Effect of microencapsulation techniques on the different properties of bioactives, vitamins and minerals.

This paper explores the impact of encapsulation techniques on bioactive compounds, vitamins, and minerals, which are crucial for delivering bioactive compounds. Due to their instability and reactivity with the environment, encapsulation is often necessary to make these compounds suitable for medical or dietary applications. The evaluation of the kinetic model of bioactives reveals that encapsulation can significantly enhance their stability.

Blood-based targeted metabolipidomics reveals altered omega fatty acid-derived lipid mediators in relapsing-remitting multiple sclerosis patients.

Unresolved and uncontrolled inflammation is considered a hallmark of pathogenesis in chronic inflammatory diseases like multiple sclerosis (MS), suggesting a defective resolution process. Inflammatory resolution is an active process partially mediated by endogenous metabolites of dietary polyunsaturated fatty acids (PUFA), collectively termed specialized pro-resolving lipid mediators (SPMs). Altered levels of resolution mediators have been reported in several inflammatory diseases and may partly explain impaired inflammatory resolution.

Immuno-Responsive Gene-1: A mitochondrial gene regulates pathogenic Th17 in CNS autoimmunity mouse model.

Pathogenic Th17 cells are crucial to CNS autoimmune diseases like multiple sclerosis (MS), though their control by endogenous mechanisms is unknown. RNAseq analysis of brain glial cells identified immuno-responsive gene 1 (), a mitochondrial-related enzyme-coding gene, as one of the highly upregulated gene under inflammatory conditions which were further validated in the spinal cord of animals with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Moreover, mRNA and protein levels in myeloid, CD4, and B cells were higher in the EAE group, raising questions about its function in CNS autoimmunity.

Profiling blood-based brain biomarkers and cytokines in experimental autoimmune encephalomyelitis model of multiple sclerosis using single-molecule array technology.

Experimental autoimmune encephalomyelitis (EAE) remains a widely used pre-clinical animal model to study multiple sclerosis (MS). Blood-based cytokines and CNS biomarkers are increasingly used as predictors of neurodegeneration, disease activity, and disability in MS. However, there exists variation in animal model characterization and disease course across animal strains/studies due to understudied confounding factors, limiting the utility of these biomarkers to predict disease activity in EAE.

An early glycolysis burst in microglia regulates mitochondrial dysfunction in oligodendrocytes under neuroinflammation.

Metabolism and energy processes governing oligodendrocyte function during neuroinflammatory disease are of great interest. However, how varied cellular environments affect oligodendrocyte activity during neuroinflammation is unknown. We demonstrate that activated microglial energy metabolism controls oligodendrocyte mitochondrial respiration and activity.

Maresin-1 promotes neuroprotection and prevents disease progression in experimental models of multiple sclerosis through metabolic reprogramming and shaping innate and adaptive disease-associated cell types.

Multiple sclerosis (MS) is one of the most common inflammatory neurodegenerative diseases in young adults and causes neurological abnormalities and disability. We studied the effect of maresin 1 (MaR1) on the progression of disease in a relapsing-remitting form of experimental allergic encephalomyelitis (RR-EAE). Treatment with MaR1 in RR-EAE accelerated inflammation resolution, protected against neurological deficits, and delayed disease progression by decreasing immune cell infiltration (CD4+IL17+ and CD4+IFNγ+) into the CNS.

Pyruvate Dehydrogenase-Dependent Metabolic Programming Affects the Oligodendrocyte Maturation and Remyelination.

The metabolic needs of the premature/premyelinating oligodendrocytes (pre-OLs) and mature oligodendrocytes (OLs) are distinct. The metabolic control of oligodendrocyte maturation from the pre-OLs to the OLs is not fully understood. Here, we show that the terminal maturation and higher mitochondrial respiration in the OLs is an integrated process controlled through pyruvate dehydrogenase complex (Pdh).

Microwave assisted fluidized bed drying of bitter gourd: Modelling and optimization of process conditions based on bioactive components.

Bitter gourds were dried under varied drying conditions in a microwave assisted fluidized bed dryer, and the process was optimized using response surface methodology. Microwave power, temperature and air velocity were used as process variables for drying and the process parameters were varied between 360 and 720 W, 40-60 °C and 10-14 m/s, respectively. The responses determined for deciding the optimal criteria were vitamin C, total phenolics, IC, total chlorophyll content, vitamin A content, rehydration ratio, hardness and total color change of the dried bitter gourd.

Effect of incorporation of wheat bran, rice bran and banana peel powder on the mesostructure and physicochemical characteristics of biscuits.

