Department of Bioscience & Bioengineering

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IIT Jodhpur

We study how the dynamics of solitary wave (SW) interactions in integrable systems is different from that in nonintegrable systems in the context of crossing of two identical SWs in the (integrable) Toda and the (non-integrable) Hertz systems. We show that the collision process in the Toda system is perfectly symmetric about the collision point, whereas in the Hertz system, the collision process involves more complex dynamics. The symmetry in the Toda system forbids the formation of secondary SWs (SSWs), while the absence of symmetry in the Hertz system allows the generation of SSWs. We next show why the experimentally observed by-products of SW-SW interactions, the SSWs, must form in the Hertz system. We present quantitative estimations of the amount of energy that transfers from the SW after collision to the SSWs using (i) dynamical simulations, (ii) a phenomenological approach using energy and momentum conservation, and (iii) using an analytical solution introduced earlier to describe the SW in the Hertz system. We show that all three approaches lead to reliable estimations of the energy in the SSWs. © 2020 Author(s).

World University root node

Chaos

Interactions of solitary waves in integrable and nonintegrable lattices

We numerically study uncompressed granular crystals excited by sinusoidal signals at 1–100 kHz. A simple system such as two beads in a line reveals that for a fixed driven frequency, incident signals can be transmitted or filtered depending on the driving amplitude. We show that using square tapered crystals with decoration it becomes possible to enhance the low frequency filtration properties of granular systems. In addition to filtration, we find that 80 % or more of the input force is attenuated using a crystal thickness of 4 grains. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.

Granular Matter

Decorated granular crystal as filter of low-frequency ultrasonic signals

Amyloids are a class of protein with unique self-aggregation properties, and their aberrant accumulation can lead to cellular dysfunctions associated with neurodegenerative diseases. While genetic and environmental factors can influence amyloid formation, molecular triggers and/or facilitators are not well defined. Growing evidence suggests that non-identical amyloid proteins may accelerate reciprocal amyloid aggregation in a prion-like fashion. While humans encode ~30 amyloidogenic proteins, the gut microbiome also produces functional amyloids. For example, curli are cell surface amyloid proteins abundantly expressed by certain gut bacteria. In mice overexpressing the human amyloid α-synuclein (α Syn), we reveal that colonization with curli-producing Escherichia coli promotes α Syn pathology in the gut and the brain. Curli expression is required for E. coli to exacerbate α Syn-induced behavioral deficits, including intestinal and motor impairments. Purified curli subunits accelerate α Syn aggregation in biochemical assays, while oral treatment of mice with a gut-restricted amyloid inhibitor prevents curli-mediated acceleration of pathology and behavioral abnormalities. We propose that exposure to microbial amyloids in the gastrointestinal tract can accelerate aSyn aggregation and disease in the gut and the brain. © Sampson et al.

Fulltext

eLife

A gut bacterial amyloid promotes a-synuclein aggregation and motor impairment in mice

Fragile X-associated tremor ataxia syndrome is an untreatable neurological and neuromuscular disorder caused by unstable expansion of 55–200 CGG nucleotide repeats in 5′ UTR of Fragile X intellectual disability 1 (FMR1) gene. The expansion of CGG repeats in the FMR1 mRNA elicits neuronal cell toxicity through two main pathogenic mechanisms. First, mRNA with CGG expanded repeats sequester specific RNA regulatory proteins resulting in splicing alterations and formation of ribonuclear inclusions. Second, repeat-associated non-canonical translation (RANT) of the CGG expansion produces a toxic homopolymeric protein, FMRpolyG. Very few small molecules are known to modulate these pathogenic events, limiting the therapeutic possibilities for FXTAS. Here, we found that a naturally available biologically active small molecule, Curcumin, selectively binds to CGG RNA repeats. Interestingly, Curcumin improves FXTAS associated alternative splicing defects and decreases the production and accumulation of FMRpolyG protein inclusion. Furthermore, Curcumin decreases cell cytotoxicity promptly by expression of CGG RNA in FXTAS cell models. In conclusion, our data suggest that small molecules like Curcumin and its derivatives may be explored as a potential therapeutic strategy against the debilitating repeats associated neurodegenerative disorders. © Copyright © 2020 Verma, Khan, Mishra, Mishra, Charlet-Berguerand and Kumar.

Frontiers in Neuroscience

Curcumin Regulates the r(CGG)exp RNA Hairpin Structure and Ameliorate Defects in Fragile X-Associated Tremor Ataxia Syndrome

This study reports for the first time an operation of an outdoor algae assisted Microbial Fuel Cell (MFC). The MFC (10 L) comprised of low-cost materials like rock phosphate blended clayware &amp; low-density polyethylene bags as anodic &amp; cathodic chamber respectively. Algae biomass after lipid extraction at 2 g/l served as electron donor at the anode. Chlorella vulgaris at cathode provided oxygen as electron acceptor and served as lipid source. The MFCs performed well in all aspects namely energy recovery, algae productivity, and cost of operation. The 5% RP-MFCs gave 0.307 kg/m3d algal productivity, 0.09 kg/m3d lipid productivity, and 11.5318 kWh/m3 of net energy recovery (NER). Rock phosphate served as a slow and constant source of phosphorus supporting algae growth. Proteobacteria (45.14%) were the dominant phyla while Alicyliphilus (5.46%) and Dechloromonas (4.74%) were the dominant genera at the anode. The estimated cost of the system was $11.225 only. © 2020 Elsevier Ltd

Department of Electrical Engineering

Bioresource Technology

Performance evaluation of algae assisted microbial fuel cell under outdoor conditions

