Fee-for-service cancer rehabilitation programs improve health-related quality of life.

BACKGROUND: Rigorously applied exercise interventions undertaken in a research setting result in improved health-related quality of life (hrqol) in cancer survivors, but research to demonstrate effective translation of that research to practice is needed. The objective of the present study was to determine the effect of fee-for-service cancer rehabilitation programs in the community on hrqol and on self-reported physical activity and its correlates. METHODS: After enrolment and 17 ± 4 weeks later, new clients (n = 48) to two fee-for-service cancer rehabilitation programs completed the 36-Item Short Form Health Survey (rand-36: rand Corporation, Santa Monica, CA, U.S.A.), the Godin Leisure-Time Exercise Questionnaire, and questions about physical activity correlates. Normal fee-for-service operations were maintained, including a fitness assessment and individualized exercise programs supervised in a group or one-on-one setting, with no minimum attendance required. Fees were associated with the assessment and with each exercise session. RESULTS: Of the 48 participants, 36 (75%) completed both questionnaires. Improvements in the physical functioning, role physical, pain, and energy/fatigue scales on the rand-36 exceeded minimally important differences and were of a magnitude similar to improvements reported in structured, rigorously applied, and free research interventions. Self-reported levels of vigorous-intensity (p = 0.021), but not moderate-intensity (p = 0.831) physical activity increased. The number of perceived barriers to exercise (p = 0.035) and the prevalence of fatigue as a barrier (p = 0.003) decreased. Exercise self-efficacy improved only in participants who attended 11 or more sessions (p = 0.002). Exercise enjoyment did not change (p = 0.629). CONCLUSIONS: Enrolment in fee-for-service cancer rehabilitation programs results in meaningful improvements in hrqol comparable to those reported by research interventions, among other benefits. The fee-for-service model could be an effective model for delivery of exercise to more cancer survivors.

Retreatment with varenicline for smoking cessation in smokers who have previously taken varenicline: a randomized, placebo-controlled trial.

The efficacy and safety of retreatment with varenicline in smokers attempting to quit were evaluated in this randomized, double-blind, placebo-controlled, multicenter trial (Australia, Belgium, Canada, the Czech Republic, France, Germany, the United Kingdom, and the United States). Participants were generally healthy adult smokers (≥ 10 cigarettes/day) with ≥ 1 prior quit attempt (≥ 2 weeks) using varenicline and no quit attempts in ≤ 3 months; they were randomly assigned (1:1) to 12 weeks' varenicline (n = 251) or placebo (n = 247) treatment, with individual counseling, plus 40 weeks' nontreatment follow-up. The primary efficacy end point was the carbon monoxide-confirmed (≤ 10 ppm) continuous abstinence rate for weeks 9-12, which was 45.0% (varenicline; n = 249) vs. 11.8% (placebo; n = 245; odds ratio: 7.08; 95% confidence interval: 4.34, 11.55; P < 0.0001). Common varenicline group adverse events were nausea, abnormal dreams, and headache, with no reported suicidal behavior. Varenicline is efficacious and well tolerated in smokers who have previously taken it. Abstinence rates are comparable with rates reported for varenicline-naive smokers.

The invariant chain gene intronic enhancer shows homology to class II promoter elements.

Coordinate expression of MHC class II proteins and the class II-associated invariant chain (Ii) is important for proper MHC class II functioning in Ag processing and presentation. The coordinate regulation of these genes results, in part, from the sharing of transcriptional regulatory regions between MHC class II and Ii genes; the Ii has previously been shown to have an upstream enhancer closely related to the essential class II promoter elements. We report here the characterization of a second enhancer in the Ii gene, located within the first intron. This intronic enhancer is contained within a 155-bp region, enhances transcription from the Ii minimal promoter, and also contains elements that are homologous to class II promoter elements X1, X2, and Y boxes.

Backscatter absorption gas imaging: a new technique for gas visualization.

This paper presents a new laser-based method of gas detection that permits real-time television images of gases to be produced. The principle of this technique [which is called backscatter absorption gas imaging (BAGI)] and the operation of two instruments used to implement it are described. These instruments use 5-W and 20-W CO(2) lasers to achieve gas imaging at ranges of approximately 30 and 125 m, respectively. Derivations of relevant BAGI signal equations that can be used to predict the performance of a gas imager are provided. The predictions of this model and the measured range performance of an extended-range gas imager are compared. Finally, the results of gas sensitivity measurements and imaging tests on flowing gases are presented. These can be used to generate a realistic estimate of the BAGI sensitivity expected in detecting leaks of many different vapors.

