158 research outputs found
Near Infrared Spectroscopy to Assess Feeding Value and Antinutritional Compounds in Legume Species
There is an increasing demand for information on the quality characteristics and chemical composition of forages in order to meet the demands of dietary specifications for feeding animals. Near Infrared (NIR) spectroscopy provides a tool for rapid and non-destructive analysis in agronomic and breeding programs of a number of chemical components of forages and grains. NIR spectroscopy in particular has the advantage of being able to simultaneously evaluate the samples for a number of qualitative traits of whole plants and seeds. In two experiments here presented, NIR Spectroscopy was used to predict: i) qualitative characteristics of field pea seeds and, as regards secondary metabolites responsible of detrimental or beneficial effects on animal nutrition ii) condensed tannins in legume forages, based on calibration sets of samples previously chemically analysed
Effects of wilting and lactic acid bacteria inoculation on fermentation quality of white lupin and fababean silages
Fababeans and lupins are short-term catch crops with a high crude protein content, which provide a high forage yield in a short growing period. Legumes are difficult to conserve as silages because of their low water soluble carbohydrates content (WSC) and high buffer capacity. To our knowledge, little information is available on the ensiling of fababeans and lupins in Southern Europe. The research was carried out in Lodi (Italy) in order to evaluate the effects of wilting and inoculation with lactic acid bacteria (LAB) on fermentation characteristics of the resulting silages. The data show that both wilting and LAB inoculant significantly improved fermentation quality of the legumes silages
Prediction of the chemical composition and nutritive value of lucerne (Medicago sativa L.) by Near Infrared Spectroscopy
Lucerne is a low input energy efficient crop that improves soil fertility, and its importance is rising with the increase of public interest in sustainable agriculture. Furthermore, it occupies a significant economic position in the animal feed market (i.e. hay, dehydrated forage, pellets and silage products) and deserves a particular interest in the Parmigiano-Reggiano and Grana Padano cheese production areas of Northern Italy (Torricelli et al., 2000)
Effects of beliefs, motivation and entrepreneurial self-efficacy on entrepreneurial intentions: The moderating role of family support
Entrepreneurship is crucial for promoting innovation, creating employment opportunities and generating social and economic wealth in a country’s economy. In order to increase entrepreneurial activity, it is important to investigate entrepreneurial behavior by analyzing the process of businesses creation and the set of factors that favor the development of entrepreneurial aspirations, intentions and actions, which is a central goal ofpsychology of entrepreneurship. This research aims to deepen the knowledge about the relationship between the entrepreneurial self-efficacy, belief, motivation, family support and entrepreneurial intentions by developing a moderated mediation model. This study suggests that entrepreneurial self-efficacy partially mediates the effect of beliefs and motivations on entrepreneurial intention. This mediation is moderated by family support, which is also directly related to the intentions. The study was conducted on a sample of 446 students from four different high schools, and results support our hypotheses. Theoretical and practical implications from this research are further examined in the study
Calcium Signalling Triggered by NAADP in T Cells Determines Cell Shape and Motility During Immune Synapse Formation
Nicotinic acid adenine dinucleotide phosphate (NAADP) has been implicated as an initial Ca(2+) trigger in T cell Ca(2+) signalling, but its role in formation of the immune synapse in CD4(+) effector T cells has not been analysed. CD4(+) T cells are activated by the interaction with peptide-MHCII complexes on the surface of antigen-presenting cells. Establishing a two-cell system including primary rat CD4(+) T cells specific for myelin basic protein and rat astrocytes enabled us to mirror this activation process in vitro and to analyse Ca(2+) signalling, cell shape changes and motility in T cells during formation and maintenance of the immune synapse. After immune synapse formation, T cells showed strong, antigen-dependent increases in free cytosolic calcium concentration ([Ca(2+)](i)). Analysis of cell shape and motility revealed rounding and immobilization of T cells depending on the amplitude of the Ca(2+) signal. NAADP-antagonist BZ194 effectively blocked Ca(2+) signals in T cells evoked by the interaction with antigen-presenting astrocytes. BZ194 reduced the percentage of T cells showing high Ca(2+) signals thereby supporting the proposed trigger function of NAADP for global Ca(2+) signalling. Taken together, the NAADP signalling pathway is further confirmed as a promising target for specific pharmacological intervention to modulate T cell activation
The Activation Status of Neuroantigen-specific T Cells in the Target Organ Determines the Clinical Outcome of Autoimmune Encephalomyelitis
