Carbohydrate Replacement of Rice or Potato with Lentils Reduces the Postprandial Glycemic Response in Healthy Adults in an Acute, Randomized, Crossover Trial.

Background: The postprandial blood glucose response (PBGR) following carbohydrate replacement of high-glycemic index (GI) foods with pulses, in a mixed meal, has not been accurately defined. Objective: We aimed to determine the extent to which PBGR and relative glycemic response (RGR) are lowered when half of the available carbohydrate (AC) from rice or potato is replaced with cooked lentils. Methods: Using a crossover design, 2 groups of 24 healthy adults randomly consumed 50 g AC from control white rice alone [mean ± SD body mass index (BMI, in kg/m2): 24.3 ± 0.5; mean ± SD age: 27.7 ± 1.2 y], instant potato alone (BMI: 24.0 ± 0.5; age: 27.4 ± 1.2 y), or the same starch source in a 50:50 AC combination with each of 3 types of commercially available lentils (large green, small green, split red). Fasting and postprandial blood samples were analyzed for glucose and insulin, and used to derive incremental area under the curve (iAUC), RGR, and maximum concentration (Cmax). Treatment effects were assessed with the use of repeated-measures ANOVA within the rice and potato treatments. Results: In comparison to rice alone, blood glucose iAUC and Cmax (P < 0.001) were lowered after consumption of rice with large green (P = 0.057), small green (P = 0.002), and split red (P = 0.006) lentils. Blood glucose iAUC and Cmax were also significantly lowered (P < 0.0001) after consumption of potato combined with each lentil, compared to potato alone. Plasma insulin iAUC and Cmax were significantly (P < 0.001) decreased when lentils were combined with potato, but not with rice. The RGRs of rice and potato were lowered by ∼20% and 35%, respectively, when half of their AC was replaced with lentils. Conclusions: Replacing half of the AC from high-GI foods with lentils significantly attenuates PBGR in healthy adults; this can contribute to defining a health claim for pulses and blood glucose lowering. This trial was registered at clinicaltrials.gov as NCT02426606.

Intervention based on social cognitive theory: evaluating adolescents' knowledge of OTC pain medications.

OBJECTIVE: To evaluate the effect of a social cognitive theory (SCT)-based intervention on the constructs of situational perception, behavioral capabilities, outcome expectations, outcome expectancies, and self-efficacy concerning over-the-counter (OTC) pain medications among an adolescent population. DESIGN: Pre-posttest control group design. SETTING: Rural high school in the southeastern United States, between February and March 2011. PARTICIPANTS: 203 high school students recruited from 10 classrooms. INTERVENTION: Classrooms were randomly assigned to an SCT-based education intervention group or the control group. Pre- and posttest data were collected from each group 2 weeks before and 2 weeks after the intervention was delivered. MAIN OUTCOME MEASURES: Change in the five selected constructs of SCT. RESULTS: Compared with the control group, significant improvements at posttest were observed in the intervention group for outcome expectations of OTC pain medications ( P ≤ 0.05) and behavioral capabilities ( P ≤ 0.05). CONCLUSION: The results suggest that lessons based on SCT to improve the outcome expectations that an adolescent population places on the consumption of OTC pain medications may assist in developing the knowledge and skills needed to consume these products properly.

Contribution of toll-like receptor signaling pathways to breast tumorigenesis and treatment.

Mounting evidence indicates that anomalies in the inflammatory and immune response pathways are essential to tumorigenesis. However, tumor-based innate immunity initiated by transformed breast epithelia tissues has received much less attention. This review summarizes published reports on the role of the toll-like receptor signaling pathway on breast cancer risk, disease progression, survival, and disease recurrence. Specifically, we discuss the underlying biological mechanisms that contribute to the tumorigenic and/or anti-tumorigenic properties of toll-like receptors and their associated agonists in relation to breast tumorigenesis and cancer treatment. Further, we use results from preclinical, clinical, and population-based studies as prompts for the exploration of new and more effective breast cancer therapies. As the knowledge base of innate immunity's involvement in breast cancer progression increases, current and new immune-modifying strategies will be refined to effectively treat breast cancer.

The influence of a patient-counseling course on the communication apprehension, outcome expectations, and self-efficacy of first-year pharmacy students.

