulation.     

Extraintestinal human infection caused by Edwardsiella tarda.

Edwardsiella tarda is an uncommon enteric bacterium which has been found generally in animal hosts and occasionally in human feces. Three cases of extraintestinal infection caused by E. tarda which are described herein include a typhoid-like illness, peritonitis with sepsis, and cellulitis from a wound acquired while fishing. The microbiology of E. tarda and the previous reports of infection due to this organism are reviewed.