The relationship between knowledge of recent HbA1c values and diabetes care understanding and self-management

OBJECTIVE: Knowledge of one's actual and target health outcomes (such as HbA(1c) values) is hypothesized to be a prerequisite for effective patient involvement in managing chronic diseases such as diabetes. We examined 1) the frequency and correlates of knowing one's most recent HbA(1c) test result and 2) whether knowing one's HbA(1c) value is associated with a more accurate assessment of diabetes control and better diabetes self-care understanding, self-efficacy, and behaviors related to glycemic control. RESEARCH DESIGN AND METHODS: We conducted a cross-sectional survey of a sample of 686 U.S. adults with type 2 diabetes in five health systems who had HbA(1c) checked in the previous 6 months. Independent variables included patient characteristics, health care provider communication, and health system type. We examined bivariate and multivariate associations between each variable and the respondents' knowledge of their last HbA(1c) values and assessed whether knowledge of HbA(1c) was associated with key diabetes care attitudes and behaviors. RESULTS: Of the respondents, 66% reported that they did not know their last HbA(1c) value and only 25% accurately reported that value. In multivariate analyses, more years of formal education and high evaluations of provider thoroughness of communication were independently associated with HbA(1c) knowledge. Respondents who knew their last HbA(1c) value had higher odds of accurately assessing their diabetes control (adjusted odds ratio 1.59, 95% CI 1.05-2.42) and better reported understanding of their diabetes care (P < 0.001). HbA(1c) knowledge was not associated with respondents' diabetes care self-efficacy or reported self-management behaviors. CONCLUSIONS: Respondents who knew their HbA(1c) values reported better diabetes care understanding and assessment of their glycemic control than those who did not. Knowledge of one's HbA(1c) level alone, however, was not sufficient to translate increased understanding of diabetes care into the increased confidence and motivation necessary to improve patients' diabetes self-management. Strategies to provide information to patients must be combined with other behavioral strategies to motivate and help patients effectively manage their diabetes.     

Scintigraphic diagnosis of tricuspid regurgitation

The authors describe a simple technique for diagnosis of tricuspid regurgitation. Red blood cells were labeled in vivo with 99mTc and 22 patients were studied with ECG-gated blood-pool imaging of the liver. A single region of interest was manually drawn around the liver and a time-activity curve obtained. The per cent change in liver counts during the cardiac cycle was found to be significantly higher in the 12 patients with tricuspid regurgitation (Group I) (mean, 4.04 +/- 1.6%; range, 1.3-21.4%) compared with the 10 controls (Group II) (mean, 0.35 +/- 0.16%; range, 0.013-1.3%) (p less than 0.05). Using a 1% change in liver counts as the criterion of a positive study, all 12 cases in Group I were diagnosed correctly, but there was one false positive in Group II; thus the sensitivity was 100% and the specificity 90%.     

Quantitative autoradiography of dopamine receptors in the brains of micro-opioid receptor knockout mice

Given the existence of functional interactions between opioidergic and dopaminergic systems, we have analyzed by quantitative autoradiography the possible long-term adaptive changes in the expression of D(1)- and D(2)-like dopamine receptors in the brains of mice lacking the micro-opioid receptor gene. An overall significant increase in D(1) and D(2) receptors (7.4 and 12.6%, respectively) across all cerebral regions examined was obtained in mutant mice relative to wild-type mice. However, region by region comparisons failed to reach significance in any individual brain area. These results indicate that only moderate changes in D(1)- and D(2)-like dopamine receptors densities occur in the brains of micro-opioid receptor knockout mice.     

No evidence for G-protein-coupled epsilon receptor in the brain of triple opioid receptor knockout mouse

Pharmacological approaches have defined the epsilon receptor as a beta-endorphin-preferring opioid receptor, described in rat vas deferens and in brain of several species. Only three opioid receptors-mu, delta and kappa-have been cloned and the existence of this additional subtype as a distinct protein remains controversial. Recently, the mouse brain epsilon receptor was detected in a G protein activation assay, as mediating residual beta-endorphin activity following pharmacological blockade of mu, delta and kappa receptors. To clarify whether this site is independent from mu, delta and kappa receptors, we performed beta-endorphin-induced [(35)S]GTPgammaS binding using mice lacking these three receptors (triple knockout mice). We tested both pons-medulla and whole brain preparations. beta-Endorphin strongly stimulated [(35)S]GTPgammaS binding in wild-type membranes but had no detectable effect in membranes from triple knockout mice. We conclude that the brain epsilon site involves mu, delta and/or kappa receptors, possibly coupled to nonclassical G proteins.     

Optimization of the preparation of 99mTc-labeled Hynic-derivatized Annexin V for human use

Hydrazino nicotinate (Hynic) is one of the most attractive bifunctional agents designed for the labeling of proteins with (99m)Tc. Recently, a (99m)Tc-labeled Hynic-Annexin V derivative has been described and successfully evaluated in animal models of apoptosis. Prior to a phase I human study, the preparation of (99m)Tc-Hynic-Annexin V has been optimized. The influence of the Hynic-load of Annexin V, amount of protein, nature and amount of reducing agent, activity and co-ligand on the labeling yield were evaluated using ITLC and size-exclusion FPLC. Optimal labeling yields were obtained when 60-90 microgram Hynic-Annexin V was labeled with up to 1.11 GBq (30 mCi) (99m)TcO(4)-using 10-20 microgram SnCl(2).2H(2)O as reducing agent and 1.5 mg tricine as the co-ligand. Biodistribution in normal mice was comparable to literature data.