Effects of the optimized resonator dimensions on the performance of the standing-wave thermoacoustic refrigerator

Thermoacoustic refrigerator is an alternative cooling system, which is environmentally safe due to the absence of any refrigerants. The resonator tube of the system is of great importance; its design and dimensions influence the design and performance of the entire refrigerator. The central component of the resonator is the stack. So this work describes the design of the stack and the resonator along with the influence of its dimensions on the performance of the standing-wave thermoacoustic refrigerator. The resonator consists of two tubes, one larger than the other, characterized by the diameter ratio of the small over the larger diameter. A Lagrange multiplier method is used as a technique to optimize the coefficient of performance (COP) of the system. The computational analyses show that the resonator small diameter tube dissipates minimum acoustic power at a diameter ratio of 0.46, which is about 17 percent (at least) less than the published values. Moreover, the results show that the resonator length increases gradually with the increase of the mean design temperature. The increase of the resonator length leads to increase of the total acoustic power dissipated by the resonator, which reduces the COP of the standing-wave thermoacoustic refrigerator

Duchenne Muscular Dystrophy (DMD) Diagnosis: Past and Present Perspectives

Duchenne muscular dystrophy (DMD) is a fatal X-linked disorder, characterized by progressive skeletal muscle wasting. The disease is caused by various types of mutations in the dystrophin gene (DMD). The disease occurs at a frequency of about 1 in 5000 male births, making it the most common severe neuro-muscular disease. In addition to clinical examinations of muscle strength and function, diagnosis of DMD usually involves a combination of immunological assays using muscle biopsies, typically immunohistochemistry and western blotting, and molecular techniques such as DMD gene sequencing or Multiplex Ligation Dependent Probe Amplification (MLPA) using blood samples. In fact, precise molecular diagnosis is a prerequisite for determining the appropriate personalized therapeutic approach such as exon-skipping, gene therapy or stem cell-based therapies in conjunction with gene editing techniques like CRISPR-Cas9. However, the quest for reliable biomarkers with high sensitivity and specificity for DMD from liquid biopsy is still a hotspot of research, as such non-invasive biomarker(s) would not only facilitate disease diagnosis but would also help in carrier detection, which will eventually result in better disease management. In this chapter, we will illustrate the detailed current and prospect strategies for disease

Differential Association between HER2/neu and Angiogenesis in Breast Cancer

The HER-2/neu oncogene encodes a transmembrane tyrosine kinase receptor and a member of the epidermal growth factor receptors (EGFR/ErbB) family. Over-expression of this oncogene is known to contribute to pathogenesis and aggressive progression in breast cancer. On the other hand, angiogenesis is a physiological process of forming new blood vessels from pre-existing ones; however it is essential for tumor growth and transitional from benign stage to malignant form and also fundamental process for metastasis of tumors. In this study the main aim was to investigate whether angiogenesis is the cause for increased aggressive behavior of HER2 overexpression subtype in breast cancer. A variety of approaches were employed to investigate the main aim: quantification of angiogenesis using a mouse cancer cells implanted model; Drabkin’s assay for hemoglobin measurement; morphology assessment of cell lines; Bio-Plex analysis of angiogenesis factors angiopoietin-2, follistatin, G-CSF, HGF, IL-8, Leptin, PDGF-BB, PECAM-1 and VEGF; and reverse transcriptase-PCR on VEGFA and HIF-1 alpha genes expression. The data from this study showed that the AU-565 cell line which over-expresses HER2 receptors showed a significant decrease in both tumor weight and hemoglobin measurement when the cells were treated with anti-HER2 implanted in nude mice. Also, the data showed an increased expression of angiogenic factors and genes (mainly VEGF, VEGFA, Angiopoietin, and IL-8) in AU-565 as compared to MCF-7 cells, which have low expression of HER2 receptors. This suggests that breast cancer with HER2/neuoncogenes is associated with more angiogenic activities that result in an increased aggressive behavior of this form of cancer

Metabolomic profiling reveals altered phenylalanine metabolism in Parkinson’s disease in an Egyptian cohort

