Loss Of Plasticity Research Articles

Cross-species evidence from human and rat brain transcriptome for growth factor signaling pathway dysregulation in major depression.

An enhanced understanding of the pathophysiology of depression would facilitate the discovery of new efficacious medications. To this end, we examined hippocampal transcriptional changes in rat models of disease and in humans to identify common disease signatures by using a new algorithm for signature-based clustering of expression profiles. The tool identified a transcriptomic signature comprising 70 probesets able to discriminate depression models from controls in both Flinders Sensitive Line and Learned Helplessness animals. To identify disease-relevant pathways, we constructed an expanded protein network based on signature gene products and performed functional annotation analysis. We applied the same workflow to transcriptomic profiles of depressed patients. Remarkably, a 171-probesets transcriptional signature which discriminated depressed from healthy subjects was identified. Rat and human signatures shared the SCARA5 gene, while the respective networks derived from protein-based significant interactions with signature genes contained 25 overlapping genes. The comparison between the most enriched pathways in the rat and human signature networks identified a highly significant overlap (p-value: 3.85 × 10-6) of 67 terms including ErbB, neurotrophin, FGF, IGF, and VEGF signaling, immune responses and insulin and leptin signaling. In conclusion, this study allowed the identification of a hippocampal transcriptional signature of resilient or susceptible responses in rat MDD models which overlapped with gene expression alterations observed in depressed patients. These findings are consistent with a loss of hippocampal neural plasticity mediated by altered levels of growth factors and increased inflammatory responses causing metabolic impairments as crucial factors in the pathophysiology of MDD.

A microstructure with improved thermal stability and creep resistance in a novel near-alpha titanium alloy

A triple-microstructure with the precipitation of silicide along the α/β phase boundaries and α2 phase in the Ti-5.8Al-3Sn-5Zr-0.5Mo-1.0Nb-1.0Ta-0.4Si-0.2Er alloy was prepared for improving thermal stability and creep resistance. The alloys were forged at 1050 °C and 1000 °C followed by solution treatment at 1000 °C for 1 h and subsequent ageing at 700 °C for 5 h. The effects of α morphology and precipitation characteristics on the thermal stability and creep performance of high-temperature titanium alloy were investigated. A triple-microstructure with the participation of silicide along the α/β phase boundary and α2 phase was a promising structure with improved thermal stability and creep resistance. The plasticity loss rate was 25.0% after thermal exposure at 650 °C for 100 h due to the participation and coarsening of α2 and silicide. Meanwhile, the plastic creep strain was 0.111% during the creep deformation at 650 °C for 100 h with an applied stress of 100 MPa, which was attributed to the inhibition of silicide and α2 phase for boundary migration and dislocation slipping. Furthermore, the mutual precipitation of coarsening silicide and α2 phase inside α matrix was a significant reason for the dramatic decrease in the thermal ability, which also worsened the inhibition for dislocation climbing of silicon element during the creep deformation.

Phase stability and tensile behavior of metastable β Ti-V-Fe and Ti-V-Fe-Al alloys

The tensile property and deformation microstructure of a series of metastable β Ti-V-Fe and Ti-V-Fe-Al alloys have been studied. The results show that although Al is an α-stabilizer element, Al addition suppresses the athermal ω phase transformation in metastable β Ti-V-Fe-Al alloys. The Ti-16V-Fe alloy plastically deforms via {332}〈113〉 mechanical twinning and stress-induced ω phase with a special habit plane of {−5052}ω//{3-3-2}β, and the Ti-14V-2Fe-Al and Ti-12V-2Fe-Al alloys via {332}〈113〉 twinning. The Ti-16V-2Fe, Ti-16V-2Fe-Al and Ti-16V-2Fe-2Al alloys with relatively high β phase stability plastically deforms mainly via dislocation glide. The Ti-16V-Fe, Ti-14V-2Fe-Al and Ti-12V-2Fe-Al alloys exhibit higher yield strength without loss of plasticity significantly than the binary β Ti-V alloys deformed via {332}〈113〉 twinning due to solid-solution strengthening effect of Fe and Al elements in the alloys.