Various types of natural fiber-rich ingredients are added into bakery-based products to improve their fiber content for health promotional purposes. But the majority of these products usually include exotic dietary fiber components. The aim of this study was to develop biscuits incorporated with wheat bran, rice bran and banana peel powder and to evaluate the effects on physicochemical properties and sensory acceptability of these different biscuit samples.

Blood-based untargeted metabolomics in relapsing-remitting multiple sclerosis revealed the testable therapeutic target.

Metabolic aberrations impact the pathogenesis of multiple sclerosis (MS) and possibly can provide clues for new treatment strategies. Using untargeted metabolomics, we measured serum metabolites from 35 patients with relapsing-remitting multiple sclerosis (RRMS) and 14 healthy age-matched controls. Of 632 known metabolites detected, 60 were significantly altered in RRMS.

Cytokine Storm and Failed Resolution in COVID-19: Taking a Cue from Multiple Sclerosis.

Introduction: Excessive inflammatory responses and failed resolution are major common causes of tissue injury and organ dysfunction in a variety of diseases, including multiple sclerosis (MS), diabetes, and most recently, COVID-19, despite the distinct pathoetiology of the diseases. The promotion of the natural process of inflammatory resolution has been long recognized to improve functional recovery and disease outcomes effectively. To mitigate the excessive inflammation in MS, scientific investigations identified a group of derivatives of omega fatty acids, known as specialized pro-resolving lipid mediators (SPM) that have been significantly effective in treating preclinical disease models of MS.

An emerging potential of metabolomics in multiple sclerosis: a comprehensive overview.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the nervous system that primarily affects young adults. Although the exact etiology of the disease remains obscure, it is clear that alterations in the metabolome contribute to this process. As such, defining a reliable and disease-specific metabolome has tremendous potential as a diagnostic and therapeutic strategy for MS.

Specialized Pro-Resolving Lipid Mediators: Emerging Therapeutic Candidates for Multiple Sclerosis.

Multiple sclerosis (MS) is a neuroinflammatory disease in which unresolved and uncontrolled inflammation disrupts normal cellular homeostasis and leads to a pathological disease state. It has long been recognized that endogenously derived metabolic by-products of omega fatty acids, known as specialized pro-resolving lipid mediators (SPMs), are instrumental in resolving the pathologic inflammation. However, there is minimal data available on the functional status of SPMs in MS, despite the fact that MS presents a classical model of chronic inflammation.

Multiple sclerosis in India: Iceberg or volcano.

Multiple sclerosis (MS) is a chronic neurodegenerative disease involving destruction of the myelin sheath around axons of the brain, spinal cord and optic nerve. There has been a tremendous transformation in its perspective across globe. In recent years, its prevalence has changed dramatically worldwide and India is no exception.

Demographic and clinical profile of Multiple Sclerosis in Kashmir: A short report.

Background: Multiple sclerosis (MS) is a chronic autoimmune and inflammatory disease of the central nervous system (CNS). There have been only few population/hospital based studies on MS in India, and at the same time there is no data on its profile in Kashmir.

Methods: A total of 41 MS patients diagnosed on the basis of 2010 Revised Mc Donald criteria were enrolled in this study from Kashmir region of India.

Multiple sclerosis in Kashmir: Where we stand.

Multiple sclerosis (MS) is a disabling neurological disorder commonly diagnosed in young adults. Its causes still remain inexplicable and presently it can only be managed by different drug treatments. There has been a remarkable shift in MS perspective across world.

Multiple Sclerosis and EIF2B5: A Paradox or a Missing Link.

Multiple sclerosis (MS) is an encumbering inflammatory condition of the central nervous system (CNS) caused by axonal demyelination. There is sufficient evidence suggesting role of eukaryotic translation initiation factor 2B (EIF2B) gene family encoding the five subunits of eIF2B complex-α, β, γ, δ and ε respectively, in causing vanishing white matter (VWM) disease of the brain. Incidentally researchers have proposed overlapping between MS and VWM in terms of clinical, biochemical and genetic aspects, which incited us to write this chapter to explore the association between EIF2B5 and MS.

No evidence for a role of Ile587Val polymorphism of EIF2B5 gene in multiple sclerosis in Kashmir Valley of India.

Multiple sclerosis (MS) is an inflammatory neurodegenerative disease of the nervous system with a profound genetic element. It is already known that alterations in Eukaryotic Translation Initiation Factor 2B (EIF2B) gene encoding the five subunits of eIF2B complex cause Vanishing White Matter (VWM) disease of the brain and emerging evidences have advocated certain resemblances between MS and VWM in terms of clinical and epidemiological characteristics, thus validating the association study between EIF2B and MS. Moreover, a recent study has implicated EIF2B5 Ile587Val (rs843358) polymorphism as a susceptibility factor for MS.