The classical criteria for the evaluation of clinical trials in cancer reflect alterations in physical well-being, but are insensitive to other important factors, such as psychosocial state, sociability, and somatic sensation that may play a critical role in determining the patients' functional response to their illness and its treatment. The Functional Living Index-Cancer is designed for easy, repeated patient self-administration. It is a 22-item questionnaire that has been validated on 837 patients in two cities over a three-year period. Criteria for validity include stability of factor analysis, concurrent validation studies against the Karnofsky, Beck Depression, Spielberger State and Trait Anxiety, and Katz Activities of Daily Living scales, as well as the scaled version of The General Health Questionnaire and The McGill/ Melzack Pain Index. The index is uncontaminated by social desirability issues. The validation studies demonstrate the lack of correlation between traditional measures of patient response and other significant functional factors such as depression and anxiety (r = 0.33), sociability and family interaction, and nausea. These findings elucidate the frequently observed discrepancies between traditional assessments of clinical response and overall functional patient outcome. The index is proposed as an adjunct to clinical trials assessment and may provide additional patient functional information on which to analyse the outcome of clinical trials or offer specific advice to individual patients.

With three independent techniques (absorption spectrophotometry, measurement of the deoxyribonucleic acid [DNA] melting temperature, and equilibrium dialysis), no evidence has been found for the binding of nalidixic acid to purified DNA. Also, no evidence has been found to support the hypothesis that nalidixic acid is permanently modified to a new, active compound by the bacterial cell. By using an in vitro DNA replication system developed by Bonhoeffer and colleagues, soluble extracts from nalidixic acid-sensitive cells have been shown to confer nalidixic acid sensitivity on the DNA synthesis of lysates from nalidixic acid-resistant cells. The activity in the extracts is only present in sensitive cells and is nondialyzable and heat sensitive. Finally, two known nalidixic acid-resistant mutants of Escherichia coli, mapping at nal A and nal B, respectively, have been tested to determine whether either of them is a transport mutant. It has been shown that nal Br is a transport mutant whereas nal Ar is not.Nalidixic acid (NAL; 1-ethyl-1,4-dihydro-7-methyl-4-oxo-1,8-naphthyridine -3 -carboxylic acid) is a specific, rapid, and reversible inhibitor of bacterial deoxyribonucleic acid (DNA) replication (3, 9). At present the mechanism of action of NAL is totally unknown. Previous work by other investigators has ruled out several possibilities. For example, none of the many purified enzymes involved in DNA metabolism are inhibited by NAL in vitro. Those (13,16,18). Consequently, NAL must be blocking some aspect of the DNA polymerization reaction itself and not just synthesis of the DNA precursors. Based on the work described above, three possibilities remain for the way in which NAL inhibits DNA replication: (i) NAL binds directly to the DNA template; (ii) NAL binds to and inactivates one of the components of the DNA replication complex (possibly an unknown replication protein); or (iii) NAL is chemically modified by metabolizing bacteria to an active form, which then functions by either (i) or (ii). In this paper we present experiments which test all three of these possribilities.In addition, we have carried out experiments with the two known NAL-resistant mutants of E. coli, mapping at nal A and nal B (10)

For women with breast cancer who are being treated with cyclophosphamide, methotrexate, and fluorouracil, the efficacy of dexamethasone and metoclopramide in controlling nausea and vomiting equaled or exceeded that of ondansetron.