Search results for: Mohammad-Javad Eslami

Authors: Mohammadjavad Sotoudeheian

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COVID-19, which began in December 2019, uses the angiotensin-converting enzyme 2 (ACE2) receptor to enter and spread through the cells. ACE2 mRNA is present in almost every organ, including nasopharynx, lung, as well as the brain. Ports of entry of SARS-CoV-2 into the central nervous system (CNS) may include arterial circulation, while viremia is remarkable. However, it is imperious to develop neurological symptoms evaluation CSF analysis in patients with COVID-19, but theoretically, ACE2 receptors are expressed in cerebellar cells and may be a target for SARS-CoV-2 infection in the brain. Recent evidence agrees that SARS-CoV-2 can impact the brain through direct and indirect injury. Two biomarkers for CNS injury, glial fibrillary acidic protein (GFAP) and neurofilament light chain (NFL) detected in the plasma of patients with COVID-19. NFL, an axonal protein expressed in neurons, is related to axonal neurodegeneration, and GFAP is over-expressed in CNS inflammation. GFAP cytoplasmic accumulation causes Schwan cells to misfunction, so affects myelin generation, reduces neuroskeletal support over NfLs during CNS inflammation, and leads to axonal degeneration. Interleukin-6 (IL-6), which extensively over-express due to interleukin storm during COVID-19 inflammation, regulates gene expression, as well as GFAP through STAT molecular pathway. IL-6 also impresses the phosphoinositide 3-kinase (PI3K)/STAT/smads pathway. The PI3K/ protein kinase B (Akt) pathway is the main modulator upstream of the mammalian target of rapamycin (mTOR), and alterations in this pathway are common in neurodegenerative diseases. Most neurodegenerative diseases show a disruption of autophagic function and display an abnormal increase in protein aggregation that promotes cellular death. Therefore, induction of autophagy has been recommended as a rational approach to help neurons clear abnormal protein aggregates and survive. The mTOR is a major regulator of the autophagic process and is regulated by cellular stressors. The mTORC1 pathway and mTORC2, as complementary and important elements in mTORC1 signaling, have become relevant in the regulation of the autophagic process and cellular survival through the extracellular signal-regulated kinase (ERK) pathway.

Keywords: mTORC1, COVID-19, PI3K, autophagy, neurodegeneration

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Authors: Majid Eslami

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Functionally graded materials (FGMs) exhibit heterogeneous microstructures in which the composition and properties gently change in specified directions. The common type of FGMs consist of a metal in which ceramic particles are distributed with a graded concentration. There are many processing routes for FGMs. An important group of these methods is casting techniques (gravity or centrifugal). However, the main problem of casting molten metal slurry with dispersed ceramic particles is a destructive chemical reaction between these two phases which deteriorates the properties of the materials. In order to overcome this problem, in the present investigation a suspension of 6061 aluminum and alumina powders in a liquid polymer was used as the starting material and subjected to centrifugal force for making FGMs. The size rang of these powders was 45-63 and 106-125 μm. The volume percent of alumina in the Al/Al2O3 powder mixture was in the range of 5 to 20%. PMMA (Plexiglas) in different concentrations (20-50 g/lit) was dissolved in toluene and used as the suspension liquid. The glass mold contaning the suspension of Al/Al2O3 powders in the mentioned liquid was rotated at 1700 rpm for different times (4-40 min) while the arm length was kept constant (10 cm) for all the experiments. After curing the polymer, burning out the binder, cold pressing and sintering , cylindrical samples (φ=22 mm h=20 mm) were produced. The density of samples before and after sintering was quantified by Archimedes method. The results indicated that by using the same sized alumina and aluminum powders particles, FGM sample can be produced by rotation times exceeding 7 min. However, by using coarse alumina and fine alumina powders the sample exhibits step concentration. On the other hand, using fine alumina and coarse alumina results in a relatively uniform concentration of Al2O3 along the sample height. These results are attributed to the effects of size and density of different powders on the centrifugal force induced on the powders during rotation. The PMMA concentration and the vol.% of alumina in the suspension did not have any considerable effect on the distribution of alumina particles in the samples. The hardness profiles along the height of samples were affected by both the alumina vol.% and porosity content. The presence of alumina particles increased the hardness while increased porosity reduced the hardness. Therefore, the hardness values did not show the expected gradient in same sample. The sintering resulted in decreased porosity for all the samples investigated.