DinCH and ESBO actual migration from PVC infusion tubings used in an oncopediatric unit

ABSTRACTPlasticizer leaching from poly(vinyl chloride) (PVC) tubing is a well‐studied phenomenon and is a real issue in medical care today. The present study focuses on the release of two plasticizers 1,2‐cyclohexane dicarboxylic acid diisononyl ester (DINCH) (primary) and epoxidized soy bean oil (ESBO) (secondary) from PVC extension tubings used in an oncopediatric unit. The release of plasticizers is calculated by comparison to unused tubings with the same batch number. Both the DINCH and ESBO ratio diminishes in used versus new extension tubings. The loss of plasticizers has not been related to the presence of a specific drug. Our results confirm the leaching of classic plasticizers like the DINCH and of secondary plasticizers like the ESBO from tubings in real life. It confirms too the existence of a complex phenomenon in which exchanges between drugs, lipids, PVC matrices, and the administration sequences can change the global release of plasticizers. Considering all the variables involved in real‐life data, the in vitro testing appears to be the most efficient way to confirm these observations. © 2018 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2018, 135, 46649.

Loss of inter-cellular cooperation by complete epithelial-mesenchymal transition supports favorable outcomes in basal breast cancer patients.

According to the sequential metastasis model, aggressive mesenchymal (M) metastasis-initiating cells (MICs) are generated by an epithelial-mesenchymal transition (EMT) which eventually is reversed by a mesenchymal-epithelial transition (MET) and outgrowth of life-threatening epithelial (E) macrometastases. Paradoxically, in breast cancer M signatures are linked with more favorable outcomes than E signatures, and M cells are often dispensable for metastasis in mouse models. Here we present evidence at the cellular and patient level for the cooperation metastasis model, according to which E cells are MICs, while M cells merely support E cell persistence through cooperation. We tracked the fates of co-cultured E and M clones and of fluorescent CDH1-promoter-driven cell lines reporting the E state derived from basal breast cancer HMLER cells. Cells were placed in suspension state and allowed to reattach and select an EMT cell fate. Flow cytometry, single cell and bulk gene expression analyses revealed that only pre-existing E cells generated E cells, mixed E/M populations, or stem-like hybrid E/M cells after suspension and that complete EMT manifest in M clones and CDH1-negative reporter cells resulted in loss of cell plasticity, suggesting full transdifferentiation. Mechanistically, E-M coculture experiments supported the persistence of pre-existing E cells where M cells inhibited EMT of E cells in a mutual cooperation via direct cell-cell contact. Consistently, M signatures were associated with more favorable patient outcomes compared to E signatures in breast cancer, specifically in basal breast cancer patients. These findings suggest a potential benefit of complete EMT for basal breast cancer patients.

Failure Analysis of Nitrile Rubber O-Rings Static Sealing for Packaging Barrel

Nitrile rubber O-rings seals for packaging barrel was stored in China tropical marine atmosphere environments for 10 years, and then the sealing function of nitrile rubber O-ring was failed. By comparing the molecular structure, cross-link density, thermal decomposition, content of elements and chemical functional groups of the original nitrile rubber seals, the surface and interior of nitrile rubber seals storage for 10 years, a long-term natural failure mechanism was studied. The results showed that: the surface content of dibutyl phthalate and dibutyl sebacate, the surface carbonyl peak height and the surface content of oxygen element were higher than that in internal; the surface cross-link density was lower than that in internal but still higher than in original sample; and surface carbon- to-oxygen ratio were lower than that in internal and original sample. After aging for 10 years, the weight loss of plasticizer decreased, and the main chain content increased. It can be inferred that nitrile rubber mainly undergoes oxygen-absorbing cross-linking reaction to form carboxylic acids and esters, which is accompanied by the migration and enrichment of two plasticizers to the surface, causing reductions in elasticity and elasticity. The residual permanent compression set was lower than the design critical value, and the sealing function for the packaging barrel was lost, and a leak occurred.

