Lowering the glycemic index of white bread using a white bean extract

<p>Abstract</p> <p>Background</p> <p>Phase 2^®is a dietary supplement derived from the common white kidney bean (Phaseolus vulgaris). Phase 2 has been shown to inhibit alpha-amylase, the complex carbohydrate digesting enzyme, in vitro. The inhibition of alpha-amylase may result in the lowering of the effective Glycemic Index (GI) of certain foods. The objective of this study was to determine whether the addition of Phase 2 would lower the GI of a commercially available high glycemic food (white bread).</p> <p>Methods</p> <p>An open-label 6-arm crossover study was conducted with 13 randomized subjects. Standardized GI testing was performed on white bread with and without the addition of Phase 2 in capsule and powder form, each in dosages of 1500 mg, 2000 mg, and 3000 mg. Statistical analysis was performed by one-way ANOVA of all seven treatment groups using unadjusted multiple comparisons (t tests) to the white bread control.</p> <p>Results</p> <p>For the capsule formulation, the 1500 mg dose had no effect on the GI and the 2000 mg and 3000 mg capsule doses caused insignificant reductions in GI. For the powder, the 1500 mg and 2000 mg doses caused insignificant reductions in the GI, and the 3000 mg dose had a significant effect (-20.23 or 34.11%, p = 0.023)</p> <p>Conclusion</p> <p>Phase 2 white bean extract appears to be a novel and potentially effective method for reducing the GI of existing foods without modifying their ingredient profile.</p> <p>Trial Registration</p> <p>Trial Registration: ISRCTN50347345</p

Does dietary calcium interact with dietary fiber against colorectal cancer? : a case-control study in Central Europe

BACKGROUND: An unfavorable trend of increasing rates of colorectal cancer has been observed across modern societies. In general, dietary factors are understood to be responsible for up to 70% of the disease’s incidence, though there are still many inconsistencies regarding the impact of specific dietary items. Among the dietary minerals, calcium intake may play a crucial role in the prevention. The purpose of this study was to assess the effect of intake of higher levels of dietary calcium on the risk of developing of colorectal cancer, and to evaluate dose dependent effect and to investigate possible effect modification. METHODS: A hospital based case–control study of 1556 patients (703 histologically confirmed colon and rectal incident cases and 853 hospital-based controls) was performed between 2000–2012 in Krakow, Poland. The 148-item semi-quantitative Food Frequency Questionnaire to assess dietary habits and level of nutrients intake was used. Data regarding possible covariates was also collected. RESULTS: After adjustment for age, gender, education, consumption of fruits, raw and cooked vegetables, fish, and alcohol, as well as for intake of fiber, vitamin C, dietary iron, lifetime recreational physical activity, BMI, smoking status, and taking mineral supplements, an increase in the consumption of calcium was associated with the decrease of colon cancer risk (OR = 0.93, 95% CI: 0.89-0.98 for every 100 mg Ca/day increase). Subjects consumed >1000 mg/day showed 46% decrease of colon cancer risk (OR = 0.54, 95% CI: 0.35-0.83). The effect of dietary calcium was modified by dietary fiber (p for interaction =0.015). Finally, consistent decrease of colon cancer risk was observed across increasing levels of dietary calcium and fiber intake. These relationships were not proved for rectal cancer. CONCLUSIONS: The study confirmed the effect of high doses of dietary calcium against the risk of colon cancer development. This relationship was observed across different levels of dietary fiber, and the beneficial effect of dietary calcium depended on the level of dietary fiber suggesting modification effect of calcium and fiber. Further efforts are needed to confirm this association, and also across higher levels of dietary fiber intake

3D Mapping of Serial Histology Sections with Anomalies Using a Novel Robust Deformable Registration Algorithm

The neuroimaging field is moving toward micron scale and molecular features in digital pathology and animal models. These require mapping to common coordinates for annotation, statistical analysis, and collaboration. An important example, the BRAIN Initiative Cell Census Network, is generating 3D brain cell atlases in mouse, and ultimately primate and human. We aim to establish RNAseq profiles from single neurons and nuclei across the mouse brain, mapped to Allen Common Coordinate Framework (CCF). Imaging includes (Forumala Presented). 500 tape-transfer cut 20 (Forumala Presented). m thick Nissl-stained slices per brain. In key areas 100 &#x0024;&#x0024;\upmu &#x0024;&#x0024; m thick slices with 0.5–2 mm diameter circular regions punched out for snRNAseq are imaged. These contain abnormalities including contrast changes and missing tissue, two challenges not jointly addressed in diffeomorphic image registration. Existing methods for mapping 3D images to histology require manual steps unacceptable for high throughput, or are sensitive to damaged tissue. Our approach jointly: registers 3D CCF to 2D slices, models contrast changes, estimates abnormality locations. Our registration uses 4 unknown deformations: 3D diffeomorphism, 3D affine, 2D diffeomorphism per-slice, 2D rigid per-slice. Contrast changes are modeled using unknown cubic polynomials per-slice. Abnormalities are estimated using Gaussian mixture modeling. The Expectation Maximization algorithm is used iteratively, with E step: compute posterior probabilities of abnormality, M step: registration and intensity transformation minimizing posterior-weighted sum-of-square-error. We produce per-slice anatomical labels using Allen Institute’s ontology, and publicly distribute results online, with several typical and abnormal slices shown here. This work has further applications in digital pathology, and 3D brain mapping with stroke, multiple sclerosis, or other abnormalities