Keywords: FGM, powder metallurgy, centrifugal method, polymeric suspension

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Authors: Maryam Mohammadi, Mohammadjavad Mahdavinejad, Mojtaba Ansari

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The main driving force for increasing movement towards the design of High-Performance Buildings (HPB) are building codes and rating systems that address the various components of the building and their impact on the environment and energy conservation through various methods like prescriptive methods or simulation-based approaches. The methods and tools developed to meet these needs, which are often based on building performance simulation tools (BPST), have limitations in terms of compatibility with the integrated design process (IDP) and HPB design, as well as use by architects in the early stages of design (when the most important decisions are made). To overcome these limitations in recent years, efforts have been made to develop Design Decision Support Systems, which are often based on artificial intelligence. Numerous needs and steps for designing and developing a Decision Support System (DSS), which complies with the early stages of energy-efficient architecture design -consisting of combinations of different methods in an integrated package- have been listed in the literature. While various review studies have been conducted in connection with each of these techniques (such as optimizations, sensitivity and uncertainty analysis, etc.) and their integration of them with specific targets; this article is a critical and holistic review of the researches which leads to the development of applicable systems or introduction of a comprehensive framework for developing models complies with the IDP. Information resources such as Science Direct and Google Scholar are searched using specific keywords and the results are divided into two main categories: Simulation-based DSSs and Meta-simulation-based DSSs. The strengths and limitations of different models are highlighted, two general conceptual models are introduced for each category and the degree of compliance of these models with the IDP Framework is discussed. The research shows movement towards Multi-Level of Development (MOD) models, well combined with early stages of integrated design (schematic design stage and design development stage), which are heuristic, hybrid and Meta-simulation-based, relies on Big-real Data (like Building Energy Management Systems Data or Web data). Obtaining, using and combining of these data with simulation data to create models with higher uncertainty, more dynamic and more sensitive to context and culture models, as well as models that can generate economy-energy-efficient design scenarios using local data (to be more harmonized with circular economy principles), are important research areas in this field. The results of this study are a roadmap for researchers and developers of these tools.

Keywords: integrated design process, design decision support system, meta-simulation based, early stage, big data, energy efficiency

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Authors: Mansour Eslami, Fereshte Habibi

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Limb length discrepancy (LLD), or anisomeric, is defined as a condition in which paired limbs are noticeably unequal. Individuals with LLD during walking use compensatory mechanisms to dynamically lengthen the short limb and shorten the long limb to minimize the displacement of the body center of mass and consequently reduce body energy expenditure. Due to the compensatory movements created, LLD greater than 1 cm increases the odds of creating lumbar problems and hip and knee osteoarthritis. Insoles are non-surgical therapies that are recommended to improve the walking pattern, pain and create greater symmetry between the two lower limbs. However, it is not yet clear what effect insoles have on the variables related to injuries during walking. The aim of the present study was to evaluate the effect of internal and external heel lift insoles on pelvic kinematic in sagittal and frontal planes and lower extremity joint moments in individuals with mild leg length discrepancy during the stance phase of walking. Biomechanical data of twenty-eight men with structural leg length discrepancy of 10-25 mm were collected while they walked under three conditions: shoes without insole (SH), with internal heel lift insoles (IHLI) in shoes, and with external heal lift insole (EHLI). The tests were performed for both short and long legs. The pelvic kinematic and joint moment were measured with a motion capture system and force plate. Five walking trials were performed for each condition. The average value of five successful trials was used for further statistical analysis. Repeated measures ANCOVA with Bonferroni post hoc test were used for between-group comparisons (p ≤ 0.05). In both internal and external heel lift insoles (IHLI, EHLI), there was a significant decrease in the peak values of lateral and anterior pelvic tilts of the long leg, hip, and knee moments of a long leg and ankle moment of short leg (p ≤ 0.05). Furthermore, significant increases in peak values of lateral and anterior pelvic tilt of short leg in IHLI and EHLI were observed as compared to Shoe (SH) condition (p ≤ 0.01). In addition, a significant difference was observed between the IHLI and EHLI conditions in peak anterior pelvic tilt of long leg and plantar flexor moment of short leg (p=0.04; p= 0.04 respectively). Our findings indicate that both IHLI and EHLI can play an important role in controlling excessive pelvic movements in the sagittal and frontal planes in individuals with mild LLD during walking. Furthermore, the EHLI may have a better effect in preventing musculoskeletal injuries compared to the IHLI.