Introduction: Parkinson’s disease (PD) is the most common motor neurodegenerative disease worldwide. Given the complexity of PD etiology and the different metabolic derangements correlated to the disease, metabolomics profiling of patients is a helpful tool to identify patho-mechanistic pathways for the disease development. Dopamine metabolism has been the target of several previous studies, of which some have reported lower phenylalanine and tyrosine levels in PD patients compared to controls.Methods: In this study, we have collected plasma from 27 PD patients, 18 reference controls, and 8 high-risk controls to perform a metabolomic study using liquid chromatography-electrospray ionization–tandem mass spectrometry (LC-ESI-MS/MS).Results: Our findings revealed higher intensities of trans-cinnamate, a phenylalanine metabolite, in patients compared to reference controls. Thus, we hypothesize that phenylalanine metabolism has been shifted to produce trans-cinnamate via L-phenylalanine ammonia lyase (PAL), instead of producing tyrosine, a dopamine precursor, via phenylalanine hydroxylase (PAH).Discussion: Given that these metabolites are precursors to several other metabolic pathways, the intensities of many metabolites such as dopamine, norepinephrine, and 3-hydroxyanthranilic acid, which connects phenylalanine metabolism to that of tryptophan, have been altered. Consequently, and in respect to Metabolic Control Analysis (MCA) theory, the levels of tryptophan metabolites have also been altered. Some of these metabolites are tryptamine, melatonin, and nicotinamide. Thus, we assume that these alterations could contribute to the dopaminergic, adrenergic, and serotonergic neurodegeneration that happen in the disease

Neuroantibody Biomarkers: Links and Challenges in Environmental Neurodegeneration and Autoimmunity

The majority of neurodegenerative (ND) and autoimmune diseases (AID) remain idiopathic. The contribution of environmental chemicals to the development of these disorders has become of great interest in recent years. A convergence of mechanism between of ND and AID development has also emerged. In the case of ND, including neurotoxicity, the focus of this review, work over the last two decade in the realm of biomarker development, indicates that the immune response provides a venue whereby humoral immunity, in the form of autoantibodies to nervous system specific proteins, or neuroantibodies (NAb), may provide, once validated, a sensitive high throughput surrogate biomarker of effect with the potential of predicting outcome in absence of overt neurotoxicity/neurodegeneration. In addition, NAb may prove to be a contributor to the progression of the nervous system pathology, as well as biomarker of stage and therapeutic efficacy. There is a compelling need for biomarkers of effect in light of the introduction of new chemicals, such as nanoengineered material, where potential neurotoxicity remains to be defined. Furthermore, the convergence of mechanisms associated with ND and AID draws attention to the neglected arena of angiogenesis in defining the link between environment, ND, and AID

Mercury and Alzheimer’s disease: a look at the links and evidence

This review paper investigates a specific environmental-disease interaction between mercury exposure and Alzheimer’s disease hallmarks. Alzheimer’s disease is a neurodegenerative disorder affecting predominantly the memory of the affected individual. It prevails mostly in the elderly, rendering many factors as possible causative agents, which potentially contribute to the disease pathogenicity cumulatively. Alzheimer’s disease affects nearly 50 million people worldwide and is considered one the most devastating diseases not only for the patient but also for their families and caregivers. Mercury is a common environmental toxin, found in the atmosphere mostly due to human activity, such as coal-burning for heating and cooking. The natural release of mercury into the atmosphere occurs by volcanic eruptions, in the form of vapor, or weathering rocks. The most toxic form of mercury to humans is methylmercury, to which humans are exposed by the ingestion of fish. Methylmercury was found to exert its toxic effects on different parts of the human body, with predominance on the brain. There is no safe concentration for mercury in the atmosphere, even trace amounts can elicit harm to humans in the long term. Mercury’s effect on Alzheimer\u27s disease hallmarks formation, extracellular senile plaques, and intracellular neurofibrillary tangles, has been widely studied. This review demonstrates the involvement of mercury, in its different forms, in the pathway of amyloid-beta deposition and tau tangles formation. It aims to understand the link between mercury exposure and Alzheimer’s disease so that, in the future, prevention strategies can be applied to halt the progression of this disease

Hepigenetics: A Review of Epigenetic Modulators and Potential Therapies in Hepatocellular Carcinoma

Hepatocellular carcinoma is the fifth most common cancer worldwide and the second most lethal, following lung cancer. Currently applied therapeutic practices rely on surgical resection, chemotherapy and radiotherapy, or a combination thereof. These treatment options are associated with extreme adversities, and risk/benefit ratios do not always work in patients’ favor. Anomalies of the epigenome lie at the epicenter of aberrant molecular mechanisms by which the disease develops and progresses. Modulation of these anomalous events poses a promising prospect for alternative treatment options, with an abundance of felicitous results reported in recent years. Herein, the most recent epigenetic modulators in hepatocellular carcinoma are recapitulated on