Immunohistochemical localization and quantification of the 3-(cystein-S-yl)-acetaminophen protein adduct in acetaminophen hepatotoxicity.

Acetaminophen overdose causes severe hepatotoxicity in humans and laboratory animals, presumably by metabolism to N-acetyl-p-benzoquinone imine: and binding to cysteine groups as 3-(cystein-S-yl)acetaminophen-protein adduct. Antiserum specific for the adduct was used immunohistochemically to demonstrate the formation, distribution, and concentration of this specific adduct in livers of treated mice and was correlated with cell injury as a function of dose and time. Within the liver lobule, immunohistochemically demonstrable adduct occurred in a temporally progressive, central-to-peripheral pattern. There was concordance between immunohistochemical staining and quantification of the adduct in hepatic 10,000g supernate, using a quantitative particle concentration fluorescence immunoassay. Findings include: 1) immunochemically detectable adduct before the appearance of centrilobular necrosis, 2) distinctive lobular zones of adduct localization with subsequent depletion during the progression of toxicity, 3) drug-protein binding in hepatocytes at subhepatotoxic doses and before depletion of total hepatic glutathione, 4) immunohistochemical evidence of drug binding in the nucleus, and 5) adduct in metabolically active and dividing hepatocytes and in macrophagelike cells in the regenerating liver.

Propanil-induced methemoglobinemia and hemoglobin binding in the rat.

Administration of [ring-U-14C]propanil (3,4-dichloropropionanilide) to male Sprague-Dawley rats (30, 100, and 300 mg/kg, ip) increased the formation of methemoglobin at the two highest doses. Following a propanil dose of 100 mg/kg, methemoglobin formation attained a maximum level of 5% by 1.5 hr and declined to normal levels (approximately 2.5%) by 12 hr. Hemoglobin binding attained a maximum level of 50 pmol/mg protein by 12 hr, and remained constant for 24 hr. Following a propanil dose of 300 mg/kg, methemoglobin formation attained a maximum level of 24% by 4.5 hr, and declined to a level of 5% by 24 hr. Hemoglobin binding attained a maximum level of 425 pmol/mg protein by 12 hr, and remained constant for 24 hr. Hemoglobin binding was also detected at the lowest propanil dose (10 pmol/mg protein) even though methemoglobin formation was not observed. HPLC analysis of alkaline-treated hemoglobin from propanil-treated rats indicated the presence of one radiolabeled compound with the same HPLC retention time as 3,4-dichloraniline. These data are consistent with the concept that propanil is converted to N-hydroxy-3,4-dichloroaniline in the liver. Subsequently, this metabolite enters the erythrocyte and is oxidized by hemoglobin to 3,4-dichloronitrosobenzene with concomitant conversion of oxyhemoglobin to methemoglobin. The 3,4-dichloronitrosobenzene binds to cysteine residues on hemoglobin as the corresponding sulfinic acid amide adduct. These data suggest that human exposure to propanil may be monitored in the absence of observable toxicity by the analysis of propanil metabolites bound to hemoglobin.

Utility of solution electrochemistry mass spectrometry for investigating the formation and detection of biologically important conjugates of acetaminophen.

On-line formation and detection of glutathione and cysteine conjugates of acetaminophen were accomplished by the interfacing of a coulometric electrochemical cell with a thermospray mass spectrometer in a flow-injection experiment using a liquid chromatographic pump. Formation of the conjugates occurred only after acetaminophen was oxidized electrochemically by a two-electron transfer to N-acetyl-p-benzoquinoneimine and reacted in a mixing tee with either glutathione or cysteine. The newly formed conjugate was detected by thermospray mass spectrometry by observing the [M + H]+ ion for the acetaminophen-glutathione conjugate at m/z 457, or the [M + H]+ ion for the acetaminophen cysteine conjugate at m/z 271. Both the glutathione and cysteine conjugates produced a common fragment ion at m/z 184. The on-line reaction of glutathione and electrochemically generated N-acetyl-p-benzoquinoneimine was monitored at varying pH. At pH 8.5 the ion intensity for the acetaminophen-glutathione conjugate was greater than at lower pH, indicating that lower proton concentration enhanced the reaction of glutathione with N-acetyl-p-benzoquinoneimine. This on-line electrochemical-thermospray mass spectrometric method demonstrated that acetaminophen conjugates may be formed and detected in the time frame of 1 s.