Influence of the Speed of High-Carbon Steel Billet in the Patenting Unit on Its Final Structure and Mechanical Properties

Prestressed ferroconcrete structures are widely used at present. As a result, compressive stress is created in the concrete and tensile stress in the reinforcing rope. The stressed reinforcing rope is better able to withstand the external loads that it experiences throughout the life of the construction. Consequently, larger loads may be applied or, with unchanged load, the size of the construction may be decreased, with accompanying savings of concrete and steel. Today, it is important to develop a manufacturing technology for nanostructured reinforcing rope that may be used in prestressed concrete-steel constructions. This technology is based on patenting, in which the steel acquires the structure of a fine ferrite–carbide mixture characterized by high strength and improved deformability. In the present work, the influence of increased billet speed in the patenting unit on the final structure and mechanical properties of steel 80, 70, and 50 is investigated, with a view to increasing the productivity in patenting, without loss of strength or plasticity of the steel, in the production of blanks for nanostructured reinforcing rope that may be used in prestressed concrete-steel constructions. To determine the heat-treatment time and temperature, the Gleeble 3500 system is used to plot diagrams of the isothermal decomposition of undercooled austenite. In qualitative and quantitative analysis of the microstructure, the interlamellar spacing of the ferrite–carbide mixture is determined for different billet speeds in the patenting system. The mechanical properties are studied in tensile tests. It is found that, for all billet speeds, the interlamellar spacing of the ferrite–carbide mixture is practically the same and is optimal for subsequent drawing: 0.1–0.2 μm. Thanks to the fine structure of the ferrite–carbide mixture formed in patenting, the strength of the billet is increased. Hence, in subsequent drawing, the billet may withstand greater compression without fracture. In the production of patented billet for nanostructured reinforcing rope, its speed in the patenting unit may be increased to 5 m/min. Consequently, the productivity may be increased without loss of strength and plasticity of the billet.

Epigallocatechin‐3‐gallate Suppressed Methylglyoxal‐Induced Apoptosis in SH‐SY5Y Cells

Glycation is an endogenous process that generates a class of compounds known as advanced glycation end products (AGEs). AGEs are found in age‐related intracellular protein deposits of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Green tea polyphenols have a role in the reversal of age‐related loss of neuronal plasticity and recovery after neuronal lesions. There are several polyphenolic catechins in green tea, where epigallocatechin‐3‐gallate (EGCG) is both the most abundant and most biologically active form. EGCG could exhibit protective effects against AGEs‐induced injury in neuronal cells through its antioxidative properties, suggesting a beneficial role for this tea catechin against neurodegenerative diseases. In the current study, efforts were made to investigate the effects of EGCG on MG‐induced apoptosis. SH‐SY5Y cell were treated with different concentrations of EGCG followed by treatment with MG. Our data exhibited that both the cleaved PARP and cleaved‐caspase‐3 were downregulated by EGCG, and the MG‐induced reduction of Bcl‐2 expression were reversed by EGCG treatment. Moreover, EGCG could protect cells from death via reverse MG‐induced promoting of ERK/JNK pathway, and associated with reduced p53 accumulation. Our results implicate that EGCG could suppress MG‐induced apoptosis.Support or Funding InformationThis study was supported by NSC 100‐2313‐B‐309‐003 to A‐C ChengThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Theasinensins A Against Methylglyoxal‐Induced Neurotoxicity via Autophagy in SH‐SY5Y Cells

Methylglyoxal (MG) is a highly reactive dicarbonyl aldehyde. MG has been proved to be toxic to neuron and may be the reason of many neurodegenerative diseases. Tea polyphenols have notable effects against various types of cancers, blood pressure, cardiovascular problems, arthritis, and atherosclerosis without inducing major toxicity consequences. Tea polyphenols have a role in the reversal of age‐related loss of neuronal plasticity and recovery after neuronal lesions. Theasinensins are a group of tea polyphenols different from green tea catechins, and they are considered as bioactive compounds in Oolong tea. During enzymatic oxidation, EGCG is fermentated and several B‐ring homodimers: theasinensins A (TSA) intermediates generated. TSA had been found to have many bioactivities, such as anti‐oxidation. However, the effect of the neuroprotective effect of this tea polyphenol remains unclear. The aim of this study is to investigate the neuroprotective effects and the molecular mechanism of TSA against MG‐induced toxicity in SH‐SY5Y cell model. The cell viability assay demonstrated that TSA treatment protected cells from MG‐induced neurotoxicity. The result of acridine orange (AO) stain, detecting AO fluoresce intensity and the level of LC3, showed that TSA could increase intracellular AVO value and induce autophagy in MG‐treated neuron cell. We expect that TSA could be reagents to protect neurodegenerative diseases.Support or Funding InformationThis study was supported by NSC 100‐2313‐B‐309‐003 to A‐C ChengThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Links between Anatomy, Systems biology, Epigenetics, etho‐eco‐morphological mismatches, evolutionary trends, and organism behavior: a unifying view of anatomical evolution

