Novel Resistant Potato Starches on Glycemia and Satiety in Humans

This study was designed to determine the efficacy of two novel type-four resistant starches (RS4) on postprandial glycemia and ratings of fullness. Volunteers (n = 10) completed completed five interventions designed to determine the glycemic and satiety (fullness) effects of the starches (38 g,) alone and when added on top of available carbohydrate. The dose of the starches provided 30 g of resistant starch per treatment. The treatments were: commercial resistant starch added to water (PF−), noncommercial resistant starch added to water (PR−), dextrose solution (DEX, 50 g), and DEX with PenFibe starch (PF+), and DEX with the non-commercial starch added (PR+). Blood glucose was measured in the fasted state and following the randomly assigned treatments at 30, 45, 60, 90, and 120 minutes post-consumption. A visual analog scale was used to determine fullness at each time point. There were no differences in the glucose incremental areas under the curve (iAUC) for PF+ and PR+ compared with DEX. The PF− and PR− treatments had decreased (P < 0.05) iAUCs for glucose compared with DEX, PF+, and PR+. There were no treatment differences for RoF. The dose (38 g) of starches did not to alter glucose responses when added on top of 50 g of dextrose

High-efficiency, high-power difference-frequency generation of 0.9–1.5 μm light in BBO

An efficient method for generation of high energy pulsed ir light between 0.9 and 1.5 μm is described. The technique uses difference frequency mixing of pulsed, visible dye and Nd:YAG laser light in a 10 mm long BBO crystal. Quantum efficiencies of up to 23% and ir pulse energies up to 4.5 mJ are demonstrated. The low shot-to-shot fluctuations of difference frequency generation in BBO make this technique an attractive alternative to the conventional optical parametric oscillator or Raman shifting methods that are currently used to access this spectral region

Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise

Citation: Teeman, C. S., Kurti, S. P., Cull, B. J., Emerson, S. R., Haub, M. D., & Rosenkranz, S. K. (2016). Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise. Nutrition & Metabolism, 13, 14. doi:10.1186/s12986-016-0142-6Postprandial lipemia is an independent risk factor for development of cardiovascular disease. Postprandial inflammation following the prolonged elevation of triglycerides occurring subsequent to ingestion of high-fat meals, provides a likely explanation for increased disease risk. Substantial evidence has shown that acute exercise is an effective modality for attenuation of postprandial lipemia following a high-fat meal. However, much of the evidence pertaining to exercise intensity, duration, and overall energy expenditure for reducing postprandial lipemia is inconsistent. The effects of these different exercise variables on postprandial inflammation is largely unknown. Long-term, frequent exercise, however, appears to effectively reduce systemic inflammation, especially in at-risk or diseased individuals. With regard to an acute postprandial response, without a recent bout of exercise, high levels of chronic exercise do not appear to reduce postprandial lipemia. This review summarizes the current literature on postprandial and inflammatory responses to high-fat meals, and the roles that both acute and chronic exercise play. This review may be valuable for health professionals who wish to provide evidence-based, pragmatic advice for reducing postprandial lipemia and cardiovascular disease risk for their patients. A brief review of proposed mechanisms explaining how high-fat meals may result in pro-inflammatory and pro-atherosclerotic environments is also included

Serotonin receptor type 3 antagonists improve obesity-associated fatty liver disease in mice

ABSTRACT Obesity is a major cause for nonalcoholic fatty liver disease (NAFLD). Previous studies suggested that alterations in intestinal motility and permeability contribute to the development of NAFLD. Serotonin and serotonin receptor type 3 (5-HT 3 R) are key factors in the regulation of intestinal motility and permeability. Therefore, we studied the effect of the 5-HT 3 R antagonists tropisetron and palonosetron on the development of NA-FLD in leptin-deficient obese mice. Four-week-old ob/ob mice and lean controls were treated for 6 weeks orally with tropisetron or palonosetron at 0.2 mg/kg per day. We determined markers of liver damage and inflammation, portal endotoxin levels, and duodenal concentrations of serotonin, serotoninreuptake transporter (SERT), occludin, and claudin-1. Tropisetron treatment significantly reduced liver fat content (Ϫ29%), liver inflammation (Ϫ56%), and liver cell necrosis (Ϫ59%) in ob/ob mice. The beneficial effects of tropisetron were accompanied by a decrease in plasma alanine aminotransferase and portal vein plasma endotoxin levels, an attenuation of enhanced MyD88 and tumor necrosis factor-␣ mRNA expression in the liver, and an increase of tight junction proteins in the duodenum. Tropisetron treatment also caused a reduction of elevated serotonin levels and an increase of SERT in the duodenum of ob/ob mice. Palonosetron had similar effects as tropisetron with regard to the reduction of liver fat and other parameters. Tropisetron and palonosetron are effective in attenuating NAFLD in a genetic mouse model of obesity. The effect involves the intestinal nervous system, resulting in a reduction of endotoxin influx into the liver and subsequently of liver inflammation and fat accumulation

A vertebrate case study of the quality of assemblies derived from next-generation sequences

