Iowa Manure Matters: Odor and Nutrient Management, Winter 2001, Vol. 4, no. 4

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2003, Vol. 6, no. 9

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2004, Vol. 7, no. 4

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2005, Vol. 8, no. 4

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2006, Vol. 9, no. 4

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2007, Vol. 10, no. 4

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2008, Vol. 11, no. 3

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Iowa Manure Matters: Odor and Nutrient Management, Winter 2002, Vol. 5, no. 4

Iowa Manure Matters: Odor and Nutrient Management is published by Iowa State University Extension, with funding support from the USDA Natural Resource Conservation Service.

Effects of usual nutrient intake and vitamin D status on markers of bone turnover in Swiss adolescents.

OBJECTIVE: To evaluate the effects of nutrient intake and vitamin D status on markers of type I collagen formation and degradation in adolescent boys and girls. DESIGN: Cross-sectional study. SETTING: Canton of Vaud, West Switzerland. SUBJECTS: A total of 92 boys and 104 girls, aged 11-16 y. Data were collected on height, weight, pubertal status (self-assessment of Tanner stage), nutrient intake (3-day dietary record) and fasting serum concentration of 25-hydroxyvitamin D (25OHD), and markers of collagen formation (P1NP) and degradation (serum C-terminal telopeptides: S-CTX). RESULTS: Tanner stage was a significant determinant of P1NP in boys and girls and S-CTX in girls. Of the nutrients examined, only the ratio of calcium to phosphorus (Ca/P) was positively associated with P1NP in boys, after adjustment for pubertal status. 25OHD decreased significantly at each Tanner stage in boys. Overall, 15% of boys and 17% of girls were identified as being vitamin D insufficient (serum 25OHD <30 nmol/l), with the highest proportion of insufficiency at Tanner stage 4-5 (29%) in boys and at Tanner stage 3 (24%) in girls. A significant association was not found between 25OHD and either bone turnover marker, nor was 25OHD insufficiency associated with higher concentrations of the bone turnover markers. CONCLUSIONS: The marked effects of puberty on bone metabolism may have obscured any possible effects of diet and vitamin D status on markers of bone metabolism. The mechanistic basis for the positive association between dietary Ca/P ratio and P1NP in boys is not clear and may be attributable to a higher Ca intake per se, a critical balance between Ca and P intake or higher dairy product consumption. A higher incidence of vitamin D insufficiency in older adolescents may reflect a more sedentary lifestyle or increased utilisation of 25OHD, and suggests that further research is needed to define their requirements. SPONSORSHIP: Nestec Ltd and The Swiss Foundation for Research in Osteoporosis.

Nutrient and light availability to white spruce seedlings in partial and clearcut harvested aspen stands

Abstract

1199-000 Soil Nutrient Mass Balance Study

Key Points: • Iowa’s exceptional agricultural productivity is dependent upon nutrient‐rich soils with high carbon and nitrogen stocks. • Soil carbon and nitrogen stocks in Iowa corn‐soybean rotations are at significant risk of long‐term decline. • Soil carbon and nitrogen stocks are a function of crop residue inputs. • Nutrient input levels that do not maximize crop yield and residue production are likely to reduce soil carbon and nitrogen stocks. • If soil carbon and nitrogen stocks decline, water quality improvements become more difficult. • Soil carbon and nitrogen balances are extremely difficult to measure, but positive balances are essential to the future of Iowa agriculture. Recommended Actions: • Accurate measurement of soil carbon and nitrogen balances is exceptionally difficult, but can be accomplished with sufficient investment and long‐term planning. • The ideal approach will include a combination of measurements from farms and experimental networks that manipulate nutrient inputs. • With proper planning and cooperation, Iowa State University and the Iowa Department of Agriculture and Land Stewardship can address the concerns raised in this report regarding the future of Iowa’s soil resource and agricultural productivity.

Transcriptome analysis of intraspecific competition in Arabidopsis thaliana reveals organ-specific signatures related to nutrient acquisition and general stress response pathways.