It is a puzzling paradox that eco‐morphological mismatches occur so frequently in an evolutionary process that often leads to macroevolutionary trends and in which organisms are said to be ‘designed’ for the habitats they inhabit. Here I present a new framework ‐ Organic Nonoptimal Constrained Evolution (ONCE) ‐ to address this paradox, and to explain why organisms look as they look: organisms themselves, and in particular their behavior, are the major active players of evolution. That is, within this framework, internal factors can both decrease and increase plasticity/hidden variation and therefore, together with epigenetic factors influenced by the external environment, can allows organisms to shift their behavior, for instance as a response to environmental changes. Importantly, due to behavioral persistence related to behavioral/ecological inheritance, organisms as diverse as bacteria, plants and animals help to construct their own niches, thus being crucial to direct evolution. Darwinian natural (external) selection then comes into play as a secondary ‐ but still crucial ‐ player. That is, due to organismal behavioral persistence, the random mutations/epigenetic factors that happen to be advantageous within the niches constructed by the organisms will be selected, further directing evolution and increasing the match between behavior, phenotype, and environment. This process can extend for long periods of time, leading to macroevolutionary morphological trends and further increasing this match, potentially resulting in successful phenotypic overspecialization. However, behavioral persistence, loss of plasticity due to natural selection, genetic drift, overspecialization, and internal constraints can often make it difficult for the organisms to respond behaviorally and/or anatomically to new environmental changes, resulting in potential mismatches between behavior, ecology and form, and eventually in extinction. This new framework about anatomical evolution therefore bridges the gap between ideas that have been long considered to be opposing views of biology since Aristotle, including internalism and externalism, Cuvier's vs. Geoffroy's take on form and function, Darwinism and Lamarkism, the ideas of Baldwin, Waddington and Goldschmidt, and current Evo‐Devo ideas such as a physicalist framework, niche construction and epigenetic plasticity. This talk therefore covers ‐ and aims to link ‐ areas as diverse as evolutionary developmental biology, paleontology, evolutionary biology, comparative anatomy, ecomorphology, functional anatomy, ecology, ethology, biological anthropology, evolutionary medicine and history and philosophy of biology.Support or Funding InformationNAThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Loss of plasticity in life‐history strategy associated with secondary invasion into stressful environments in invasive narrowleaf plantain (Plantago lanceolata L.)

AbstractAdaptation to changing environments is a fundamental process occurring throughout a species’ range, particularly under novel and stressful conditions at the range‐edges of invasive species. However, the evolutionary consequences associated with adaptation are still poorly understood. Secondary invasion into stressful areas may incur fitness costs that could limit range expansion. In addition, developmental plasticity is predicted to be lost under strong selection in stressful habitats. We assessed populations across a range transect of an invasive plant (Plantago lanceolata L.) for a loss of developmental plasticity and for adaptation costs, where there was prior expansion inland into stressful and novel areas from relatively benign areas closer to the coast. In the glasshouse, we grew plants from seed originating from two secondary invasion locations (near‐edge and edge), and from the range centre location representing the area of primary invasion. Plants were exposed to high or low nutrient treatment, and novel copper stress and control (no copper) treatment to assess adaptation costs associated with secondary invasion. In addition, we compared the costs in near‐edge and edge plants. Developmental plasticity in life‐history traits was lost for secondary invasion plants compared to plants from the range centre. Plants from secondary invasion locations expressed a slower life‐history under both nutrient treatments. In contrast, range‐centre plants were able to switch to a faster life‐history under high nutrient treatment. Our copper treatment had only slight effects on plants, where they expressed intermediate specific leaf area (SLA) under copper treatment. Near‐edge plants had the lowest plant size and reproduction. The loss of plasticity associated with secondary invasion may have implications on evolution in range‐edge populations. Phenotypic plasticity may have initially mediated ecological adaptation to stressful habitats; however, adaptation to stressful conditions can also have the consequence of inhibiting further range expansion in invasive species.