The unparalleled efficiency of next-generation sequencing (NGS) has prompted widespread adoption, but significant problems remain in the use of NGS data for whole genome assembly. We explore the advantages and disadvantages of chicken genome assemblies generated using a variety of sequencing and assembly methodologies. NGS assemblies are equivalent in some ways to a Sanger-based assembly yet deficient in others. Nonetheless, these assemblies are sufficient for the identification of the majority of genes and can reveal novel sequences when compared to existing assembly references

Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise

Citation: Teeman, C. S., Kurti, S. P., Cull, B. J., Emerson, S. R., Haub, M. D., & Rosenkranz, S. K. (2016). Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise. Nutrition & Metabolism, 13, 14. doi:10.1186/s12986-016-0142-6Postprandial lipemia is an independent risk factor for development of cardiovascular disease. Postprandial inflammation following the prolonged elevation of triglycerides occurring subsequent to ingestion of high-fat meals, provides a likely explanation for increased disease risk. Substantial evidence has shown that acute exercise is an effective modality for attenuation of postprandial lipemia following a high-fat meal. However, much of the evidence pertaining to exercise intensity, duration, and overall energy expenditure for reducing postprandial lipemia is inconsistent. The effects of these different exercise variables on postprandial inflammation is largely unknown. Long-term, frequent exercise, however, appears to effectively reduce systemic inflammation, especially in at-risk or diseased individuals. With regard to an acute postprandial response, without a recent bout of exercise, high levels of chronic exercise do not appear to reduce postprandial lipemia. This review summarizes the current literature on postprandial and inflammatory responses to high-fat meals, and the roles that both acute and chronic exercise play. This review may be valuable for health professionals who wish to provide evidence-based, pragmatic advice for reducing postprandial lipemia and cardiovascular disease risk for their patients. A brief review of proposed mechanisms explaining how high-fat meals may result in pro-inflammatory and pro-atherosclerotic environments is also included

The impact of economic recession on maternal and infant mortality: lessons from history

<p>Abstract</p> <p>Background</p> <p>The effect of the recent world recession on population health has featured heavily in recent international meetings. Maternal health is a particular concern given that many countries were already falling short of their MDG targets for 2015.</p> <p>Methods</p> <p>We utilise 20^thcentury time series data from 14 high and middle income countries to investigate associations between previous economic recession and boom periods on maternal and infant outcomes (1936 to 2005). A first difference logarithmic model is used to investigate the association between short run fluctuations in GDP per capita (individual incomes) and changes in health outcomes. Separate models are estimated for four separate time periods.</p> <p>Results</p> <p>The results suggest a modest but significant association between maternal and infant mortality and economic growth for early periods (1936 to 1965) but not more recent periods. Individual country data display markedly different patterns of response to economic changes. Japan and Canada were vulnerable to economic shocks in the post war period. In contrast, mortality rates in countries such as the UK and Italy and particularly the US appear little affected by economic fluctuations.</p> <p>Conclusions</p> <p>The data presented suggest that recessions do have a negative association with maternal and infant outcomes particularly in earlier stages of a country's development although the effects vary widely across different systems. Almost all of the 20 least wealthy countries have suffered a reduction of 10% or more in GDP per capita in at least one of the last five decades. The challenge for today's policy makers is the design and implementation of mechanisms that protect vulnerable populations from the effects of fluctuating national income.</p

Apolipoprotein E controls the development of monocyte-derived alveolar macrophages upon pulmonary inflammatory adaptation

The lung is constantly exposed to the outside world and optimal adaptation of immune responses is crucial for efficient pathogen clearance. However, mechanisms that lead to lung-associated macrophages' functional and developmental adaptation remain elusive. To reveal such mechanisms, we developed a reductionist model of environmental intranasal β-glucan exposure, allowing for the detailed interrogation of molecular mechanisms of pulmonary macrophage adaptation. Employing single-cell transcriptomics, high dimensional imaging, and flow cytometric characterization paired with in vivo and ex vivo challenge models, we reveal that pulmonary low-grade inflammation results in the development of Apolipoprotein E (ApoE) -dependent monocyte-derived alveolar macrophages (ApoE+CD11b+ AM). ApoE+CD11b+ AMs expressed high levels of CD11b, ApoE, Gpnmb, and Ccl6, were glycolytic, highly phagocytic, and produced large amounts of interleukin 6 upon restimulation. Functional differences were cell intrinsic and myeloid cell-specific ApoE ablation inhibited Ly6c+ monocyte to ApoE+CD11b+ AM differentiation dependent on M-CSF secretion, promoting ApoE+CD11b+ AM cell death and thus impeding ApoE+CD11b+ AM maintenance. In vivo, β-glucan-elicited ApoE+CD11b+ AMs limited the bacterial burden of Legionella pneumophilia post-infection and improved the disease outcome in vivo and ex vivo in a murine lung fibrosis model. Collectively these data identify ApoE+CD11b+ AMs generated uponenvironmental cues, under the control of ApoE signaling, as an essential determinant for lung adaptation enhancing tissue resilience