bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genome‐wide association mapping and biochemical markers reveal that seed ageing and longevity are intricately affected by genetic background and developmental and environmental conditions in barley
Authors: NAGEL MANUELA , KRANNER ILSE , NEUMANN KERSTIN , ROLLETSCHEK HARDY , SEAL CHARLOTTE E. , COLVILLE LOUISE , FERNÁNDEZ‐MARÍN BEATRIZ , BÖRNER ANDREAS 
Published: October 2014

AbstractGlobally, over 7.4 million accessions of crop seeds are stored in gene banks, and conservation of genotypic variation is pivotal for breeding. We combined genetic and biochemical approaches to obtain a broad overview of factors that influence seed storability and ageing in barley (Hordeum vulgare). Seeds from a germplasm collection of 175 genotypes from four continents grown in field plots with different nutrient supply were subjected to two artificial ageing regimes. Genome‐wide association mapping revealed 107 marker trait associations, and hence, genotypic effects on seed ageing. Abiotic and biotic stresses were found to affect seed longevity. To address aspects of abiotic, including oxidative, stress, two major antioxidant groups were analysed. No correlation was found between seed deterioration and the lipid‐soluble tocochromanols, nor with oil, starch and protein contents. Conversely, the water‐soluble glutathione and related thiols were converted to disulphides, indicating a strong shift towards more oxidizing intracellular conditions, in seeds subjected to long‐term dry storage at two temperatures or to two artificial ageing treatments. The data suggest that intracellular pH and (bio)chemical processes leading to seed deterioration were influenced by the type of ageing or storage. Moreover, seed response to ageing or storage treatment appears to be significantly influenced by both maternal environment and genetic background.
Photoisomerization of cis‐1,2‐di(1‐Methyl‐2‐naphthyl)ethene at 77 K in Glassy Media
Authors: Redwood Christopher , Ratheesh Kumar V. K. , Hutchinson Stuart , Mallory Frank B. , Mallory Clelia W. , Clark Ronald J. , Dmitrenko Olga , Saltiel Jack 
Published: October 2014

Abstractcis‐1,2‐Di(1‐methyl‐2‐naphthyl)ethene, c‐1,1, undergoes photoisomerization in methylcyclohexane, isopentane and diethyl ether/isopentane/ethanol glasses at 77 K. On 313 nm excitation the fluorescence of c‐1,1 is replaced by fluorescence from t‐1,1. Singular value decomposition reveals that the spectral matrices behave as two component systems suggesting conversion of a stable c‐1,1 conformer to a stable t‐1,1 conformer. However, the fluorescence spectra are λexc dependent. Analysis of global spectral matrices shows that c‐1,1 is a mixture of two conformers, each of which gives one of four known t‐1,1 conformers. The λexc dependence of the c‐1,1 fluorescence spectrum is barely discernible. Structure assignments to the resolved fluorescence spectra are based on the principle of least motion and on calculated geometries, energy differences and spectra of the conformers. The relative shift of the c‐1,1 conformer spectra is consistent with the shift of the calculated absorption spectra. The calculated structure of the most stable conformer of c‐1,1 agrees well with the X‐ray crystal structure. Due to large deviations of the naphthyl groups from the ethenic plane in the conformers of both c‐ and t‐1,1 isomers, minimal motion of these bulky substituents accomplishes cis → trans interconversion by rotation about the central bond.
Systemic jasmonic acid modulation in mycorrhizal tomato plants and its role in induced resistance against Alternaria alternata
Authors: Nair A. , Kolet S. P. , Thulasiram H. V. , Bhargava S. 
Published: October 2014