Centrality of Early Synaptopathy in Parkinson's Disease.

Significant advances have been made in the understanding of the numerous mechanisms involved in Parkinson’s disease (PD) pathogenesis. The identification of PD pathogenic mutations and the use of different animal models have contributed to better elucidate the processes underlying the disease. Here, we report a brief survey of some relevant cellular mechanisms, including autophagic–lysosomal dysfunction, endoplasmic reticulum stress, and mitochondrial impairment, with the main aim to focus on their potential convergent roles in determining early alterations at the synaptic level, mainly consisting in a decrease in dopamine release at nigrostriatal terminals and loss of synaptic plasticity at corticostriatal synapses. In a number of experimental models, this synaptopathy has been shown to be an initial, central event in PD pathogenesis, preceding neuronal damage, thereby representing a valuable tool for testing potential disease-modifying treatments.

Age-Dependent Decline in Fate Switch from NG2 Cells to Astrocytes After Olig2 Deletion.

NG2 cells are a resident glial progenitor cell population that is uniformly distributed throughout the developing and mature mammalian CNS. Those in the postnatal CNS generate exclusively myelinating and non-myelinating oligodendrocytes and are thus equated with oligodendrocyte precursor cells. Prenatally, NG2 cells in the ventral gray matter of the forebrain generate protoplasmic astrocytes as well as oligodendrocytes. The fate conversion from NG2 cells into protoplasmic astrocytes is dependent on downregulation of the key oligodendrocyte transcription factor Olig2. We showed previously that constitutive deletion of Olig2 in NG2 cells converts NG2 cells in the neocortex into protoplasmic astrocytes at the expense of oligodendrocytes. In this study, we show that postnatal deletion of Olig2 caused NG2 cells in the neocortex but not in other gray matter regions to become protoplasmic astrocytes. However, NG2 cells in the neocortex became more resistant to astrocyte fate switch over the first 3 postnatal weeks. Fewer NG2 cells differentiated into astrocytes and did so with longer latency after Olig2 deletion at postnatal day 18 (P18) compared with deletion at P2. The high-mobility group transcription factor Sox10 was not downregulated for at least 1 month after Olig2 deletion at P18 despite an early transient upregulation of the astrocyte transcription factor NFIA. Furthermore, inhibiting cell proliferation in slice culture reduced astrocyte differentiation from Olig2-deleted perinatal NG2 cells, suggesting that cell division might facilitate nuclear reorganization needed for astrocyte transformation.SIGNIFICANCE STATEMENT NG2 cells are glial progenitor cells that retain a certain degree of lineage plasticity. In the normal postnatal neocortex, they generate mostly oligodendrocyte lineage cells. When the oligodendrocyte transcription factor Olig2 is deleted in NG2 cells in the neocortex, they switch their fate to protoplasmic astrocytes. However, the efficiency of the fate switch decreases with age over the first 3 postnatal weeks and is reduced when cell proliferation is inhibited. As the neocortex matures, sustained expression of the oligodendrocyte lineage-specific key transcription factor Sox10 becomes less dependent on Olig2. Together, our findings suggest a gradual stabilization of the oligodendrocyte lineage genes and loss of lineage plasticity during the first 3 weeks after birth, possibly due to nuclear reorganization.

МОДЕЛИРОВАНИЕ ПОВЕДЕНИЯ МАТЕРИАЛОВ И ЭЛЕМЕНТОВ КОНСТРУКЦИЙ, НАХОДЯЩИХСЯ ПОД ВОЗДЕЙСТВИЕМ АГРЕССИВНЫХ СРЕД (ОБЗОР)

