Estimating everyday portion size using a 'method of constant stimuli': in a student sample, portion size is predicted by gender, dietary behaviour, and hunger, but not BMI

This paper (i) explores the proposition that body weight is associated with large portion sizes and (ii) introduces a new technique for measuring everyday portion size. In our paradigm, the participant is shown a picture of a food portion and is asked to indicate whether it is larger or smaller than their usual portion. After responding to a range of different portions an estimate of everyday portion size is calculated using probit analysis. Importantly, this estimate is likely to be robust because it is based on many responses. First-year undergraduate students (N=151) completed our procedure for 12 commonly consumed foods. As expected, portion sizes were predicted by gender and by a measure of dieting and dietary restraint. Furthermore, consistent with reports of hungry supermarket shoppers, portion-size estimates tended to be higher in hungry individuals. However, we found no evidence for a relationship between BMI and portion size in any of the test foods. We consider reasons why this finding should be anticipated. In particular, we suggest that the difference in total energy expenditure of individuals with a higher and lower BMI is too small to be detected as a concomitant difference in portion size (at least in our sample)

Dopamine D_2-receptor activation elicits akinesia, rigidity, catalepsy, and tremor in mice expressing hypersensitive 4 nicotinic receptors via a cholinergic-dependent mechanism

Recent studies suggest that high-affinity neuronal nicotinic acetylcholine receptors (nAChRs) containing α4 and β2 subunits (α4β2*) functionally interact with G-protein-coupled dopamine (DA) D_2 receptors in basal ganglia. We hypothesized that if a functional interaction between these receptors exists, then mice expressing an M2 point mutation (Leu9'Ala) rendering 4 nAChRs hypersensitive to ACh may exhibit altered sensitivity to a D_2-receptor agonist. When challenged with the D_(2)R agonist, quinpirole (0.5–10 mg/kg), Leu9'Ala mice, but not wild-type (WT) littermates, developed severe, reversible motor impairment characterized by rigidity, catalepsy, akinesia, and tremor. While striatal DA tissue content, baseline release, and quinpirole-induced DA depletion did not differ between Leu9'Ala and WT mice, quinpirole dramatically increased activity of cholinergic striatal interneurons only in mutant animals, as measured by increased c-Fos expression in choline acetyltransferase (ChAT)-positive interneurons. Highlighting the importance of the cholinergic system in this mouse model, inhibiting the effects of ACh by blocking muscarinic receptors, or by selectively activating hypersensitive nAChRs with nicotine, rescued motor symptoms. This novel mouse model mimics the imbalance between striatal DA/ACh function associated with severe motor impairment in disorders such as Parkinson’s disease, and the data suggest that a D_(2)R–α4*-nAChR functional interaction regulates cholinergic interneuron activity.—Zhao-Shea, R., Cohen, B. N., Just, H., McClure-Begley, T., Whiteaker, P., Grady, S. R., Salminen, O., Gardner, P. D., Lester, H. A., Tapper, A. R. Dopamine D2-receptor activation elicits akinesia, rigidity, catalepsy, and tremor in mice expressing hypersensitive α4 nicotinic receptors via a cholinergic-dependent mechanism

Motor control strategies differ between monoarticular and biarticular quadriceps muscles during bipedal squats

The interplay between biarticular and monoarticular muscles of the knee and hip joints during bipedal squats (SQBP ) requires adequate central-nervous control mechanisms to enable smooth and dynamic movements. Here, we investigated motor control between M. vastus medialis (VM), M. vastus lateralis (VL), and M. rectus femoris (RF) in 12 healthy male recreational athletes during SQBP with three load levels (50%, 62.5% & 75% of 3-repetition maximum) following a standardized strength training protocol (3 sets of 10 repetitions). To quantify differences in motor control mechanisms in both time and frequency domains, we analyzed (1) muscle covariation via correlation analyses, as well as (2) common neural input via intermuscular coherence (IMC) between RF, VM, and VL. Our results revealed significantly higher gamma IMC between VM-VL compared to RF-VL and RF-VM for both legs. Correlation analyses demonstrated significantly higher correlation coefficients during ascent periods compared to descent periods across all analyzed muscle pairs. However, no load-dependent modulation of motor control could be observed. Our study provides novel evidence that motor control during SQBP is characterized by differences in common input between biarticular and monoarticular muscles. Additionally, muscle activation patterns show higher similarity during ascent compared to descent periods. Future research should aim to validate and extend our observations as insights into the underlying control mechanisms offer the possibility for practical implications to optimize training concepts in elite sports and rehabilitation

Degradation of human kininogens with the release of kinin peptides by extracellular proteinases of Candida spp.