AbstractTomato plants colonised with the arbuscular mycorrhizal (AM) fungus Glomus fasciculatum show systemic induced resistance to the foliar pathogen Alternaria alternata, as observed in interactions of other AM‐colonised plants with a range of pathogens. The role of jasmonic (JA) and salicylic (SA) acid in expression of this mycorrhiza‐induced resistance (MIR) against A. alternata was studied by measuring: (i) activity of enzymes reported to be involved in their biosynthesis, namely lipoxygenase (LOX) and phenylammonia lyase (PAL); and (ii) levels of methyl jasmonate (MeJA) and SA. Transcript abundance of some defence genes associated with JA and SA response pathways were also studied. Both LOX and PAL activity increased twofold in response to pathogen application to control plants. AM‐colonised plants had three‐fold higher LOX activity compared to control plants, but unlike controls, this did not increase further in response to pathogen application. Higher LOX activity in AM‐colonised plants correlated with four‐fold higher MeJA in leaves of AM‐colonised plants compared to controls. Treatment of plants with the JA biosynthesis inhibitor salicylhydroxamic acid (SHAM) led to 50% lower MeJA in both control and AM‐colonised plants and correlated with increased susceptibility to A. alternata, suggesting a causal role for JA in expression of MIR against the pathogen. Genes involved in JA biosynthesis (OPR3) and response (COI1) showed six‐ and 42‐fold higher expression, respectively, in leaves of AM‐colonised plants compared to controls. AM‐colonised plants also showed increased expression of the SA response gene PR1 and that of the wound‐inducible polypeptide prosystemin. Our results suggest that the systemic increase in JA in response to AM colonisation plays a key role in expression of MIR against A. alternata.
Vote as you Think: Determinants of Consistent Decision Making in Direct Democracy
Authors: Lanz Simon , Nai Alessandro 
Published: October 2014

AbstractThis study investigates the conditions under which Swiss citizens take consistent decisions, that is, decisions that reflect their argument‐based opinions, during direct‐democratic ballots. In line with recent work on cognitive political behavior, we expect the drivers of consistent voting to be found at the individual and contextual level. At the individual level, we argue that political knowledge positively affects consistent decisions. At the contextual level, we anticipate a positive effect for campaign intensity, complexity and negativism. We estimate hierarchical logistic models based on VOX survey data (1999‐2005) and original data that captures the nature of political campaigns. Our results support our expectations for the situational level and (partially) for the individual factors.
Rice SNF2 family helicase ENL1 is essential for syncytial endosperm development
Authors: Hara Tomomi , Katoh Hirokazu , Ogawa Daisuke , Kagaya Yasuaki , Sato Yutaka , Kitano Hidemi , Nagato Yasuo , Ishikawa Ryo , Ono Akemi , Kinoshita Tetsu , Takeda Shin , Hattori Tsukaho 
Published: October 2014

SummaryThe endosperm of cereal grains represents the most important source of human nutrition. In addition, the endosperm provides many investigatory opportunities for biologists because of the unique processes that occur during its ontogeny, including syncytial development at early stages. Rice endospermless 1 (enl1) develops seeds lacking an endosperm but carrying a functional embryo. The enl1 endosperm produces strikingly enlarged amoeboid nuclei. These abnormal nuclei result from a malfunction in mitotic chromosomal segregation during syncytial endosperm development. The molecular identification of the causal gene revealed that ENL1 encodes an SNF2 helicase family protein that is orthologous to human Plk1‐Interacting Checkpoint Helicase (PICH), which has been implicated in the resolution of persistent DNA catenation during anaphase. ENL1‐Venus (enhanced yellow fluorescent protein (YFP)) localizes to the cytoplasm during interphase but moves to the chromosome arms during mitosis. ENL1‐Venus is also detected on a thread‐like structure that connects separating sister chromosomes. These observations indicate the functional conservation between PICH and ENL1 and confirm the proposed role of PICH. Although ENL1 dysfunction also affects karyokinesis in the root meristem, enl1 plants can grow in a field and set seeds, indicating that its indispensability is tissue‐dependent. Notably, despite the wide conservation of ENL1/PICH among eukaryotes, the loss of function of the ENL1 ortholog in Arabidopsis (CHR24) has only marginal effects on endosperm nuclei and results in normal plant development. Our results suggest that ENL1 is endowed with an indispensable role to secure the extremely rapid nuclear cycle during syncytial endosperm development in rice.
Stoichiometry and novel gating mechanism within the cystic fibrosis transmembrane conductance regulator channel
Authors: Qian Feng , Li Tao , Yang Fei , Liu Lian 
Published: October 2014

New Findings
What is the central question of this study?
We aimed to demonstrate the possibility that the cystic fibrosis transmembrane conductance regulator (CFTR) forms higher‐order multimers during channel pore formation and/or channel gating using functional evidence.