Keywords: kinematic, leg length discrepancy, shoe insole, walking

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Authors: Hamed Khosravi, Reza Eslami-Farsani

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Increased interest in lightweight and efficient structural components has created the need for selecting materials with improved mechanical properties. To do so, composite materials are being widely used in many applications, due to durability, high strength and modulus, and low weight. Among the various composite structures, grid-stiffened structures are extensively considered in various aerospace and aircraft applications, because of higher specific strength and stiffness, higher impact resistance, superior load-bearing capacity, easy to repair, and excellent energy absorption capability. Although there are a good number of publications on the design aspects and fabrication of grid structures, little systematic work has been reported on their material modification to improve their properties, to our knowledge. Therefore, the aim of this research is to study the reinforcing effect of silica nanoparticles on the flexural properties of epoxy/E-glass isogrid panels under three-point bending test. Samples containing 0, 1, 3, and 5 wt.% of the silica nanoparticles, with 44 and 48 vol.% of the glass fibers in the ribs and skin components respectively, were fabricated by using a manual filament winding method. Ultrasonic and mechanical routes were employed to disperse the nanoparticles within the epoxy resin. To fabricate the ribs, the unidirectional fiber rovings were impregnated with the matrix mixture (epoxy + nanoparticles) and then laid up into the grooves of a silicone mold layer-by-layer. At once, four plies of woven fabrics, after impregnating into the same matrix mixture, were layered on the top of the ribs to produce the skin part. In order to conduct the ultimate curing and to achieve the maximum strength, the samples were tested after 7 days of holding at room temperature. According to load-displacement graphs, the bellow trend was observed for all of the samples when loaded from the skin side; following an initial linear region and reaching a load peak, the curve was abruptly dropped and then showed a typical absorbed energy region. It would be worth mentioning that in these structures, a considerable energy absorption was observed after the primary failure related to the load peak. The results showed that the flexural properties of the nanocomposite samples were always higher than those of the nanoparticle-free sample. The maximum enhancement in flexural maximum load and energy absorption was found to be for the incorporation of 3 wt.% of the nanoparticles. Furthermore, the flexural stiffness was continually increased by increasing the silica loading. In conclusion, this study suggested that the addition of nanoparticles is a promising method to improve the flexural properties of grid-stiffened fibrous composite structures.

Keywords: grid-stiffened composite structures, nanocomposite, three point flexural test , energy absorption

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Authors: Mohammadjavad Sotoudeheian

Abstract:

Heart failure (HF) prevalence, as a global cardiovascular problem, is increasing gradually. A variety of molecular mechanisms contribute to HF. Proteins involved in cardiac contractility regulation, such as ion channels and calcium handling proteins, are altered. Additionally, epigenetic modifications and gene expression can lead to altered cardiac function. Moreover, inflammation and oxidative stress contribute to HF. The progression of HF can be attributed to mitochondrial dysfunction that impairs energy production and increases apoptosis. Molecular mechanisms such as these contribute to the development of cardiomyocyte defects and HF and can be therapeutically targeted. The heart's contractile function is controlled by cardiomyocytes. Calpain, and its related molecules, including Bax, VEGF, and AMPK, are among the proteins involved in regulating cardiomyocyte function. Apoptosis is facilitated by Bax. Cardiomyocyte apoptosis is regulated by this protein. Furthermore, cardiomyocyte survival, contractility, wound healing, and proliferation are all regulated by VEGF, which is produced by cardiomyocytes during inflammation and cytokine stress. Cardiomyocyte proliferation and survival are also influenced by AMPK, an enzyme that plays an active role in energy metabolism. They all play key roles in apoptosis, angiogenesis, hypertrophy, and metabolism during myocardial inflammation. The role of calpains has been linked to several molecular pathways. The calpain pathway plays an important role in signal transduction and apoptosis, as well as autophagy, endocytosis, and exocytosis. Cell death and survival are regulated by these calcium-dependent cysteine proteases that cleave proteins. As a result, protein fragments can be used for various cellular functions. By cleaving adhesion and motility proteins, calcium proteins also contribute to cell migration. HF may be brought about by calpain-mediated pathways. Many physiological processes are mediated by the calpain molecular pathways. Signal transduction, cell death, and cell migration are all regulated by these molecular pathways. Calpain is activated by calcium binding to calmodulin. In the presence of calcium, calmodulin activates calpain. Calpains are stimulated by calcium, which increases matrix metalloproteinases (MMPs). In order to develop novel treatments for these diseases, we must understand how this pathway works. A variety of myocardial remodeling processes involve calpains, including remodeling of the extracellular matrix and hypertrophy of cardiomyocytes. Calpains also play a role in maintaining cardiac homeostasis through apoptosis and autophagy. The development of HF may be in part due to calpain-mediated pathways promoting cardiomyocyte death. Numerous studies have suggested the importance of the Ca2+ -dependent protease calpain in cardiac physiology and pathology. Therefore, it is important to consider this pathway to develop and test therapeutic options in humans that targets calpain in HF. Apoptosis, autophagy, endocytosis, exocytosis, signal transduction, and disease progression all involve calpain molecular pathways. Therefore, it is conceivable that calpain inhibitors might have therapeutic potential as they have been investigated in preclinical models of several conditions in which the enzyme has been implicated that might be treated with them. Ca 2+ - dependent proteases and calpains contribute to adverse ventricular remodeling and HF in multiple experimental models. In this manuscript, we will discuss the calpain molecular pathway's important roles in HF development.

Keywords: calpain, heart failure, autophagy, apoptosis, cardiomyocyte

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Authors: Mohammadjavad Sotoudeheian, Soroush Nematollahi

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Crohn’s disease (CD) is a chronic gastrointestinal segment inflammation encompassing immune dysregulation in a genetically susceptible individual in response to the environmental triggers and interaction between the microbiome and immune system. Uncontrolled inflammation leads to long-term complications, including fibrotic strictures and enteric fistulae. Increased production of Th1 and Th17-cell cytokines and defects in T-regulatory cells have been associated with CD. Th17-cells are essential for protection against extracellular pathogens, but their atypical activity can cause autoimmunity. Intrinsic defects in the control of programmed cell death in the mucosal T-cell compartment are strongly implicated in the pathogenesis of CD. The apoptosis defect in mucosal T-cells in CD has been endorsed as an imbalance of the Bcl-2 and the Bax. The immune system encounters foreign antigens through microbial colonization of mucosal surfaces or infections. In addition, FOSL downregulated IL-26 expression, a cytokine that marks inflammatory Th17-populations in patients suffering from CD. Furthermore, the expression of IL-23 is associated with the transcription factor primary leucine zipper transcription factor ATF-like (Batf). Batf-deficiency demonstrated the crucial role of Batf in colitis development. Batf and IL-23 mediate their effects by inducing IL-6 production. Strong association of IL-23R, Stat3, and Stat4 with IBD susceptibility point to a critical involvement of T-cells. IL-23R levels in transfer fistula were dependent on the AP-1 transcription factor JunB that additionally controlled levels of RORγt by facilitating DNA binding of Batf. T lymphocytes lacking JunB failed to induce IL-23- and Th17-mediated experimental colitis highlighting the relevance of JunB for the IL-23/ Th17 pathway. The absence of T-bet causes unrestrained Th17-cell differentiation. T-cells are central parts of immune-mediated colon fistula. Especially Th17-cells were highly prevalent in inflamed IBD tissues, as RORγt is effective in preventing colitis. Intraepithelial lymphocytes (IEL) contain unique T-cell subsets, including cells expressing RORγt. Increased activated Th17 and decreased T-regulatory cells in inflamed intestinal tissues had been seen. T-cells differentiate in response to many cytokines, including IL-1β, IL-6, IL-23, and TGF-β, into Th17-cells, a process which is critically dependent on the Batf. IL-23 promotes Th17-cell in the colon. Batf manages the generation of IL-23 induced IL-23R+ Th17-cells. Batf is necessary for TGF-β/IL-6-induced Th17-polarization. Batf-expressing T-cells are the core of T-cell-mediated colitis. The human-specific parts of three AP-1 transcription factors, FOSL1, FOSL2, and BATF, are essential during the early stages of Th17 differentiation. BATF supports the Th17 lineage. FOSL1, FOSL2, and BATF make possession of regulatory loci of genes in the Th17 lineage cascade. The AP1 transcription factor Batf is identified to control intestinal inflammation and seems to regulate pathways within lymphocytes, which could theoretically control the expression of several genes. It shows central regulatory properties over Th17-cell development and is intensely upregulated within IBD-affected tissues. Here, we demonstrated that targeting Batf in IBD appears as a therapeutic approach that reduces colitogenic T-cell activities during fistula formation while aiming to affect inflammation in the gut epithelial cells.

