Influence of tied ridging technology on the rate of surface runoff and erosion in potato cultivation

ArticleWater management and securing good condition of soil is becoming an important factor in agriculture one of the reasons being adaptation to the increasingly frequent extremes in weather. Tied ridging technology enables to reduce significantly the loss of water and soil from arable land. The effect of a tied ridger mounted on 2-row planter and effect of 6-row tied ridger on basin renewal was tested in potato cultivation on plots of land with length of 10 m. During entire season lasting 135 days the technology helped achieve 78% of efficiency in reduction of surface water runoff and 88% of efficiency in case of soil loss. In the case of furrows with only tied ridging the water retained represented additional 15% of total water from rainfall (37.5 mm of 250 mm) over untreated furrows. In the case of basins formed in furrows with wheel trails the water retained represented 15% of total water from rainfalls in the trail. This water retained on the land would have otherwise flown off and would not have been utilized without this technology. The renewal of dams after 1/3 of the season increased significantly the efficiency of this technology. The technology of tied ridging significantly contributes to sustainable agriculture management

The PYRIN Domain-only Protein POP1 Inhibits Inflammasome Assembly and Ameliorates Inflammatory Disease

SummaryIn response to infections and tissue damage, ASC-containing inflammasome protein complexes are assembled that promote caspase-1 activation, IL-1β and IL-18 processing and release, pyroptosis, and the release of ASC particles. However, excessive or persistent activation of the inflammasome causes inflammatory diseases. Therefore, a well-balanced inflammasome response is crucial for the maintenance of homeostasis. We show that the PYD-only protein POP1 inhibited ASC-dependent inflammasome assembly by preventing inflammasome nucleation, and consequently interfered with caspase-1 activation, IL-1β and IL-18 release, pyroptosis, and the release of ASC particles. There is no mouse ortholog for POP1, but transgenic expression of human POP1 in monocytes, macrophages, and dendritic cells protected mice from systemic inflammation triggered by molecular PAMPs, inflammasome component NLRP3 mutation, and ASC danger particles. POP1 expression was regulated by TLR and IL-1R signaling, and we propose that POP1 provides a regulatory feedback loop that shuts down excessive inflammatory responses and thereby prevents systemic inflammation

Stability of scaling regimes in d≥2d\geq 2 developed turbulence with weak anisotropy

The fully developed turbulence with weak anisotropy is investigated by means of renormalization group approach (RG) and double expansion regularization for dimensions $d\ge 2$. Some modification of the standard minimal substraction scheme has been used to analyze stability of the Kolmogorov scaling regime which is governed by the renormalization group fixed point. This fixed point is unstable at $d=2$; thus, the infinitesimally weak anisotropy destroyes above scaling regime in two-dimensional space. The restoration of the stability of this fixed point, under transition from $d=2$ to $d=3,$ has been demonstrated at borderline dimension $2<d_c<3$. The results are in qualitative agreement with ones obtained recently in the framework of the usual analytical regularization scheme.Comment: 23 pages, 2 figure

Report From the American Society of Transplantation Conference on Donor Heart Selection in Adult Cardiac Transplantation in the United States

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138918/1/ajt14354.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138918/2/ajt14354_am.pd

Evidence of Glycolysis Up-Regulation and Pyruvate Mitochondrial Oxidation Mismatch During Mechanical Unloading of the Failing Human Heart: Implications for Cardiac Reloading and Conditioning

This study sought to investigate the effects of mechanical unloading on myocardial energetics and the metabolic perturbation of heart failure (HF) in an effort to identify potential new therapeutic targets that could enhance the unloading-induced cardiac recovery. The authors prospectively examined paired human myocardial tissue procured from 31 advanced HF patients at left ventricular assist device (LVAD) implant and at heart transplant plus tissue from 11 normal donors. They identified increased post-LVAD glycolytic metabolites without a coordinate increase in early, tricarboxylic acid (TCA) cycle intermediates. The increased pyruvate was not directed toward the mitochondria and the TCA cycle for complete oxidation, but instead, was mainly converted to cytosolic lactate. Increased nucleotide concentrations were present, potentially indicating increased flux through the pentose phosphate pathway. Evaluation of mitochondrial function and structure revealed a lack of post-LVAD improvement in mitochondrial oxidative functional capacity, mitochondrial volume density, and deoxyribonucleic acid content. Finally, post-LVAD unloading, amino acid levels were found to be increased and could represent a compensatory mechanism and an alternative energy source that could fuel the TCA cycle by anaplerosis. In summary, the authors report evidence that LVAD unloading induces glycolysis in concert with pyruvate mitochondrial oxidation mismatch, most likely as a result of persistent mitochondrial dysfunction. These findings suggest that interventions known to improve mitochondrial biogenesis, structure, and function, such as controlled cardiac reloading and conditioning, warrant further investigation to enhance unloading-induced reverse remodeling and cardiac recovery

Co-Regulation of NF-κB and Inflammasome-Mediated Inflammatory Responses by Myxoma Virus Pyrin Domain-Containing Protein M013

NF-κB and inflammasomes both play central roles in orchestrating anti-pathogen responses by rapidly inducing a variety of early-response cytokines and chemokines following infection. Myxoma virus (MYXV), a pathogenic poxvirus of rabbits, encodes a member of the cellular pyrin domain (PYD) superfamily, called M013. The viral M013 protein was previously shown to bind host ASC-1 protein and inhibit the cellular inflammasome complex that regulates the activation and secretion of caspase 1-regulated cytokines such as IL-1β and IL-18. Here, we report that human THP-1 monocytic cells infected with a MYXV construct deleted for the M013L gene (vMyxM013-KO), in stark contrast to the parental MYXV, rapidly induce high levels of secreted pro-inflammatory cytokines like TNF, IL-6, and MCP-1, all of which are regulated by NF-κB. The induction of these NF-κB regulated cytokines following infection with vMyxM013-KO was also confirmed in vivo using THP-1 derived xenografts in NOD-SCID mice. vMyxM013-KO virus infection specifically induced the rapid phosphorylation of IKK and degradation of IκBα, which was followed by nuclear translocation of NF-κB/p65. Even in the absence of virus infection, transiently expressed M013 protein alone inhibited cellular NF-κB-mediated reporter gene expression and nuclear translocation of NF-κB/p65. Using protein/protein interaction analysis, we show that M013 protein also binds directly with cellular NF-κB1, suggesting a direct physical and functional linkage between NF-κB1 and ASC-1. We further demonstrate that inhibition of the inflammasome with a caspase-1 inhibitor did not prevent the induction of NF-κB regulated cytokines following infection with vMyxM013-KO virus, but did block the activation of IL-1β. Thus, the poxviral M013 inhibitor exerts a dual immuno-subversive role in the simultaneous co-regulation of both the cellular inflammasome complex and NF-κB-mediated pro-inflammatory responses

Evaluation of Nod-Like Receptor (NLR) Effector Domain Interactions

Members of the Nod-like receptor (NLR) family recognize intracellular pathogens and recruit a variety of effector molecules, including pro-caspases and kinases, which in turn are implicated in cytokine processing and NF-κB activation

Flexible prey handling, preference and a novel capture technique in invasive, sub-adult Chinese mitten crabs

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