What is the main finding and its importance?
The majority of our electrophysiological data suggested that the CFTR channel pore is formed by transmembrane domains of only one CFTR molecule as a monomer. However, we also observed functional upregulation of CFTR activation in patches, which implies interprotein interactions among CFTR molecules. Our findings will help to resolve many contradictions among previous reports regarding whether CFTR is a monomer or a multimer.

Despite its fundamental importance to the molecular mechanism underlying cystic fibrosis, many details of the structural basis for the cystic fibrosis transmembrane conductance regulator (CFTR) remain unknown. In addition, the possible interactions among the CFTR proteins have not been clearly demonstrated. In order to identify whether the CFTR channel pore is formed as a monomer or a multimer, we analysed the single‐channel properties in patches of cell membrane that coexpressed selected CFTR mutants having significantly different single‐channel properties. No hybrid channel opening patterns were observed. We therefore propose that the CFTR channel pore is indeed composed of a monomer. However, we also observed that coexisting CFTR monomers in the cell membrane facilitated the activation of individual CFTR channels. The functional upregulation of this CFTR channel opening probability and the different gating behaviour suggest dynamic conformational changes among the interacting CFTR proteins within the multimeric CFTR complex. Our findings regarding the CFTR monomer channel pore and the novel synergistic gating behaviour within the CFTR channel complex will help to resolve the remaining contradictions among previous studies regarding whether CFTR is a monomer or a multimer.
Enhanced pan‐peroxisome proliferator‐activated receptor gene and protein expression in adipose tissue of diet‐induced obese mice treated with telmisartan
Authors: Penna‐de‐Carvalho Aline , Graus‐Nunes Francielle , Rabelo‐Andrade Júlia , Mandarim‐de‐Lacerda Carlos Alberto , Souza‐Mello Vanessa 
Published: October 2014

New Findings

What is the central question of this study?
Telmisartan, an antihypertensive, has beneficial side‐effects through its peroxisome proliferator‐activated receptor (PPAR) β/δ agonism in white adipose tissue, besides its well‐known property of partial PPARγ agonism. Here, we investigated a potential pan‐PPAR role of this drug in the white and brown adipose tissues.

What is the main finding and its importance?
Telmisartan enhanced pan‐PPAR gene and protein expression in adipose tissue (white and brown) in obese mice, with downstream effects that resulted in the management of insulin resistance, anti‐inflammatory adipokine profile and thermogenesis induction. These findings are relevant and should be explored as new targets for controlling obesity and comorbidities through pan‐PPAR‐related effects.

Telmisartan has previously been used to target obesity, showing peroxisome proliferator‐activated receptor (PPAR) β/δ‐related effects in white adipose tissue (WAT). We sought to evaluate whether telmisartan enhances gene and protein expression of all PPAR isoforms in WAT and brown adipose tissue (BAT), as well as their downstream effects upon insulin resistance, adipokine profile and adaptive thermogenesis. Male C57BL/6 mice were fed standard chow (SC; 10% lipids) or high‐fat diet (HF; 50% lipids) for 10 weeks. Animals were then randomly allocated into the following four groups: SC, SC‐T, HF and HF‐T. Telmisartan [10 mg (kg diet)−1] was administered for 4 weeks in the diet. Animals in the HF group were overweight and exhibited hypertension, insulin resistance, decreased energy expenditure, a pro‐inflammatory adipokine profile and abnormal fat pad mass distribution. Animals in the HF group showed decreased expression of PPARα, β/δ and γ in WAT and BAT, resulting in impaired glucose uptake and insufficient thermogenesis. Due to the improvement in the adipokine profile and enhanced insulin sensitivity with adequate insulin‐stimulated glucose uptake after treatment with telmisartan, the activation of all PPAR isoforms in WAT was beneficial. In BAT, telmisartan induced sustained sympathetic activation, because the β3‐adrenergic receptor was induced by PPARβ/δ, while uncoupling protein 1 was induced by PPARα to promote thermogenesis. Telmisartan exerted anti‐obesity effects through higher pan‐PPAR gene and protein expression. Upon PPARα, β/δ and γ (pan‐PPAR) agonism in adipose tissue of obese mice, telmisartan ameliorates inflammation and insulin resistance, as well as inducing non‐shivering thermogenesis. Our results point to new therapeutic targets for the control of obesity and comorbidities through pan‐PPAR‐related effects.
Distinct roles of L‐ and T‐type voltage‐dependent Ca2+ channels in regulation of lymphatic vessel contractile activity
Authors: Lee Stewart , Roizes Simon , von der Weid Pierre‐Yves 
Published: October 2014