Keywords: immune system, Crohn’s Disease, BATF, T helper cells, Bcl, interleukin, FOSL

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Authors: Mohammadjavad Sotoudeheian, Navid Farahmandian

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Kawasaki disease (KD) is the primary cause of acquired pediatric heart disease as an acute vasculitis. In children with prolonged fever, rash, and inflammation of the mucosa KD must be considered as a clinical diagnosis. There is a persuasive suggestion of immune-mediated damage as the pathophysiologic cascade of KD. For example, the invasion of cytotoxic T-cells supports a viral etiology and the inflammasome of the innate immune system is a critical component in the vasculitis formation in KD. Animal models of KD propose the cytokine profiles, such as increased IL-1 and GM-CSF, which cause vascular damage. CRP and IFN-γ elevated expression and the upregulation of IL-6, and IL-10 production are also described in previous studies. Untreated KD is a critical risk factor for coronary artery diseases and myocardial infarction. Vascular damage may encompass amplified T-cell activity. SMAD3 is an essential molecule in down-regulating T-cells and increasing expression of FoxP3. It has a critical effect in the differentiation of regulatory T-cells. The discrepancy of regulatory T-cells and pro-inflammatory Th17 has been studied in acute coronary syndrome during KD. However in the coronary artery damaged lymphocytes and IgA plasma cells are seen at the lesion locations, the major immune cells in the coronary lesions are monocytes/macrophages and neutrophils. These cells secrete TNF-α, and activates matrix metalloprotease (MMP)-9, reducing the integrity of vessels and prompting patients to arise aneurysm. MMPs can break down the components of the extracellular matrix and assist immune cell movement. IVIG as an effective form of treatment clarified the role of the immune system, which may target pathogenic antigens and regulate cytokine production. Several reports have revealed that in the coronary arteries, high expression of MMP-9 in monocyte/macrophage results in pathologic cascades. Curcumin is a potent antioxidant and anti-inflammatory molecule. Curcumin decreases the production of reactive oxygen and nitrogen species and inhibits transcription factors like AP-1 and NF-κB. Curcumin also contains the characteristics of inhibitory effects on MMPs, especially MMP-9. The upregulation of MMP-9 is an important cellular response. Curcumin treatment caused a reverse effect and down-regulates MMP-9 gene expression which may fund the anti-inflammatory effect. Curcumin inhibits MMP-9 expression via PKC and AMPK-dependent pathways in Human monocytes cells. Elevated expression and activity of MMP-9 are correlated with advanced vascular lesions. AMPK controls lipid metabolism and oxidation, and protein synthesis. AMPK is also necessary for the MMP-9 activity and THP-1 cell adhesion to endothelial cells. Curcumin was shown to inhibit the activation of AMPKα. Compound C (AMPK inhibitor) inhibits MMP-9 expression level. Therefore, through inactivating AMPKs and PKC, curcumin decreases the MMP-9 level, which results in inhibiting monocyte/macrophage differentiation. Compound C also suppress the phosphorylation of three major classes of MAP kinase signaling, suggesting that curcumin may suppress MMP-9 level by inactivation of MAPK pathways. MAPK cascades are activated to induce the expression of MMP-9. Curcumin inhibits MAPKs phosphorylation, which contributes to the down-regulation of MMP-9. This study demonstrated that the potential inhibitory properties of curcumin over MMP-9 lead to a therapeutic strategy to reduce the risk of coronary artery involvement during KD.

