Nutrition therapy is essential for diabetes treatment, and assessment of dietary intake can be time consuming. The purpose of this study was to develop a reliable and valid instrument to measure diabetic patients’ adherence to Canadian diabetes nutrition recommendations. Specific information derived from three, repeated 24-h dietary recalls of 64 type 2 diabetic patients, aged 59.2 ± 9.7 years, was correlated with a total score and individual items of the Perceived Dietary Adherence Questionnaire (PDAQ). Test-retest reliability was completed by 27 type 2 diabetic patients, aged 62.8 ± 8.4 years. The correlation coefficients for PDAQ items versus 24-h recalls ranged from 0.46 to 0.11. The intra-class correlation (0.78) was acceptable, indicating good reliability. The results suggest that PDAQ is a valid and reliable measure of diabetes nutrition recommendations. Because it is quick to administer and score, it may be useful as a screening tool in research and as a clinical tool to monitor dietary adherence.

Herein, orthorhombic BP crystals were successfully synthesized by low-pressure mineralization and the phase transitions at every stage were revealed systematically and were accurately confirmed.

Speckle-type POZ domain protein (SPOP), an adaptor in the E3 ubiquitin ligase complex, recognizes substrates and promotes protein degradation via the ubiquitin-proteasome system. It appears to help regulate progression of several cancers, and we show here that it acts as a tumor suppressor in pancreatic cancer. Our analysis of patient tissues showed decreased SPOP expression, which was associated with poor prognosis. SPOP knockdown in SW1990 (in vitro/vivo) and PANC-1 (in vitro) cells led to significantly greater proliferation, migration, and invasion. Co-immunoprecipitation experiments in SW1990 cells showed that SPOP interacted with the stem-cell marker NANOG, and this interaction has recently been shown to play a critical role in regulating progression of prostate cancer. We showed that, in one patient with pancreatic cancer, the expression of a truncated form of SPOP (p.Q360*) lacking the nuclear localization signal led to nuclear accumulation of NANOG, which promoted growth and metastasis of pancreatic cancer cells. Our results suggest that SPOP suppresses progression of pancreatic cancer by promoting the ubiquitination and subsequent degradation of NANOG. These results identify the SPOP-NANOG interaction as a potential therapeutic target against pancreatic cancer.