The secretion of proteolytic enzymes by pathogenic microorganisms is one of the most successful strategies used by pathogens to colonize and infect the host organism. The extracellular microbial proteinases can seriously deregulate the homeostatic proteolytic cascades of the host, including the kinin-forming system, repeatedly reported to he activated during bacterial infection. The current study assigns a kinin-releasing activity to secreted proteinases of Candida spp. yeasts, the major fungal pathogens of humans. Of several Candida species studied, C. parapsilosis and C. albicans in their invasive filamentous forms are shown to produce proteinases which most effectively degrade proteinaceous kinin precursors, the kininogens. These enzymes, classified as aspartyl proteinases, have the highest kininogen-degrading activity at low pH (approx. 3.5), but the associated production of bradykinin-related peptides from a small fraction of kininogen molecules is optimal at neutral pH (6.5). The peptides effectively interact with cellular B2-type kinin receptors. Moreover, kinin-related peptides capable of interacting with inflammation-induced B1-type receptors are also formed, but with a reversed pH dependence. The presented variability of the potential extracellular kinin production by secreted aspartyl proteinases of Candida spp. is consistent with the known adaptability of these opportunistic pathogens to different niches in the host organism

Microwave pyrolysis of Laminaria digitata to produce unique seaweed-derived bio-oils

Microwave pyrolysis has become an attractive form of processing technology to generate bio-oil, bio-char and syngas from different biomass feedstocks. In this study, microwave pyrolysis was performed on the UK native seaweed Laminaria digitata and its extract residue from a bio-refinery process. Pyrolysis of these two feedstocks was successfully achieved without the requirement of microwave susceptors, as pelletizing the biomass was sufficient to allow microwave pyrolysis to occur. It was found that average energy requirements as low as 1.84–2.83 kJ g−1 were required to pyrolyse 55–70% of both feedstocks and bio-oil yields of 5–8% and 10–14% for native and extraction residue L. digitata were produced, respectively. Maximum microwave pyrolysis processing times were in the order of 200 s. The bio-oil generated from both feedstocks contained no phenolic based compounds, but a greater number of nitrogen-containing compounds and compounds derived from macroalgal polysaccharides. Yields of certain compounds differed in bio-oils generated from the two L. digitata feedstocks, however it was observed that specific energy did not have a direct influence on bio-oil compound yield. Furthermore, the identification of a particular nitrogen-containing compound L-Proline, 1-methyl-5-oxo-, methylester is thought to be a unique product of microwave pyrolysis when carbon-based additives are avoided

Paternal nicotine exposure alters hepatic xenobiotic metabolism in offspring

Paternal environmental conditions can influence phenotypes in future generations, but it is unclear whether offspring phenotypes represent specific responses to particular aspects of the paternal exposure history, or a generic response to paternal \u27quality of life\u27. Here, we establish a paternal effect model based on nicotine exposure in mice, enabling pharmacological interrogation of the specificity of the offspring response. Paternal exposure to nicotine prior to reproduction induced a broad protective response to multiple xenobiotics in male offspring. This effect manifested as increased survival following injection of toxic levels of either nicotine or cocaine, accompanied by hepatic upregulation of xenobiotic processing genes, and enhanced drug clearance. Surprisingly, this protective effect could also be induced by a nicotinic receptor antagonist, suggesting that xenobiotic exposure, rather than nicotinic receptor signaling, is responsible for programming offspring drug resistance. Thus, paternal drug exposure induces a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics

Integrated miRNA-/mRNA-Seq of the Habenulo-Interpeduncular Circuit During Acute Nicotine Withdrawal

Tobacco use is the leading preventable cause of mortality in the world. The limited number of smoking cessation aids currently available are minimally effective, highlighting the need for novel therapeutic interventions. We describe a genome-wide approach to identify potential candidates for such interventions. Next-generation sequencing was performed using RNA isolated from the habenulo-interpeduncular circuit of male mice withdrawn from chronic nicotine treatment. This circuit plays a central role in the nicotine withdrawal response. Differentially expressed miRNAs and mRNAs were validated using RT-qPCR. Many of the differentially expressed mRNAs are predicted targets of reciprocally expressed miRNAs. We illustrate the utility of the dataset by demonstrating that knockdown in the interpeduncular nucleus of a differentially expressed mRNA, that encoding profilin 2, is sufficient to induce anxiety-related behavior. Importantly, profilin 2 knockdown in the ventral tegmental area did not affect anxiety behavior. Our data reveal wide-spread changes in gene expression within the habenulo-interpeduncular circuit during nicotine withdrawal. This dataset should prove to be a valuable resource leading to the identification of substrates for the design of innovative smoking cessation aids

Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms

Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL, but the contribution of inherited factors is poorly characterized. Using a three-stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with genome-wide significance in JAK2V617F-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 × 10−10) and rs2201862 (MECOM; meta-analysis P=1.96 × 10−9). Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide significance when including JAK2V617F-positive cases. rs9376092 has a stronger effect in JAK2V617F-negative cases with CALR and/or MPL mutations (Breslow–Day P=4.5 × 10−7), whereas in JAK2V617F-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (allelic χ2 P=7.3 × 10−7). Reduced MYB expression, previously linked to development of an ET-like disease in model systems, associates with rs9376092 in normal myeloid cells. These findings demonstrate that multiple germline variants predispose to MPN and link constitutional differences in MYB expression to disease phenotype