Keywords: MMP-9, coronary artery aneurysm, Kawasaki’s disease, curcumin, AMPK, immune system, NF-κB, MAPK

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Authors: Mohammadjavad Sotoudeheian, Navid Farahmandian

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Cardiac hypertrophy arises in response to persistent increases in hemodynamic loads. In comparison, diabetic cardiomyopathy is defined by an abnormal myocardial changes without other cardiac-related risk factors. Pathological cardiac hypertrophy and myocardial remodeling are hallmarks of cardiovascular diseases and are risk factors for heart failure. The transcription factor forkhead box class O (FOXOs) can protect heart tissue by hostile oxidative stress and stimulating apoptosis and autophagy. FOXO proteins, as sensitive elements and mediators in response to environmental changes, have been revealed to prevent and inverse cardiac hypertrophy. FOXOs are inhibited by insulin and are critical mediators of insulin action. Insulin deficiency and uncontrolled diabetes lead to a catabolic state. FOXO1 acts downstream of the insulin-dependent pathways, which are dysregulated in diabetes. It regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K/Akt activation, which are critical regulators of cardiac hypertrophy. The complex network of signaling pathways comprising insulin/IGF-1 signaling, AMPK, JNK, and Sirtuins regulate the development of cardiovascular dysfunction by modulating the activity of FOXOs. Insulin receptors and IGF1R act via the PI3k/Akt and the MAPK/ERK pathways. Activation of Akt in response to insulin or IGF-1 induces phosphorylation of FOXOs. Increased protein synthesis induced by activation of the IGF-I/Akt/mTOR signaling pathway leads to hypertrophy. This pathway and the myostatin/Smad pathway are potent negative muscle development regulators. In cardiac muscle, insulin receptor substrates (IRS)-1 or IRS-2 activates the Akt signaling pathway and inactivate FOXO1. Under metabolic stress, p38 MAPK promotes degradation of IRS-1 and IRS-2 in cardiac myocytes and activates FOXO1, leading to cardiomyopathy. Sirt1 and FOXO1 interaction play an essential role in starvation-induced autophagy in cardiac metabolism. Inhibition of Angiotensin-II induced cardiomyocyte hypertrophy is associated with reduced FOXO1 acetylation and activation of Sirt1. The NF-κB, ERK, and FOXOs are de-acetylated by SIRT1. De-acetylation of FOXO1 induces the expression of genes involved in autophagy and stimulates autophagy flux. Therefore, under metabolic stress, FOXO1 can cause diabetic cardiomyopathy. The overexpression of FOXO1 leads to decreased cardiomyocyte size and suppresses cardiac hypertrophy through inhibition of the calcineurin–NFAT pathway. Diabetes mellitus is associated with elevation of O-GlcNAcylation. Some of its binding partners regulate the substrate selectivity of O-GlcNAc transferase (OGT). O-GlcNAcylation of essential contractile proteins may inhibit protein-protein interactions, reduce calcium sensitivity, and modulate contractile function. Uridine diphosphate (UDP)-GlcNAc is the obligatory substrate of OGT, which catalyzes a reversible post-translational protein modification. The increase of O-GlcNAcylation is accompanied by impaired cardiac hypertrophy in diabetic hearts. Inhibition of O-GlcNAcylation blocks activation of ERK1/2 and hypertrophic growth. O-GlcNAc modification on NFAT is required for its translocation from the cytosol to the nucleus, where NFAT stimulates the transcription of various hypertrophic genes. Inhibition of O-GlcNAcylation dampens NFAT-induced cardiac hypertrophic growth. Transcriptional activity of FOXO1 is enriched by improved O-GlcNAcylation upon high glucose stimulation or OGT overexpression. In diabetic conditions, the modification of FOXO1 by O-GlcNAc is promoted in cardiac troponin I and myosin light chain 2. Therefore targeting O-GlcNAcylation represents a potential therapeutic option to prevent hypertrophy in the diabetic heart.