OBJECTIVES: To evaluate first-year doctor of pharmacy (PharmD) students' communication apprehension, outcome expectations, and self-efficacy for communication over the duration of a 15-week patient-counseling course. DESIGN: First-year PharmD students (n=94) were asked to complete a 47-item, self-administered questionnaire on 3 occasions over the duration of the Nonprescription Drugs/Patient-Counseling course during the fall 2009 and 2010 semesters. ASSESSMENT: Eighty-seven of 94 students completed the survey instrument across data collection periods. There were significant reductions in total communication apprehension scores and in the communication apprehension subscores for meetings and public speaking, and significant increases in self-efficacy over time. No differences were found for outcome expectations of communication scores or the subscores for interpersonal conversations and group discussion. CONCLUSIONS: Communication apprehension may be decreased and self-efficacy for communication increased in first-year PharmD students through a 15-week Nonprescription Drugs/Patient-Counseling course using small-group practice sessions, case studies, and role-play exercises in conjunction with classroom lectures.

Chemokine Ligand 5 (CCL5) and chemokine receptor (CCR5) genetic variants and prostate cancer risk among men of African Descent: a case-control study.

BACKGROUND: Chemokine and chemokine receptors play an essential role in tumorigenesis. Although chemokine-associated single nucleotide polymorphisms (SNPs) are associated with various cancers, their impact on prostate cancer (PCA) among men of African descent is unknown. Consequently, this study evaluated 43 chemokine-associated SNPs in relation to PCA risk. We hypothesized inheritance of variant chemokine-associated alleles may lead to alterations in PCA susceptibility, presumably due to variations in antitumor immune responses. METHODS: Sequence variants were evaluated in germ-line DNA samples from 814 African-American and Jamaican men (279 PCA cases and 535 controls) using Illumina's Goldengate genotyping system. RESULTS: Inheritance of CCL5 rs2107538 (AA, GA+AA) and rs3817655 (AA, AG, AG+AA) genotypes were linked with a 34-48% reduction in PCA risk. Additionally, the recessive and dominant models for CCR5 rs1799988 and CCR7 rs3136685 were associated with a 1.52-1.73 fold increase in PCA risk. Upon stratification, only CCL5 rs3817655 and CCR7 rs3136685 remained significant for the Jamaican and U.S. subgroups, respectively. CONCLUSIONS: In summary, CCL5 (rs2107538, rs3817655) and CCR5 (rs1799988) sequence variants significantly modified PCA susceptibility among men of African descent, even after adjusting for age and multiple comparisons. Our findings are only suggestive and require further evaluation and validation in relation to prostate cancer risk and ultimately disease progression, biochemical/disease recurrence and mortality in larger high-risk subgroups. Such efforts will help to identify genetic markers capable of explaining disproportionately high prostate cancer incidence, mortality, and morbidity rates among men of African descent.

Interaction among apoptosis-associated sequence variants and joint effects on aggressive prostate cancer.

BACKGROUND: Molecular and epidemiological evidence demonstrate that altered gene expression and single nucleotide polymorphisms in the apoptotic pathway are linked to many cancers. Yet, few studies emphasize the interaction of variant apoptotic genes and their joint modifying effects on prostate cancer (PCA) outcomes. An exhaustive assessment of all the possible two-, three- and four-way gene-gene interactions is computationally burdensome. This statistical conundrum stems from the prohibitive amount of data needed to account for multiple hypothesis testing. METHODS: To address this issue, we systematically prioritized and evaluated individual effects and complex interactions among 172 apoptotic SNPs in relation to PCA risk and aggressive disease (i.e., Gleason score ≥ 7 and tumor stages III/IV). Single and joint modifying effects on PCA outcomes among European-American men were analyzed using statistical epistasis networks coupled with multi-factor dimensionality reduction (SEN-guided MDR). The case-control study design included 1,175 incident PCA cases and 1,111 controls from the prostate, lung, colo-rectal, and ovarian (PLCO) cancer screening trial. Moreover, a subset analysis of PCA cases consisted of 688 aggressive and 488 non-aggressive PCA cases. SNP profiles were obtained using the NCI Cancer Genetic Markers of Susceptibility (CGEMS) data portal. Main effects were assessed using logistic regression (LR) models. Prior to modeling interactions, SEN was used to pre-process our genetic data. SEN used network science to reduce our analysis from > 36 million to < 13,000 SNP interactions. Interactions were visualized, evaluated, and validated using entropy-based MDR. All parametric and non-parametric models were adjusted for age, family history of PCA, and multiple hypothesis testing. RESULTS: Following LR modeling, eleven and thirteen sequence variants were associated with PCA risk and aggressive disease, respectively. However, none of these markers remained significant after we adjusted for multiple comparisons. Nevertheless, we detected a modest synergistic interaction between AKT3 rs2125230-PRKCQ rs571715 and disease aggressiveness using SEN-guided MDR (p = 0.011). CONCLUSIONS: In summary, entropy-based SEN-guided MDR facilitated the logical prioritization and evaluation of apoptotic SNPs in relation to aggressive PCA. The suggestive interaction between AKT3-PRKCQ and aggressive PCA requires further validation using independent observational studies.