Key points
Lymph transport is promoted by lymphatic pumping, a robust phasic contractile activity of the collecting lymphatic vessels. This contractile function, critical for tissue fluid homeostasis and immune cell transport to lymph nodes, is regulated by the amount of lymph entering the vessels and subsequent distension of the vessel wall.

While lymphatic pumping relies on influx of Ca2+ through voltage‐dependent Ca2+ channels, characterization of these channels and details of their contribution to the regulation of stretch‐activated contractions are lacking.

Here we report the expression of L‐ and T‐type Ca2+ channels in rat mesenteric lymphatic vessels and their differential role in regulating strength and frequency of lymphatic contractions.

This study fosters our knowledge on the mechanisms that drive stretch‐activated lymphatic contractions. It may help in providing a basis to developing agents able to enhance lymphatic function, which could be of therapeutic benefit during lymphatic impairment such as lymphoedema.

AbstractLymph drainage maintains tissue fluid homeostasis and facilitates immune response. It is promoted by phasic contractions of collecting lymphatic vessels through which lymph is propelled back into the blood circulation. This rhythmic contractile activity (i.e. lymphatic pumping) increases in rate with increase in luminal pressure and relies on activation of nifedipine‐sensitive voltage‐dependent Ca2+ channels (VDCCs). Despite their importance, these channels have not been characterized in lymphatic vessels. We used pressure‐ and wire‐myography as well as intracellular microelectrode electrophysiology to characterize the pharmacological and electrophysiological properties of L‐type and T‐type VDCCs in rat mesenteric lymphatic vessels and evaluated their particular role in the regulation of lymphatic pumping by stretch. We complemented our study with PCR and confocal immunofluorescence imaging to investigate the expression and localization of these channels in lymphatic vessels. Our data suggest a delineating role of VDCCs in stretch‐induced lymphatic vessel contractions, as the stretch‐induced increase in force of lymphatic vessel contractions was significantly attenuated in the presence of L‐type VDCC blockers nifedipine and diltiazem, while the stretch‐induced increase in contraction frequency was significantly decreased by the T‐type VDCC blockers mibefradil and nickel. The latter effect was correlated with a hyperpolarization. We propose that activation of T‐type VDCCs depolarizes membrane potential, regulating the frequency of lymphatic contractions via opening of L‐type VDCCs, which drive the strength of contractions.
Ageing and muscular dystrophy differentially affect murine pharyngeal muscles in a region‐dependent manner
Authors: Randolph Matthew E. , Luo Qingwei , Ho Justin , Vest Katherine E. , Sokoloff Alan J. , Pavlath Grace K. 
Published: October 2014