The review of a number of scientific works in the field of modeling processes of interaction of an aggressive medium with materials and structural elements and their behavior under the action of loads is offered. The investigated phenomena are described using theoretical-experimental methods for the further prediction of short-term and long-term strength characteristics of materials and structural elements subject to the influence of an aggressive medium. In view of the complexity of the phenomena under consideration, an interdisciplinary scientific approach is used that takes into account both the physics-chemical interaction of the aggressive medium with materials and the systematization of mechanical-mathematical (phenomenological) models. The main attention is paid to the study and modeling of high-temperature corrosion damage of materials and structural elements. It is taken into account both the diffusion penetration of the aggressive medium and the chemical interaction of its elements with the material. The effect of various factors, such as liquidmetal media and radiation exposure; oxide films formed on corroding surfaces; cracking of stressed stainless steels in the conditions of hydrogen embrittlement, on the corrosion process is presented. The dependence of corrosion rate on the stressed state with elastoplastic deformations also is represented. Publications with various versions of phenomenological models of corrosion wear processes, loss of plasticity and embrittlement in aggressive media are given, as well as publications using the probabilistic-statistic approach to modeling corrosive failure. An extensive list of wellknown literature sources, that reflect scientific research taking into account all aspects of interaction of the material with an aggressive environment is given. Keywords: modeling, physics-chemical models, mechanical-mathematical models, aggressive environment, liquid metal environment, strength, corrosion, corrosion layer, corrosion failure, diffusion, chemical reaction, ionizing radiation, experiment.

Effects of propofol on the developing brain

Background Propofol is commonly used in pediatric surgery, while its detrimental effects on neurobehavior in children subjected to surgery are recognized in the field, and attract more and more attention from scientists. Objective To describe the adverse effects of propofol on the developing brain, and to summarize potential interventional and therapeutic strategies to prevent or reverse neurobehavioral dysfunctions following propofol anesthesia. Content Propofol confers its anesthetic efficacy by regulating gamma amino acid(GABA) and N-methyl-D-aspartate (NMDA) receptors. Because of the unique characteristics of neurons and neural circuit connections in the developing brain, propofol exceptionally interferes brain functions at both cellular and circuit levels. Propofol has been demonstrated to disrupt calcium homeostasis, elevating intracellular calcium concentrations, and to inhibit the synthesis of mature neurotrophic factors. These cellular events may contribute to propofol-induced cellular and circuit outcomes, such as, neuronal apoptosis, imbalance of excitatory and inhibitory drives to neurons, loss of synaptic plasticity, and enhancement of inflammatory reaction. Accumulating experimental evidence shows that 17--estradiol, dexmedetomidine, acetyl-L-carnitine, erythropoietin, and lithium salts have therapeutic potentials to propofol-induced dysfunctions on developing brain. Trend Most toxicological and therapeutic experiments were conducted in animals. More sophisticated mechanistic experiments and clinical trials are warranted to advance our understanding of neuro-pathophysiological bases of propofol, and to provide new avenue for interventional and therapeutic strategies to treat Propofol-induced neural dysfunctions. Key words: Propofol; Developing brain

Analysis of the effects of chemical ageing of ethylene-propylene diene monomer by chemical, spectroscopic, and thermal means

Ethylene-propylene diene monomer (EPDM) failures due to material degradation poses a major risk in the biopharmaceutical industry, which can result in long periods of production downtime. It is suspected that a key cause of this EPDM degradation is due to the chemical solutions used in equipment cleaning processes, resulting in crosslinking of the EPDM polymer bulk. However, the mechanisms responsible for crosslink formation, and whether other degradation sources are also present, has never been investigated in the public domain. Twenty four virgin samples were utilised for testing, twelve of which were subject to common chemical cleaning solutions used in the biopharmaceutical sector. The chemical solutions under investigation were aqueous solutions of NaOH, NaClO, H3PO4, and the interaction between 100 °C H2O and NaClO. The characterisation of the degradation process was conducted via chemical, spectroscopic and thermal means. The results show that degradation of the polymer bulk proceeds predominantly via crosslinking for all exposure types, due to oxidative damage and the formation and recombination of free radicals. Loss of plasticiser in the polymer matrix and thermo-oxidative damage are contributory degradation mechanisms. NaOH and H3PO4 exposure results in an accelerated rate of crosslinking compared to NaClO in the early stages of exposure.

