Tunable order in colloids of hard magnetic hexaferrite nanoplatelets

Structural ordering in the concentrated magnetic colloids containing 50×5 nm hard magnetic disc-like SrFe₁₂O₁₉ nanoparticles was investigated by cryogenic scanning electron microscopy,optical microscopy,magnetic measurements,and small-angle X-ray scattering.It was revealed that macroscopically homogeneous magnetic liquid consists of dynamic threads of stacked nanoparticles.The threads align into quasiperiodic arrays with the distances between individual threads of a few micrometers.They also can form pseudodomain structures with -90°domain boundaries realized through T-type thread interconnects.The effects of magnetic attraction and electrostatic repulsion on the equilibrium interplatelet distance in the threads were studied.It was demonstrated that this distance can be tuned by the control of the particles charge and electric double layer screening from Stern layer thickness(-1 nm)to tens of nanometers.It was shown that the permanent magnetic field is not able to cause any structural changes in the ordered magnetic liquid phase,while alternating field draws particles apart by their vibrations.External variation of interparticle distance up to 6%was achieved using an alternating magnetic field of low intensity.Experimental data were complemented by the theoretical models of screened electrostatic interactions between spherical and platelike magnetic particles.The last model provides good predictive power and correlates with the experimental data.The stabilization energy of the condensed phase in the order of 1-10 kBT was derived from the model.An approach allows controlling of an equilibrium interparticle distance and interparticle distance distribution by adjusting the magnetization and surface charge of the particles as well as the ionic strength of the solvent.     

Aging of Vascular System Is a Complex Process: The Cornerstone Mechanisms

Aging is one of the most intriguing processes of human ontogenesis. It is associated with the development of a wide variety of diseases affecting all organs and their systems. The victory over aging is the most desired goal of scientists; however, it is hardly achievable in the foreseeable future due to the complexity and ambiguity of the process itself. All body systems age, lose their performance, and structural disorders accumulate. The cardiovascular system is no exception. And it is cardiovascular diseases that occupy a leading position as a cause of death, especially among the elderly. The aging of the cardiovascular system is well described from a mechanical point of view. Moreover, it is known that at the cellular level, a huge number of mechanisms are involved in this process, from mitochondrial dysfunction to inflammation. It is on these mechanisms, as well as the potential for taking control of the aging of the cardiovascular system, that we focused on in this review.     

Synergistic and suppressive effects of dietary phenolic acids and other phytochemicals from cereal extracts on nuclear factor kappa B activity

In this study the combinatorial action of the main phenolic acids (ferulic, caffeic, p-coumaric and sinapic acids) found in extracts of free (ME) and bound phenolic acids (HE) from oat, barley and wheat flour on the modulation of NF-κB activity was investigated. The results show that combination of phenolic acids in low concentrations (<0.1 μg/ml) has a significant synergistic, or enhanced effect, on NF-κB activity, while their combination in high concentrations (0.3–70 μg/ml) helps to suppress the strong effect obtained by individual solutions of ferulic and p-coumaric acids. The modulation of NF-κB activity observed by HE extracts is the effect of combinatorial action of the phenolic acids present therein, while the modulation of NF-κB activity observed with ME extracts is the result of combinatorial action of phenolic acids together with other phenolic compounds present in the extracts. These results increase the knowledge about the health promoting effect from cereal consumption and dietary phenolic acids.     

Rheological properties of wheat dough supplemented with functional by-products of food processing: Brewer’s spent grain and apple pomace

The physicochemical properties of brewer’s spent grain (BSG) and apple pomace (AP), and their effect on dough rheological properties were investigated. BSG had high protein content and both by-products were found to be high in dietary fibre. The rheological and the pasting properties of dough were significantly altered by the addition of by-products, with the main effects being due to the presence of dietary fibre. The biaxial extensional viscosity was significantly higher for the supplemented doughs; the strain hardening index decreased with increasing the levels of flour substitution. The replacement of wheat flour with the by-products significantly reduced the uniaxial extensibility, while the storage modulus, G″, was found to increase, indicating changes in the structural properties of dough. These changes were reflected in the ability of dough to rise during proofing.     

Antibacterial Activity of Copper Nanoparticles against Xanthomonas campestris pv. vesicatoria in Tomato Plants

Copper-based bactericides have appeared as a new tool in crop protection and offer an effective solution to combat bacterial resistance. In this work, two copper nanoparticle products that were previously synthesized and evaluated against major bacterial and fungal pathogens were tested on their ability to control the bacterial spot disease of tomato. Growth of Xanthomonas campestris pv. vesicatoria, the causal agent of the disease, was significantly suppressed by both nanoparticles, which had superior function compared to conventional commercial formulations of copper. X-ray fluorescence spectrometry measurements in tomato leaves revealed that bioavailability of copper is superior in the case of nanoparticles compared to conventional formulations and is dependent on synthesis rather than size. This is the first report correlating bioavailability of copper to nanoparticle efficacy.     

