Biomedical subjects
Publications and source records attributed to M Cushing.
Lateral epicondylitis is a common affliction that can be treated nonsurgically. However, surgical treatment is rarely indicated, and results are usually effective in more than 90% of patients. Although complications have been described, ours is the first report of heterotopic ossification after an uncomplicated lateral epicondylectomy.
Leishmania major-infected C57BL / 6 skin-dendritic cells (DC) are activated and release cytokines (including IL-12 p70), and likely initiate protective Th1 immunity in vivo (von Stebut, E. et al., J. Exp. Med. 188: 1547 - 1552). To characterize differences in DC function in mice that are genetically susceptible (BALB / c) and resistant (C57BL / 6) to cutaneous leishmaniasis, we analyzed the effects of L. major on Langerhans cell-like, fetal skin-derived DC (FSDDC) from both strains. BALB / c- and C57BL / 6-FSDDC ingested similar numbers of amastigotes, but did not ingest metacyclic promastigotes. Like C57BL / 6-FSDDC, infection of BALB / c-FSDDC led to up-regulation of MHC class I and II antigens, CD40, CD54, and CD86 within 18 h. L. major-induced BALB / c DC activation also led to the release of TNF-alpha, IL-6 and IL-12 p40 into 18-h supernatants. Infected BALB / c- and C57BL / 6-DC both released small amounts of IL-12 p70 within 72 h. Additional stimulation with IFN-gamma and / or anti-CD40 induced the release of more IL-12 p70 from infected BALB / c-DC than C57BL / 6-DC. Co-culture of control or infected BALB / c- and C57BL / 6-DC with naive syngeneic CD4(+) T cells and soluble anti-CD3 resulted in mixed, IFN-gamma-predominant responses after restimulation with immobilized anti-CD3. Finally, syngeneic L. major-infected DC effectively vaccinated BALB / c mice against cutaneous leishmaniasis. Genetic susceptibility to L. major that results from induction of Th2 predominant immune responses after infection does not appear to reflect failure of skin DC to internalize or respond to parasites, or the inability of BALB / c T cells to mount a Th1 response to DC-associated Leishmania antigens.
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OBJECTIVES: Pathologists differ in their definition of "dysplasia." This study was done to test the hypothesis that experienced oral pathologists are consistent in diagnosing epithelial dysplasia. STUDY DESIGN: Six board-certified oral pathologists examined 120 oral biopsies exhibiting simple hyperkeratosis to severe dysplasia. No clinical information was given, and presence of dysplasia was judged by histomorphology. Examiners' diagnoses were compared with sign-out diagnoses for each case. Months later, each examiner viewed 60 relabeled slides from the original 120. Each diagnosis was compared with the diagnosis in the first round. RESULTS: Exact agreement with the sign-out diagnosis averaged 50.5% (within one histologic grade 90.4%). Examiners agreed exactly with their own diagnoses 50.8% of the time (within one histologic grade 92.4%). Agreement distinguishing dysplasia from no dysplasia compared with original sign-out diagnosis was 81.5%. Agreement with themselves distinguishing dysplasia from no dysplasia was 80.3%. CONCLUSIONS: Accurate reproducible agreement among experienced board-certified oral pathologists diagnosing oral epithelial dysplasia is difficult to achieve.
In summary, analysis of the P01 program indicates that differences exist in scores and funding requirements between purely basic and translational P01s; P01 funding has been stable and the P01 policies consistent; growth in average costs for P01s has lagged compared to R01s; P01 grantees have a higher success rate than R01 grantees; priority score compression reduces the P01 payline without reducing the number of grants funded; exception funding in P01s expands the number of grants awarded and helps to meet the scientific program needs of the NCI; almost all R01 and P01 applications in the first quartile are funded; comparably ranked R01s and P01s are funded at equivalent percentages of recommended funding levels; the percentage of approved funds awarded declines as scores for R01s and P01s become less favorable. Because the resources available are finite, the NCI carefully considers the competing demands for RPG funds. On balance, however, the P01 program is still in good health. In combination with the other methods we use to make RPG awards, the P01 program is a vital component of our research grant program. Faced with budget realities, however, some difficult decisions have to be made. The NCI is open to suggestions on how to distribute research funds to best promote cancer research throughout the country. The NCI is particularly interested in hearing researchers' perceptions of problems so that, whenever it is appropriate, we can modify our course. There are important questions to consider for the future. Should there be greater or lesser use of RFAs in allocating resources for P01 grants? What algorithm optimally distributes resources among R01s, P01s, and other funding instruments in the RPGs? Should exceptions be used more or less heavily in the P01 funding process? Should other grant programs outside the RPG budget, such as the P50 SPORE program, be used to relieve pressures on the P01 budget? Should the number of projects within P01s be limited? How can peer review groups be given opportunities to provide priority scores that better reflect distinguishable differences in highly meritorious P01s? Should P01 scores be normalized? How could the R01 percentile concept be applied to P01s? How can the results from standing study sections be synchronized with results from ad hoc review groups? What changes in peer review procedures would promote equitable score distributions and budget recommendations across years? How can the NCI provide stability for established P01s without impinging on the ability of new P01s to enter the system?(ABSTRACT TRUNCATED AT 400 WORDS)
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