Hyperthyroidism presenting with hyperglycemia in an adolescent female.

A 15-year-old female presented to a pediatric emergency department with glycosuria, ketonuria, and hyperglycemia and was admitted with a presumed diagnosis of diabetes mellitus. The patient required no insulin therapy and only minor dietary modification to maintain euglycemia. Clinical examination and laboratory findings revealed a primary diagnosis of Graves' hyperthyroidism with associated impaired glucose tolerance. Here, we review the mechanisms of thyrotoxicosis resulting in impaired glucose metabolism.

Congenital plaque-type glomuvenous malformations presenting in childhood.

BACKGROUND: Glomuvenous malformations (GVMs) are now considered a separate entity from venous malformations. The rarest type of GVM is the generalized congenital plaque-type GVM. OBSERVATIONS: We present 10 new cases of congenital plaque-type GVM and describe their clinical progression and treatment. Mutations in the glomulin gene were found in those patients who participated in the genetic study. CONCLUSIONS: Congenital plaque-type GVMs are unique in their congenital nature, extensive distribution, difficult to diagnose and treat, and progressive involvement after birth. Most cases are familial, yet affected relatives usually have only minor lesions. The lesions of congenital plaque-type GVM are severe, visible at birth, and usually mistaken for extensive venous malformations. Vascular malformations are divided by hemodynamic type into slow-flow and fast-flow lesions. Slow-flow lesions are subcategorized as capillary, lymphatic, and venous.(1) Capillary malformations are flat, sharply demarcated, red-pink vascular stains of the skin commonly referred to as port-wine stains. These persist throughout life and are characterized histologically by dilated capillaries within the dermis. They slowly increase in size with age. Lymphatic malformations are spongelike collections of abnormal channels and spaces that contain clear lymphatic fluid, causing an excess of fluid to accumulate and dilate the lymphatic channels. This results in swelling of the affected area and, if extensive, can cause enlargement of soft tissues and bones.

Dendritic spine and dendritic field characteristics of layer V pyramidal neurons in the visual cortex of fragile-X knockout mice.

Fragile-X syndrome is a common form of mental retardation resulting from the inability to produce the fragile-X mental retardation protein. The specific function of this protein is unknown; however, it has been proposed to play a role in developmental synaptic plasticity. Examination of human brain autopsy material has shown that fragile-X patients exhibit abnormalities in dendritic spine structure and number, suggesting a failure of normal developmental dendritic spine maturation and pruning in this syndrome. Similar results using a knockout mouse model have previously been described; however, it was noted in retrospect that the mice used in that study may have carried a mutation for retinal degeneration, which may have affected cell morphology in the visual cortex of those animals. In this study, dendritic spines on layer V pyramidal cells of visual cortices, taken from fragile-X knockout and wild-type control mice without the retinal degeneration mutation and stained using the Golgi-Cox method, were investigated for comparison with the human condition. Quantitative analyses of the lengths, morphologies, and numbers of dendritic spines, as well as amount of dendritic arbor and dendritic branching complexity, were conducted. The fragile-X mice exhibited significantly more long dendritic spines and significantly fewer short dendritic spines than control mice. Similarly, fragile-X mice exhibited significantly more dendritic spines with an immature-like morphology and significantly fewer with a more mature type morphology. However, unlike the human condition, fragile-X mice did not exhibit statistically significant dendritic spine density differences from controls. Fragile-X mice also did not demonstrate any significant differences from controls in dendritic tree complexity or dendritic arbor. Long dendritic spines with immature morphologies are characteristic of early development or a lack of sensory experience. These results are similar to those found in the human condition and further support a role for the fragile-X mental retardation protein specifically in normal dendritic spine developmental processes. They also support the validity of these mice as a model of fragile-X syndrome.