Keywords: diabetes, cardiac hypertrophy, O-GlcNAcylation, FOXO1, Akt, PI3K, AMPK, insulin

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Authors: Jocelyn Doucet, Jean-Philippe Laviolette, Ali Eslami

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The end-of-life management and recycling of polymer wastes remains a key environment issue in on-going efforts to increase resource efficiency and attaining GHG emission reduction targets. Half of all the plastics ever produced were made in the last 13 years, and only about 16% of that plastic waste is collected for recycling, while 25% is incinerated, 40% is landfilled, and 19% is unmanaged and leaks in the environment and waterways. In addition to the plastic collection issue, the UN recently published a report on chemicals in plastics, which adds another layer of challenge when integrating recycled content containing toxic products into new products. To tackle these important issues, innovative solutions are required. Chemical recycling of plastics provides new complementary alternatives to the current recycled plastic market by converting waste material into a high value chemical commodity that can be reintegrated in a variety of applications, making the total market size of the output – virgin-like, high value products - larger than the market size of the input – plastic waste. Access to high-quality feedstock also remains a major obstacle, primarily due to material contamination issues. Pyrowave approaches this challenge with its innovative nano-recycling technology, which purifies polymers at the molecular level, removing undesirable contaminants and restoring the resin to its virgin state without having to depolymerise it. This breakthrough approach expands the range of plastics that can be effectively recycled, including mixed plastics with various contaminants such as lead, inorganic pigments, and flame retardants. The technology allows yields below 100ppm, and purity can be adjusted to an infinitesimal level depending on the customer's specifications. The separation of the polymer and contaminants in Pyrowave's nano-recycling process offers the unique ability to customize the solution on targeted additives and contaminants to be removed based on the difference in molecular size. This precise control enables the attainment of a final polymer purity equivalent to virgin resin. The patented process involves dissolving the contaminated material using a specially formulated solvent, purifying the mixture at the molecular level, and subsequently extracting the solvent to yield a purified polymer resin that can directly be reintegrated in new products without further treatment. Notably, this technology offers simplicity, effectiveness, and flexibility while minimizing environmental impact and preserving valuable resources in the manufacturing circuit. Pyrowave has successfully applied this nano-recycling technology to decontaminate polymers and supply purified, high-quality recycled plastics to critical industries, including food-contact compliance. The technology is low-carbon, electrified, and provides 100% traceable resins with properties identical to those of virgin resins. Additionally, the issue of low recycling rates and the limited market for traditionally hard-to-recycle plastic waste has fueled the need for new complementary alternatives. Chemical recycling, such as Pyrowave's microwave depolymerization, presents a sustainable and efficient solution by converting plastic waste into high-value commodities. By employing microwave catalytic depolymerization, Pyrowave enables a truly circular economy of plastics, particularly in treating polystyrene waste to produce virgin-like styrene monomers. This revolutionary approach boasts low energy consumption, high yields, and a reduced carbon footprint. Pyrowave offers a portfolio of sustainable, low-carbon, electric solutions to give plastic waste a second life and paves the way to the new circular economy of plastics. Here, particularly for polystyrene, we show that styrene monomer yields from Pyrowave’s polystyrene microwave depolymerization reactor is 2,2 to 1,5 times higher than that of the thermal conventional pyrolysis. In addition, we provide a detailed understanding of the microwave assisted depolymerization via analyzing the effects of microwave power, pyrolysis time, microwave receptor and temperature on the styrene product yields. Furthermore, we investigate life cycle environmental impact assessment of microwave assisted pyrolysis of polystyrene in commercial-scale production. Finally, it is worth pointing out that Pyrowave is able to treat several tons of polystyrene to produce virgin styrene monomers and manage waste/contaminated polymeric materials as well in a truly circular economy.

Keywords: nanorecycling, nanomaterials, plastic recycling, depolymerization

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