Effects of intermittent fasting on experimental autoimune encephalomyelitis in C57BL/6 mice

Several religions recommend periods of fasting. One of the most frequently asked questions of MS patients before the holy month of Ramadan is weather fasting might have an unfavorable effect on their disease course. This debate became more challenging after the publication of experimental studies suggesting that calorie restriction prior to disease induction attenuates disease severity. We conducted this study to assess early and late effects of fasting on the animal model of MS, known as autoimmune encephalomyelitis. EAE was induced in the C57BL/6 mice, using Myelin Oligodendrocyte Glycopeptide (MOG) 35-55 and they fasted every other day either after the appearance of the first clinical sign or 30 days after disease induction for ten days. Thereafter, the mice were sacrificed for further histological and immunological evaluations. Intermittent fasting after the establishment of EAE did not have any unfavorable effect on the course of disease. Moreover, fasting at the early phase of disease alleviated EAE severity by ameliorating spinal cord demyelination. Fasting suppressed the secretion of IFN-γ, TNF-α and raised IL-10 production in splenocytes. Fasting was also associated with a lower percent of cytotoxicity. Intermittent fasting not only had no unfavorable effect on EAE but also reduced EAE severity if started at early phase of disease. © Summer 2016, Iran J Allergy Asthma Immunol. All rights reserved

Effect of oral genistein administration in early and late phases of allergic encephalomyelitis

Objective(s): Experimental allergic encephalomyelitis (EAE) is an autoimmune disease validated as animal model of multiple sclerosis (MS). Administration of genistein, a phytoestrogenic component of soy, to mice at the onset of EAE is known to attenuate the clinical signs of the disease. The potential effects of genistein on established EAE is less studied. In the current study, we aimed to compare the effects of genistein administration on EAE severity in early and late phases of the disease. Materials and Methods: The C57BL/6 mice were induced with EAE, using MOG 35-55 and gavaged with genistein (300 mg/kg) either after the appearance of the first clinical sign or 30 days post disease induction for ten days. 24 hr after the last gavage, mice were sacrificed. Brains and spleens were removed for assessing lymphocyte proliferation, cell cytotoxicity, and cytokine profile. Spinal cords were dissected to assess the amount of demyelination using Luxol fast blue/cresyl violet staining. Results: Administering mice with genistein, after the establishment of EAE, did not reverse the clinical signs of disease. However, treating with genistein at the onset of disease alleviated the clinical signs by reducing neuronal demyelination. Genistein suppressed the production of IFN-γ and enhanced IL-10 secretion in splenocyte and brain. Genistein also reduced IL-12 and TNF-α secretion in splenocytes, suppressed the proliferation of T-cells, and reduced the cell cytotoxicity. Conclusion: Genistein oral therapy might only reduce EAE severity if started in early phases of the disease

A Combined Approach of Structured and Non-structured IR in Multimodal Domain

We present a generic model for multimodal information retrieval, leveraging different information sources to improve the effectiveness of a retrieval system. The proposed method is able to take into account both explicit and latent semantics present in the data and can be used to answer complex queries, not currently answerable neither by document retrieval systems, nor by semantic web systems. By providing a hybrid approach combining IR and structured search techniques, we prepare a framework applicable to multimodal data collections. To test its effectiveness, we instantiate the model for an image retrieval task

CO2 Capture by Metal-Organic Framework based Mixed Matrix Membranes (MMMs)

Membrane separation is an energy efficient technology with a small physical footprint in which the membrane is the core of process. Membranes need to be further developed to be specifically applied in the field of gas separation. The most challenging target in designing membranes is to improve the permeation and selectivity, simultaneously. This goal cannot be achieved without acquiring the knowledge of material science to tune the membrane material properties. This PhD thesis focusses on designing mixed matrix membranes (MMMs) by using a new class of crystalline materials known as metal organic frameworks (MOFs) as filler. In combination with polymers as continuous phase it was expected to improve both the processability and separation performance of this composite material in comparison with the polymer only. This work has been performed in the framework of the FP7-EU project M4CO2 ('MOF-based Mixed Matrix Membranes for energy efficient CO2 capture', grant agreement n° 608490). Therefore the focus in this thesis was on, but not limited to, membranes for the separation of CO2 from N2, as a model for stack gases in coal combustion ('post-combustion separation'). To this aim, the overall concept of this thesis is divided into three parts in which the most relevant aspects of design in mixed matrix membranes are carefully studied. Part I (Chapter 2) elucidated the influence of MOF pore structure and topology on the MMMs separation performance. In part II (Chapter 3 and 4) the effect of MOF morphology and polymer free volume is studied. Finally, part III (Chapter 5) reports a study on free-standing and thin supported MOF nanosheet based membranes by using industrially viable methods. The summary of each Chapter in this thesis is presented as follows...ChemE/Catalysis Engineerin

Neural pathways that control the glucose counterregulatory response

Glucose is an essential metabolic substrate for all bodily tissues. The brain depends particularly on a constant supply of glucose to satisfy its energy demands. Fortunately, a complex physiological system has evolved to keep blood glucose at a constant level. The consequences of poor glucose homeostasis are well-known: hyperglycemia associated with uncontrolled diabetes can lead to cardiovascular disease, neuropathy and nephropathy, while hypoglycemia can lead to convulsions, loss of consciousness, coma, and even death. The glucose counterregulatory response involves detection of declining plasma glucose levels and secretion of several hormones including glucagon, adrenaline, cortisol, and growth hormone (GH) to orchestrate the recovery from hypoglycemia. Low blood glucose leads to a low brain glucose level that is detected by glucose-sensing neurons located in several brain regions such as the ventromedial hypothalamus, the perifornical region of the lateral hypothalamus, the arcuate nucleus (ARC), and in several hindbrain regions. This review will describe the importance of the glucose counterregulatory system and what is known of the neurocircuitry that underpins it

Adrenaline: insights into its metabolic roles in hypoglycaemia and diabetes

Adrenaline is a hormone that has profound actions on the cardiovascular system and is also a mediator of the fight-or-flight response. Adrenaline is now increasingly recognized as an important metabolic hormone that helps mobilize energy stores in the form of glucose and free fatty acids in preparation for physical activity or for recovery from hypoglycaemia. Recovery from hypoglycaemia is termed counter-regulation and involves the suppression of endogenous insulin secretion, activation of glucagon secretion from pancreatic α-cells and activation of adrenaline secretion. Secretion of adrenaline is controlled by presympathetic neurons in the rostroventrolateral medulla, which are, in turn, under the control of central and/or peripheral glucose-sensing neurons. Adrenaline is particularly important for counter-regulation in individuals with type 1 (insulin-dependent) diabetes because these patients do not produce endogenous insulin and also lose their ability to secrete glucagon soon after diagnosis. Type 1 diabetic patients are therefore critically dependent on adrenaline for restoration of normoglycaemia and attenuation or loss of this response in the hypoglycaemia unawareness condition can have serious, sometimes fatal, consequences. Understanding the neural control of hypoglycaemia-induced adrenaline secretion is likely to identify new therapeutic targets for treating this potentially life-threatening condition.A. J. M. Verberne, W. S. Korim, A. Sabetghadam, I. J. Llewellyn‐Smit