ABSTRACT: BACKGROUND: Plants are sessile and therefore have to perceive and adjust to changes in their environment. The presence of neighbours leads to a competitive situation where resources and space will be limited. Complex adaptive responses to such situation are poorly understood at the molecular level. RESULTS: Using microarrays, we analysed whole-genome expression changes in Arabidopsis thaliana plants subjected to intraspecific competition. The leaf and root transcriptome was strongly altered by competition. Differentially expressed genes were enriched in genes involved in nutrient deficiency (mainly N, P, K), perception of light quality, and responses to abiotic and biotic stresses. Interestingly, performance of the generalist insect Spodoptera littoralis on densely grown plants was significantly reduced, suggesting that plants under competition display enhanced resistance to herbivory. CONCLUSIONS: This study provides a comprehensive list of genes whose expression is affected by intraspecific competition in Arabidopsis. The outcome is a unique response that involves genes related to light, nutrient deficiency, abiotic stress, and defence responses.

Nutrient-based dietary patterns and the risk of head and neck cancer: a pooled analysis in the International Head and Neck Cancer Epidemiology consortium.

Background The association between dietary patterns and head and neck cancer has rarely been addressed. Patients and methods We used individual-level pooled data from five case-control studies (2452 cases and 5013 controls) participating in the International Head and Neck Cancer Epidemiology consortium. A posteriori dietary patterns were identified through a principal component factor analysis carried out on 24 nutrients derived from study-specific food-frequency questionnaires. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using unconditional logistic regression models on quintiles of factor scores. Results We identified three major dietary patterns named 'animal products and cereals', 'antioxidant vitamins and fiber', and 'fats'. The 'antioxidant vitamins and fiber' pattern was inversely related to oral and pharyngeal cancer (OR = 0.57, 95% CI 0.43-0.76 for the highest versus the lowest score quintile). The 'animal products and cereals' pattern was positively associated with laryngeal cancer (OR = 1.54, 95% CI 1.12-2.11), whereas the 'fats' pattern was inversely associated with oral and pharyngeal cancer (OR = 0.78, 95% CI 0.63-0.97) and positively associated with laryngeal cancer (OR = 1.69, 95% CI 1.22-2.34). Conclusions These findings suggest that diets rich in animal products, cereals, and fats are positively related to laryngeal cancer, and those rich in fruit and vegetables inversely related to oral and pharyngeal cancer.

Liquid fructose down-regulates liver insulin receptor substrate 2 and gluconeogeneic enzymes by modifying nutrient sensing factors in rats

High consumption of fructose-sweetened beverages has been linked to a high prevalence of chronic metabolic diseases. We have previously shown that a short course of fructose supplementation as a liquid solution induces glucose intolerance in female rats. In the present work, we characterized the fructose-driven changes in the liver and the molecular pathways involved. To this end, female rats were supplemented or not with liquid fructose (10%, w/v) for 7 or 14 days. Glucose and pyruvate tolerance tests were performed, and the expression of genes related to insulin signaling, gluconeogenesis and nutrient sensing pathways was evaluated. Fructose-supplemented rats showed increased plasma glucose excursions in glucose and pyruvate tolerance tests and reduced hepatic expression of several genes related to insulin signaling, including insulin receptor substrate 2 (IRS-2). However, the expression of key gluconeogenic enzymes, glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, was reduced. These effects were caused by an inactivation of hepatic forkhead box O1 (FoxO1) due to an increase in its acetylation state driven by a reduced expression and activity of sirtuin 1 (SIRT1). Further contributing to FoxO1 inactivation, fructose consumption elevated liver expression of the spliced form of X-box-binding-protein-1 as a consequence of an increase in the activity of the mammalian target of rapamycin 1 and protein 38-mitogen activated protein kinase (p38-MAPK). Liquid fructose affects both insulin signaling (IRS-2 and FoxO1) and nutrient sensing pathways (p38-MAPK, mTOR and SIRT1), thus disrupting hepatic insulin signaling without increasing the expression of key gluconeogenic enzymes.