Development of simple, robust, and noninvasive therapeutic approaches to treat cancers and improve survival rates is a grand challenge in clinical biomedicine. In particular, the sizes and shape of the nanomaterials play a vital role in dictating their biodistribution and clearance pathways. It remains elusive how the size and shape of a nanomaterial affect its therapeutic efficacy in cancer diagnosis and treatments. To tackle the above problem, the effects of size and shape of Cu2(OH)PO4 nanostructures (nanosheets and quantum dots) on the photodynamic therapy (PDT) in destroying malignant drug-resistant lung tumors and on combating the tumor hypoxia problem are investigated and compared. The photocatalytic mechanism of Cu2(OH)PO4 nanostructures mainly involves the generation of reactive oxygen species (ROS), such as hydroxyl radical (·OH) and singlet oxygen (1O2). Under an oxygen deprivation condition, Cu2(OH)PO4 nanosheets still can generate OH radicals to kill cancer cells upon near-infrared (NIR) light irradiation. Overall, in vitro and in vivo experiments show that Cu2(OH)PO4 nanosheets can overcome tumor hypoxia problems and effectively mediate dual modal PDT and photothermal therapeutic (PTT) effects on destruction of NCI-H23 lung tumors in mice using ultralow doses (350 mW cm−2) of NIR (915 nm) light. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

Particle and Particle Systems Characterization

Size and Shape Effects of Near-Infrared Light-Activatable Cu2(OH)PO4 Nanostructures on Phototherapeutic Destruction of Drug-Resistant Hypoxia Tumors

Microglia are resident innate immune cells of the central nervous system (CNS). Microglia play a critical role during development, in maintaining homeostasis, and during infection or injury. Several independent research groups have highlighted the central role that microglia play in autoimmune diseases, autoinflammatory syndromes and cancers. The activation of microglia in some neurological diseases may directly participate in pathogenic processes. Primary microglia are a powerful tool to understand the immune responses in the brain, cell-cell interactions and dysregulated microglia phenotypes in disease. Primary microglia mimic in vivo microglial properties better than immortalized microglial cell lines. Human adult microglia exhibit distinct properties as compared to human fetal and rodent microglia. This protocol provides an efficient method for isolation of primary microglia from adult human brain. Studying these microglia can provide critical insights into cell-cell interactions between microglia and other resident cellular populations in the CNS including, oligodendrocytes, neurons and astrocytes. Additionally, microglia from different human brains may be cultured for characterization of unique immune responses for personalized medicine and a myriad of therapeutic applications. © 2020 JoVE Journal of Visualized Experiments.

Journal of Visualized Experiments

Obtaining human microglia from adult human brain tissue

Apoptosis associated speck like protein containing CARD (ASC) is widely researched and recognized as an adaptor protein participating in inflammasome assembly and pyroptosis. It contains a bipartite structure comprising of a pyrin and a caspase recruitment domain (CARD) domain. These two domains help ASC function as an adaptor molecule. ASC is encoded by the gene PYCARD. ASC plays pivotal role in various diseases as well as different homeostatic processes. ASC plays a regulatory role in different cancers showing differential regulation with respect to tissue and stage of disease. Besides cancer, ASC also plays a central role in sensing, regulation, and/or disease progression in bacterial infections, viral infections and in varied inflammatory diseases. ASC is expressed in different types of immune and non-immune cells. Its localization pattern also varies with different kinds of stimuli encountered by cell. This review will summarize the literature on the structure cellular and tissue expression, localization and disease association of ASC. © 2020, Springer Nature B.V.

Molecular Biology Reports

Comprehensive review of ASC structure and function in immune homeostasis and disease

Triple-negative breast cancer (TNBC), defined as loss of estrogen, progesterone, and Her2 receptors, is a subtype of highly aggressive breast cancer with worse prognosis and poor survival rate. Macrophage migration inhibitory factor (MIF) is a pleiotropic pro-inflammatory cytokine aberrantly expressed in many solid tumors and known to promote tumor progression and metastasis. However, its role in TNBC progression and metastasis is unexplored. Here we have shown that in TNBC patients, MIF expression was significantly enriched in the tumor compared to adjacent normal tissue. Using publically available patient datasets, we showed that MIF overexpression correlates with worse survival in TNBC compared to other hormonal status. Orthotopic implantation of TNBC cells into MIF knockout mice showed reduced tumor growth compared to wild-type mice. In addition, we have shown that MIF downregulation inhibits TNBC growth and progression in a syngeneic mouse model. We further showed that CPSI-1306, a small-molecule MIF inhibitor, inhibits the growth of TNBC cells in vitro. Mechanistic studies revealed that CPSI-1306 induces intrinsic apoptosis by alteration in mitochondrial membrane potential, cytochrome c (Cyt c) release, and activation of different caspases. In addition, CPSI-1306 inhibits the activation of cell survival and proliferation-related molecules. CPSI-1306 treatment also reduced the tumor growth and metastasis in orthotopic mouse models of mammary carcinoma. CPSI-1306 treatment of tumor-bearing mice significantly inhibited TNBC growth and pulmonary metastasis in a dose-dependent manner. Histological analysis of xenograft tumors revealed a higher number of apoptotic cells in CPSI-1306-treated tumors compared to vehicle controls. Our studies, for the first time, show that MIF overexpression in TNBC enhances growth and metastasis. Taken together, our results indicate that using small molecular weight MIF inhibitors could be a promising strategy to inhibit TNBC progression and metastasis. © 2020, The Author(s).