The clinical picture of experimental autoimmune encephalomyelitis (EAE) is critically dependent on the nature of the target autoantigen and the genetic background of the experimental animals. Potentially lethal EAE is mediated by myelin basic protein (MBP)–specific T cells in Lewis rats, whereas transfer of S100β- or myelin oligodendrocyte glycoprotein (MOG)–specific T cells causes intense inflammatory response in the central nervous system (CNS) with minimal disease. However, in Dark Agouti rats, the pathogenicity of MOG-specific T cells resembles the one of MBP-specific T cells in the Lewis rat. Using retrovirally transduced green fluorescent T cells, we now report that differential disease activity reflects different levels of autoreactive effector T cell activation in their target tissue. Irrespective of their pathogenicity, the migratory activity, gene expression patterns, and immigration of green fluorescent protein+ T cells into the CNS were similar. However, exclusively highly pathogenic T cells were significantly reactivated within the CNS. Without local effector T cell activation, production of monocyte chemoattractants was insufficient to initiate and propagate a full inflammatory response. Low-level reactivation of weakly pathogenic T cells was not due to anergy because these cells could be activated by specific antigen in situ as well as after isolation ex vivo
Ketogenic diet uncovers differential metabolic plasticity of brain cells
To maintain homeostasis, the body, including the brain, reprograms its metabolism in response to altered nutrition or disease. However, the consequences of these challenges for the energy metabolism of the different brain cell types remain unknown. Here, we generated a proteome atlas of the major central nervous system (CNS) cell types from young and adult mice, after feeding the therapeutically relevant low-carbohydrate, high-fat ketogenic diet (KD) and during neuroinflammation. Under steady-state conditions, CNS cell types prefer distinct modes of energy metabolism. Unexpectedly, the comparison with KD revealed distinct cell type–specific strategies to manage the altered availability of energy metabolites. Astrocytes and neurons but not oligodendrocytes demonstrated metabolic plasticity. Moreover, inflammatory demyelinating disease changed the neuronal metabolic signature in a similar direction as KD. Together, these findings highlight the importance of the metabolic cross-talk between CNS cells and between the periphery and the brain to manage altered nutrition and neurological disease
Microglia facilitate repair of demyelinated lesions via post-squalene sterol synthesis
The repair of inflamed, demyelinated lesions as in multiple sclerosis (MS) necessitates the clearance of cholesterol-rich myelin debris by microglia/macrophages and the switch from a pro-inflammatory to an anti-inflammatory lesion environment. Subsequently, oligodendrocytes increase cholesterol levels as a prerequisite for synthesizing new myelin membranes. We hypothesized that lesion resolution is regulated by the fate of cholesterol from damaged myelin and oligodendroglial sterol synthesis. By integrating gene expression profiling, genetics and comprehensive phenotyping, we found that, paradoxically, sterol synthesis in myelin-phagocytosing microglia/macrophages determines the repair of acutely demyelinated lesions. Rather than producing cholesterol, microglia/macrophages synthesized desmosterol, the immediate cholesterol precursor. Desmosterol activated liver X receptor (LXR) signaling to resolve inflammation, creating a permissive environment for oligodendrocyte differentiation. Moreover, LXR target gene products facilitated the efflux of lipid and cholesterol from lipid-laden microglia/macrophages to support remyelination by oligodendrocytes. Consequently, pharmacological stimulation of sterol synthesis boosted the repair of demyelinated lesions, suggesting novel therapeutic strategies for myelin repair in MS. Efficient repair of demyelinated CNS lesions involves the resolution of inflammation and induction of remyelination. Berghoff et al. show that sterol synthesis in microglia is key to both processes, which can be supported by squalene therapy
M tuberculosis in the adjuvant modulates time of appearance of CNS-specific effector T cells in the spleen through a polymorphic site of TLR2
DC deliver information regulating trafficking of effector T cells along T-cell priming. However, the role of pathogen-derived motives in the regulation of movement of T cells has not been studied. We hereinafter report that amount of M tuberculosis in the adjuvant modulates relocation of PLP139-151 specific T cells. In the presence of a low dose of M tuberculosis in the adjuvant, T cells (detected by CDR3 BV-BJ spectratyping, the so-called "immunoscope") mostly reach the spleen by day 28 after immunization ("late relocation") in the SJL strain, whereas T cells reach the spleen by d 14 with a high dose of M tuberculosis ("early relocation"). The C57Bl/6 background confers a dominant "early relocation" phenotype to F1 (SJL
7C57Bl/6) mice, allowing early relocation of T cells in the presence of low dose M tuberculosis. A single non-synonymous polymorphism of TLR2 is responsible for "early/late" relocation phenotype. Egress of T lymphocytes is regulated by TLR2 expressed on T cells. Thus, pathogens engaging TLR2 on T cells regulate directly T-cell trafficking, and polymorphisms of TLR2 condition T-cell trafficking upon a limiting concentration of ligand
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