Influence of External Conditions on the Relation between the Physical and Chemical Processes in the Thermodegradation of Plasticized Poly(Vinyl Chloride)

The heat-induced loss of plasticizer from and dehydrochlorination of poly(vinyl chloride) plasticized with dioctyl phthalate is studied by thermogravimetric analysis, IR spectroscopy, and colorimetry. Specific features and general regularities of the processes at high (200–320°C) and medium (100–132°C) temperatures are established. It is shown that the dehydrochlorination and oxidation processes dominate in confined space whereas, in unconfined space, plasticizer is lost largely through evaporation. The activation energies of the initial stages of the processes are determined.

Sex Differences in the Cognitive and Hippocampal Effects of Streptozotocin in an Animal Model of Sporadic AD.

More than 95% of Alzheimer's disease (AD) belongs to sporadic AD (sAD), and related animal models are the important research tools for investigating the pathogenesis and developing new drugs for sAD. An intracerebroventricular infusion of streptozotocin (ICV-STZ) is commonly employed to generate sporadic AD animal model. Moreover, the potential impact of sex on brain function is now emphasized in the field of AD. However, whether sex differences exist in AD animal models remains unknown. Here we reported that ICV-STZ remarkably resulted in learning and memory impairment in the Sprague-Dawley male rats, but not in the female rats. We also found tau hyperphosphorylation, an increase of Aβ40/42 as well as increase in both GSK-3β and BACE1 activities, while a loss of dendritic and synaptic plasticity was observed in the male STZ rats. However, STZ did not induce above alterations in the female rats. Furthermore, estradiol levels of serum and hippocampus of female rats were much higher than that of male rats. In conclusion, sex differences exist in this sporadic AD animal model (Sprague-Dawley rats induced by STZ), and this should be considered in future AD research.

MicroRNA in Alzheimer's disease revisited: implications for major neuropathological mechanisms.

Pathology of Alzheimer's disease (AD) goes far beyond neurotoxicity resulting from extracellular deposition of amyloid β (Aβ) plaques. Aberrant cleavage of amyloid precursor protein and accumulation of Aβ in the form of the plaque or neurofibrillary tangles are the known primary culprits of AD pathogenesis and target for various regulatory mechanisms. Hyper-phosphorylation of tau, a major component of neurofibrillary tangles, precipitates its aggregation and prevents its clearance. Lipid particles, apolipoproteins and lipoprotein receptors can act in favor or against Aβ and tau accumulation by altering neural membrane characteristics or dynamics of transport across the blood-brain barrier. Lipids also alter the oxidative/anti-oxidative milieu of the central nervous system (CNS). Irregular cell cycle regulation, mitochondrial stress and apoptosis, which follow both, are also implicated in AD-related neuronal loss. Dysfunction in synaptic transmission and loss of neural plasticity contribute to AD. Neuroinflammation is a final trail for many of the pathologic mechanisms while playing an active role in initiation of AD pathology. Alterations in the expression of microRNAs (miRNAs) in AD and their relevance to AD pathology have long been a focus of interest. Herein we focused on the precise pathomechanisms of AD in which miRNAs were implicated. We performed literature search through PubMed and Scopus using the search term: ('Alzheimer Disease') OR ('Alzheimer's Disease') AND ('microRNAs' OR 'miRNA' OR 'MiR') to reach for relevant articles. We show how a limited number of common dysregulated pathways and abnormal mechanisms are affected by various types of miRNAs in AD brain.

Reduction of myocardial ischemia reperfusion injury in pigs by (over) expression of human membrane co-factor protein

Edible films and barriers derived from polysaccharides, proteins and lipids provide several functions which prevent mass transfer, for example, water vapor, gas, and volatile compounds, between foods and environment. The preparation of materials can be either by solution casting commonly used in the laboratory or a more commercially extrusion process. Plasticizers are used to increase deformability reducing the glass transition temperature (Tg) of the materials which can be determined using differential scanning calorimetry (DSC) and dynamic mechanical thermal analysis (DMTA). This chapter also demonstrates the effects of plasticizers, other components, and treatments on the Tg values of various edible films. Moreover, the non-equilibrium state of the edible film matrices causes several time-dependent changes during storage or “aging,” for example, plasticizer loss, lipid destabilization, and crystallization which subsequently impacts functional and mechanical properties of the films.