Autotaxin Has a Negative Role in Systemic Inflammation

The pathogenesis of sepsis involves complex interactions and a systemic inflammatory response leading eventually to multiorgan failure. Autotaxin (ATX, ENPP2) is a secreted glycoprotein largely responsible for the extracellular production of lysophosphatidic acid (LPA), which exerts multiple effects in almost all cell types through its at least six G-protein-coupled LPA receptors (LPARs). Here, we investigated a possible role of the ATX/LPA axis in sepsis in an animal model of endotoxemia as well as in septic patients. Mice with 50% reduced serum ATX levels showed improved survival upon lipopolysaccharide (LPS) stimulation compared to their littermate controls. Similarly, mice bearing the inducible inactivation of ATX and presenting with >70% decreased ATX levels were even more protected against LPS-induced endotoxemia; however, no significant effects were observed upon the chronic and systemic transgenic overexpression of ATX. Moreover, the genetic deletion of LPA receptors 1 and 2 did not significantly affect the severity of the modelled disease, suggesting that alternative receptors may mediate LPA effects upon sepsis. In translation, ATX levels were found to be elevated in the sera of critically ill patients with sepsis in comparison with their baseline levels upon ICU admission. Therefore, the results indicate a role for ATX in LPS-induced sepsis and suggest possible therapeutic benefits of pharmacologically targeting ATX in severe, systemic inflammatory disorders.     

The mTOR Signaling Pathway in Multiple Sclerosis; from Animal Models to Human Data

This article recapitulates the evidence on the role of mammalian targets of rapamycin (mTOR) complex pathways in multiple sclerosis (MS). Key biological processes that intersect with mTOR signaling cascades include autophagy, inflammasome activation, innate (e.g., microglial) and adaptive (B and T cell) immune responses, and axonal and neuronal toxicity/degeneration. There is robust evidence that mTOR inhibitors, such as rapamycin, ameliorate the clinical course of the animal model of MS, experimental autoimmune encephalomyelitis (EAE). New, evolving data unravel mechanisms underlying the therapeutic effect on EAE, which include balance among T-effector and T-regulatory cells, and mTOR effects on myeloid cell function, polarization, and antigen presentation, with relevance to MS pathogenesis. Radiologic and preliminary clinical data from a phase 2 randomized, controlled trial of temsirolimus (a rapamycin analogue) in MS show moderate efficacy, with significant adverse effects. Large clinical trials of indirect mTOR inhibitors (metformin) in MS are lacking; however, a smaller prospective, non-randomized study shows some potentially promising radiological results in combination with ex vivo beneficial effects on immune cells that might warrant further investigation. Importantly, the study of mTOR pathway contributions to autoimmune inflammatory demyelination and multiple sclerosis illustrates the difficulties in the clinical application of animal model results. Nevertheless, it is not inconceivable that targeting metabolism in the future with cell-selective mTOR inhibitors (compared to the broad inhibitors tried to date) could be developed to improve efficacy and reduce side effects.     

The Gestational Effects of Maternal Bone Marker Molecules on Fetal Growth,Metabolism and Long-Term Metabolic Health: A Systematic Review

Fetal exposure in adverse environmental factors during intrauterine life can lead to various biological adjustments, affecting not only in utero development of the conceptus, but also its later metabolic and endocrine wellbeing. During human gestation, maternal bone turnover increases, as reflected by molecules involved in bone metabolism, such as vitamin D, osteocalcin, sclerostin, sRANKL, and osteoprotegerin; however, recent studies support their emerging role in endocrine functions and glucose homeostasis regulation. Herein, we sought to systematically review current knowledge on the effects of aforementioned maternal bone biomarkers during pregnancy on fetal intrauterine growth and metabolism, neonatal anthropometric measures at birth, as well as on future endocrine and metabolic wellbeing of the offspring. A growing body of literature converges on the view that maternal bone turnover is likely implicated in fetal growth, and at least to some extent, in neonatal and childhood body composition and metabolic wellbeing. Maternal sclerostin and sRANKL are positively linked with fetal abdominal circumference and subcutaneous fat deposition, contributing to greater birthweights. Vitamin D deficiency correlates with lower birthweights, while research is still needed on intrauterine fetal metabolism, as well as on vitamin D dosing supplementation during pregnancy, to diminish the risks of low birthweight or SGA neonates in high-risk populations.     

A Scoping Review on Lipocalin-2 and Its Role in Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma

Excess calorie intake and a sedentary lifestyle have made non-alcoholic fatty liver disease (NAFLD) one of the fastest growing forms of liver disease of the modern world. It is characterized by abnormal accumulation of fat in the liver and can range from simple steatosis and non-alcoholic steatohepatitis (NASH) to cirrhosis as well as development of hepatocellular carcinoma (HCC). Biopsy is the golden standard for the diagnosis and differentiation of all NAFLD stages, but its invasiveness poses a risk for patients, which is why new, non-invasive ways of diagnostics ought to be discovered. Lipocalin-2 (LCN2), which is a part of the lipocalin transport protein family, is a protein formally known for its role in iron transport and in inflammatory response. However, in recent years, its implication in the pathogenesis of NAFLD has become apparent. LCN2 shows significant upregulation in several benign and malignant liver diseases, making it a good candidate for the NAFLD biomarker or even a therapeutic target. What makes LCN2 more interesting to study is the fact that it is overexpressed in HCC development induced by chronic NASH, which is one of the primary causes of cancer-related deaths. However, to this day, neither its role as a biomarker for NAFLD nor the molecular mechanisms of its implication in NAFLD pathogenesis have been completely elucidated. This review aims to gather and closely dissect the current knowledge about, sometimes conflicting, evidence on LCN2 as a biomarker for NAFLD, its involvement in NAFLD, and NAFLD-HCC related pathogenesis, while comparing it to the findings in similar pathologies.