Key points
Millions of elderly individuals have dysphagia, a debilitating and life‐threatening condition in which the ability to swallow is impaired.
Several muscles surround the three regions of the pharynx, which are essential for proper swallowing, yet the effects of ageing and disease on these muscles are not well understood.
We demonstrate that the fibre size of murine pharyngeal muscles is differentially affected by ageing and muscular dystrophy depending on their location within the pharynx.
Using a mouse model of an age‐associated dysphagic disease (oculopharyngeal muscular dystrophy), we show that overexpression of wild‐type polyadenylate binding nuclear protein 1 in muscle tissue prevents age‐related dysphagia and age‐related muscle atrophy of laryngopharyngeal muscles.
These results demonstrate that mice are an excellent model for studying mechanisms of ageing and disease on pharyngeal muscle physiology, and such studies could lead to new therapies for individuals with dysphagia.
AbstractThe inability to swallow, or dysphagia, is a debilitating and life‐threatening condition that arises with ageing or disease. Dysphagia results from neurological or muscular impairment of one or more pharyngeal muscles, which function together to ensure proper swallowing and prevent the aspiration of food or liquid into the lungs. Little is known about the effects of age or disease on pharyngeal muscles as a group. Here we show ageing affected pharyngeal muscle growth and atrophy in wild‐type mice depending on the particular muscle analysed. Furthermore, wild‐type mice also developed dysphagia with ageing. Additionally, we studied pharyngeal muscles in a mouse model for oculopharyngeal muscular dystrophy, a dysphagic disease caused by a polyalanine expansion in the RNA binding protein, PABPN1. We examined pharyngeal muscles of mice overexpressing either wild‐type A10 or mutant A17 PABPN1. Overexpression of mutant A17 PABPN1 differentially affected growth of the palatopharyngeus muscle dependent on its location within the pharynx. Interestingly, overexpression of wild‐type A10 PABPN1 was protective against age‐related muscle atrophy in the laryngopharynx and prevented the development of age‐related dysphagia. These results demonstrate that pharyngeal muscles are differentially affected by both ageing and muscular dystrophy in a region‐dependent manner. These studies lay important groundwork for understanding the molecular and cellular mechanisms that regulate pharyngeal muscle growth and atrophy, which may lead to novel therapies for individuals with dysphagia.
Evidence for cyclooxygenase‐dependent sweating in young males during intermittent exercise in the heat
Authors: Fujii Naoto , McGinn Ryan , Stapleton Jill M. , Paull Gabrielle , Meade Robert D. , Kenny Glen P. 
Published: October 2014

Key points
Previous studies implicate nitric oxide (NO) in the control of sweating during exercise in the heat; however, it is unclear whether cyclooxygenase (COX) is also involved.
We demonstrated that exercise‐induced sweating at a moderate heat production (400 W, ∼40% was similarly reduced when COX and NO synthase were inhibited separately and in combination.
Alternatively, inhibiting COX and/or NO synthase did not influence exercise‐induced sweating at a high heat production (700 W, ∼70%
We show that both COX and NO are involved in sweating during exercise at moderate heat production and that the effects may not be independent. However, roles for COX and NO are less evident when heat production is elevated.
The results lead to better understanding of the mechanisms of sweating and indicate that COX inhibitors (e.g. aspirin) may impair core body temperature regulation and thereby increase the risk of heat‐related illness.
AbstractOur recent work implicated nitric oxide (NO) in the control of sweating during intermittent exercise; however, it is unclear if cyclooxygenase (COX) is also involved. On separate days, ten healthy young (24 ± 4 years) males cycled in the heat (35°C). Two 30 min exercise bouts were performed at either a moderate (400 W, moderate heat load) or high (700 W, high heat load) rate of metabolic heat production and were followed by 20 and 40 min of recovery, respectively. Forearm sweating (ventilated capsule) was evaluated at four skin sites that were continuously perfused via intradermal microdialysis with: (1) lactated Ringer solution (Control), (2) 10 mm ketorolac (a non‐selective COX inhibitor), (3) 10 mm NG‐nitro‐l‐arginine methyl ester (l‐NAME; a non‐selective NO synthase inhibitor) or (4) a combination of 10 mm ketorolac + 10 mm
l‐NAME. During the last 5 min of the first exercise at moderate heat load, forearm sweating (mg min−1 cm−2) was equivalently reduced with ketorolac (0.54 ± 0.08), l‐NAME (0.55 ± 0.07) and ketorolac+l‐NAME (0.56 ± 0.08) compared to Control (0.67 ± 0.06) (all P < 0.05). Similar results were obtained for the second exercise at moderate heat load (all P < 0.05). However, forearm sweating was similar between the four sites during exercise at high heat load and during recovery regardless of exercise intensity (all P > 0.05). We show that (1) although both COX and NO modulate forearm sweating during intermittent exercise bouts in the heat at a moderate heat load, the effects are not additive, and (2) the contribution of both enzymes to forearm sweating is less evident during intermittent exercise when the heat load is high and during recovery.